Archive for the ‘Female Genetics’ Category

acquired trait: A phenotypic characteristic, acquired during growth and development, that is not genetically based and therefore cannot be passed on to the next generation (for example, the large muscles of a weightlifter).

adaptation: Any heritable characteristic of an organism that improves its ability to survive and reproduce in its environment. Also used to describe the process of genetic change within a population, as influenced by natural selection.

adaptive landscape: A graph of the average fitness of a population in relation to the frequencies of genotypes in it. Peaks on the landscape correspond to genotypic frequencies at which the average fitness is high, valleys to genotypic frequencies at which the average fitness is low. Also called a fitness surface.

adaptive logic: A behavior has adaptive logic if it tends to increase the number of offspring that an individual contributes to the next and following generations. If such a behavior is even partly genetically determined, it will tend to become widespread in the population. Then, even if circumstances change such that it no longer provides any survival or reproductive advantage, the behavior will still tend to be exhibited -- unless it becomes positively disadvantageous in the new environment.

adaptive radiation: The diversification, over evolutionary time, of a species or group of species into several different species or subspecies that are typically adapted to different ecological niches (for example, Darwin's finches). The term can also be applied to larger groups of organisms, as in "the adaptive radiation of mammals."

adaptive strategies: A mode of coping with competition or environmental conditions on an evolutionary time scale. Species adapt when succeeding generations emphasize beneficial characteristics.

agnostic: A person who believes that the existence of a god or creator and the nature of the universe is unknowable.

algae: An umbrella term for various simple organisms that contain chlorophyll (and can therefore carry out photosynthesis) and live in aquatic habitats and in moist situations on land. The term has no direct taxonomic significance. Algae range from macroscopic seaweeds such as giant kelp, which frequently exceeds 30 m in length, to microscopic filamentous and single-celled forms such as Spirogyra and Chlorella.

allele: One of the alternative forms of a gene. For example, if a gene determines the seed color of peas, one allele of that gene may produce green seeds and another allele produce yellow seeds. In a diploid cell there are usually two alleles of any one gene (one from each parent). Within a population there may be many different alleles of a gene; each has a unique nucleotide sequence.

allometry: The relation between the size of an organism and the size of any of its parts. For example, an allometric relation exists between brain size and body size, such that (in this case) animals with bigger bodies tend to have bigger brains. Allometric relations can be studied during the growth of a single organism, between different organisms within a species, or between organisms in different species.

allopatric speciation: Speciation that occurs when two or more populations of a species are geographically isolated from one another sufficiently that they do not interbreed.

allopatry: Living in separate places. Compare with sympatry.

amino acid: The unit molecular building block of proteins, which are chains of amino acids in a certain sequence. There are 20 main amino acids in the proteins of living things, and the properties of a protein are determined by its particular amino acid sequence.

amino acid sequence: A series of amino acids, the building blocks of proteins, usually coded for by DNA. Exceptions are those coded for by the RNA of certain viruses, such as HIV.

ammonoid: Extinct relatives of cephalopods (squid, octopi, and chambered nautiluses), these mollusks had coiled shells and are found in the fossil record of the Cretaceous period.

amniotes: The group of reptiles, birds, and mammals. These all develop through an embryo that is enclosed within a membrane called an amnion. The amnion surrounds the embryo with a watery substance, and is probably an adaptation for breeding on land.

amphibians: The class of vertebrates that contains the frogs, toads, newts, and salamanders. The amphibians evolved in the Devonian period (about 370 million years ago) as the first vertebrates to occupy the land. They have moist scaleless skin which is used to supplement the lungs in gas exchange. The eggs are soft and vulnerable to drying, therefore reproduction commonly occurs in water. Amphibian larvae are aquatic, and have gills for respiration; they undergo metamorphosis to the adult form. Most amphibians are found in damp environments and they occur on all continents except Antarctica.

analogous structures: Structures in different species that look alike or perform similar functions (e.g., the wings of butterflies and the wings of birds) that have evolved convergently but do not develop from similar groups of embryological tissues, and that have not evolved from similar structures known to be shared by common ancestors. Contrast with homologous structures. Note: The recent discovery of deep genetic homologies has brought new interest, new information, and discussion to the classical concepts of analogous and homologous structures.

anatomy: (1) The structure of an organism or one of its parts. (2) The science that studies those structures.

ancestral homology: Homology that evolved before the common ancestor of a set of species, and which is present in other species outside that set of species. Compare with derived homology.

anthropoid: A member of the group of primates made up of monkeys, apes, and humans.

antibacterial: Having the ability to kill bacteria.

antibiotics: Substances that destroy or inhibit the growth of microorganisms, particularly disease-causing bacteria.

antibiotic resistance: A heritable trait in microorganisms that enables them to survive in the presence of an antibiotic.

aperture: Of a camera, the adjustable opening through which light passes to reach the film. The diameter of the aperture determines the intensity of light admitted. The pupil of a human eye is a self-adjusting aperture.

aquatic: Living underwater.

arboreal: Living in trees.

archeology: The study of human history and prehistory through the excavation of sites and the analysis of physical remains, such as graves, tools, pottery, and other artifacts.

archetype: The original form or body plan from which a group of organisms develops.

artifact: An object made by humans that has been preserved and can be studied to learn about a particular time period.

artificial selection: The process by which humans breed animals and cultivate crops to ensure that future generations have specific desirable characteristics. In artificial selection, breeders select the most desirable variants in a plant or animal population and selectively breed them with other desirable individuals. The forms of most domesticated and agricultural species have been produced by artificial selection; it is also an important experimental technique for studying evolution.

asexual reproduction: A type of reproduction involving only one parent that ususally produces genetically identical offspring. Asexual reproduction occurs without fertilization or genetic recombination, and may occur by budding, by division of a single cell, or by the breakup of a whole organism into two or more new individuals.

assortative mating: The tendency of like to mate with like. Mating can be assortative for a certain genotype (e.g., individuals with genotype AA tend to mate with other individuals of genotype AA) or phenotype (e.g., tall individuals mate with other tall individuals).

asteroid: A small rocky or metallic body orbitting the Sun. About 20,000 have been observed, ranging in size from several hundred kilometers across down to dust particles.

atheism: The doctrine or belief that there is no god.

atomistic: (as applied to theory of inheritance) Inheritance in which the entities controlling heredity are relatively distinct, permanent, and capable of independent action. Mendelian inheritance is an atomistic theory because in it, inheritance is controlled by distinct genes.

australopithecine: A group of bipedal hominid species belonging to the genus Australopithecus that lived between 4.2 and 1.4 mya.

Australopithecus afarensis: An early australopithecine species that was bipedal; known fossils date between 3.6 and 2.9 mya (for example, Lucy).

autosome: Any chromosome other than a sex chromosome.

avian: Of, relating to, or characteristic of birds (members of the class Aves).

bacteria: Tiny, single-celled, prokaryotic organisms that can survive in a wide variety of environments. Some cause serious infectious diseases in humans, other animals, and plants.

base: The DNA molecule is a chain of nucleotide units; each unit consists of a backbone made of a sugar and a phosphate group, with a nitrogenous base attached. The base in a unit is one of adenine (A), guanine (G), cytosine (C), or thymine (T). In RNA, uracil (U) is used instead of thymine. A and G belong to the chemical class called purines; C, T, and U are pyrimidines.

Batesian mimicry: A kind of mimicry in which one non-poisonous species (the Batesian mimic) mimics another poisonous species.

belemnite: An extinct marine invertebrate that was related to squid, octopi, and chambered nautiluses. We know from the fossil record that belemnites were common in the Jurassic period and had bullet-shaped internal skeletons.

big bang theory: The theory that states that the universe began in a state of compression to infinite density, and that in one instant all matter and energy began expanding and have continued expanding ever since.

biodiversity (or biological diversity): A measure of the variety of life, biodiversity is often described on three levels. Ecosystem diversity describes the variety of habitats present; species diversity is a measure of the number of species and the number of individuals of each species present; genetic diversity refers to the total amount of genetic variability present.

bioengineered food: Food that has been produced through genetic modification using techniques of genetic engineering.

biogenetic law: Name given by Haeckel to recapitulation.

biogeography: The study of patterns of geographical distribution of plants and animals across Earth, and the changes in those distributions over time.

biological species concept: The concept of species, according to which a species is a set of organisms that can interbreed among each other. Compare with cladistic species concept, ecological species concept, phenetic species concept, and recognition species concept.

biometrics: The quantitative study of characters of organisms.

biosphere: The part of Earth and its atmosphere capable of sustaining life.

bipedalism: Of hominids, walking upright on two hind legs; more generally, using two legs for locomotion.

bivalve: A mollusk that has a two-part hinged shell. Bivalves include clams, oysters, scallops, mussels, and other shellfish.

Blackmore, Susan: A psychologist interested in memes and the theory of memetics, evolutionary theory, consciousness, the effects of meditation, and why people believe in the paranormal. A recent book, The Meme Machine, offers an introduction to the subject of memes.

blending inheritance: The historically influential but factually erroneous theory that organisms contain a blend of their parents' hereditary factors and pass that blend on to their offspring. Compare with Mendelian inheritance.

botanist: A scientist who studies plants.

brachiopod: Commonly known as "lamp shells," these marine invertebrates resemble bivalve mollusks because of their hinged shells. Brachiopods were at their greatest abundance during the Paleozoic and Mesozoic eras.

Brodie, Edmund D., III: A biologist who studies the causes and evolutionary implications of interactions among traits in predators and their prey. Much of his work concentrates on the coevolutionary arms race between newts that posess tetrodotoxin, one of the most potent known toxins, and the resistant garter snakes who prey on them.

Brodie, Edmund D., Jr.: A biologist recognized internationally for his work on the evolution of mechanisms in amphibians that allow them to avoid predators. These mechanisms include toxins carried in skin secretions, coloration, and behavior.

Bruner, Jerome: A psychologist and professor at Harvard and Oxford Universities, and a prolific author whose book, The Process of Education, encouraged curriculum innovation based on theories of cognitive development.

bryozoan: A tiny marine invertebrate that forms a crust-like colony; colonies of bryozoans may look like scaly sheets on seaweed.

Burney, David: A biologist whose research has focused on endangered species, paleoenvironmental studies, and causes of extinction in North America, Africa, Madagascar, Hawaii, and the West Indies.

carbon isotope ratio: A measure of the proportion of the carbon-14 isotope to the carbon-12 isotope. Living material contains carbon-14 and carbon-12 in the same proportions as exists in the atmosphere. When an organism dies, however, it no longer takes up carbon from the atmosphere, and the carbon-14 it contains decays to nitrogen-14 at a constant rate. By measuring the carbon-14-to-carbon-12 ratio in a fossil or organic artifact, its age can be determined, a method called radiocarbon dating. Because most carbon-14 will have decayed after 50,000 years, the carbon isotope ratio is mainly useful for dating fossils and artifacts younger than this. It cannot be used to determine the age of Earth, for example.

carnivorous: Feeding largely or exclusively on meat or other animal tissue.

Carroll, Sean: Developmental geneticist with the Howard Hughes Medical Institute and professor at the University of Wisconsin-Madison. From the large-scale changes that distinguish major animal groups to the finely detailed color patterns on butterfly wings, Dr. Carroll's research has centered on those genes that create the "molecular blueprint" for body pattern and play major roles in the origin of new features. Coauthor, with Jennifer Grenier and Scott Weatherbee, of From DNA to Diversity: Molecular Genetics and the Evolution of Animal Design.

Carson, Rachel: A scientist and writer fascinated with the workings of nature. Her best-known publication, Silent Spring, was written over the years 1958 to 1962. The book looks at the effects of insecticides and pesticides on songbird populations throughout the United States. The publication helped set off a wave of environmental legislation and galvanized the emerging ecological movement.

Castle, W.E.: An early experimental geneticist, his 1901 paper was the first on Mendelism in America. His Genetics of Domestic Rabbits, published in 1930 by Harvard University Press, covers such topics as the genes involved in determining the coat colors of rabbits and associated mutations.

cell: The basic structural and functional unit of most living organisms. Cell size varies, but most cells are microscopic. Cells may exist as independent units of life, as in bacteria and protozoans, or they may form colonies or tissues, as in all plants and animals. Each cell consists of a mass of protein material that is differentiated into cytoplasm and nucleoplasm, which contains DNA. The cell is enclosed by a cell membrane, which in the cells of plants, fungi, algae, and bacteria is surrounded by a cell wall. There are two main types of cell, prokaryotic and eukaryotic.

Cenozoic: The era of geologic time from 65 mya to the present, a time when the modern continents formed and modern animals and plants evolved.

centromere: A point on a chromosome that is involved in separating the copies of the chromosome produced during cell division. During this division, paired chromosomes look somewhat like an X, and the centromere is the constriction in the center.

cephalopod: Cephalopods include squid, octopi, cuttlefish, and chambered nautiluses. They are mollusks with tentacles and move by forcing water through their bodies like a jet.

character: Any recognizable trait, feature, or property of an organism. In phylogenetic studies, a character is a feature that is thought to vary independantly of other features, and to be derived from a corresponding feature in a common ancestor of the organisms being studied. A "character state" is one of the possible alternative conditions of the character. For example, "present" and "absent" are two states of the character "hair" in mammals. Similarly, a particular position in a DNA sequence is a character, and A, T, C, and G are its possible states (see bases.)

character displacement: The increased difference between two closely related species where they live in the same geographic region (sympatry) as compared with where they live in different geographic regions (allopatry). Explained by the relative influences of intra- and inter-specific competition in sympatry and allopatry.

chloroplast: A structure (or organelle) found in some cells of plants; its function is photosynthesis.

cholera: An acute infectious disease of the small intestine, caused by the bacterium Vibrio cholerae which is transmitted in drinking water contaminated by feces of a patient. After an incubation period of 1-5 days, cholera causes severe vomiting and diarrhea, which, if untreated, leads to dehydration that can be fatal.

chordate: A member of the phylum Chordata, which includes the tunicates, lancelets, and vertebrates. They are animals with a hollow dorsal nerve cord; a rodlike notochord that forms the basis of the internal skeleton; and paired gill slits in the wall of the pharynx behind the head, although in some chordates these are apparent only in early embryonic stages. All vertebrates are chordates, but the phylum also contains simpler types, such as sea-squirts, in which only the free-swimming larva has a notochord.

chromosomal inversion: See inversion.

chromosome: A structure in the cell nucleus that carries DNA. At certain times in the cell cycle, chromosomes are visible as string-like entities. Chromosomes consist of the DNA with various proteins, particularly histones, bound to it.

chronology: The order of events according to time.

Clack, Jenny: A paleontologist at Cambridge University in the U.K., Dr. Clack studies the origin, phylogeny, and radiation of early tetrapods and their relatives among the lobe-finned fish. She is interested in the timing and sequence of skeletal and other changes which occurred during the transition, and the origin and relationships of the diverse tetrapods of the late Paleozoic.

clade: A set of species descended from a common ancestral species. Synonym of monophyletic group.

cladism: Phylogenetic classification. The members of a group in a cladistic classification share a more recent common ancestor with one another than with the members of any other group. A group at any level in the classificatory hierarchy, such as a family, is formed by combining a subgroup at the next lowest level (the genus, in this case) with the subgroup or subgroups with which it shares its most recent common ancestor. Compare with evolutionary classification and phenetic classification.

cladistic species concept: The concept of species, according to which a species is a lineage of populations between two phylogenetic branch points (or speciation events). Compare with biological species concept, ecological species concept, phenetic species concept, and recognition species concept.

cladists: Evolutionary biologists who seek to classify Earth's life forms according to their evolutionary relationships, not just overall similarity.

cladogram: A branching diagram that illustrates hypotheses about the evolutionary relationships among groups of organisms. Cladograms can be considered as a special type of phylogenetic tree that concentrates on the order in which different groups branched off from their common ancestors. A cladogram branches like a family tree, with the most closely related species on adjacent branches.

class: A category of taxonomic classification between order and phylum, a class comprises members of similar orders. See taxon.

classification: The arrangement of organisms into hierarchical groups. Modern biological classifications are Linnaean and classify organisms into species, genus, family, order, class, phylum, kingdom, and certain intermediate categoric levels. Cladism, evolutionary classification, and phenetic classification are three methods of classification.

cline: A geographic gradient in the frequency of a gene, or in the average value of a character.

clock: See molecular clock.

clone: A set of genetically identical organisms asexually reproduced from one ancestral organism.

coadaptation: Beneficial interaction between (1) a number of genes at different loci within an organism, (2) different parts of an organism, or (3) organisms belonging to different species.

codon: A triplet of bases (or nucleotides) in the DNA coding for one amino acid. The relation between codons and amino acids is given by the genetic code. The triplet of bases that is complementary to a condon is called an anticodon; conventionally, the triplet in the mRNA is called the codon and the triplet in the tRNA is called the anticodon.

coelacanth: Although long thought to have gone extinct about 65 million years ago, one of these deep-water, lungless fish was caught in the 1930s. Others have since been caught and filmed in their natural habitat.

coevolution: Evolution in two or more species, such as predator and its prey or a parasite and its host, in which evolutionary changes in one species influence the evolution of the other species.

cognitive: Relating to cognition, the mental processes involved in the gathering, organization, and use of knowledge, including such aspects as awareness, perception, reasoning, and judgement. The term refers to any mental "behaviors" where the underlying characteristics are abstract in nature and involve insight, expectancy, complex rule use, imagery, use of symbols, belief, intentionality, problem-solving, and so forth.

common ancestor: The most recent ancestral form or species from which two different species evolved.

comparative biology: The study of patterns among more than one species.

comparative method: The study of adaptation by comparing many species.

concerted evolution: The tendency of the different genes in a gene family to evolve in concert; that is, each gene locus in the family comes to have the same genetic variant.

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Supercourse: Epidemiology, the Internet, and Global Health

Elephants are large mammals of the family Elephantidae and the order Proboscidea. Two species are traditionally recognised, the African elephant (Loxodonta africana) and the Asian elephant (Elephas maximus), although some evidence suggests that African bush elephants and African forest elephants are separate species (L.africana and L.cyclotis respectively). Elephants are scattered throughout sub-Saharan Africa, South Asia, and Southeast Asia. Elephantidae is the only surviving family of the order Proboscidea; other, now extinct, members of the order include deinotheres, gomphotheres, mammoths, and mastodons. Male African elephants are the largest extant terrestrial animals and can reach a height of 4m (13ft) and weigh 7,000kg (15,000lb). All elephants have several distinctive features, the most notable of which is a long trunk or proboscis, used for many purposes, particularly breathing, lifting water and grasping objects. Their incisors grow into tusks, which can serve as weapons and as tools for moving objects and digging. Elephants' large ear flaps help to control their body temperature. Their pillar-like legs can carry their great weight. African elephants have larger ears and concave backs while Asian elephants have smaller ears and convex or level backs.

Elephants are herbivorous and can be found in different habitats including savannahs, forests, deserts and marshes. They prefer to stay near water. They are considered to be keystone species due to their impact on their environments. Other animals tend to keep their distance where predators such as lions, tigers, hyenas, and wild dogs usually target only the young elephants (or "calves"). Females ("cows") tend to live in family groups, which can consist of one female with her calves or several related females with offspring. The groups are led by an individual known as the matriarch, often the oldest cow. Elephants have a fissionfusion society in which multiple family groups come together to socialise. Males ("bulls") leave their family groups when they reach puberty, and may live alone or with other males. Adult bulls mostly interact with family groups when looking for a mate and enter a state of increased testosterone and aggression known as musth, which helps them gain dominance and reproductive success. Calves are the centre of attention in their family groups and rely on their mothers for as long as three years. Elephants can live up to 70 years in the wild. They communicate by touch, sight, smell and sound; elephants use infrasound, and seismic communication over long distances. Elephant intelligence has been compared with that of primates and cetaceans. They appear to have self-awareness and show empathy for dying or dead individuals of their kind.

African elephants are listed as vulnerable by the International Union for Conservation of Nature (IUCN), while the Asian elephant is classed as endangered. One of the biggest threats to elephant populations is the ivory trade, as the animals are poached for their ivory tusks. Other threats to wild elephants include habitat destruction and conflicts with local people. Elephants are used as working animals in Asia. In the past they were used in war; today, they are often controversially put on display in zoos, or exploited for entertainment in circuses. Elephants are highly recognisable and have been featured in art, folklore, religion, literature and popular culture.

The word "elephant" is based on the Latin elephas (genitive elephantis) ("elephant"), which is the Latinised form of the Greek (elephas) (genitive (elephantos)),[1] probably from a non-Indo-European language, likely Phoenician.[2] It is attested in Mycenaean Greek as e-re-pa (genitive e-re-pa-to) in Linear B syllabic script.[3][4] As in Mycenaean Greek, Homer used the Greek word to mean ivory, but after the time of Herodotus, it also referred to the animal.[1] The word "elephant" appears in Middle English as olyfaunt (c.1300) and was borrowed from Old French oliphant (12th century).[2]Loxodonta, the generic name for the African elephants, is Greek for "oblique-sided tooth".[5]

Elephants belong to the family Elephantidae, the sole remaining family within the order Proboscidea. Their closest extant relatives are the sirenians (dugongs and manatees) and the hyraxes, with which they share the clade Paenungulata within the superorder Afrotheria.[6] Elephants and sirenians are further grouped in the clade Tethytheria.[7] Traditionally, two species of elephants are recognised; the African elephant (Loxodonta africana) of sub-Saharan Africa, and the Asian elephant (Elephas maximus) of South and Southeast Asia. African elephants have larger ears, a concave back, more wrinkled skin, a sloping abdomen and two finger-like extensions at the tip of the trunk. Asian elephants have smaller ears, a convex or level back, smoother skin, a horizontal abdomen that occasionally sags in the middle and one extension at the tip of the trunk. The looped ridges on the molars are narrower in the Asian elephant while those of the African are more diamond-shaped. The Asian elephant also has dorsal bumps on its head and some patches of depigmentation on its skin.[8] In general, African elephants are larger than their Asian cousins.

Swedish zoologist Carl Linnaeus first described the genus Elephas and an elephant from Sri Lanka (then known as Ceylon) under the binomial Elephas maximus in 1758. In 1798, Georges Cuvier classified the Indian elephant under the binomial Elephas indicus. Dutch zoologist Coenraad Jacob Temminck described the Sumatran elephant in 1847 under the binomial Elephas sumatranus. English zoologist Frederick Nutter Chasen classified all three as subspecies of the Asian elephant in 1940.[9] Asian elephants vary geographically in their colour and amount of depigmentation. The Sri Lankan elephant (Elephas maximus maximus) inhabits Sri Lanka, the Indian elephant (E.m.indicus) is native to mainland Asia (on the Indian subcontinent and Indochina), and the Sumatran elephant (E.m.sumatranus) is found in Sumatra.[8] One disputed subspecies, the Borneo elephant, lives in northern Borneo and is smaller than all the other subspecies. It has larger ears, a longer tail, and straighter tusks than the typical elephant. Sri Lankan zoologist Paules Edward Pieris Deraniyagala described it in 1950 under the trinomial Elephas maximus borneensis, taking as his type an illustration in National Geographic.[10] It was subsequently subsumed under either E.m.indicus or E.m.sumatranus. Results of a 2003 genetic analysis indicate its ancestors separated from the mainland population about 300,000years ago.[11] A 2008 study found that Borneo elephants are not indigenous to the island but were brought there before 1521 by the Sultan of Sulu from Java, where elephants are now extinct.[10]

The African elephant was first named by German naturalist Johann Friedrich Blumenbach in 1797 as Elephas africana.[12] The genus Loxodonta was commonly believed to have been named by Georges Cuvier in 1825. Cuvier spelled it Loxodonte and an anonymous author romanised the spelling to Loxodonta; the International Code of Zoological Nomenclature recognises this as the proper authority.[13] In 1942, 18 subspecies of African elephant were recognised by Henry Fairfield Osborn, but further morphological data has reduced the number of classified subspecies,[14] and by the 1990s, only two were recognised, the savannah or bush elephant (L.a.africana) and the forest elephant (L.a.cyclotis);[15] the latter has smaller and more rounded ears and thinner and straighter tusks, and is limited to the forested areas of western and Central Africa.[16] A 2000 study argued for the elevation of the two forms into separate species (L.africana and L.cyclotis respectively) based on differences in skull morphology.[17] DNA studies published in 2001 and 2007 also suggested they were distinct species,[18][19] while studies in 2002 and 2005 concluded that they were the same species.[20][21] Further studies (2010, 2011, 2015) have supported African savannah and forest elephants' status as separate species.[22][23][24] The two species are believed to have diverged 6 million years ago.[25] The third edition of Mammal Species of the World lists the two forms as full species[13] and does not list any subspecies in its entry for Loxodonta africana.[13] This approach is not taken by the United Nations Environment Programme's World Conservation Monitoring Centre nor by the IUCN, both of which list L.cyclotis as a synonym of L.africana.[26][27] Some evidence suggests that elephants of western Africa are a separate species,[28] although this is disputed.[21][23] The pygmy elephants of the Congo Basin, which have been suggested to be a separate species (Loxodonta pumilio) are probably forest elephants whose small size and/or early maturity are due to environmental conditions.[29]

Over 161 extinct members and three major evolutionary radiations of the order Proboscidea have been recorded. The earliest proboscids, the African Eritherium and Phosphatherium of the late Paleocene, heralded the first radiation.[30] The Eocene included Numidotherium, Moeritherium and Barytherium from Africa. These animals were relatively small and aquatic. Later on, genera such as Phiomia and Palaeomastodon arose; the latter likely inhabited forests and open woodlands. Proboscidean diversity declined during the Oligocene.[31] One notable species of this epoch was Eritreum melakeghebrekristosi of the Horn of Africa, which may have been an ancestor to several later species.[32] The beginning of the Miocene saw the second diversification, with the appearance of the deinotheres and the mammutids. The former were related to Barytherium, lived in Africa and Eurasia,[33] while the latter may have descended from Eritreum[32] and spread to North America.[33]

The second radiation was represented by the emergence of the gomphotheres in the Miocene,[33] which likely evolved from Eritreum[32] and originated in Africa, spreading to every continent except Australia and Antarctica. Members of this group included Gomphotherium and Platybelodon.[33] The third radiation started in the late Miocene and led to the arrival of the elephantids, which descended from, and slowly replaced, the gomphotheres.[34] The African Primelephas gomphotheroides gave rise to Loxodonta, Mammuthus and Elephas. Loxodonta branched off earliest, around the Miocene and Pliocene boundary, while Mammuthus and Elephas diverged later during the early Pliocene. Loxodonta remained in Africa, while Mammuthus and Elephas spread to Eurasia, and the former reached North America. At the same time, the stegodontids, another proboscidean group descended from gomphotheres, spread throughout Asia, including the Indian subcontinent, China, southeast Asia and Japan. Mammutids continued to evolve into new species, such as the American mastodon.[35]

At the beginning of the Pleistocene, elephantids experienced a high rate of speciation. Loxodonta atlantica became the most common species in northern and southern Africa but was replaced by Elephas iolensis later in the Pleistocene. Only when Elephas disappeared from Africa did Loxodonta become dominant once again, this time in the form of the modern species. Elephas diversified into new species in Asia, such as E.hysudricus and E.platycephus;[36] the latter the likely ancestor of the modern Asian elephant.[37]Mammuthus evolved into several species, including the well-known woolly mammoth.[36] In the Late Pleistocene, most proboscidean species vanished during the Quaternary glaciation which killed off 50% of genera weighing over 5kg (11lb) worldwide.[38] The Pleistocene also saw the arrival of Palaeoloxodon namadicus, the largest terrestrial mammal of all time.[39]

Proboscideans experienced several evolutionary trends, such as an increase in size, which led to many giant species that stood up to 5m (16ft) tall.[39] As with other megaherbivores, including the extinct sauropod dinosaurs, the large size of elephants likely developed to allow them to survive on vegetation with low nutritional value.[40] Their limbs grew longer and the feet shorter and broader. Early proboscideans developed longer mandibles and smaller craniums, while more advanced ones developed shorter mandibles, which shifted the head's centre of gravity. The skull grew larger, especially the cranium, while the neck shortened to provide better support for the skull. The increase in size led to the development and elongation of the mobile trunk to provide reach. The number of premolars, incisors and canines decreased.[41] The cheek teeth (molars and premolars) became larger and more specialized, especially after elephants started to switch from C3-plants to C4-grasses, which caused their teeth to undergo a three-fold increase in teeth height as well as substantial multiplication of lamellae after about five million years ago. Only in the last million year or so did they return to a diet mainly consisting of C3 trees and shrubs.[42][43] The upper second incisors grew into tusks, which varied in shape from straight, to curved (either upward or downward), to spiralled, depending on the species. Some proboscideans developed tusks from their lower incisors.[41] Elephants retain certain features from their aquatic ancestry such as their middle ear anatomy and the internal testes of the males.[44]

There has been some debate over the relationship of Mammuthus to Loxodonta or Elephas. Some DNA studies suggest Mammuthus is more closely related to the former,[45][46] while others point to the latter.[7] However, analysis of the complete mitochondrial genome profile of the woolly mammoth (sequenced in 2005) supports Mammuthus being more closely related to Elephas.[18][22][24][47]Morphological evidence supports Mammuthus and Elephas as sister taxa, while comparisons of protein albumin and collagen have concluded that all three genera are equally related to each other.[48] Some scientists believe a cloned mammoth embryo could one day be implanted in an Asian elephant's womb.[49]

Several species of proboscideans lived on islands and experienced insular dwarfism. This occurred primarily during the Pleistocene, when some elephant populations became isolated by fluctuating sea levels, although dwarf elephants did exist earlier in the Pliocene. These elephants likely grew smaller on islands due to a lack of large or viable predator populations and limited resources. By contrast, small mammals such as rodents develop gigantism in these conditions. Dwarf proboscideans are known to have lived in Indonesia, the Channel Islands of California, and several islands of the Mediterranean.[50]

Elephas celebensis of Sulawesi is believed to have descended from Elephas planifrons. Elephas falconeri of Malta and Sicily was only 1m (3ft), and had probably evolved from the straight-tusked elephant. Other descendants of the straight-tusked elephant existed in Cyprus. Dwarf elephants of uncertain descent lived in Crete, Cyclades and Dodecanese, while dwarf mammoths are known to have lived in Sardinia.[50] The Columbian mammoth colonised the Channel Islands and evolved into the pygmy mammoth. This species reached a height of 1.21.8m (46ft) and weighed 2002,000kg (4404,410lb). A population of small woolly mammoths survived on Wrangel Island, now 140km (87mi) north of the Siberian coast, as recently as 4,000 years ago.[50] After their discovery in 1993, they were considered dwarf mammoths.[51] This classification has been re-evaluated and since the Second International Mammoth Conference in 1999, these animals are no longer considered to be true "dwarf mammoths".[52]

Elephants are the largest living terrestrial animals. African elephants stand 34m (1013ft) and weigh 4,0007,000kg (8,80015,400lb) while Asian elephants stand 23.5m (711ft) and weigh 3,0005,000kg (6,60011,000lb).[8] In both cases, males are larger than females.[9][12] Among African elephants, the forest form is smaller than the savannah form.[16] The skeleton of the elephant is made up of 326351 bones.[53] The vertebrae are connected by tight joints, which limit the backbone's flexibility. African elephants have 21 pairs of ribs, while Asian elephants have 19 or 20 pairs.[54]

An elephant's skull is resilient enough to withstand the forces generated by the leverage of the tusks and head-to-head collisions. The back of the skull is flattened and spread out, creating arches that protect the brain in every direction.[55] The skull contains air cavities (sinuses) that reduce the weight of the skull while maintaining overall strength. These cavities give the inside of the skull a honeycomb-like appearance. The cranium is particularly large and provides enough room for the attachment of muscles to support the entire head. The lower jaw is solid and heavy.[53] Because of the size of the head, the neck is relatively short to provide better support.[41] Lacking a lacrimal apparatus, the eye relies on the harderian gland to keep it moist. A durable nictitating membrane protects the eye globe. The animal's field of vision is compromised by the location and limited mobility of the eyes.[56] Elephants are considered dichromats[57] and they can see well in dim light but not in bright light.[58] The core body temperature averages 35.9C (97F), similar to a human. Like all mammals, an elephant can raise or lower its temperature a few degrees from the average in response to extreme environmental conditions.[59]

Elephant ears have thick bases with thin tips. The ear flaps, or pinnae, contain numerous blood vessels called capillaries. Warm blood flows into the capillaries, helping to release excess body heat into the environment. This occurs when the pinnae are still, and the animal can enhance the effect by flapping them. Larger ear surfaces contain more capillaries, and more heat can be released. Of all the elephants, African bush elephants live in the hottest climates, and have the largest ear flaps.[60] Elephants are capable of hearing at low frequencies and are most sensitive at 1 kHz.[61]

The trunk, or proboscis, is a fusion of the nose and upper lip, although in early fetal life, the upper lip and trunk are separated.[41] The trunk is elongated and specialised to become the elephant's most important and versatile appendage. It contains up to 150,000 separate muscle fascicles, with no bone and little fat. These paired muscles consist of two major types: superficial (surface) and internal. The former are divided into dorsals, ventrals and laterals, while the latter are divided into transverse and radiating muscles. The muscles of the trunk connect to a bony opening in the skull. The nasal septum is composed of tiny muscle units that stretch horizontally between the nostrils. Cartilage divides the nostrils at the base.[62] As a muscular hydrostat, the trunk moves by precisely coordinated muscle contractions. The muscles work both with and against each other. A unique proboscis nerve formed by the maxillary and facial nerves runs along both sides of the trunk.[63]

Elephant trunks have multiple functions, including breathing, olfaction, touching, grasping, and sound production.[41] The animal's sense of smell may be four times as sensitive as that of a bloodhound.[64] The trunk's ability to make powerful twisting and coiling movements allows it to collect food, wrestle with conspecifics,[65] and lift up to 350kg (770lb).[41] It can be used for delicate tasks, such as wiping an eye and checking an orifice,[65] and is capable of cracking a peanut shell without breaking the seed.[41] With its trunk, an elephant can reach items at heights of up to 7m (23ft) and dig for water under mud or sand.[65] Individuals may show lateral preference when grasping with their trunks: some prefer to twist them to the left, others to the right.[63] Elephants can suck up water both to drink and to spray on their bodies.[41] An adult Asian elephant is capable of holding 8.5L (2.2USgal) of water in its trunk.[62] They will also spray dust or grass on themselves.[41] When underwater, the elephant uses its trunk as a snorkel.[44]

The African elephant has two finger-like extensions at the tip of the trunk that allow it to grasp and bring food to its mouth. The Asian elephant has only one, and relies more on wrapping around a food item and squeezing it into its mouth.[8] Asian elephants have more muscle coordination and can perform more complex tasks.[62] Losing the trunk would be detrimental to an elephant's survival,[41] although in rare cases individuals have survived with shortened ones. One elephant has been observed to graze by kneeling on its front legs, raising on its hind legs and taking in grass with its lips.[62]Floppy trunk syndrome is a condition of trunk paralysis in African bush elephants caused by the degradation of the peripheral nerves and muscles beginning at the tip.[66]

Elephants usually have 26 teeth: the incisors, known as the tusks, 12 deciduous premolars, and 12 molars. Unlike most mammals, which grow baby teeth and then replace them with a single permanent set of adult teeth, elephants are polyphyodonts that have cycles of tooth rotation throughout their lives. The chewing teeth are replaced six times in a typical elephant's lifetime. Teeth are not replaced by new ones emerging from the jaws vertically as in most mammals. Instead, new teeth grow in at the back of the mouth and move forward to push out the old ones. The first chewing tooth on each side of the jaw falls out when the elephant is two to three years old. The second set of chewing teeth falls out when the elephant is four to six years old. The third set is lost at 915 years of age, and set four lasts until 1828 years of age. The fifth set of teeth lasts until the elephant is in its early 40s. The sixth (and usually final) set must last the elephant the rest of its life. Elephant teeth have loop-shaped dental ridges, which are thicker and more diamond-shaped in African elephants.[67]

The tusks of an elephant are modified incisors in the upper jaw. They replace deciduous milk teeth when the animal reaches 612 months of age and grow continuously at about 17cm (7in) a year. A newly developed tusk has a smooth enamel cap that eventually wears off. The dentine is known as ivory and its cross-section consists of crisscrossing line patterns, known as "engine turning", which create diamond-shaped areas. As a piece of living tissue, a tusk is relatively soft; it is as hard as the mineral calcite. Much of the incisor can be seen externally, while the rest is fastened to a socket in the skull. At least one-third of the tusk contains the pulp and some have nerves stretching to the tip. Thus it would be difficult to remove it without harming the animal. When removed, ivory begins to dry up and crack if not kept cool and moist. Tusks serve multiple purposes. They are used for digging for water, salt, and roots; debarking or marking trees; and for moving trees and branches when clearing a path. When fighting, they are used to attack and defend, and to protect the trunk.[68]

Like humans, who are typically right- or left-handed, elephants are usually right- or left-tusked. The dominant tusk, called the master tusk, is generally more worn down, as it is shorter with a rounder tip. For the African elephants, tusks are present in both males and females, and are around the same length in both sexes, reaching up to 3m (10ft),[68] but those of males tend to be thicker.[69] In earlier times elephant tusks weighing over 200 pounds (more than 90kg) were not uncommon, though it is rare today to see any over 100 pounds (45kg).[70]

In the Asian species, only the males have large tusks. Female Asians have very small ones, or none at all.[68] Tuskless males exist and are particularly common among Sri Lankan elephants.[71] Asian males can have tusks as long as Africans', but they are usually slimmer and lighter; the largest recorded was 3.02m (10ft) long and weighed 39kg (86lb). Hunting for elephant ivory in Africa[72] and Asia[73] has led to natural selection for shorter tusks[74][75] and tusklessness.[76][77]

An elephant's skin is generally very tough, at 2.5cm (1in) thick on the back and parts of the head. The skin around the mouth, anus and inside of the ear is considerably thinner. Elephants typically have grey skin, but African elephants look brown or reddish after wallowing in coloured mud. Asian elephants have some patches of depigmentation, particularly on the forehead and ears and the areas around them. Calves have brownish or reddish hair, especially on the head and back. As elephants mature, their hair darkens and becomes sparser, but dense concentrations of hair and bristles remain on the end of the tail as well as the chin, genitals and the areas around the eyes and ear openings. Normally the skin of an Asian elephant is covered with more hair than its African counterpart.[78]

An elephant uses mud as a sunscreen, protecting its skin from ultraviolet light. Although tough, an elephant's skin is very sensitive. Without regular mud baths to protect it from burning, insect bites, and moisture loss, an elephant's skin suffers serious damage. After bathing, the elephant will usually use its trunk to blow dust onto its body and this dries into a protective crust. Elephants have difficulty releasing heat through the skin because of their low surface-area-to-volume ratio, which is many times smaller than that of a human. They have even been observed lifting up their legs, presumably in an effort to expose their soles to the air.[78]

To support the animal's weight, an elephant's limbs are positioned more vertically under the body than in most other mammals. The long bones of the limbs have cancellous bone in place of medullary cavities. This strengthens the bones while still allowing haematopoiesis.[79] Both the front and hind limbs can support an elephant's weight, although 60% is borne by the front.[80] Since the limb bones are placed on top of each other and under the body, an elephant can stand still for long periods of time without using much energy. Elephants are incapable of rotating their front legs, as the ulna and radius are fixed in pronation; the "palm" of the manus faces backward.[79] The pronator quadratus and the pronator teres are either reduced or absent.[81] The circular feet of an elephant have soft tissues or "cushion pads" beneath the manus or pes, which distribute the weight of the animal.[80] They appear to have a sesamoid, an extra "toe" similar in placement to a giant panda's extra "thumb", that also helps in weight distribution.[82] As many as five toenails can be found on both the front and hind feet.[8]

Elephants can move both forwards and backwards, but cannot trot, jump, or gallop. They use only two gaits when moving on land, the walk and a faster gait similar to running.[79] In walking, the legs act as pendulums, with the hips and shoulders rising and falling while the foot is planted on the ground. With no "aerial phase", the fast gait does not meet all the criteria of running, although the elephant uses its legs much like other running animals, with the hips and shoulders falling and then rising while the feet are on the ground.[83] Fast-moving elephants appear to 'run' with their front legs, but 'walk' with their hind legs and can reach a top speed of 18km/h (11mph).[84] At this speed, most other quadrupeds are well into a gallop, even accounting for leg length. Spring-like kinetics could explain the difference between the motion of elephants and other animals.[85] During locomotion, the cushion pads expand and contract, and reduce both the pain and noise that would come from a very heavy animal moving.[80] Elephants are capable swimmers. They have been recorded swimming for up to six hours without touching the bottom, and have travelled as far as 48km (30mi) at a stretch and at speeds of up to 2.1km/h (1mph).[86]

The brain of an elephant weighs 4.55.5kg (1012lb) compared to 1.6kg (4lb) for a human brain. While the elephant brain is larger overall, it is proportionally smaller. At birth, an elephant's brain already weighs 3040% of its adult weight. The cerebrum and cerebellum are well developed, and the temporal lobes are so large that they bulge out laterally.[59] The throat of an elephant appears to contain a pouch where it can store water for later use.[41]

The heart of an elephant weighs 1221kg (2646lb). It has a double-pointed apex, an unusual trait among mammals.[59] When standing, the elephant's heart beats approximately 30 times per minute. Unlike many other animals, the heart rate speeds up by 8 to 10 beats per minute when the elephant is lying down.[87] The lungs are attached to the diaphragm, and breathing relies mainly on the diaphragm rather than the expansion of the ribcage.[59]Connective tissue exists in place of the pleural cavity. This may allow the animal to deal with the pressure differences when its body is underwater and its trunk is breaking the surface for air,[44] although this explanation has been questioned.[88] Another possible function for this adaptation is that it helps the animal suck up water through the trunk.[44] Elephants inhale mostly through the trunk, although some air goes through the mouth. They have a hindgut fermentation system, and their large and small intestines together reach 35m (115ft) in length. The majority of an elephant's food intake goes undigested despite the process lasting up to a day.[59]

A male elephant's testes are located internally near the kidneys. The elephant's penis can reach a length of 100cm (39in) and a diameter of 16cm (6in) at the base. It is S-shaped when fully erect and has a Y-shaped orifice. The female has a well-developed clitoris at up to 40cm (16in). The vulva is located between the hind legs instead of near the tail as in most mammals. Determining pregnancy status can be difficult due to the animal's large abdominal cavity. The female's mammary glands occupy the space between the front legs, which puts the suckling calf within reach of the female's trunk.[59] Elephants have a unique organ, the temporal gland, located in both sides of the head. This organ is associated with sexual behaviour, and males secrete a fluid from it when in musth.[89] Females have also been observed with secretions from the temporal glands.[64]

The African bush elephant can be found in habitats as diverse as dry savannahs, deserts, marshes, and lake shores, and in elevations from sea level to mountain areas above the snow line. Forest elephants mainly live in equatorial forests, but will enter gallery forests and ecotones between forests and savannahs.[16] Asian elephants prefer areas with a mix of grasses, low woody plants and trees, primarily inhabiting dry thorn-scrub forests in southern India and Sri Lanka and evergreen forests in Malaya.[9] Elephants are herbivorous and will eat leaves, twigs, fruit, bark, grass and roots.[16] They are born with sterile intestines, and require bacteria obtained from their mothers feces to digest vegetation.[90] African elephants are mostly browsers while Asian elephants are mainly grazers. They can consume as much as 150kg (330lb) of food and 40L (11USgal) of water in a day. Elephants tend to stay near water sources.[16] Major feeding bouts take place in the morning, afternoon and night. At midday, elephants rest under trees and may doze off while standing. Sleeping occurs at night while the animal is lying down.[79][91] Elephants average 34 hours of sleep per day.[92] Both males and family groups typically move 1020km (612mi) a day, but distances as far as 90180km (56112mi) have been recorded in the Etosha region of Namibia.[93] Elephants go on seasonal migrations in search of food, water and mates. At Chobe National Park, Botswana, herds travel 325km (202mi) to visit the river when the local waterholes dry up.[94]

Because of their large size, elephants have a huge impact on their environments and are considered keystone species. Their habit of uprooting trees and undergrowth can transform savannah into grasslands; when they dig for water during drought, they create waterholes that can be used by other animals. They can enlarge waterholes when they bathe and wallow in them. At Mount Elgon, elephants excavate caves that are used by ungulates, hyraxes, bats, birds and insects.[95] Elephants are important seed dispersers; African forest elephants ingest and defecate seeds, with either no effect or a positive effect on germination. The seeds are typically dispersed in large amounts over great distances.[96] In Asian forests, large seeds require giant herbivores like elephants and rhinoceros for transport and dispersal. This ecological niche cannot be filled by the next largest herbivore, the tapir.[97] Because most of the food elephants eat goes undigested, their dung can provide food for other animals, such as dung beetles and monkeys.[95] Elephants can have a negative impact on ecosystems. At Murchison Falls National Park in Uganda, the overabundance of elephants has threatened several species of small birds that depend on woodlands. Their weight can compact the soil, which causes the rain to run off, leading to erosion.[91]

Elephants typically coexist peacefully with other herbivores, which will usually stay out of their way. Some aggressive interactions between elephants and rhinoceros have been recorded. At Aberdare National Park, Kenya, a rhino attacked an elephant calf and was killed by the other elephants in the group.[91] At HluhluweUmfolozi Game Reserve, South Africa, introduced young orphan elephants went on a killing spree that claimed the lives of 36 rhinos during the 1990s, but ended with the introduction of older males.[98] The size of adult elephants makes them nearly invulnerable to predators,[9] though there are rare reports of adult elephants falling prey to tigers.[99] Calves may be preyed on by lions, spotted hyenas, and wild dogs in Africa[12] and tigers in Asia.[9] The lions of Savuti, Botswana, have adapted to hunting juvenile elephants during the dry season, and a pride of 30 lions has been recorded killing juvenile individuals between the ages of four and eleven years.[100] Elephants appear to distinguish between the growls of larger predators like tigers and smaller ones like leopards (which have not been recorded killing calves); the latter they react less fearfully and more aggressively to.[101] Elephants tend to have high numbers of parasites, particularly nematodes, compared to other herbivores. This is due to lower predation pressures that would otherwise kill off many of the individuals with significant parasite loads.[102]

Female elephants spend their entire lives in tight-knit matrilineal family groups, some of which are made up of more than ten members, including three pairs of mothers with offspring, and are led by the matriarch which is often the eldest female.[103] She remains leader of the group until death[12] or if she no longer has the energy for the role;[104] a study on zoo elephants showed that when the matriarch died, the levels of faecal corticosterone ('stress hormone') dramatically increased in the surviving elephants.[105] When her tenure is over, the matriarch's eldest daughter takes her place; this occurs even if her sister is present.[12] The older matriarchs tend to be more effective decision-makers.[106]

The social circle of the female elephant does not necessarily end with the small family unit. In the case of elephants in Amboseli National Park, Kenya, a female's life involves interaction with other families, clans, and subpopulations. Families may associate and bond with each other, forming what are known as bond groups. These are typically made of two family groups. During the dry season, elephant families may cluster together and form another level of social organisation known as the clan. Groups within these clans do not form strong bonds, but they defend their dry-season ranges against other clans. There are typically nine groups in a clan. The Amboseli elephant population is further divided into the "central" and "peripheral" subpopulations.[103]

Some elephant populations in India and Sri Lanka have similar basic social organisations. There appear to be cohesive family units and loose aggregations. They have been observed to have "nursing units" and "juvenile-care units". In southern India, elephant populations may contain family groups, bond groups and possibly clans. Family groups tend to be small, consisting of one or two adult females and their offspring. A group containing more than two adult females plus offspring is known as a "joint family". Malay elephant populations have even smaller family units, and do not have any social organisation higher than a family or bond group. Groups of African forest elephants typically consist of one adult female with one to three offspring. These groups appear to interact with each other, especially at forest clearings.[103]

The social life of the adult male is very different. As he matures, a male spends more time at the edge of his group and associates with outside males or even other families. At Amboseli, young males spend over 80% of their time away from their families when they are 1415. The adult females of the group start to show aggression towards the male, which encourages him to permanently leave. When males do leave, they either live alone or with other males. The former is typical of bulls in dense forests. Asian males are usually solitary, but occasionally form groups of two or more individuals; the largest consisted of seven bulls. Larger bull groups consisting of over 10 members occur only among African bush elephants, the largest of which numbered up to 144 individuals.[107] A dominance hierarchy exists among males, whether they range socially or solitarily. Dominance depends on the age, size and sexual condition.[107] Old bulls appear to control the aggression of younger ones and prevent them from forming "gangs".[108] Adult males and females come together for reproduction. Bulls appear to associate with family groups if an oestrous cow is present.[107]

Adult males enter a state of increased testosterone known as musth. In a population in southern India, males first enter musth at the age of 15, but it is not very intense until they are older than 25. At Amboseli, bulls under 24 do not go into musth, while half of those aged 2535 and all those over 35 do. Young bulls appear to enter musth during the dry season (JanuaryMay), while older bulls go through it during the wet season (JuneDecember). The main characteristic of a bull's musth is a fluid secreted from the temporal gland that runs down the side of his face. He may urinate with his penis still in his sheath, which causes the urine to spray on his hind legs. Behaviours associated with musth include walking with the head held high and swinging, picking at the ground with the tusks, marking, rumbling and waving only one ear at a time. This can last from a day to four months.[109]

Males become extremely aggressive during musth. Size is the determining factor in agonistic encounters when the individuals have the same condition. In contests between musth and non-musth individuals, musth bulls win the majority of the time, even when the non-musth bull is larger. A male may stop showing signs of musth when he encounters a musth male of higher rank. Those of equal rank tend to avoid each other. Agonistic encounters typically consist of threat displays, chases and minor sparring with the tusks. Serious fights are rare.[109]

Elephants are polygynous breeders,[110] and copulations are most frequent during the peak of the wet season.[111] A cow in oestrus releases chemical signals (pheromones) in her urine and vaginal secretions to signal her readiness to mate. A bull will follow a potential mate and assess her condition with the flehmen response, which requires the male to collect a chemical sample with his trunk and bring it to the vomeronasal organ.[112] The oestrous cycle of a cow lasts 1416 weeks with a 46-week follicular phase and an 810-week luteal phase. While most mammals have one surge of luteinizing hormone during the follicular phase, elephants have two. The first (or anovulatory) surge, could signal to males that the female is in oestrus by changing her scent, but ovulation does not occur until the second (or ovulatory) surge.[113] Fertility rates in cows decline around 4550 years of age.[104]

Bulls engage in a behaviour known as mate-guarding, where they follow oestrous females and defend them from other males. Most mate-guarding is done by musth males, and females actively seek to be guarded by them, particularly older ones.[114] Thus these bulls have more reproductive success.[107] Musth appears to signal to females the condition of the male, as weak or injured males do not have normal musths.[115] For young females, the approach of an older bull can be intimidating, so her relatives stay nearby to provide support and reassurance.[116] During copulation, the male lays his trunk over the female's back.[117] The penis is very mobile, being able to move independently of the pelvis.[118] Prior to mounting, it curves forward and upward. Copulation lasts about 45 seconds and does not involve pelvic thrusting or ejaculatory pause.[119]

Homosexual behaviour is frequent in both sexes. As in heterosexual interactions, this involves mounting. Male elephants sometimes stimulate each other by playfighting and "championships" may form between old bulls and younger males. Female same-sex behaviours have been documented only in captivity where they are known to masturbate one another with their trunks.[120]

Gestation in elephants typically lasts around two years with interbirth intervals usually lasting four to five years. Births tend to take place during the wet season.[121] Calves are born 85cm (33in) tall and weigh around 120kg (260lb).[116] Typically, only a single young is born, but twins sometimes occur.[122][123] The relatively long pregnancy is maintained by five corpus luteums (as opposed to one in most mammals) and gives the foetus more time to develop, particularly the brain and trunk.[122] As such, newborn elephants are precocial and quickly stand and walk to follow their mother and family herd.[124] A new calf is usually the centre of attention for herd members. Adults and most of the other young will gather around the newborn, touching and caressing it with their trunks. For the first few days, the mother is intolerant of other herd members near her young. Alloparenting where a calf is cared for by someone other than its mother takes place in some family groups. Allomothers are typically two to twelve years old.[116] When a predator is near, the family group gathers together with the calves in the centre.[125]

For the first few days, the newborn is unsteady on its feet, and needs the support of its mother. It relies on touch, smell and hearing, as its eyesight is poor. It has little precise control over its trunk, which wiggles around and may cause it to trip. By its second week of life, the calf can walk more firmly and has more control over its trunk. After its first month, a calf can pick up, hold and put objects in its mouth, but cannot suck water through the trunk and must drink directly through the mouth. It is still dependent on its mother and keeps close to her.[124]

For its first three months, a calf relies entirely on milk from its mother for nutrition after which it begins to forage for vegetation and can use its trunk to collect water. At the same time, improvements in lip and leg coordination occur. Calves continue to suckle at the same rate as before until their sixth month, after which they become more independent when feeding. By nine months, mouth, trunk and foot coordination is perfected. After a year, a calf's abilities to groom, drink, and feed itself are fully developed. It still needs its mother for nutrition and protection from predators for at least another year. Suckling bouts tend to last 24 min/hr for a calf younger than a year and it continues to suckle until it reaches three years of age or older. Suckling after two years may serve to maintain growth rate, body condition and reproductive ability.[124] Play behaviour in calves differs between the sexes; females run or chase each other, while males play-fight. The former are sexually mature by the age of nine years[116] while the latter become mature around 1415 years.[107] Adulthood starts at about 18 years of age in both sexes.[126][127] Elephants have long lifespans, reaching 6070 years of age.[67]Lin Wang, a captive male Asian elephant, lived for 86 years.[128]

Touching is an important form of communication among elephants. Individuals greet each other by stroking or wrapping their trunks; the latter also occurs during mild competition. Older elephants use trunk-slaps, kicks and shoves to discipline younger ones. Individuals of any age and sex will touch each other's mouths, temporal glands and genitals, particularly during meetings or when excited. This allows individuals to pick up chemical cues. Touching is especially important for mothercalf communication. When moving, elephant mothers will touch their calves with their trunks or feet when side-by-side or with their tails if the calf is behind them. If a calf wants to rest, it will press against its mother's front legs and when it wants to suckle, it will touch her breast or leg.[129]

Visual displays mostly occur in agonistic situations. Elephants will try to appear more threatening by raising their heads and spreading their ears. They may add to the display by shaking their heads and snapping their ears, as well as throwing dust and vegetation. They are usually bluffing when performing these actions. Excited elephants may raise their trunks. Submissive ones will lower their heads and trunks, as well as flatten their ears against their necks, while those that accept a challenge will position their ears in a V shape.[130]

Elephants produce several sounds, usually through the larynx, though some may be modified by the trunk. Perhaps the most well known is the trumpet, which is made during excitement, distress or aggression.[131] Fighting elephants may roar or squeal, and wounded ones may bellow.[132]Rumbles are produced during mild arousal[133] and some appear to be infrasonic.[134] Infrasonic calls are important, particularly for long-distance communication,[131] in both Asian and African elephants. For Asian elephants, these calls have a frequency of 1424Hz, with sound pressure levels of 8590dB and last 1015 seconds.[134] For African elephants, calls range from 1535Hz with sound pressure levels as high as 117dB, allowing communication for many kilometres, with a possible maximum range of around 10km (6mi).[135]

At Amboseli, several different infrasonic calls have been identified. A greeting rumble is emitted by members of a family group after having been separated for several hours. Contact calls are soft, unmodulated sounds made by individuals that have been separated from their group and may be responded to with a "contact answer" call that starts out loud, but becomes softer. A "let's go" soft rumble is emitted by the matriarch to signal to the other herd members that it is time to move to another spot. Bulls in musth emit a distinctive, low-frequency pulsated rumble nicknamed the "motorcycle". Musth rumbles may be answered by the "female chorus", a low-frequency, modulated chorus produced by several cows. A loud postcopulatory call may be made by an oestrous cow after mating. When a cow has mated, her family may produce calls of excitement known as the "mating pandemonium".[133]

Elephants are known to communicate with seismics, vibrations produced by impacts on the earth's surface or acoustical waves that travel through it. They appear to rely on their leg and shoulder bones to transmit the signals to the middle ear. When detecting seismic signals, the animals lean forward and put more weight on their larger front feet; this is known as the "freezing behaviour". Elephants possess several adaptations suited for seismic communication. The cushion pads of the feet contain cartilaginous nodes and have similarities to the acoustic fat found in marine mammals like toothed whales and sirenians. A unique sphincter-like muscle around the ear canal constricts the passageway, thereby dampening acoustic signals and allowing the animal to hear more seismic signals.[136] Elephants appear to use seismics for a number of purposes. An individual running or mock charging can create seismic signals that can be heard at great distances.[137] When detecting the seismics of an alarm call signalling danger from predators, elephants enter a defensive posture and family groups will pack together. Seismic waveforms produced by locomotion appear to travel distances of up to 32km (20mi) while those from vocalisations travel 16km (10mi).[138]

Elephants exhibit mirror self-recognition, an indication of self-awareness and cognition that has also been demonstrated in some apes and dolphins.[139] One study of a captive female Asian elephant suggested the animal was capable of learning and distinguishing between several visual and some acoustic discrimination pairs. This individual was even able to score a high accuracy rating when re-tested with the same visual pairs a year later.[140] Elephants are among the species known to use tools. An Asian elephant has been observed modifying branches and using them as flyswatters.[141] Tool modification by these animals is not as advanced as that of chimpanzees. Elephants are popularly thought of as having an excellent memory. This could have a factual basis; they possibly have cognitive maps to allow them to remember large-scale spaces over long periods of time. Individuals appear to be able to keep track of the current location of their family members.[58]

Scientists debate the extent to which elephants feel emotion. They appear to show interest in the bones of their own kind, regardless of whether they are related.[142] As with chimps and dolphins, a dying or dead elephant may elicit attention and aid from others, including those from other groups. This has been interpreted as expressing "concern",[143] however, others would dispute such an interpretation as being anthropomorphic;[144][145] the Oxford Companion to Animal Behaviour (1987) advised that "one is well advised to study the behaviour rather than attempting to get at any underlying emotion".[146]

Distribution of elephants

African elephants were listed as vulnerable by the International Union for Conservation of Nature (IUCN) in 2008, with no independent assessment of the conservation status of the two forms.[26] In 1979, Africa had an estimated minimum population of 1.3million elephants, with a possible upper limit of 3.0million. By 1989, the population was estimated to be 609,000; with 277,000 in Central Africa, 110,000 in eastern Africa, 204,000 in southern Africa, and 19,000 in western Africa. About 214,000 elephants were estimated to live in the rainforests, fewer than had previously been thought. From 1977 to 1989, elephant populations declined by 74% in East Africa. After 1987, losses in elephant numbers accelerated, and savannah populations from Cameroon to Somalia experienced a decline of 80%. African forest elephants had a total loss of 43%. Population trends in southern Africa were mixed, with anecdotal reports of losses in Zambia, Mozambique and Angola, while populations grew in Botswana and Zimbabwe and were stable in South Africa.[147] Conversely, studies in 2005 and 2007 found populations in eastern and southern Africa were increasing by an average annual rate of 4.0%.[26] Due to the vast areas involved, assessing the total African elephant population remains difficult and involves an element of guesswork. The IUCN estimates a total of around 440,000 individuals for 2012.[148]

African elephants receive at least some legal protection in every country where they are found, but 70% of their range exists outside protected areas. Successful conservation efforts in certain areas have led to high population densities. As of 2008, local numbers were controlled by contraception or translocation. Large-scale cullings ceased in 1988, when Zimbabwe abandoned the practice. In 1989, the African elephant was listed under Appendix I by the Convention on International Trade in Endangered Species of Wild Fauna and Flora (CITES), making trade illegal. Appendix II status (which allows restricted trade) was given to elephants in Botswana, Namibia and Zimbabwe in 1997 and South Africa in 2000. In some countries, sport hunting of the animals is legal; Botswana, Cameroon, Gabon, Mozambique, Namibia, South Africa, Tanzania, Zambia, and Zimbabwe have CITES export quotas for elephant trophies.[26] In June 2016 the First Lady of Kenya, Margaret Kenyatta, helped launch the East Africa Grass-Root Elephant Education Campaign Walk, organised by elephant conservationist Jim Nyamu. The event was conducted to raise awareness of the value of elephants and rhinos, to help mitigate human-elephant conflicts, and to promote anti-poaching activities.[149][150]

In 2008, the IUCN listed the Asian elephant as endangered due to a 50% population decline over the past 6075 years,[151] while CITES lists the species under Appendix I.[151] Asian elephants once ranged from Syria and Iraq (the subspecies Elephas maximus asurus), to China (up to the Yellow River)[152] and Java. It is now extinct in these areas,[151] and the current range of Asian elephants is highly fragmented.[152] The total population of Asian elephants is estimated to be around 40,00050,000, although this may be a loose estimate. It is likely that around half of the population is in India. Although Asian elephants are declining in numbers overall, particularly in Southeast Asia, the population in the Western Ghats appears to be increasing.[151]

The poaching of elephants for their ivory, meat and hides has been one of the major threats to their existence.[151] Historically, numerous cultures made ornaments and other works of art from elephant ivory, and its use rivalled that of gold.[153] The ivory trade contributed to the African elephant population decline in the late 20th century.[26] This prompted international bans on ivory imports, starting with the United States in June 1989, and followed by bans in other North American countries, western European countries, and Japan.[153] Around the same time, Kenya destroyed all its ivory stocks.[154] CITES approved an international ban on ivory that went into effect in January 1990.[153] Following the bans, unemployment rose in India and China, where the ivory industry was important economically. By contrast, Japan and Hong Kong, which were also part of the industry, were able to adapt and were not badly affected.[153] Zimbabwe, Botswana, Namibia, Zambia, and Malawi wanted to continue the ivory trade and were allowed to, since their local elephant populations were healthy, but only if their supplies were from elephants that had been culled or died of natural causes.[154]

The ban allowed the elephant to recover in parts of Africa.[153] In January 2012, 650 elephants in Bouba Njida National Park, Cameroon, were killed by Chadian raiders.[155] This has been called "one of the worst concentrated killings" since the ivory ban.[154] Asian elephants are potentially less vulnerable to the ivory trade, as females usually lack tusks. Still, members of the species have been killed for their ivory in some areas, such as Periyar National Park in India.[151] China was the biggest market for poached ivory but announced they would phase out the legal domestic manufacture and sale of ivory products in May, 2015, and in September 2015 China and the United States "said they would enact a nearly complete ban on the import and export of ivory."[156]

Other threats to elephants include habitat destruction and fragmentation.[26] The Asian elephant lives in areas with some of the highest human populations. Because they need larger amounts of land than other sympatric terrestrial mammals, they are the first to be affected by human encroachment. In extreme cases, elephants may be confined to small islands of forest among human-dominated landscapes. Elephants cannot coexist with humans in agricultural areas due to their size and food requirements. Elephants commonly trample and consume crops, which contributes to conflicts with humans, and both elephants and humans have died by the hundreds as a result. Mitigating these conflicts is important for conservation.[151] One proposed solution is the provision of urban corridors which allow the animals access to key areas.[157]

Elephants have been working animals since at least the Indus Valley Civilization[158] and continue to be used in modern times. There were 13,00016,500 working elephants employed in Asia as of 2000. These animals are typically captured from the wild when they are 1020 years old, when they can be trained quickly and easily, and will have a longer working life.[159] They were traditionally captured with traps and lassos, but since 1950, tranquillisers have been used.[160] Individuals of the Asian species are more commonly trained to be working animals, although the practice has also been attempted in Africa. The taming of African elephants in the Belgian Congo began by decree of Leopold II of Belgium during the 19th century and continues to the present with the Api Elephant Domestication Centre.[161]

Asian elephants perform tasks such as hauling loads into remote areas, moving logs into trucks, transporting tourists around national parks, pulling wagons and leading religious processions.[159] In northern Thailand, the animals are used to digest coffee beans for Black Ivory coffee.[162] They are valued over mechanised tools because they can work in relatively deep water, require relatively little maintenance, need only vegetation and water as fuel and can be trained to memorise specific tasks. Elephants can be trained to respond to over 30 commands.[159] Musth bulls can be difficult and dangerous to work with and are chained until the condition passes.[163] In India, many working elephants are alleged to have been subject to abuse. They and other captive elephants are thus protected under the The Prevention of Cruelty to Animals Act of 1960.[164]

In both Myanmar and Thailand, deforestation and other economic factors have resulted in sizable populations of unemployed elephants resulting in health problems for the elephants themselves as well as economic and safety problems for the people amongst whom they live.[165][166]

Historically, elephants were considered formidable instruments of war. They were equipped with armour to protect their sides, and their tusks were given sharp points of iron or brass if they were large enough. War elephants were trained to grasp an enemy soldier and toss him to the person riding on them or to pin the soldier to the ground and impale him.[167]

One of the earliest references to war elephants is in the Indian epic Mahabharata (written in the 4th century BCE, but said to describe events between the 11th and 8th centuries BCE). They were not used as much as horse-drawn chariots by either the Pandavas or Kauravas. During the Magadha Kingdom (which began in the 6th century BCE), elephants began to achieve greater cultural importance than horses, and later Indian kingdoms used war elephants extensively; 3,000 of them were used in the Nandas (5th and 4th centuries BCE) army, while 9,000 may have been used in the Mauryan army (between the 4th and 2nd centuries BCE). The Arthashastra (written around 300 BCE) advised the Mauryan government to reserve some forests for wild elephants for use in the army, and to execute anyone who killed them.[168] From South Asia, the use of elephants in warfare spread west to Persia[167] and east to Southeast Asia.[169] The Persians used them during the Achaemenid Empire (between the 6th and 4th centuries BCE),[167] while Southeast Asian states first used war elephants possibly as early as the 5th century BCE and continued to the 20th century.[169]

Alexander the Great trained his foot soldiers to injure the animals and cause them to panic during wars with both the Persians and Indians. Ptolemy, who was one of Alexander's generals, used corps of Asian elephants during his reign as the ruler of Egypt (which began in 323 BCE). His son and successor Ptolemy II (who began his rule in 285 BCE) obtained his supply of elephants further south in Nubia. From then on, war elephants were employed in the Mediterranean and North Africa throughout the classical period. The Greek king Pyrrhus used elephants in his attempted invasion of Rome in 280 BCE. While they frightened the Roman horses, they were not decisive and Pyrrhus ultimately lost the battle. The Carthaginian general Hannibal took elephants across the Alps during his war with the Romans and reached the Po Valley in 217 BCE with all of them alive, but they later succumbed to disease.[167]

Elephants were historically kept for display in the menageries of Ancient Egypt, China, Greece and Rome. The Romans in particular pitted them against humans and other animals in gladiator events. In the modern era, elephants have traditionally been a major part of zoos and circuses around the world. In circuses, they are trained to perform tricks. The most famous circus elephant was probably Jumbo (1861 15 September 1885), who was a major attraction in the Barnum & Bailey Circus.[170] These animals do not reproduce well in captivity, due to the difficulty of handling musth bulls and limited understanding of female oestrous cycles. Asian elephants were always more common than their African counterparts in modern zoos and circuses. After CITES listed the Asian elephant under Appendix I in 1975, the number of African elephants in zoos increased in the 1980s, although the import of Asians continued. Subsequently, the US received many of its captive African elephants from Zimbabwe, which had an overabundance of the animals.[171] As of 2000, around 1,200 Asian and 700 African elephants were kept in zoos and circuses. The largest captive population is in North America, which has an estimated 370 Asian and 350 African elephants. About 380 Asians and 190 Africans are known to exist in Europe, and Japan has around 70 Asians and 67 Africans.[171]

Keeping elephants in zoos has met with some controversy. Proponents of zoos argue that they offer researchers easy access to the animals and provide money and expertise for preserving their natural habitats, as well as safekeeping for the species. Critics claim that the animals in zoos are under physical and mental stress.[172] Elephants have been recorded displaying stereotypical behaviours in the form of swaying back and forth, trunk swaying or route tracing. This has been observed in 54% of individuals in UK zoos.[173] Elephants in European zoos appear to have shorter lifespans than their wild counterparts at only 17 years, although other studies suggest that zoo elephants live as long those in the wild.[174]

The use of elephants in circuses has also been controversial; the Humane Society of the United States has accused circuses of mistreating and distressing their animals.[175] In testimony to a US federal court in 2009, Barnum & Bailey Circus CEO Kenneth Feld acknowledged that circus elephants are struck behind their ears, under their chins and on their legs with metal-tipped prods, called bull hooks or ankus. Feld stated that these practices are necessary to protect circus workers and acknowledged that an elephant trainer was reprimanded for using an electric shock device, known as a hot shot or electric prod, on an elephant. Despite this, he denied that any of these practices harm elephants.[176] Some trainers have tried to train elephants without the use of physical punishment. Ralph Helfer is known to have relied on gentleness and reward when training his animals, including elephants and lions.[177] In January 2016 Ringling Bros. and Barnum and Bailey circus announced it would retire its touring elephants in May 2016.[178]

Like many mammals, elephants can contract and transmit diseases to humans, one of which is tuberculosis. In 2012, two elephants in Tete dOr zoo, Lyon were diagnosed with the disease. Due to the threat of transmitting tuberculosis to other animals or visitors to the zoo, their euthanasia was initially ordered by city authorities but a court later overturned this decision.[179] At an elephant sanctuary in Tennessee, a 54-year-old African elephant was considered to be the source of tuberculosis infections among eight workers.[180]

As of 2015[update], tuberculosis appears to be widespread among captive elephants in the US. It is believed that the animals originally acquired the disease from humans, a process called reverse zoonosis. Because the disease can spread through the air to infect both humans and other animals, it is a public health concern affecting circuses and zoos.[181][182]

Elephants can exhibit bouts of aggressive behaviour and engage in destructive actions against humans.[183] In Africa, groups of adolescent elephants damaged homes in villages after cullings in the 1970s and 1980s. Because of the timing, these attacks have been interpreted as vindictive.[108][184] In India, male elephants regularly enter villages at night, destroying homes and killing people. Elephants killed around 300 people between 2000 and 2004 in Jharkhand, while in Assam 239 people were reportedly killed between 2001 and 2006.[183] Local people have reported their belief that some elephants were drunk during their attacks, although officials have disputed this explanation.[185][186] Purportedly drunk elephants attacked an Indian village a second time in December 2002, killing six people, which led to the killing of about 200 elephants by locals.[187]

Elephants have been represented in art since Paleolithic times. Africa in particular contains many rock paintings and engravings of the animals, especially in the Sahara and southern Africa.[188] In the Far East, the animals are depicted as motifs in Hindu and Buddhist shrines and temples.[189] Elephants were often difficult to portray by people with no first-hand experience with them.[190] The ancient Romans, who kept the animals in captivity, depicted anatomically accurate elephants on mosaics in Tunisia and Sicily. At the beginning of the Middle Ages, when Europeans had little to no access to the animals, elephants were portrayed more like fantasy creatures. They were often depicted with horse- or bovine-like bodies with trumpet-like trunks and tusks like a boar; some were even given hooves. Elephants were commonly featured in motifs by the stonemasons of the Gothic churches. As more elephants began to be sent to European kings as gifts during the 15th century, depictions of them became more accurate, including one made by Leonardo da Vinci. Despite this, some Europeans continued to portray them in a more stylised fashion.[191]Max Ernst's 1921 surrealist painting The Elephant Celebes depicts an elephant as a silo with a trunk-like hose protruding from it.[192]

Elephants have been the subject of religious beliefs. The Mbuti people believe that the souls of their dead ancestors resided in elephants.[189] Similar ideas existed among other African tribes, who believed that their chiefs would be reincarnated as elephants. During the 10th century AD, the people of Igbo-Ukwu buried their leaders with elephant tusks.[193] The animals' religious importance is only totemic in Africa[194] but is much more significant in Asia. In Sumatra, elephants have been associated with lightning. Likewise in Hinduism, they are linked with thunderstorms as Airavata, the father of all elephants, represents both lightning and rainbows.[189] One of the most important Hindu deities, the elephant-headed Ganesha, is ranked equal with the supreme gods Shiva, Vishnu, and Brahma.[195] Ganesha is associated with writers and merchants and it is believed that he can give people success as well as grant them their desires.[189] In Buddhism, Buddha is said to have been a white elephant reincarnated as a human.[196] In Islamic tradition, the year 570, when Muhammad was born, is known as the Year of the Elephant.[197] Elephants were thought to be religious themselves by the Romans, who believed that they worshipped the sun and stars.[189] The 'Land of a Million Elephants' was the name of the ancient kingdom of Lan Xang and later the Lan Chang Province and it is now a nickname for Laos.

Elephants are ubiquitous in Western popular culture as emblems of the exotic, especially since as with the giraffe, hippopotamus and rhinoceros there are no similar animals familiar to Western audiences.[198] The use of the elephant as a symbol of the US Republican Party began with an 1874 cartoon by Thomas Nast.[199] As characters, elephants are most common in children's stories, in which they are generally cast as models of exemplary behaviour. They are typically surrogates for humans with ideal human values. Many stories tell of isolated young elephants returning to a close-knit community, such as "The Elephant's Child" from Rudyard Kipling's Just So Stories, Disney's Dumbo and Kathryn and Byron Jackson's The Saggy Baggy Elephant. Other elephant heroes given human qualities include Jean de Brunhoff's Babar, David McKee's Elmer and Dr. Seuss's Horton.[198]

Several cultural references emphasise the elephant's size and exotic uniqueness. For instance, a "white elephant" is a byword for something expensive, useless and bizarre.[198] The expression "elephant in the room" refers to an obvious truth that is ignored or otherwise unaddressed.[200] The story of the blind men and an elephant teaches that reality may be viewed by different perspectives.[201]

Excerpt from:
Elephant - Wikipedia, the free encyclopedia

The mission of the Department of Science and Health Department at UC Clermont is to provide outstanding, comprehensive undergraduate programs for careers in the biological and chemical sciences and in allied health professions. We strive to nurture a classroom environment which demonstrates and inculcates in our students the understanding and ability to acquire and critically interpret knowledge of basic facts and theories of the basic and clinical sciences, strive to add to the body of scientific knowledge through research, and encourage our students to communicate their understanding to others.We use every opportunity in our classrooms to encourage curiosity, propose hypotheses, construct scientifically valid tests for hypotheses, and nurture critical thinking skills. We teach our students the tools needed to create hypothetical answers to new questions, to make an educated guess.

Our laboratories emphasize hands-on experiments or manipulations which demonstrate principles presented in lecture. Each student will be taught the use of specialized scientific or clinical equipment and the performance of important lab or clinical techniques.

We provide a classroom environment which favors the learning process through small class size and lively classroom discussions. We test in a manner which enhances student improvement to more effectively engage them in their learning process. We believe that all of the material we teach should relate directly or indirectly to a students life or professional interests. Our curriculum is organized around these shared values.

See original here:
Science & Health, Colleges Around Cincinnati, University ...

Homosexuality is the condition of "sexual desire or behavior directed toward a person or persons of one's own sex."[1]

Homosexuality has a number of causal factors that influence its ultimate origination in individuals; these factors will be addressed shortly. In addition, homosexuality has a variety of effects on individuals and society. Next, some of the historical events, religious matters, and legal matters relating to homosexuality will be covered. Finally, the latter part of the 20th century has seen a large body of research on the causes and effects of homosexuality.

For more information please see: Homosexuality and biblical interpretation and Homosexuality and the Bible and Atheism and homosexuality and Atheism and the persecution of homosexuals

Below are several Bible verses that condemn homosexuality:

In addition, there are numerous other references that also condemn the lifestyle, such as 1 Kings 22:46 (NASB): "The remnant of the sodomites who remained in the days of his father Asa, he expelled from the land."

For more information please see: Causes of Homosexuality

Homosexuality is sometimes also defined in terms of an attraction, preference, orientation, or identity. The term "orientation" is particularly favored by those who are promoting public acceptance of homosexuality.[2]

For more information please see: Homosexuality and Genetics

A common argument is that an inclination to homosexuality is inborn and immutable. It is widely believed that the public will become more accepting of homosexuality if they are convinced that it is inborn and immutable. For example, neuroscientist and homosexual Simon Levay stated: "...people who think that gays and lesbians are born that way are also more likely to support gay rights."[3]

Eight major studies of identical twins in the United States, Australia and Scandinavia during the last two decades indicate that homosexuals were not born that way.[4]Research into the issue of the origins of homosexuality suggests that adoptive brothers are more likely to both be homosexuals than the biological brothers, who share half their genes which suggests that homosexuality is not genetically caused. [5][6] This data prompted the journal Science to report "this . . . suggests that there is no genetic component, but rather an environmental component shared in families".[7][8] However, in regards to psychosocial and biological theories in regards to the origin of homosexuality, Columbia University psychiatry professors Drs. William Byrne and Bruce Parsons stated in 1994: "There is no evidence that at present to substantiate a biological theory. [T]he appeal of current biological explanations for sexual orientation may derive more from dissatisfaction with the present status of psychosocial explanations than from a substantiating body of experimental data".[9]

Dr. Tahir I. Jaz, M.D., Winnipeg, Canada states: "The increasing claims of being "born that way" parallels the rising political activism of homosexual organizations, who politicize the issue of homosexual origins. In the 1970s, approximately ten percent of homosexuals claimed to be "born homosexual" according to a large scale survey....However, in a survey in the 1980s, with the homosexual rights movement increasingly becoming active, thirty-five percent claimed to be born that way.[10]

For more information please see: Religious Upbringing and Culture Affects Rates of Homosexuality

Dr. Neil Whitehead is a research scientist and biochemist from New Zealand and his wife Briar Whitehead is a writer.[11] Dr. Whitehead coauthored a book with with his wife entitled My Genes Made Me Do it - a scientific look at sexual orientation which argues that there is no genetic determinism in regards to homosexuality (homosexuals are "not born that way") and that there is abundant documentation that individuals are able to leave homosexuality and become heterosexuals.[12]

Dr. Whitehead and Briar Whitehead declared:

This evidence comes from missionaries who commonly spend 25 years of their lives living in one culture, far more than almost any anthropologist....Overall they can be considered as reliable witnesses. For example, in contrast to groups like the Sambia in the New Guinea highlands, where homosexuality was compulsory, only about 2-3 percent of Western Dani (also in the New Guinea highlands) practiced it. However, in another group of Dani who were genetically related, homosexuality was totally unknown. Missionaries report that when they were translating the Bible into Dani for this group, their tribal assistants, who knew their own culture intimately, were nonplused by references to homosexuality in Romans 1; they did not understand the concept. Another missionary, with the same group for 25 years, overheard many jests and sexually ribald exchanges among the men, but never a single mention of homosexuality in all that time. When Dani went to help with missionary work among the Sambia, they were astounded at some of the homosexual practices they saw for the first time. Although it is always difficult for a foreigner to be completely sure whether a rare and stigmatized behavior exists, it is certainly true that if three such different experiences of homosexuality can occur in groups of people so closely related genetically, genetically enforced homosexuality is an impossibility.[13]

The religious leader and civil rights leader Martin Luther King (MLK) never championed the homosexual agenda. In fact, MLK saw homosexuality as probably a culturally induced "problem" and he believed that homosexuals could become ex-homosexuals. (see: Overcoming homosexuality).[14]

King wrote in a 1958 column: The type of feeling that you have toward boys is probably not an innate tendency, but something that has been culturally acquired, . You are already on the right road toward a solution, since you honestly recognize the problem and have a desire to solve it.[15]

In 1994, the book Sex in America: A definitive survey by Robert T. Michael, John H. Gagnon, Edward O. Laumann, and Gina Kolata stated the following:

The aforementioned authors Dr. Whitehead and Briar Whitehead similarly wrote:

For more information please see: Failure of Experiments to Show Genetic Determinism For Homosexuality

Dr. Dean Hamer is a researcher often cited to show that there is empirical data supporting the notion of genetic determinism in regards to homosexuality. News organizations like National Public Radio and Newsweek have done news stories regarding his work.[18] In respect to the press trumpeting various findings genetics-of-behavior research uncritically the science journal Science stated the following in 1994:

The Gallup Organization reported: "The Family Research Report says 'around 2-3% of men, and 2% of women, are homosexual or bisexual.'"[20] The U.S Department of Health and Human Services reported: "While the percentage of women and men aged 18-44 years who reported they were either heterosexual or homosexual was similar (94% of women and 96% of men said they were heterosexual while 1.1% of women and 1.7% of men said they were homosexual or gay), the percentage of women who reported they were bisexual was more than 3 times as high as men (3.5% of women vs. 1.1% of men)."[21][22]

In regards to the issue of homosexuality and choice, given the existence of ex-homosexuals and given the existence of human cultures where homosexuality has apparently not existed, the position that homosexuality is ultimately a choice in individuals or at the very least can be a choice in individuals has strong evidential support. In short, there is a strong argument that one can leave homosexuality.

Also, in 2012 ABC News reported concerning actress Cynthia Nixon: "Cynthia Nixon stands by her statement that she is gay by choice, despite the backlash shes received from members of the gay community."[23] In addition, given that the homosexual population has significantly higher rates of many diseases and the homosexual population also has significantly lower rates of various measures of mental health it can be strongly argued that engaging in homosexual acts is a bad choice for individuals. Another other factor that makes engaging in homosexual acts a bad choice for individuals is the significantly higher rates of domestic violence in homosexual couples. In addition, according to experts homosexual murders are relatively or quite common and often homosexual murders are very brutal. Also, the homosexual population has a greater propensity to engage in illegal drug use.

A 2003 poll done by Ellison Research of Phoenix, Arizona stated that 82% of all American Protestant ministers agreed with the statement homosexuality is a choice people make".[24]

Immutability is the inability of a thing to be changed. For example, it is impossible to change a dog into a cat. Likewise, it is impossible to change one's race, although with makeup or plastic surgery has made it possible to alter one's racial appearance. The immutability of membership in a group is an important consideration in determining the level of scrutiny given to a law against that group under the Equal Protection Clause.

There has been much debate over whether homosexuality is immutable despite the existence of ex-homosexuals. Often the argument is made that it's either genetically determined (and thus immutable), or that it is entirely a matter of choice. Given this dichotomy, the premise that "I didn't choose to be gay" yields the conclusion that it must be genetically determined. However, the search for a "gay gene" has proved elusive. Many others, including most scientists, have a much less 'black and white' view. They propose that it is determined by a complex interaction of many factors, some of which could be genetic, but probably also include psychological, environmental and cognitive factors, and is shaped at a very early age.

Simon LeVay wrote: "It's important to stress what I didn't find. I did not prove that homosexuality is genetic, or find a genetic cause for being gay. I didn't show that gay men are born that way, the most common mistake people make in interpreting my work. Nor did I locate a gay center in the brain. ... Since I look at adult brains, we don't know if the differences I found were there at birth or if they appeared later."[25]

See also: Homosexuality and frontal lobe injury and Religiosity and larger frontal lobes and Atheism and brain function

The frontal lobe plays a role in controlling sexual behavior.[28][29]

According to the 2007 medical journal article (and its abstract) entitled Neurological control of human sexual behaviour: insights from lesion studies which was published in the Journal of Neurology, Neurosurgery, and Psychiatry:

Disinhibited sexual behaviour has been reported following damage to the frontal lobes, particularly the orbitofrontal region of the limbic system.

Kolarsky and colleagues54 examined the relationships between sexual deviation, age of lesion onset and localisation of lesion (temporal vs extratemporal). The authors defined two diagnostic categories: (1) sexual deviation, involving a deviation of sexual object (for example, paedophilia). Homosexuality was included in this category, which would now be considered inappropriate, and (2) sexual disturbances other than deviations, including orgasm in response to stimuli unrelated to the subject's sexual preference, hypersexuality and hyposexuality...

An association between temporal lobe abnormalities and paedophilia has been reported by Mendez and colleagues.[30]

For more information please see: Ex-Homosexuals and Overcoming Homosexuality and Resources on becoming a Christian

In regards to the question of whether or not homosexuality is a permanent condition, one of the earliest historical records regarding of the existence of ex-homosexuals is a letter of the Apostle Paul to the Corinthian Christian church.

The Apostle Paul taught that homosexuality is a sin when he wrote the following:

Today people still report leaving homosexuality and becoming heterosexual through their Christian faith.[31]

Peter LaBarbera is the President of Americans for Truth which is a organization which counters the homosexual agenda. Peter LaBarbera stated the following regarding Christian ex-homosexuals who reported being transformed by the power of God:

In respect to Peter LaBarbera's statement above regarding homosexuals overcoming homosexuality through the power of God, in 1980 a study was published in the American Journal of Psychiatry and eleven men participated in this study. The aforementioned study in the American Journal of Psychiatry stated that eleven homosexual men became heterosexuals "without explicit treatment and/or long-term psychotherapy" through their participation in a Pentecostal church.[33] The Apostle Paul in a letter to the church of Corinth indicated that Christians were able to overcome being drunkards through the power of Jesus Christ (I Corinthians 6:9-11).

Dr. Whitehead and Briar Whitehead state in their aforementioned book the following regarding ex-homosexuals overcoming homosexuality:

West mentions one man who was exclusively homosexual for eight years, then became heterosexual...

Another well known author in the field, Hatterer, who believes in sexual orientation change, said, Ive heard of hundreds of ... men who went from a homosexual to a heterosexual adjustment on their own.[34]

See: Hate Crime Law Misapplied to Ex-homosexual

See also: Denials that ex-homosexuals exist

Commonly homosexual activists fallaciously argue that ex-homosexuals must never have been really gay at all (see: No true Scotsman fallacy) or is just deluding himself. [35] For example, when the alleged homosexual, male penguin "Harry" mated with a female penguin (see: Homosexuality in animals myth), the homosexual activist Wayne Besen angrily exclaimed "There is no ex-gay sexual orientation. Harry is simply in denial. Hes living what I call the big lie.[36] In Madison, Wisconsin an ex-homosexual was forced to do 50 hours of community service and undergo "tolerance training" (or face jail time and fines) due to a discussion he had with a homosexual (see: Hate Crime Law Misapplied to Ex-homosexual).

The denial that homosexuality is a choice by homosexual activists and liberals is similar to the behavior of fat acceptance movement activists who insist that being overweight is never a choice and ostracize ex-overweight people (see: fat acceptance movement for details).

Two of the more popular anti-homosexuality blogs are Americans For Truth and Gay Christian Movement Watch. The blog Americans For Truth is run by Peter LaBarbera and the blog Gay Christian Movement Watch is run by Pastor D.L. Foster.

A 2006 survey finds homosexual men seek to leave homosexual lifestyle to heal emotional pain and for spiritual reasons rather than outside pressure. In addition, there is other data that supports the above 2006 survey findings.

For additional information please see: Homosexuality and biblical interpretation and Homosexuality and the Bible and Atheism and homosexuality

In respect to homosexuality and the Bible, sound Bible exegesis and Bible exposition demonstrates that the Bible condemns homosexuality.[38][39][40][41] In addition, Christian apologist JP Holding refutes various arguments that assert that the Bible does not condemn homosexuality.[42][43][44][45][46] In his essay which examines the biblical passages regarding homosexuality, Pastor and Associate Professor of Pastoral Ministries at The Master's Seminary Dr. Alex D. Montoya states that "The Christian needs to befriend and witness to the homosexual with such love, compassion, and wisdom that such will respond to the saving grace of God."[47]

The Bible clearly associates the city of Sodom with homosexuality (Genesis 19:4-9), although the Bible associates with Sodom other sins as well. Claims that the primary reason for Sodom's judgment was inhospitality are not supported by sound Bible exegesis.[48][49]

The Bible states regarding Sodom:

...the LORD rained on Sodom and Gomorrah brimstone and fire from the LORD out of heaven, and He overthrew those cities, and all the valley, and all the inhabitants of the cities, and what grew on the ground. Genesis 19:24-25

The following was reported in respect to Dr. Bryant Wood's archaeological work in relating to the biblical city of Sodom:

Dr. Bryant Wood, in describing these charnel houses, stated that a fire began on the roofs of these buildings. Eventually the burning roof collapsed into the interior and spread inside the building. This was the case in every house they excavated. Such a massive fiery destruction would match the biblical account that the city was destroyed by fire that rained down from heaven. Wood states, "The evidence would suggest that this site of Bab edh-Drha is the biblical city of Sodom."[50]

Dr. Wood provides some additional material in relation to the find being the biblical city of Sodom.[51][52]

For related information see: Homosexuality and promiscuity and Homosexuality Statistics

A 2004 article by Michael Foust states:

According to the researchers, 42.9 percent of homosexual men in Chicago's Shoreland area have had more than 60 sexual partners, while an additional 18.4 percent have had between 31 and 60 partners. All total, 61.3 percent of the area's homosexual men have had more than 30 partners, and 87.8 percent have had more than 15, the research found.

As a result, 55.1 percent of homosexual males in Shoreland -- known as Chicago's "gay center" -- have at least one sexually transmitted disease, researchers said.

The three-year study on the sexual habits of Chicago's citizens will appear in the upcoming book, "The Sexual Organization of The City" (University of Chicago Press), due out this spring.[53][54]

For more information please see: Homosexual Couples and Domestic Violence and Gay bashing

Studies report that homosexual couples have significantly higher incidences of violent behavior. For example, a recent study by the Canadian government states that "violence was twice as common among homosexual couples compared with heterosexual couples".[55] According the American College of Pediatricians who cite several studies, "Violence among homosexual partners is two to three times more common than among married heterosexual couples."[56] In addition, the American College of Pediatricians states the following: "Homosexual partnerships are significantly more prone to dissolution than heterosexual marriages with the average homosexual relationship lasting only two to three years."[57]

In June of 2004, the journal Nursing Clinics of North America reported the following regarding homosexuality and domestic violence:

Male-on-male same-sex domestic violence also has been reported in couples where one or both persons are HIV-positive. Intimate partner abuse and violence include humilation, threatening to disclose HIV status, withholding HIV therapy, and harming family members or pets.[58]

For more information please see: Homosexuality and Murders

Vernon J. Geberth, M.S., M.P.S. who is a former commander of Bronx homicide for the New York City Police Department stated in 1995 concerning homosexuality and murders that homosexual murders are relatively common and these murders may involve male victims murdered by other males or may involve female victims who are in some type of lesbian relationship and they are murdered by another female.[59] In 2005, Dr. Harnam Singh, Dr. Luv Sharma, and Dr. Dhattarwal reported in the Journal of Indian Academy of Forensic Medicine in respect to homosexuality and murders that homosexual murders are quite common and that these murders may involve both sexes either as victims or as assailants.[60]

There have been a number of forensic journal articles on the issue of homosexual homicides and overkill.[61][62][63][64][65] In 1996, the forensic journal The American Journal of Forensic Medicine and Pathology published an article entitled Homicide in homosexual victims: a study of 67 cases from the Broward County, Florida, Medical Examiner's office (1982-1992), with special emphasis on "overkill". The abstract for the journal article states:

According to the New York Times, Dr. William Eckert was a world-renowned authority in the field of pathology and he worked on major murder cases including the assassination of Senator Robert F. Kennedy and the Charles Manson murders.[67] Dr. Eckert founded the American Journal of Forensic Medicine and Pathology.[68][69] According to Time magazine, Dr. Eckert was a pioneer who encouraged collaborative effort between law-enforcement and forensics teams.[70]

Dr. Eckert wrote concerning homosexual murders:

The Encyclopedia of Serial Killers by Michael Newton reports:

The previously cited pathology textbook by Knight and Saukko stated the following: "In addition, quite a number of fatal altercations arise because a heterosexual man becomes violent when importuned by a homosexual."[74]

Women who engage in homosexuality are called lesbians (after the ancient Greek island of Lesbos). Recently, the former lesbian activist Charlene Cothran left homosexuality and converted her pro-homosexuality magazine to one that helps homosexuals find freedom and deliverance through faith in Jesus Christ.[75][76] Lesbian activist Yvette Cantu Schneider also became a Christian and left homosexuality.[77][78]

In 2007, WorldNetDaily published the following regarding a lesbian woman:

For more information please see: Homosexuality and health and Gay bathhouses

A review of the history of homosexuality and AIDS, indicates the original spread of AIDS is generally attributed to the aforementioned promiscuity of homosexual men. Originally the syndrome was called the "gay disease" because the overwhelming majority of patients were homosexual men.

In September of 2010, Reuters reported: "Nearly one in five gay and bisexual men in 21 major U.S. cities are infected with HIV, and nearly half of them do not know it".[80] A September 2010 report of the Centers for Disease Control and Prevention (CDC) reported: "Gay, bisexual, and other men who have sex with men (MSM) represent approximately 2% of the US population, yet are the population most severely affected by HIV and are the only risk group in which new HIV infections have been increasing steadily since the early 1990s. In 2006, MSM accounted for more than half (53%) of all new HIV infections in the United States..."[81]

In August of 2009, LifeSiteNews reported: "An official with the Centers for Disease Control and Prevention (CDC) announced the CDC's estimate Monday that in the United States AIDS is fifty times more prevalent among men who have sex with men ('MSM') than the rest of the population."[82] This is a dramatic recent increase. In June of 2004, the journal Nursing Clinics of North America reported that homosexual men and men who have sex with men "are nine times more likely to become infected with HIV than their heterosexual counterparts".[83] Of newly diagnosed HIV infections in the United States during the year 2003, the Centers for Disease Control and Prevention (CDC) estimated that about 63% were among men who were infected through sexual contact with other men.[84] As of 1998, fifty-four percent of all AIDS cases in the United States were homosexual men, and the CDC stated that nearly ninety percent of these men acquired HIV through sexual activity with other men.[85]

In 2004, Jeffrey D. Klausner, Robert Kohn, and Charlotte Kent reported in the journal Clinical Infectious Diseases the following: "Proctitis, or inflammation of the rectum, is a condition that is not uncommon among men who have sex with men (MSM), and, in HIV-negative men, greatly increases the risk of acquiring HIV infection. With the recent increases in bacterial sexually transmitted diseases (STDs) among MSM in the United States and Europe, there has been a concomitant increase in the number of cases of clinical proctitis."[86] On March 15, 2004 Medscape published an article by John G. Bartlett, M.D. entitled New Look at "Gay Bowel Syndrome" in which they commented on the aforementioned 2004 journal article Etiology of clinical proctitis among men who have sex with men published by JD Klausner and C. Kent in the journal Clinical Infectious Diseases. The article in Medscape stated the following:

Johns Hopkins HIV Guide website has a duplicate of the aforementioned article by John G. Bartlett, M.D. at Medscape which was entitled New Look at "Gay Bowel Syndrome".[88][89]

In 2004, the prominent medical website, WebMD, stated the following: "Men who have sex with men and women are a "significant bridge for HIV to women," the CDC's new data suggest."[90]

See: Teenage homosexuality and Teenage AIDS

In relation to homosexuality and MRSA, on January 15, 2008 the newspaper San Francisco Chronicle had a news article entitled San Francisco gay community an epicenter for new strain of virulent staph.[91] The San Francisco Chronicle news article stated the following in regards to homosexuality and MRSA:

On February 19, 2008 the Annals of Internal Medicine published a study regarding antiobiotic resistant staph infection in relation to men who have sex with men and the abstract for the article states the following in relation to homosexuality and MRSA:

Syphilis is an infection caused by the bacteria Treponema pallidum. An early publication to propose the link between homosexuality contributing to the spread of sexually transmitted disease was the English publication Proceedings of the Royal Society of Medicine in 1962.[94] The Proceedings of the Royal Society of Medicine made the following statement: "The importance of homosexual practices in the spread of venereal diseases has attracted particular attention recently. It almost seems that these practices are keeping syphilis alive in this country." [95]

The news organization Cybercast News Service reported the following about homosexuality and syphilis:

In a report on sexually transmitted diseases (STDs) issued Tuesday, the government said syphilis, a disease that was almost eliminated as a public health threat less than 10 years ago, is on the rise -- with cases increasing each year since 2000.[96]

In relation to homosexuality and gonorrhea, in 2006, the American Association of Family Physicians reported: "Men who have sex with men (MSM) have high rates of gonococcal infection. In San Francisco, more than one half of these infections occur in MSM, and previous cross-sectional studies have reported a prevalence of up to 15.3 percent in this group."[97]

In 2007, the medical journal Sexually Transmitted Diseases published an article entitled Sexually Transmitted Infections in Western Europe Among HIV-Positive Men Who Have Sex With Men which stated the following regarding homosexuality and gonorrhea:

In Denmark (19941999), gonorrhea incidence was 6 times higher among known HIV-positive MSM [men who have sex with men]... A study in a Parisian clinic showed that at least one-third (30/92) of MSM diagnosed with gonorrhea between January 1999 and May 2001 were HIV-positive... In Sweden, 5.4% (4/74) of gonorrhea cases were in HIV-positive MSM in 2000. By comparison, at sentinel sites in England and Wales, 32% (123/381) of MSM with gonorrhea were HIV-positive in 2004.[98]

Lymphogranuloma venereum is a sexually transmitted disease that mainly infects the lymphatics.[99] According to the recent medical literature, there have been recent outbreaks of lymphogranuloma venereum in Europe and North America and the outbreaks have been limited to the homosexual community.

In 2006, the The Medical Journal of Australia reported the following:

Amoebiasis has become endemic in MSM in Japan and causes significant morbidity and mortality; complications such as colitis and liver abscesses occur more frequently in homosexual and bisexual men than in heterosexual men. Similar findings on amoebiasis are reported from Taiwan, with MSM at increased risk for invasive amoebiasis and intestinal colonisation with E. histolytica.[101]

In 2001, The journal Internal Medicine (Tokyo, Japan) published an article entitled Amebiasis in acquired immunodeficiency syndrome in which they stated the following the following:

Sexually transmitted diseases that cause proctitis include syphilis, gonorrhea, lymphogranuloma venereum, and amebiasis and as noted earlier the homosexual community has significant problems in regards to these illnesses.[104] In addition, as mentioned earlier proctitis significant risk factor in respect to HIV infection.[105][106] According to the Mayo Clinic, "proctitis in general mainly affects adult males".[107]Proctitis, syphilis, gonorrhea, lymphogranuloma venereum, and amebiasis are all maladies that are associated with gay bowel syndrome which why John G. Bartlett, M.D. stated at the Johns Hopkins HIV Guide website and at Medscape that gay bowel syndrome is still currently an issue.[108][109]

For more information please see: Homosexuality and Hepatitis

In relation to homosexuality and hepatitis, according to the Centers for Disease Control and Prevention (CDC) both Hepatitis A and Hepatitis B disproportionately affects men who have sex with men (MSM).[110][111]

In a 2007 article entitled Advances in the Management of Viral Hepatitis B and Hepatitis C Infection in HIV-Coinfected Patients Vincent V. Soriano, MD, PhD reported in Medscape the following regarding homosexuality and Hepatitis C viral infections:

Viral hepatitis is one of the illnesses of gay bowel syndrome.

Go here to read the rest:
Homosexuality - Conservapedia

The genetics of cat coat coloration, pattern, length, and texture is a complex subject, and many different genes are involved.

Cat coat genetics can produce a variety of colors and coat patterns. These are physical properties and should not be confused with a breed of cat. Furthermore, cats may show the color and/or pattern particular to a certain breed without actually being of that breed. For example, cats may have point coloration, but not be Siamese.

A cat with Oo and white spotting genes is commonly called a calico. The reason for the patchwork effect in female cats heterozygous for the O gene (Oo) is X-inactivation one or the other X chromosome in every cell in the embryo is randomly inactivated (see Barr body), and the gene in the other X chromosome is expressed.

For a cat to be tortoiseshell, calico, or one of the variants such as blue-cream or chocolate tortoiseshell, the cat must simultaneously express two alleles, O and o, which are located on the X chromosome. Males normally cannot do this, as they have only one X chromosome, and therefore only one allele, and so calico cats are normally only female. Male tortoiseshell or calico cats occur only if they have chromosomal abnormalities such as the genotype XXY (in which case they are sterile), chromosomal mosaicism (only portions of their cells have the genotype XXY, so these cats may be fertile), or chimerism (a single individual formed from two fused embryos, at least one of which was male). Approximately 1 in 3,000 calico/tortoiseshell cats are male.[4] Chimericism (which may result in fertile male cats) appears to be the most common mechanism.

One can deduce that a grey male cat with a white bib and paws, but showing no tabby pattern:

Tabby cats (AA or Aa), normally have:

Most or all striping disappears in the chinchilla or shaded cat, but it is still possible to identify the cat as a tabby from these other features.

The genetics involved in producing the ideal tabby, tipped, shaded, or smoke cat is complex. Not only are there many interacting genes, but genes sometimes do not express themselves fully, or conflict with one another. For example, the melanin inhibitor gene sometimes does a poor job blocking pigment, resulting in an excessively gray undercoat, or in tarnishing (yellowish or rusty fur).

Likewise, poorly-expressed non-agouti or over-expression of melanin inhibitor will cause a pale, washed out black smoke. Various polygenes (sets of related genes), epigenetic factors, or modifier genes, as yet unidentified, are believed to result in different phenotypes of coloration, some deemed more desirable than others by fanciers.

Here are the genetic influences on tipped or shaded cats:

Cat fur length is governed by the Long hair gene in which the dominant form, L, codes for short hair, and the recessive l codes for long hair. In the longhaired cat, the transition from anagen (hair growth) to catagen (cessation of hair growth) is delayed due to this mutation. A rare recessive shorthair gene has been observed in some lines of Persian cat (silvers) where two longhaired parents have produced shorthaired offspring.

There have been many genes identified that result in unusual cat fur. These genes were discovered in random-bred cats and selected for. Some of the genes are in danger of going extinct because the cats are not sold beyond the region where the mutation originated or there is simply not enough demand for cats expressing the mutation.

In many breeds, coat gene mutations are unwelcome. An example is the rex allele which appeared in Maine Coons in the early 1990s. Rexes appeared in America, Germany and the UK, where one breeder caused consternation by calling them "Maine Waves". Two UK breeders did test mating which indicated that this was probably a new rex mutation and that it was recessive. The density of the hair was similar to normally coated Maine Coons, but consisted only of down type hairs with a normal down type helical curl, which varied as in normal down hairs. Whiskers were more curved, but not curly. Maine Coons do not have awn hairs, and after moulting, the rexes had a very thin coat.

There are various genes producing curly coated or "rex" cats. New types of rex pop up spontaneously in random-bred cats now and then. Here are some of the rex genes that breeders have selected for:

There are also genes for hairlessness:

Some rex cats are prone to temporary hairlessness, known as baldness, during moulting.

Here are a few other genes resulting in unusual fur:

More:
Cat coat genetics - Wikipedia, the free encyclopedia

About Cloning

What is Cloning?

Learn the basics about cloning and see how its done.

Why Clone?

Evaluate the reasons for using cloning technologies.

The History of Cloning

Explore the history of cloning technologies.

Cloning Myths

Here we help you separate the facts from the fiction.

Click and Clone

Try it yourself in the mouse cloning laboratory.

Is it Cloning? Or Not?

Test your cloning savvy with this interactive quiz.

APA format:

Genetic Science Learning Center. (2014, July 10) Cloning. Retrieved August 24, 2016, from http://learn.genetics.utah.edu/content/cloning/

CSE format:

Cloning [Internet]. Salt Lake City (UT): Genetic Science Learning Center; 2014 [cited 2016 Aug 24] Available from http://learn.genetics.utah.edu/content/cloning/

Chicago format:

Genetic Science Learning Center. "Cloning." Learn.Genetics.July 10, 2014. Accessed August 24, 2016. http://learn.genetics.utah.edu/content/cloning/.

The rest is here:
Cloning - Learn Genetics

Historians of homosexuality will judge much twentieth-century "science" harshly when they come to reflect on the prejudice, myth, and downright dishonesty that litter modern academic research on sexuality. Take, for example, the lugubrious statements of-once respected investigators. Here is Sandor Feldman, a well-known psychotherapist, in 1956:

Or consider the remarks of the respected criminologist Herbert Hendin:

The notion of the homosexual as a deeply disturbed deviant in need of treatment was the orthodoxy until only recently. Bernard Oliver, Jr., a psychiatrist specializing in sexual medicine, wrote in 1967 that Dr. Edmond Bergler feels that the homosexual's real enemy is not so much his perversion but [sic] ignorance of the possibility that he can be helped, plus his psychic masochism which leads him to shun treatment....

There is good reason to believe now, more than ever before, that many homosexuals can be successfully treated by psychotherapy, and we should encourage homosexuals to seek this help.[3]

Such views about the origin of homosexual preferences have become part of American political culture as well. When, in 1992, Vice-President Dan Quayle offered the view that homosexuality "is more of a choice than a biological situation.... It is a wrong choice,"[4] he merely reasserted the belief that homosexuality reflected psychological conditioning with little biological basis, and certainly without being influenced by a person's biological inheritance.

And now we have the much publicized spectacle--Time magazine has taken up the story in a dramatic feature entitled "Search for a Gay Gene"[5] --of homosexuality's origins being revealed in the lowly fruit fly, Drosophila.[6] Males and females of this, one has to admit, rather distant relation adopt courtship behavior that has led two researchers at the US National Institutes of Health to draw extravagant parallels with human beings.

Shang-Ding Zhang and Ward F. Odenwald found that what they took to be homosexual behavior among male fruit flies--touching male partners with forelegs, licking their genitalia, and curling their bodies to allow genital contact--could be induced by techniques that abnormally activated a gene called w (for "white," so called because of its effect on eye color). Widespread activation (or "expression") of the white gene in Drosophila produced male-to-male rituals that took place in chains or circles of five or more flies. If female fruit flies lurked nearby, male flies would only rarely be tempted away from their male companions. These findings, which have apparently been reproduced by others, have led the investigators to conclude that "w misexpression has a profound effect on male sexual behavior."

Zhang and Odenwald go on to speculate that the expression of w could lead to severe shortages of serotonin, an important chemical signal that enables nerve cells to communicate with one another. The authors conjecture that mass activation of w diminishes brain serotonin by promoting its use elsewhere in the body. Indeed, cats, rabbits, and rats all show some elements of "gay" behavior when their brain serotonin concentrations fall. Intriguing and, you might think, convincing evidence.

Yet, although w is found in modified form in human beings, it is a huge (and, it seems to me, a dangerous) leap to extrapolate observations from fruit flies to humans. In truth, when the recent data are interpreted literally we find that (a) the w gene induces male group sex behavior in highly ritualized linear or circular configurations, and (b) while these tend more toward homosexual than straight preferences, they are truly bisexual (as pointed out by Larry Thompson in Time). Zhang and Odenwald force their experimental results with fruit flies to fit their preconceived notions of homosexuality. How simplistic it seems to equate genital licking in Drosophila with complex individual and social homosexual behavior patterns in humans. Can notions of homosexuality apply uniformly across the biological gulf that divides human beings and insects? Such arguments by analogy seem hopelessly inadequate.

By contrast, the work of Simon LeVay, Dean Hamer, and a small group of researchers concerned to distinguish biological and genetic influences on sexual behavior has discredited much of the loose rhetoric that has been used about homosexuality. In August 1991, LeVay, a neuroscientist who now directs the Institute of Gay and Lesbian Education in southern California, published in the magazine Science findings from autopsies of men and women of known sexual preference. He found that a tiny region in the center of the brain--the interstitial nucleus of the anterior hypothalamus (INAH) 3--was, on average, substantially smaller in nineteen gay men who died from AIDS than among sixteen heterosexual men.[7]

The observation that the male brain could take two different forms, depending on one's sexual preference, was a stunning discovery. The hypothalamus-a small, intricate mass of cells lying at the base of the brain-was long believed to have a role in sexual behavior, but direct evidence that it did so was weak. Yet LeVay expressed caution. Although his data showed that human sexual preference "is amenable to study at the biological level," he noted that it was impossible to be certain whether the anatomical differences between the brains of gay and straight men were a cause or a consequence of their preference.[8]

In the thirteen persuasive essays that make up The Sexual Brain, LeVay takes account of the current bio-behavioral controversy over the science of sex. From the union of wiry sperm and bloated ovum to the child-rearing practices of mammals and humans, for which mothers are largely responsible, he writes (metaphorically), the "male is little more than a parasite who takes advantage of [the female's] dedication to reproduction." He goes on to draw from a wide range of sources to support his contentious assertion that "there are separate centers within the hypothalamus for the generation of male-typical and female-typical sexual behavior and feelings." He argues that a connection--the details of which remain mysterious--between brain and behavior exists through hormones such as testosterone.

The most convincing evidence he puts forward to support his view comes from women with congenital adrenal hyperplasia. This condition, in which masculine characteristics, such as androgenized genitalia, including clitoral enlargement and partially fused labia, become pronounced in women, is caused by excessive testosterone production and leads, in adulthood, to an increased frequency of lesbianism affecting up to half of all the women who have the condition. The theory, still unproven, that is proposed to explain these behavioral effects of hormones is that one or more chemical signals act during a brief early critical period in the development of most males to alter permanently both the brain and the pattern of their later adult behavior. Unless this hormonal influence is switched on, a female pattern of development will follow automatically.

What might be the origin of biological differences underlying male sexual preference? In 1993 Dean Hamer and his colleagues at the National Cancer Institute discovered a preliminary but nevertheless tantalizing clue.[9] Hamer began his painstaking search for a genetic contribution to sexual behavior by studying the rates of homosexuality among male relatives of seventy-six known gay men. He found that the incidence of homosexual preference in these family members was strikingly higher (13.5 percent) than the rate of homosexuality among the whole sample (2 percent). When he looked at the patterns of sexual orientation among these families, he discovered more gay relatives on the maternal side. Homosexuality seemed, at least, to be passed from generation to generation through women.

Maternal inheritance could be explained if there was a gene influencing sexual orientation on the X chromosome, one of the two human sex chromosomes that bear genes determining the sex of offspring.[10] Men have both X and Y chromosomes, while women have two X chromosomes. A male sex-determining gene, called SRY, is found on the Y chromosome. Indeed, the Y chromosome is the most obvious site for defining male sexuality since it is the only one of the forty-six human chromosomes to be found in men alone. The SRY gene is the most likely candidate both to turn on a gene that prevents female development and to trigger testosterone production. Since the female has no Y chromosome, she lacks this masculinizing gene. In forty pairs of homosexual brothers, Hamer and his team looked for associations between the DNA on the X chromosome and the homosexual trait. They found that thirty-three pairs of brothers shared the same five X chromosomal DNA "markers," or genetic signatures, at a region near the end of the long arm of the X chromosome designated Xq28.[11] The possibility that this observation could have occurred by chance was only 1 in 10,000.

LeVay takes a broad philosophical perspective in his discussion of human sexuality by placing his research in the context of animal evolution. Hamer, on the other hand, has written, with the assistance of the journalist Peter Copeland, a more focused popular account of his research. He conceived his project after reflecting on a decade of laborious research on yeast genes. Although the project was approved by the National Institutes of Health after navigating a labyrinthine course through government agencies, it remained rather meagerly funded.

Taken together, the scientific papers of both LeVay and Hamer and the books that their first reports have now spawned[12] make a forceful but by no means definitive case for the view that biological and genetic influences have an important--perhaps even decisive--part in determining sexual preference among males. LeVay writes, for example, that "...the scientific evidence presently available points to a strong influence of nature, and only a modest influence of nurture." But there is no broad scientific agreement on these findings. They have become mired in a quasi-scientific debate that threatens to let obscurantism triumph over inquiry. What happened?

To begin with, we must ask what LeVay and Hamer have not shown. LeVay has found no proof of any direct link between the size of INAH 3 and sexual behavior. Size differences alone prove nothing. He was also unable to exclude the possibility that AIDS has an influence on brain structure, although this seemed unlikely, since six of the heterosexual men he studied also had AIDS. Moreover, Hamer did not find a gene for homosexuality; what he discovered was data suggesting some influence of one or more genes on one particular type of sexual preference in one group of people. Seven pairs of brothers did not have the Xq28 genetic marker, yet these brothers were all gay. Xq28 is clearly not a sine qua non for homosexuality; it is neither a necessary nor a sufficient cause by itself.

And what about women? Although the genitalia of women as well as men are clearly biologically determined, no data exist to prove a genetic link, or a link based on brain structure, with female sexual preferences, whether heterosexual or homosexual. Finally, neither study has been replicated by other researchers, the necessary standard of scientific proof. Indeed, there is every reason to suppose that the INAH 3 data will be extremely difficult to confirm. Only a few years ago INAH 1 (located close to INAH 3) was also thought to be larger in men than in women. Two groups, including LeVay's, have failed to reproduce this result.

Most of these limitations are clearly acknowledged by both LeVay and Hamer in their original scientific papers and are reinforced at length in their books. But reactions to their findings have nevertheless been harshly critical. For instance, after pointing out several potential weaknesses in Hamer's study and criticizing his decision to publish in Science at a time when gay "lives are at stake," two biologists, Anne Fausto-Sterling and Evan Balaban, asked "whether it might not have been prudent for the authors and the editors of Science to have waited until more of the holes in the study had been plugged...."[13] Fortunately, their somewhat hysterical reaction has been followed by more careful comment by other scientists.[14]

Lack of prudence also characterized the response in the press. In London, the conservative Daily Telegraph ran the clumsy headline, "Claim that homosexuality is inherited prompts fears that science could be used to eradicate it." Another story began, "A lot of mothers are going to feel guilty," while another was entitled "Genetic tyranny."

These headlines are part of the popular rhetoric about DNA, which supposes that a gene represents an irreducible and immutable unit of the human self. The correlation between a potentially active gene and a behavior pattern is assumed to indicate cause and effect. Was Hamer himself guilty of over-interpretation? In his original paper, he went to extraordinary lengths to qualify his findings. He and his co-authors offer no fewer than ten statements advising a cautious reading of their data, and they note that "replication and confirmation of our results are essential." Neither the hyperbolic press response with its relentless message of genetic determinism nor the ill-judged scientific criticism was appropriate.

Nevertheless, there are three conceptual issues raised by these reports --namely, heritability, sexual categorization, and the meaning of the phrase "biological basis of behavior" --which have been largely ignored in the scramble to publish instant analyses of the findings of LeVay and Hamer, among others.

Heritability is a measure of the resemblance between relatives; it is expressed as the proportion of variability in an observable characteristic that can be attributed to genetic factors. Eye color, for example, is 100 percent heritable, whereas we know that most behavioral traits have genetic contributions of well below 50 percent. Heritability is a quarrelsome issue among geneticists, and its proportional value is often quoted without the necessary qualifications. Variation in any trait is accounted for by the influence of genes (including, importantly, the interaction among genes), environment (the family and one's wider life experience), and the interaction between one or more genes and one or more environmental variables. The standard measure of heritability is the sum of all genetic influences, and it ignores potentially complex interactions--for example, the influence of the family milieu on the behavioral expression of a gene influencing sexual preference. The most common error made by those who discuss genetic contributions to behavior is to forget that heritability is a property only of the population under study at one particular time. It cannot be generalized to characterize the behavior itself.

When we apply these considerations to Hamer's data, we make a surprising discovery. If we accept his own hypothesis of the relation between the Xq28 marker and the behavioral trait, the maximum heritability of homosexuality in the group he studied is 67 percent, which may seem a remarkably high figure. Yet this group was a particularly selected one: the seventy-six study participants openly acknowledged being gay, and had volunteered for the study. What Hamer's results do not tell us is what the influence of the Xq28 marker in the general population might be. He infers from various mathematical calculations "that Xq28 plays some role in about 5 to 30 percent of gay men." But he admits that this is merely a preliminary estimate and that accurate measuring of Xq28 heritability in the general population remains to be done. In fact, a frequent criticism of Hamer's Science paper was that he did not measure the incidence of Xq28 markers among heterosexual brothers of gay sibling pairs. Without this information, it is impossible to guess the influence of any genes that might be located at Xq28. Their effects will be unpredictable at best, and any interaction with the environment will assume critical importance.

At this point, science inches uneasily toward dogma and diatribe. Hamer cites Richard Lewontin's Not in Our Genes[15] as one of his early inspirations to change the direction of his research. Hamer writes that he

knew that [Lewontin] had criticized the idea that behavior is genetic, arguing instead that it is a product of class-based social structures....Why was Lewontin, a formidable geneticist, so determined not to believe that behavior could be inherited? He couldn't disprove the genetics of behavior in a lab, so he wrote a political polemic against it.

Indeed, Lewontin has frequently provided cogent arguments against the view that heritability can help delineate the effects of genes on human behavior.[16] He has described the separation of behavioral variation into genetic and environmental contributions and the interaction between the two as "illusory."[17] For him and his co-writers, such a model "cannot produce information about causes of phenotypic difference," i.e., differences in observable physical and mental traits. The precise meaning of heritability forces the inevitable conclusion, Lewontin has written, that whatever proportion is quoted, it "is nearly equivalent to no information at all for any serious problem in human genetics."

Imagine Dean Hamer's astonishment, therefore, when he received a letter from Richard Lewontin in 1992. A Harvard professor teaching genetics and behavior had invited Hamer to submit a pamphlet describing his research as an example of "conceptual advances" in "modern behavior genetic studies." He had willingly complied, but only later discovered that it had been ruled "scientifically unacceptable" by Ruth Hubbard, an emeritus professor at the Harvard Biological Laboratories deeply skeptical about determinism. In his letter, Hamer writes, Lewontin

went on to theorize that human behaviors must be "very, very far from the genes" because "there are some at least that we know for sure are not influenced by genes as, for example, the particular language one speaks." That made about as much sense as saying that since some people eat tacos and some eat hamburgers, there is no biological drive to eat.

Hamer, tongue firmly in cheek, offered to give Lewontin's students a lecture on how good research into behavior genetics is done. Lewontin accepted. On the day of his scheduled talk, Hamer faced not only Lewontin but also Ruth Hubbard and Evan Balaban (a co-author of the hostile letter later published in Science). Hamer described his methods carefully and stressed that his research could identify only potential genetic influences and not isolate specific genetic causes of behavior. At the end of the lecture, Lewontin indicated that he had no dispute with Hamer after all, and left the classroom without further comment. One wonders from this if Lewontin has modified his views on studying genetic contributions to human behavior.

Although it is true that heritability is only a crude measure of genetic influence, it remains a valuable research tool if, as one scientist has said, the researchers realize that

genetic influence on behavior appears to involve multiple genes rather than one or two major genes, and nongenetic sources of variance are at least as important as genetic factors....This should not be interpreted to mean that genes do not affect human behavior; it only demonstrates that genetic influence on behavior is not due to major-gene effects.[18]

More importantly, one can move beyond the "lump sum" theory of genetic influences to study the way in which genes affect behavior over time, or to discover how a gene influences different but possibly related behaviors, for instance both sexual preference and aggression.

Lewontin also cited the "terrible mischief" that could result from a research program based on heritability as his reason to suggest stopping "the endless search for better methods of estimating useless quantities."" Hamer agrees that precise genetic determinacy is an impossible goal; his 1993 article for Science on DNA markers also ended with an unusual admonition:

We believe that it would be fundamentally unethical to use [this] information to try to assess or alter a person's current or future sexual orientation, either heterosexual or homosexual, or other normal attributes of human behavior. Rather, scientists, educators, policy-makers, and the public should work together to ensure that such research is used to benefit all members of society.

If scientists who have opposed research on heritability would accept that it can have, when it is carried out in this spirit, an important place in the study of behavior, that would add much-needed weight to calls to expand, and improve, research on human sexuality.

Although Hamer and LeVay have both expressed cautious confidence in their results, they are evidently uneasy about their own categorizations of men as either gay or straight. Hamer writes that,

In truth, I don't think that there is such a thing as "the" rate of homosexuality in the population at large. It all depends on the definition, how it's measured, and who is measured.

Classifying sexuality into homosexual and heterosexual categories may have benefits of simplicity for researchers, but how closely does this division fit the real world? Poorly is the answer. Sexual behavior and styles of life among men and women vary from day to day and year to year, and a conclusion about whether or not sexual experience is characterized as homosexual frequently depends on the definition one uses.[20] The slippery nature of our crude categories should alert us to beware of conclusions about groups labeled as "homosexual" or "heterosexual."

Moreover, the concept of sexuality itself cannot easily be analyzed. It exists at several levels--chromosomal, genital, brain, preference, gender self-image, gender role, and a range of subtle influences on behavior (hair color, eye color, and many more). Each of these can be grouped together with the others to produce a single measurable component on a scale, devised by Alfred Kinsey in the 1940s, that allegedly shows a person's degree of homosexual preference. Hamer used this scale somewhat uncritically to categorize his volunteers. Stephen Levine, a medical expert on sexual behavior, has noted that the conflated and crude Kinsey scale "does not do justice to the diversity among homosexual women and men."[21]

One of Hamer's severest critics, Anne Fausto-Sterling, a developmental geneticist at Brown University, has tried to extend sexual categories beyond the binary divisions of male and female[(22] She suggests adding three more groups based on "intersex" humans: herms (true hermaphrodites who possess one testis and one ovary), merms (individuals who have testes, no ovaries, but some female genitalia), and ferms (who have ovaries, no testes, but some male characteristics). This attempt to create multiple categories is, however, futile. It tries to systematize the un-systematizable by proposing a neatly divided-up continuum of sexuality, while, in fact, very different and mutually exclusive factors may be at work in particular cases. It is an impossible and intellectually misguided task.

Two major studies examining the historical origins of modern sexual categories show how social groupings that evolve over time can mislead one into supposing that inherent biological classes exist in some unchangeable sense. Michel Foucault chronicled the history of sexual norms by concentrating on the fluid notion of "homosexuality."[23] He denounced what he called "Freud's conformism" in taking heterosexuality to be the normal standard in psychoanalysis. He concluded:

We must not forget that the psychological, psychiatric, medical category of homosexuality was constituted from the moment it was characterized--Westphal's famous article of 1870 on "contrary sexual sensations" can stand as its date of birth[24]--less by a type of sexual relations than by a certain quality of sexual sensibility.... The sodomite had been a temporary aberration; the homosexual was now a species.

This analysis, it seems to me, points to a critical error in the research of both Hamer and LeVay. Both, in spite of their qualifications, adopt the idea of the homosexual as a physical "species" different from the heterosexual. But there are no convincing historical grounds for this view. As Foucault points out, at the time of Plato,

People did not have the notion of two distinct appetites allotted to different individuals or at odds with each other in the same soul; rather, they saw two ways of enjoying one's pleasure...

The cultural historian Jonathan Katz has recently attacked the naive partitioning of sexual orientation by tracing the dominance of the norm--heterosexuality --throughout history.[25] He provides a convincing argument that the "just-is hypothesis" of heterosexuality--i.e., that the word corresponds to a true behavioral norm--is an "invented tradition." He shows that the categories of gay and straight are gradually dissolving as notions of the family become more various. Basing his view more on intuition than on sociological evidence, he predicts "the declining significance of sexual orientation."

The final issue that has confused the interpretation of research into sexuality is the meaning of "biological influence." Unfortunately, both LeVay and Hamer, in their effort to popularize their findings, ignore the subtlety of this question. As has been noted, LeVay is unambiguous about his own position on biological determinism,

The most promising area for exploration is the identification of genes that influence sexual behavior and the study of when, where, and how these genes exert their effects.

Both researchers ignore the central issue in the debate over nature and nurture. The question is: How do genes get you from a biochemical program that instructs cells to make proteins to an unpredictable interplay of behavioral impulses--fantasy, courtship, arousal, sexual selection--that constitutes "sexuality"? The question remains unresolved. The classic fall-back position is to claim that genes merely provide a basis, at most a predisposition, to a particular behavior. But such statements lack a precise or testable meaning.

Perhaps we are asking the wrong question when we set out to find whether there is a gene for sexual orientation. We know that genes are responsible for the development of our lungs, larynx, mouth, and the speech areas of our brain. And we understand that this complexity cannot be collapsed into the notion of a gene for "talking." Similarly, what possible basis can there be for concluding that there is a single gene for sexuality, even though we accept that there are genes that direct the development of our penises, vaginas, and brains? This analogy is not to deny the importance of genes, but merely to recast their role in a different conceptual setting, one devoid of dualist prejudice.

The search for a single dominant gene--the "O-GOD" (one gene, one disorder) hypothesis--that would influence a behavioral variant is likely to be fruitless. Many different genes, together with many different environmental factors, will interact in unpredictable ways to guide behavioral preferences. Each component will contribute small quanta of influence. One result of such a quantum theory of behavior is that it makes irrelevant the overstretched speculations of both Hamer and LeVay about why a gene for homosexuality still exists when it apparently has little apparent survival value in evolutionary terms. The quest for a teleological explanation to identify a reason for the existence of a "gay gene" becomes pointless when one understands that there is not now, and never was, a single and final reason for being gay or straight, or having any other identity along the continuum of sexual preference.

Does this complexity, together with an adverse and polarized social milieu, preclude successful research efforts concerning human sexuality? In 1974, Lewontin wrote that reconstruction of man's genetic past is "an activity of leisure rather than of necessity."[26] Perhaps so. But, as Robert Plomin argues, the value of studying inheritance in behavior lies in its importance

per se rather than in its usefulness for revealing how genes work. Some of society's most pressing problems, such as drug abuse, mental illness, and mental retardation, are behavioral problems. Behavior is also a key in health as well as illness, in abilities as well as disabilities, and in the personal pluses of life, such as sense of well-being and the ability to love and work.[27]

What research into human sexuality, then, lies ahead? Dean Hamer has repeated his initial work among male homosexuals in an entirely new group of families and has included a much-needed analysis of women. He has also compared the frequency of the Xq28 marker among pairs of gay siblings and their heterosexual brothers, important control data that he did not acquire the first time around. This work has been submitted to the journal Nature Genetics. Two other teams--one recently formed at the National Institutes of Health and a Canadian group that has reached some preliminary results--are attempting to replicate Hamer's initial findings. All Hamer will say about his latest data is that they have not discouraged him from continuing with his project.

To track down and sequence the DNA from one or more relevant genes at Xq28, from a total of about two hundred candidates, seems an almost insuperable task. To read the molecular script of DNA involves deciphering millions of constituent elements. Moreover, each gene will have to be studied individually and many more pairs of gay brothers will be needed to achieve this goal. The work will be extremely difficult for a single laboratory to undertake on its own. Hamer's request for a federally funded center for research into sexuality--a National Institute of Sexual Health--is therefore timely, for the study of differences between the sexes has reached a critical, though admittedly fragmented, stage and a coordinated research program would be valuable.

The concerns of such an institute should be broad. For example, it might have included the recent work reported from Yale which overturns the conventional view that language function is identical for both men and women.[28] By studying which brain areas were activated during various linguistic tasks, the Yale scientists found that women used regions in both their right and left brain cortices in certain instances, while men used only the left side of their brains. If functional brain differences for sophisticated behaviors exist between the sexes, the task for the future would be to link function to structure and to describe how both evolve from a background of genetic and environmental influence.

Inevitably, the idea of biological determinism carries with it the threat of manipulating the genes or the brain in order to adapt to the prevailing norm. As I have noted, Hamer was acutely aware of this possibility when he wrote his paper. But the prospects for pinpointing genetic risk have moved rapidly and worryingly forward with the recent availability of genetic screening techniques for, among other diseases, several cancers, including a small proportion of cancers of the breast, colon, and thyroid. Most such techniques are used without any current prospect for gene therapy or for any other effective treatment of the conditions identified. Geneticists such as Francis Collins, director of the Human Genome Project, have opposed unrestricted and unregulated screening techniques, describing their recent uses as "alarming"[29] because we are "treading into a territory which the genetics community has felt rather strongly is still [in the stage of] research." Hamer's fine words opposing genetic manipulation are likely to mean little in the marketplace if his work eventually leads to the isolation of a gene that has an effect on sexual preference, even if it has only a small effect that is present in only a limited number of people. US state legislatures are slowly responding to these issues. Colorado recently became the eleventh state to enact a law preventing information derived from genetic testing to be used in a discriminatory fashion.

In recognition of the emerging risks from dubious applications of preliminary discoveries, NIH launched a Task Force on Genetic Testing in April. The twenty-member committee includes representatives from industry, managed-care organizations, and patient-advocacy groups, and is chaired by Neil A. Holtzman, a professor of pediatrics and health policy at Johns Hopkins University. Far from being a friend to the hyperbolists, Holtzman has written that "physicians should be at the forefront of decrying florid genetic determinism and its dire implications for health and welfare reform."[30] His committee is charged with performing a two-year study of genetic technologies, which will look specifically at the accuracy, safety, reliability, and social implications of new testing procedures. This move is not without self-interest on the part of the geneticists at the NIH. Members of the US Congressional House Appropriations Committee, which closely monitors NIH spending, have said that they may freeze the Human Genome Project's $153 million grant if ethics issues are not given close attention.

But sex-based research has already run into political trouble. The Council for Citizens Against Government Waste has charged that some NIMH research is a misuse of taxpayer's money. Tom Schatz, CCAGW's president, has criticized twenty such studies, including one involving research into sex offenders. Rex Cowdry, acting director of the National Institute of Mental Health, argues that "for these grants, I think first you have to believe that the factors that motivate and control sexual behavior are worth knowing about...you have to believe that knowing more about how men and women are both similar and different is important."[31]

With such partisan pressures dominating the future of the research agenda, the circulation of uninformed opinions couched in scholarly prose is a cause for anxiety. In an otherwise superb and iconoclastic critique of the history of heterosexuality, Jonathan Katz ends with a sweeping and badly informed declaration:

Biological determinism is misconceived intellectually, as well as politically loathsome...Contrary to today's bio-belief, the heterosexual/homosexual binary is not in nature, but is socially constructed, therefore deconstructable.

LeVay and Hamer on the one hand, and Katz, on the other, evidently have taken completely antithetical positions. But Katz's extreme intellectual reductionism makes him as guilty as the more simplistic biologists and journalists who inflate claims about every new genetic discovery. After convincingly undermining the distinction between gay and straight, he then accepts the naive dualism of nature vs. nurture. It is such attempts as Katz's to put into opposition forces that are not in opposition which argue so strongly for planned research free from the ideological temptations that he succumbs to. Biological research into sexuality will indeed be misconceived if we assume that we already understand the differences between the sexes. In part the results of that research often contradict any such assumption. Katz demands that "we need to look less to oracles [presumably biological], and trust more in our desires, visions, and political organizing." But to take this path risks perpetuating a debate based on ignorance rather than one based on evidence.

It is true that the research of Hamer and LeVay presents technical and conceptual difficulties and that their preliminary findings obviously need replication or refutation. Yet their work represents a genuine epistemological break away from the past's rigid and withered conceptions of sexual preference. The pursuit of understanding about the origins of human sexuality --the quest to find an answer to the question, What does it mean to be gay and/or straight?--offers the possibility of eliminating what can be the most oppressive of cultural forces, the prejudiced social norm.

1 See Perversions: Psychodynamics and Therapy, edited by Sandor Lorand and Michael Balint (Ortolan Press, 1965; first edition, Random House, 1956), p. 75.

2 Quoted in Kenneth Lewes, The Psychoanalytic Theory of Male Homosexuality (Simon and Schuster, 1988), p. 188.

3 See Bernard J. Oliver, Jr., Sexual Deviation in American Society (College and University Press, 1967), p. 146.

4 See Karen de Witt, "Quayle Contends Homosexuality Is a Matter of Choice, Not Biology," The New York Times, September 14, 1992, p. A17.

5 See Larry Thompson, "Search for a Gay Gene," Time (June 12, 1995), pp. 60-61.

6 See Shang-Ding Zhang and Ward F. Odenwald, "Misexpression of the White (w) Gene Triggers Male-male Courtship in Drosophila," Proceedings of the National Academy of Sciences, USA, Vol. 92 (June 6, 1995), pp. 5525-5529.

7 See Simon LeVay, "A Difference in Hypothalamic Structure Between Heterosexual and Homosexual Men," Science (August 30, 1991), pp. 1034-1037.

8 The suprachiasmatic nucleus, also located in the hypothalamus, is larger in homosexual men than in either heterosexual men or women. The anterior commissure of the corpus callosum (a band of tissue that connects the right and left hemispheres of the brain) is also larger in gay men.

9 See Dean H. Hamer et al., "A Linkage Between DNA Markers on the X Chromosome and Male Sexual Orientation," Science (July 16, 1993), pp. 321-327.

10. The normal complement of human chromosomes is forty-six per individual, two of which are designated sex chromosomes. In the male, the sex chromosomal makeup is XY, while in the female it is XX. If a gene for homosexuality (Xh) was transmitted through the maternal line, one can see how the subsequent offspring would be affected.

(Chart omitted)

Suppose the unaffected female carrier for homosexuality (XXh) produced offspring with a non-Xh male (XY). Half of all female children would be carriers of Xh (like their mothers), while half of all male offspring would carry Xh unopposed by another X. The Xh trait -- homosexuality -- would then be able to express itself.

11 By chance, one would expect each pair of brothers to share half their DNA. So, assuming that there was no gene for homosexuality, one would expect twenty of the forty pairs of brothers to share the X chromosome marker.

12 LeVay has recently completed a second book in collaboration with Elisabeth Nonas--City of Friends--that surveys gay and lesbian culture; it will be published by MIT Press in November. He is currently working on Queer Science, a study of how scientific research has affected the lives of gays and lesbians.

13 See Anne Fausto-Sterling and Evan Balaban, "Genetics and Male Sexual Orientation," Science (September 3, 1993), p. 1257.

14 For example, see David Weatherall, Science and the Quiet Art (Norton, 1995) who notes that "these findings should not surprise us. Almost every condition...reveals a complex mixture of nature and nurture," p. 287.

15 See R.C. Lewontin, S. Rose, and L. J. Kamin, Not in Our Genes (Pantheon, 1984).

16 Lewontin is not a total skeptic about the importance of molecular genetics research in medicine. For instance, he accepts "that some fraction of cancers arise on a background of genetic predisposition." See R.C. Lewontin, "The Dream of the Human Genome," The New York Review (May 28, 1992), pp. 31-40.

17 See M. W. Feldman and R. C. Lewontin, "The Heritability Hang-up," Science (December 19, 1975), pp. 1163-1168.

18 See Robert Plomin, "The Role of Inheritance in Behavior," Science (April 13, 1990), pp. 183-188.

19 See R.C. Lewontin, "The Analysis of Variance and the Analysis of Causes," The American Journal of Human Genetics, Vol. 26 (1974), pp. 400-411.

20 For example, in a UK study (see Anne M. Johnson, "Sexual lifestyles and HIV risks," Nature [December 3, 1992], pp. 410-412), although only 1.4 percent of men reported a male partner during the past five years, 6.1 percent of men reported having experienced some same-gender behavior.

21 See Stephen B Levine, Sexual Life: A Clinician's Guide (Plenum, 1992). The Kinsey scale has seven levels ranging from exclusively heterosexual (0) to exclusively gay (6). Hamer applied this scale to four aspects of sexuality: self-identification, attraction, fantasy, and behavior.

22 See Anne Fausto-Sterling, "The Five Sexes: Why Male and Female Are Not Enough," The Sciences (March/April, 1993), pp. 20-24.

23 See Michel Foucault, The History of Sexuality, Vols. One and Two (Vintage, 1990).

24 Dr. K.F.O. Westphal became the first modern author to publish an account of what he described as a "contrary sexual feeling" (Die contrare Sexualempfindung), although the word homosexual was first used in a private letter written by Karl Maria Kertbeny on May 6, 1868. This linguistic history is described in detail by Jonathan Katz (see note 25).

25 See Jonathan Ned Katz, The Invention of Heterosexuality (Dutton, 1995).

26 R.C. Lewontin, "The Analysis of Variance and the Analysis of Causes," The American Journal of Human Genetics, Vol. 26 (1974), pp. 400-411.

27. Robert Plomin, "The Role of Inheritance in Behavior," Science (April 13, 1990), pp. 183-188.

28. See Bennett A. Shaywitz et al., "Sex differences in the functional organization of the brain for language," Nature (February 16, 1995), pp. 607-609.

29 See Gina Kolata, "Tests to Assess Risks for Cancer Raising Questions," The New York Times (March 27, 1995), p. A1.

30 See Neil A. Holtzman, "Genetics," Journal of the American Medical Association (April 26, 1995), pp. 1304-1306.

31 See "NIMH's Cowdry Defends Institute's Research Against Appropriations Committee, Watchdog Group Criticism," The Blue Sheet (March 29, 1995), pp. 5-6.

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A gay Gene - Is Homosexuality Inherited Assault On Gay ...

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Name:_____________________________________

**In fruit flies, eye color is a sex linked trait. Red is dominant to white.**

1. What are the sexes and eye colors of flies with the following genotypes?

X R X r _________ X R Y __________ X r X r __________

X R X R ____________ X r Y ____________

2. What are the genotypes of these flies:

white eyed, male ____________ red eyed female (heterozygous) ________

white eyed, female ___________ red eyed, male ___________

3. Show the cross of a white eyed female X r X r with a red-eyed male X R Y .

4. Show a cross between a pure red eyed female and a white eyed male. What are the genotypes of the parents:

___________ and _______________

How many are:

white eyed, male ____ white eyed, female ____ red eyed, male ____ red eyed, female ____

5. Show the cross of a red eyed female (heterozygous) and a red eyed male.

What are the genotypes of the parents?

___________ & ________________

How many are:

white eyed, male ____ white eyed, female ____ red eyed, male ____ red eyed, female ____

Math: What if in the above cross, 100 males were produced and 200 females. How many total red-eyed flies would there be? ________

6. In humans, hemophilia is a sex linked trait. Females can be normal, carriers, or have the disease. Males will either have the disease or not (but they wont ever be carriers)

X h Y= male, hemophiliac

Show the cross of a man who has hemophilia with a woman who is a carrier.

What is the probability that their children will have the disease? __________

7. A woman who is a carrier marries a normal man. Show the cross. What is the probability that their children will have hemophilia? What sex will a child in the family with hemophilia be?

8. A woman who has hemophilia marries a normal man. How many of their children will have hemophilia, and what is their sex?

9. In cats, the gene for calico (multicolored) cats is codominant. Females that receive a B and an R gene have black and oRange splotches on white coats. Males can only be black or orange, but never calico.

Heres what a calico females genotype would look like: X B X R

Show the cross of a female calico cat with a black male?

What percentage of the kittens will be black and male? _________ What percentage of the kittens will be calico and male? _________ What percentage of the kittens will be calico and female? _________

10. Show the cross of a female black cat, with a male orange cat.

What percentage of the kittens will be calico and female? _____What color will all the male cats be? ______

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Genetics - X Linked Problems - The Biology Corner

What Are Chromosomes?

Our bodies are made up of about 60 trillion cells. Each one of those cells manufactures proteins. The kinds of proteins any given cell makes determine its particular characteristics, which in turn create the characteristics of the entire body.

The instructions for making these proteins are stored in chemicals or molecules called DNA, which is organized into chromosomes. Chromosomes are found in the center, or nucleus, of all of our cells, including the eggs and sperm.

Female Chromosomes

Male Chromosomes

Chromosomes are passed down from generation to generation through the egg and sperm. Typically, we all have 46 chromosomes in our cells, two of which are sex chromosomes. In females, these are two Xs; in males they are an X and a Y.

Genes are sections of DNA that are passed from generation to generation and perform one function. If we think of DNA as letters in the alphabet, the genes are words and the chromosome is a full sentence. All 46 chromosomes then make up the whole book.

There are many genes on each chromosome; we all have tens of thousands of genes that instruct our bodies on how to develop.

Genes are given names to identify them and the gene responsible for fragile X syndrome is called FMR1. The FMR1 Gene is on the X chromosome.

The FMR1 gene appears in four forms that are defined by the number of repeats of a pattern of DNA called CGG repeats.

Individuals with less than 45 CGG repeats have a normal FMR1 gene. Those with 45-54 CGG repeats have what is called an intermediate or grey zone allele, which does not cause any of the known fragile X associated disorders.

Individuals with 55-200 CGG repeats have a premutation, which means they carry an unstable mutation of the gene that can expand in future generations and thus cause fragile X syndrome in their children or grandchildren. Individuals with a premutation can also develop FXTAS or FXPOI themselves.

Individuals with over 200 CGG repeats have a full mutation of the FMR1 gene, which causes fragile X syndrome.

The full mutation causes the FMR1 gene to shut down or methylate in one region. Normally, the FMR1 gene produces an important protein called FMRP. When the gene is turned off, the individual does not make this protein. The lack of this specific protein is what causes fragile X syndrome.

Fragile X-associated Disorders are a group of conditions called trinucleotide repeat disorders. A common feature of these conditions is that the gene can change sizes over generations, becoming more unstable, and thus the conditions may occur more frequently or severely in subsequent generations. These conditions are often caused by a gene change that begins with a premutation and then expands to a full mutation in subsequent generations.

Approximately 1 in 151 females and 1 in 468 males carry the FMR1 premutation. They are thus carriers of the premutation.

Premutations are defined as having 55-200 CGG repeats and can occur in both males and females. When a father passes the premutation on to his daughters, it usually does not expand to a full mutation. A man never passes the fragile X gene to his sons, since he passes only his Y chromosome to them, which does not contain a fragile X gene.

A female with the FMR1 premutation will often pass on a larger version of the mutation to her children (more on this point below). She also has a 50 percent chance of passing on her normal X chromosome in each pregnancy, since usually only one of her X chromosomes has the FMR1 mutation.

The chance of the premutation expanding to a full mutation is related to the size of the mothers premutation. The larger the mothers CGG repeat number, the higher the chance that it will expand to a full mutation if it is passed on.

Typically, the premutation has no immediate and observable impact on a persons appearance or health. However, some females with a premutation will experience fragile X-associated primary ovarian insufficiency (FXPOI), which causes infertility, irregular or missed menstrual cycles, and/or early menopause.

Additionally, some older adults with a premutation may develop a neurological condition called FXTAS, (fragile X-associated tremor/ataxia syndrome), an adult onset neurodegenerative disorder.

FXTAS and FXPOI are part of the family of conditions called Fragile X-associated Disorders.

A full mutation is defined as having over 200 CGG repeats and causes that indicate the presence of fragile X syndrome in males and some females. Most full mutation expansions have some degree of Methylation (the process which turns off the gene). Males with a full mutation will have Fragile X Syndrome, though with varying degrees of severity

About 65-70 percent of females with a full mutation exhibit some difficulties with cognitive, learning, behavioral, or social functioning, and may also have some of the physical features of FXS (such as large ears or a long face). The remaining 30-35 percent are at risk to develop mental health issues such as anxiety or depression, or they may have no observable effects of the full mutation.

Fragile X in an X-linked condition, which means that the gene is on the X chromosome.

Since a woman has two X chromosomes a woman with a premutation or full mutation has a 50% chance of passing on the X with the mutation in each pregnancy, and a 50% chance of passing on her normal X.

If she has a premutation, and it is passed on (to either males or females), it can remain a premutation or it can expand to a full mutation. If she has a full mutation and it is passed on (to either males or females), it will remain a full mutation.

Because males have only one X chromosome, fathers who carry the premutation will pass it on to all their daughters and none of their sons (they pass their Y chromosome on to their sons). There have been no reports of premutations that are passed from a father to his daughter expanding to a full mutation. This appears to only occur when passed from a mother to her children.

In many X-linked conditions only males who inherit the abnormal gene are affected. Fragile X syndrome is one of the X-linked conditions that can also affect females.

Additionally, in other X-linked conditions all males who carry the abnormal form of the gene are affected. In fragile X syndrome, unaffected males can carry the gene in the premutation form while themselves having no symptoms of the condition.

Follow this link:
Genetics and Inheritance - National Fragile X Foundation

The long-term objectives of our research team are:

a. to understand the molecular etiology in the development of human cancer, and b. to identify and characterize cancer molecules for cancer detection, diagnosis, and therapy.

We use ovarian carcinoma as a disease model because it is one of the most aggressive neoplastic diseases in women. For the first research direction, we aim to identify and characterize the molecular alterations during initiation and progression of ovarian carcinomas. Previous genome-wide analyses from our team have identified molecular alterations in several new cancer-associated genes including Rsf-1, NAC-1, and Notch3 among several others. We have demonstrated the essential roles of these gene products in sustaining tumor growth and survival. Current projects are focusing on elucidating the mechanisms by which these genes function in cancer cells and delineating the cross-talks between those genes and other signaling pathways. Specifically, we are identifying their downstream targets and pathways, and are determining their roles in maintaining cancer stem cell-like features, invasion and drug resistance. The second research direction is a translation-based study. We are assessing the clinical significance of an array of new cancer-associated genes in predicting clinical outcome and in the developing potential target-based therapy in mouse preclinical models. We are also establishing innovative assays for cancer detection and diagnosis by identifying new tumor-associated genetic and protein biomarkers through serial analysis of gene expression, gene expression arrays, proteomics and methylation profiling. The purpose is to develop new tools in detecting human cancer using body fluid samples. In collaboration with several investigators, we are integrating new technologic platforms such as microfluidics, nanotechnology and systems biology in our studies.

In addition to ovarian cancer genetics, we are interested in the diagnostic pathology and basic research of gestational trophoblastic diseases. Please visit "Pathology of Trophoblastic Lesions" for details.

Click here for the Ovarian Cancer Prevention Website

Click here for the Ovarian Cancer Research Program

"What we observe is not nature itself, but nature exposed to our method of questioning." -- Werner Heisenberg, Physics and Philosophy, 1958

Tian-Li Wang, PhD tlw@jhmi.edu

Professor Departments of Pathology, Oncology, and Gynecology & Obstetrics Faculty in Pathobiology Graduate Program Johns Hopkins Medical Institutions

National Taiwan University, BS Johns Hopkins University School of Medicine, PhD University of Pennsylvania, School of Medicine, Post-doc fellow (Neuroscience) Howard Hughes Medical Institutions, Associate (Cancer Genetics)

Ie-Ming Shih, MD, PhD Co-director, Breast & Ovarian Cancer Program Sidney Kimmel Comprehensive Cancer Center ishih@jhmi.edu

Richard W. TeLinde Professor Department of Gynecology & Obstetrics Departments of Pathology and Oncology Faculty in Pathobiology Graduate Program Johns Hopkins University School of Medicine

Taipei Medical University, MD University of Pennsylvania, PhD Johns Hopkins University, Residency (Pathology) Johns Hopkins University, Fellowships (Gynecologic Pathology and Cancer Genetics)

See more here:
Molecular Genetics Laboratory of Female Reproductive Cancer

The Y chromosome is one of two sex chromosomes (allosomes) in mammals, including humans, and many other animals. The other is the X chromosome. Y is the sex-determining chromosome in many species, since it is the presence or absence of Y that determines the male or female sex of offspring produced in sexual reproduction. In mammals, the Y chromosome contains the gene SRY, which triggers testis development. The DNA in the human Y chromosome is composed of about 59 million base pairs.[2] The Y chromosome is passed only from father to son. With a 30% difference between humans and chimpanzees, the Y chromosome is one of the fastest evolving parts of the human genome.[3] To date, over 200 Y-linked genes have been identified.[4] All Y-linked genes are expressed and (apart from duplicated genes) hemizygous (present on only one chromosome) except in the cases of aneuploidy such as XYY syndrome or XXYY syndrome. (See Y linkage.)

The Y chromosome was identified as a sex-determining chromosome by Nettie Stevens at Bryn Mawr College in 1905 during a study of the mealworm Tenebrio molitor. Edmund Beecher Wilson independently discovered the same mechanisms the same year. Stevens proposed that chromosomes always existed in pairs and that the Y chromosome was the pair of the X chromosome discovered in 1890 by Hermann Henking. She realized that the previous idea of Clarence Erwin McClung, that the X chromosome determines sex, was wrong and that sex determination is, in fact, due to the presence or absence of the Y chromosome. Stevens named the chromosome "Y" simply to follow on from Henking's "X" alphabetically.[5][6]

The idea that the Y chromosome was named after its similarity in appearance to the letter "Y" is mistaken. All chromosomes normally appear as an amorphous blob under the microscope and only take on a well-defined shape during mitosis. This shape is vaguely X-shaped for all chromosomes. It is entirely coincidental that the Y chromosome, during mitosis, has two very short branches which can look merged under the microscope and appear as the descender of a Y-shape.[7]

Most mammals have only one pair of sex chromosomes in each cell. Males have one Y chromosome and one X chromosome, while females have two X chromosomes. In mammals, the Y chromosome contains a gene, SRY, which triggers embryonic development as a male. The Y chromosomes of humans and other mammals also contain other genes needed for normal sperm production.

There are exceptions, however. For example, the platypus relies on an XY sex-determination system based on five pairs of chromosomes.[8] Platypus sex chromosomes in fact appear to bear a much stronger homology (similarity) with the avian Z chromosome,[9] and the SRY gene so central to sex-determination in most other mammals is apparently not involved in platypus sex-determination.[10] Among humans, some men have two Xs and a Y ("XXY", see Klinefelter syndrome), or one X and two Ys (see XYY syndrome), and some women have three Xs or a single X instead of a double X ("X0", see Turner syndrome). There are other exceptions in which SRY is damaged (leading to an XY female), or copied to the X (leading to an XX male). For related phenomena, see Androgen insensitivity syndrome and Intersex.

Many ectothermic vertebrates have no sex chromosomes. If they have different sexes, sex is determined environmentally rather than genetically. For some of them, especially reptiles, sex depends on the incubation temperature; others are hermaphroditic (meaning they contain both male and female gametes in the same individual).

The X and Y chromosomes are thought to have evolved from a pair of identical chromosomes,[11][12] termed autosomes, when an ancestral mammal developed an allelic variation, a so-called 'sex locus' simply possessing this allele caused the organism to be male.[13] The chromosome with this allele became the Y chromosome, while the other member of the pair became the X chromosome. Over time, genes which were beneficial for males and harmful to (or had no effect on) females either developed on the Y chromosome, or were acquired through the process of translocation.[14]

Until recently, the X and Y chromosomes were thought to have diverged around 300 million years ago. However, research published in 2010,[15] and particularly research published in 2008 documenting the sequencing of the platypus genome,[9] has suggested that the XY sex-determination system would not have been present more than 166 million years ago, at the split of the monotremes from other mammals.[10] This re-estimation of the age of the therian XY system is based on the finding that sequences that are on the X chromosomes of marsupials and eutherian mammals are present on the autosomes of platypus and birds.[10] The older estimate was based on erroneous reports that the platypus X chromosomes contained these sequences.[8][16]

Recombination between the X and Y chromosomes proved harmfulit resulted in males without necessary genes formerly found on the Y chromosome, and females with unnecessary or even harmful genes previously only found on the Y chromosome. As a result, genes beneficial to males accumulated near the sex-determining genes, and recombination in this region was suppressed in order to preserve this male specific region.[13] Over time, the Y chromosome changed in such a way as to inhibit the areas around the sex determining genes from recombining at all with the X chromosome. As a result of this process, 95% of the human Y chromosome is unable to recombine. Only the tips of the Y and X chromosomes recombine. The tips of the Y chromosome that could recombine with the X chromosome are referred to as the pseudoautosomal region. The rest of the Y chromosome is passed on to the next generation intact. It is because of this disregard for the rules that the Y chromosome is such a superb tool for investigating recent human evolution from a male perspective.

By one estimate, the human Y chromosome has lost 1,393 of its 1,438 original genes over the course of its existence, and linear extrapolation of this 1,393-gene loss over 300 million years gives a rate of genetic loss of 4.6 genes per million years.[17] Continued loss of genes at the 4.6 genes per million year rate would result in a Y chromosome with no functional genes that is the Y chromosome would lose complete function within the next 10 million years, or half that time with the current age estimate of 160 million years.[13][18] Comparative genomic analysis reveals that many mammalian species are experiencing a similar loss of function in their heterozygous sex chromosome. Degeneration may simply be the fate of all non-recombining sex chromosomes, due to three common evolutionary forces: high mutation rate, inefficient selection, and genetic drift.[13]

However, comparisons of the human and chimpanzee Y chromosomes (first published in 2005) show that the human Y chromosome has not lost any genes since the divergence of humans and chimpanzees between 67 million years ago,[19] and a scientific report in 2012 stated that only one gene had been lost since humans diverged from the rhesus macaque 25 million years ago.[20] These facts provide direct evidence that the linear extrapolation model is flawed and suggest that the current human Y chromosome is either no longer shrinking or is shrinking at a much slower rate than the 4.6 genes per million years estimated by the linear extrapolation model.

The human Y chromosome is particularly exposed to high mutation rates due to the environment in which it is housed. The Y chromosome is passed exclusively through sperm, which undergo multiple cell divisions during gametogenesis. Each cellular division provides further opportunity to accumulate base pair mutations. Additionally, sperm are stored in the highly oxidative environment of the testis, which encourages further mutation. These two conditions combined put the Y chromosome at a greater risk of mutation than the rest of the genome.[13] The increased mutation risk for the Y chromosome is reported by Graves as a factor 4.8.[13] However, her original reference obtains this number for the relative mutation rates in male and female germ lines for the lineage leading to humans.[21]

Without the ability to recombine during meiosis, the Y chromosome is unable to expose individual alleles to natural selection. Deleterious alleles are allowed to "hitchhike" with beneficial neighbors, thus propagating maladapted alleles in to the next generation. Conversely, advantageous alleles may be selected against if they are surrounded by harmful alleles (background selection). Due to this inability to sort through its gene content, the Y chromosome is particularly prone to the accumulation of "junk" DNA. Massive accumulations of retrotransposable elements are scattered throughout the Y.[13] The random insertion of DNA segments often disrupts encoded gene sequences and renders them nonfunctional. However, the Y chromosome has no way of weeding out these "jumping genes". Without the ability to isolate alleles, selection cannot effectively act upon them.

A clear, quantitative indication of this inefficiency is the entropy rate of the Y chromosome. Whereas all other chromosomes in the human genome have entropy rates of 1.51.9 bits per nucleotide (compared to the theoretical maximum of exactly 2 for no redundancy), the Y chromosome's entropy rate is only 0.84.[22] This means the Y chromosome has a much lower information content relative to its overall length; it is more redundant.

Even if a well adapted Y chromosome manages to maintain genetic activity by avoiding mutation accumulation, there is no guarantee it will be passed down to the next generation. The population size of the Y chromosome is inherently limited to 1/4 that of autosomes: diploid organisms contain two copies of autosomal chromosomes while only half the population contains 1 Y chromosome. Thus, genetic drift is an exceptionally strong force acting upon the Y chromosome. Through sheer random assortment, an adult male may never pass on his Y chromosome if he only has female offspring. Thus, although a male may have a well adapted Y chromosome free of excessive mutation, it may never make it in to the next gene pool.[13] The repeat random loss of well-adapted Y chromosomes, coupled with the tendency of the Y chromosome to evolve to have more deleterious mutations rather than less for reasons described above, contributes to the species-wide degeneration of Y chromosomes through Muller's ratchet.[23]

As it has been already mentioned, the Y chromosome is unable to recombine during meiosis like the other human chromosomes; however, in 2003, researchers from MIT discovered a process which may slow down the process of degradation. They found that human Y chromosome is able to "recombine" with itself, using palindrome base pair sequences.[24] Such a "recombination" is called gene conversion.

In the case of the Y chromosomes, the palindromes are not noncoding DNA; these strings of bases contain functioning genes important for male fertility. Most of the sequence pairs are greater than 99.97% identical. The extensive use of gene conversion may play a role in the ability of the Y chromosome to edit out genetic mistakes and maintain the integrity of the relatively few genes it carries. In other words, since the Y chromosome is single, it has duplicates of its genes on itself instead of having a second, homologous, chromosome. When errors occur, it can use other parts of itself as a template to correct them.

Findings were confirmed by comparing similar regions of the Y chromosome in humans to the Y chromosomes of chimpanzees, bonobos and gorillas. The comparison demonstrated that the same phenomenon of gene conversion appeared to be at work more than 5 million years ago, when humans and the non-human primates diverged from each other.

In the terminal stages of the degeneration of the Y chromosome, other chromosomes increasingly take over genes and functions formerly associated with it. Finally, the Y chromosome disappears entirely, and a new sex-determining system arises.[13] Several species of rodent in the sister families Muridae and Cricetidae have reached these stages,[25][26] in the following ways:

Outside of the rodent family, the black muntjac, Muntiacus crinifrons, evolved new X and Y chromosomes through fusions of the ancestral sex chromosomes and autosomes.[32]

Fisher's principle outlines why almost all species using sexual reproduction have a sex ratio of 1:1, meaning that 50% of offspring will receive a Y chromosome, and 50% will not. W.D. Hamilton gave the following basic explanation in his 1967 paper on "Extraordinary sex ratios",[33] given the condition that males and females cost equal amounts to produce:

In humans, the Y chromosome spans about 58 million base pairs (the building blocks of DNA) and represents approximately 1% of the total DNA in a male cell.[34] The human Y chromosome contains over 200 genes, at least 72 of which code for proteins.[2] Traits that are inherited via the Y chromosome are called holandric traits (although biologists will usually just say 'Y-linked').

Some cells, especially in older men and smokers, lack a Y-chromosome. It has been found that men with a higher percentage of hematopoietic stem cells in blood lacking the Y-chromosome (and perhaps a higher percentage of other cells lacking it) have a higher risk of certain cancers and have a shorter life expectancy. Men with "loss of Y" (which was defined as no Y in at least 18% of their hematopoietic cells) have been found to die 5.5 years earlier on average than others. This has been interpreted as a sign that the Y-chromosome plays a role going beyond sex determination and reproduction[35] (although the loss of Y may be an effect rather than a cause). And yet women, who have no Y-chromosome, have lower rates of cancer. Male smokers have between 1.5 and 2 times the risk of non-respiratory cancers as female smokers.[36][37]

The human Y chromosome is normally unable to recombine with the X chromosome, except for small pieces of pseudoautosomal regions at the telomeres (which comprise about 5% of the chromosome's length). These regions are relics of ancient homology between the X and Y chromosomes. The bulk of the Y chromosome, which does not recombine, is called the "NRY" or non-recombining region of the Y chromosome.[38] It is the SNPs (single-nucleotide polymorphism) in this region that are used to trace direct paternal ancestral lines.

Not including pseudoautosomal genes, genes include:

Y-Chromosome-linked diseases can be of more common types, or very rare ones. Yet, the rare ones still have importance in understanding the function of the Y-chromosome in the normal case.

No vital genes reside only on the Y chromosome, since roughly half of humans (females) do not have a Y chromosome. The only well-defined human disease linked to a defect on the Y chromosome is defective testicular development (due to deletion or deleterious mutation of SRY). However, having two X chromosomes and one Y chromosome has similar effects. On the other hand, having Y chromosome polysomy has other effects than masculinization.

Y chromosome microdeletion (YCM) is a family of genetic disorders caused by missing genes in the Y chromosome. Many affected men exhibit no symptoms and lead normal lives. However, YCM is also known to be present in a significant number of men with reduced fertility or reduced sperm count.

This results in the person presenting a female phenotype (i.e., is born with female-like genitalia) even though that person possesses an XY karyotype. The lack of the second X results in infertility. In other words, viewed from the opposite direction, the person goes through defeminization but fails to complete masculinization.

The cause can be seen as an incomplete Y chromosome: the usual karyotype in these cases is 44X, plus a fragment of Y. This usually results in defective testicular development, such that the infant may or may not have fully formed male genitalia internally or externally. The full range of ambiguity of structure may occur, especially if mosaicism is present. When the Y fragment is minimal and nonfunctional, the child is usually a girl with the features of Turner syndrome or mixed gonadal dysgenesis.

Klinefelter syndrome (47, XXY) is not an aneuploidy of the Y chromosome, but a condition of having an extra X chromosome, which usually results in defective postnatal testicular function. The mechanism is not fully understood; the extra X does not seem to be due to direct interference with expression of Y genes.

47,XYY syndrome (simply known as XYY syndrome) is caused by the presence of a single extra copy of the Y chromosome in each of a male's cells. 47, XYY males have one X chromosome and two Y chromosomes, for a total of 47 chromosomes per cell. Researchers have found that an extra copy of the Y chromosome is associated with increased stature and an increased incidence of learning problems in some boys and men, but the effects are variable, often minimal, and the vast majority do not know their karyotype. When chromosome surveys were done in the mid-1960s in British secure hospitals for the developmentally disabled, a higher than expected number of patients were found to have an extra Y chromosome. The patients were mischaracterized as aggressive and criminal, so that for a while an extra Y chromosome was believed to predispose a boy to antisocial behavior (and was dubbed the 'criminal karyotype'). Subsequently, in 1968 in Scotland the only ever comprehensive nationwide chromosome survey of prisons found no over-representation of 47,XYY men, and later studies found 47,XYY boys and men had the same rate of criminal convictions as 46,XY boys and men of equal intelligence. Thus, the "criminal karyotype" concept is inaccurate and obsolete.[citation needed]

The following Y chromosome-linked diseases are rare, but notable because of their elucidating of the nature of the Y chromosome.

Greater degrees of Y chromosome polysomy (having more than one extra copy of the Y chromosome in every cell, e.g., XYYY) are rare. The extra genetic material in these cases can lead to skeletal abnormalities, decreased IQ, and delayed development, but the severity features of these conditions are variable.

XX male syndrome occurs when there has been a recombination in the formation of the male gametes, causing the SRY-portion of the Y chromosome to move to the X chromosome. When such an X chromosome contributes to the child, the development will lead to a male, because of the SRY gene.

In human genetic genealogy (the application of genetics to traditional genealogy), use of the information contained in the Y chromosome is of particular interest because, unlike other chromosomes, the Y chromosome is passed exclusively from father to son, on the patrilineal line. Mitochondrial DNA, maternally inherited to both sons and daughters, is used in an analogous way to trace the matrilineal line.

Research is currently investigating whether male-pattern neural development is a direct consequence of Y chromosome-related gene expression or an indirect result of Y chromosome-related androgenic hormone production.[39]

The presence of male chromosomes in fetal cells in the blood circulation of women was discovered in 1974.[40] In 1996, it was found that male fetal progenitor cells could persist postpartum in the maternal blood stream for as long as 27 years.[41]

A 2004 study at the Fred Hutchinson Cancer Research Center, Seattle investigated the origin of male chromosomes found in the peripheral blood of women who had not had male progeny. A total of 120 subjects (women who had never had sons) were investigated and it was found that 21% of them had male DNA. The subjects were categorised into four groups based on their case histories:[42]

The study noted that 10% of the women had never been pregnant before, raising the question where the Y Chromosomes in their blood could have come from? The study suggests that possible reasons for occurrence of male chromosome microchimerism could be one of the following:[42]

A 2012 study, at the same institute, has detected cells with the Y chromosome in multiple areas of the brains of dead women.[43]

Many groups of organisms in addition to mammals have Y chromosomes, but these Y chromosomes do not share common ancestry with mammalian Y chromosomes. Such groups include Drosophila, some other insects, some fish, some reptiles, and some plants. In Drosophila melanogaster, the Y chromosome does not trigger male development. Instead, sex is determined by the number of X chromosomes. The D. melanogaster Y chromosome does contain genes necessary for male fertility. So XXY D. melanogaster are female, and D. melanogaster with a single X (X0), are male but sterile. There are some species of Drosophila in which X0 males are both viable and fertile.

Other organisms have mirror image sex chromosomes: the female is "XY" and the male is "XX", but by convention biologists call a "female Y" a W chromosome and the other a Z chromosome. For example, female birds, snakes, and butterflies have ZW sex chromosomes, and males have ZZ sex chromosomes.

There are some species, such as the Japanese rice fish, where the Y chromosome is not inverted and can still swap genes with the X. Because the Y does not have male-specific genes and can interact with the X, XX males can be formed as well as XY and YY females.[44]

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Y chromosome - Wikipedia, the free encyclopedia

Value Genetics Bull & Female Sale

Saturday March 5, 2016 12:30 p.m. Clinton Livestock Auction, Clinton, OK View Sale Book View Videos

Davis Angus began in 1973 when Bud Davis, Jim's father purchased ten registered Angus cows from Al Rutledge. Jim and wife Debbie, later added cattle from the UT, Allen Greer and Pat O'Brian, and B&L dispersals. The first AI sires were introduced in 1995; Davis Angus chose BR New Design 323 and TC Dividend 963. Through the technological advances of breeding and the use of artificial insemination inspiration developed, a dream that cattle could be produced that had all the desired carcass traits with the show ring appeal. This idea led Davis Angus to produce the cattle you see today. Cattle that have Carcass and Conformation without Compromise.

The 2007 Davis Angus calf crop was very successful with 100% of the steers grading choice, 60% went CAB and prime, producing a 46% yield grade 1 and 2, this allowed Davis Angus to receive a premium of $106.95 per head above the market while costing only $0.78 per pound with corn costing $6.00 per bushel.

Davis Angus was very successful in the show ring with several champions; we encourage you to view our "Hall of Champions" page and view the results!

In the past decade we have become very successful in the show ring as well as winning several carcass competitions.

We encourage you to come visit us at Davis Angus, let us put you in the winner's circle!

Read the rest here:
Davis Angus Foss, Oklahoma

The X chromosome is one of the two sex-determining chromosomes (allosomes) in many animal species, including mammals (the other is the Y chromosome), and is found in both males and females. It is a part of the XY sex-determination system and X0 sex-determination system. The X chromosome was named for its unique properties by early researchers, which resulted in the naming of its counterpart Y chromosome, for the next letter in the alphabet, after it was discovered later.[2]

The X chromosome in humans spans more than 153 million base pairs (the building material of DNA). It represents about 2000 out of 20,000 - 25,000 genes. Each person normally has one pair of sex chromosomes in each cell. Females have two X chromosomes, whereas males have one X and one Y chromosome. Both males and females retain one of their mother's X chromosomes, and females retain their second X chromosome from their father. Since the father retains his X chromosome from his mother, a human female has one X chromosome from her paternal grandmother (father's side), and one X chromosome from her mother.

Identifying genes on each chromosome is an active area of genetic research. Because researchers use different approaches to predict the number of genes on each chromosome, the estimated number of genes varies. The X chromosome contains about 2000[3] genes compared to the Y chromosome containing 78[4] genes, out of the estimated 20,000 to 25,000 total genes in the human genome. Genetic disorders that are due to mutations in genes on the X chromosome are described as X linked.

The X chromosome carries a couple of thousand genes but few, if any, of these have anything to do directly with sex determination. Early in embryonic development in females, one of the two X chromosomes is randomly and permanently inactivated in nearly all somatic cells (cells other than egg and sperm cells). This phenomenon is called X-inactivation or Lyonization, and creates a Barr body. If X-inactivation in the somatic cell meant a complete de-functionalizing of one of the X-chromosomes, it would ensure that females, like males, had only one functional copy of the X chromosome in each somatic cell. This was previously assumed to be the case. However, recent research suggests that the Barr body may be more biologically active than was previously supposed.[5]

It is theorized by Ross et al. 2005 and Ohno 1967 that the X chromosome is at least partially derived from the autosomal (non-sex-related) genome of other mammals, evidenced from interspecies genomic sequence alignments.

The X chromosome is notably larger and has a more active euchromatin region than its Y chromosome counterpart. Further comparison of the X and Y reveal regions of homology between the two. However, the corresponding region in the Y appears far shorter and lacks regions that are conserved in the X throughout primate species, implying a genetic degeneration for Y in that region. Because males have only one X chromosome, they are more likely to have an X chromosome-related disease.

It is estimated that about 10% of the genes encoded by the X chromosome are associated with a family of "CT" genes, so named because they encode for markers found in both tumor cells (in cancer patients) as well as in the human testis (in healthy patients).[6]

Klinefelter syndrome:

Triple X syndrome (also called 47,XXX or trisomy X):

Turner syndrome:

XX male syndrome is a rare disorder, where the SRY region of the Y chromosome has recombined to be located on one of the X chromosomes. As a result, the XX combination after fertilization has the same effect as a XY combination, resulting in a male. However, the other genes of the X chromosome cause feminization as well.

X-linked endothelial corneal dystrophy is an extremely rare disease of cornea associated with Xq25 region. Lisch epithelial corneal dystrophy is associated with Xp22.3.

Megalocornea 1 is associated with Xq21.3-q22[medical citation needed]

The X-chromosome has played a crucial role in the development of sexually selected characteristics for over 300 million years. During that time it has accumulated a disproportionate number of genes concerned with mental functions. For reasons that are not yet understood, there is an excess proportion of genes on the X-chromosome that are associated with the development of intelligence, with no obvious links to other significant biological functions.[11][12] There has also been interest in the possibility that haploin sufficiency for one or more X-linked genes has a specific impact on development of the Amygdala and its connections with cortical centres involved in socialcognition processing or the social brain'.[11][13][clarification needed]

It was first noted that the X chromosome was special in 1890 by Hermann Henking in Leipzig. Henking was studying the testicles of Pyrrhocoris and noticed that one chromosome did not take part in meiosis. Chromosomes are so named because of their ability to take up staining. Although the X chromosome could be stained just as well as the others, Henking was unsure whether it was a different class of object and consequently named it X element,[14] which later became X chromosome after it was established that it was indeed a chromosome.[15]

The idea that the X chromosome was named after its similarity to the letter "X" is mistaken. All chromosomes normally appear as an amorphous blob under the microscope and only take on a well defined shape during mitosis. This shape is vaguely X-shaped for all chromosomes. It is entirely coincidental that the Y chromosome, during mitosis, has two very short branches which can look merged under the microscope and appear as the descender of a Y-shape.[16]

It was first suggested that the X chromosome was involved in sex determination by Clarence Erwin McClung in 1901 after comparing his work on locusts with Henking's and others. McClung noted that only half the sperm received an X chromosome. He called this chromosome an accessory chromosome and insisted, correctly, that it was a proper chromosome, and theorized, incorrectly, that it was the male determining chromosome.[14]

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X chromosome - Wikipedia, the free encyclopedia

for 1st YEAR STUDENTS X-LINKED INHERITANCE

hen the locus for a gene for a particular trait or disease lies on the X chromosome, the disease is said to be X-linked. The inheritance pattern for X-linked inheritance differs from autosomal inheritance only because the X chromosome has no homologous chromosome in the male, the male has an X and a Y chromosome. Very few genes have been discovered on the Y chromosome.

The inheritance pattern follows the pattern of segregation of the X and Y chromosomes in meiosis and fertilization. A male child always gets his X from one of his mother's two X's and his Y chromosome from his father. X-linked genes are never passed from father to son. A female child always gets the father's X chromosome and one of the two X's of the mother. An affected female must have an affected father. Males are always hemizygous for X linked traits, that is, they can never be heterozygoses or homozygotes. They are never carriers. A single dose of a mutant allele will produce a mutant phenotype in the male, whether the mutation is dominant or recessive. On the other hand, females must be either homozygous for the normal allele, heterozygous, or homozygous for the mutant allele, just as they are for autosomal loci.

When an X-linked gene is said to express dominant inheritance, it means that a single dose of the mutant allele will affect the phenotype of the female. A recessive X-linked gene requires two doses of the mutant allele to affect the female phenotype. The following are the hallmarks of X-linked dominant inheritance:

The following Punnett Squares explain the first three hallmarks of X-linked dominant inheritance. X represents the X chromosome with the normal allele, XA represents the X chromosome with the mutant dominant allele, and Y represents the Y chromosome. Note that the affected father never passes the trait to his sons but passes it to all of his daughters, since the heterozygote is affected for dominant traits. On the other hand, an affected female passes the disease to half of her daughters and half of her sons.

Males are usually more severely affected than females because in each affected female there is one normal allele producing a normal gene product and one mutant allele producing the non-functioning product, while in each affected male there is only the mutant allele with its non-functioning product and the Y chromosome, no normal gene product at all. Affected females are more prevalent in the general population because the female has two X chromosomes, either of which could carry the mutant allele, while the male only has one X chromosome as a target for the mutant allele. When the disease is no more deleterious in males than it is in females, females are about twice as likely to be affected as males. As shown in Pedigree 5 below, X-linked dominant inheritance has a unique heritability pattern.

The key for determining if a dominant trait is X-linked or autosomal is to look at the offspring of the mating of an affected male and a normal female. If the affected male has an affected son, then the disease is not X-linked. All of his daughters must also be affected if the disease is X-linked. In Pedigree 5, both of these conditions are met.

What happens when males are so severely affected that they can't reproduce? Suppose they are so severely affected they never survive to term, then what happens? This is not uncommon in X-linked dominant diseases. There are no affected males to test for X-linked dominant inheritance to see if the produce all affected daughters and no affected sons. Pedigree 6 shows the effects of such a disease in a family. There are no affected males, only affected females, in the population. Living females outnumber living males two to one when the mother is affected. The ratio in the offspring of affected females is: 1 affected female: 1 normal female: 1 normal male.

You will note that in Pedigree 6 there have also been several spontaneous abortions in the offspring of affected females. Normally, in the general population of us normal couples, one in six recognized pregnancies results in a spontaneous abortion. Here the ratio is much higher. Presumably many of the spontaneous abortions shown in Pedigree 6 are males that would have been affected had they survived to term.

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Human Genetics - Mendelian Inheritance 5

Androgenetic alopecia is a common form of hair loss in both men and women. In men, this condition is also known as male-pattern baldness. Hair is lost in a well-defined pattern, beginning above both temples. Over time, the hairline recedes to form a characteristic "M" shape. Hair also thins at the crown (near the top of the head), often progressing to partial or complete baldness.

The pattern of hair loss in women differs from male-pattern baldness. In women, the hair becomes thinner all over the head, and the hairline does not recede. Androgenetic alopecia in women rarely leads to total baldness.

Androgenetic alopecia in men has been associated with several other medical conditions including coronary heart disease and enlargement of the prostate. Additionally, prostate cancer, disorders of insulin resistance (such as diabetes and obesity), and high blood pressure (hypertension) have been related to androgenetic alopecia. In women, this form of hair loss is associated with an increased risk of polycystic ovary syndrome (PCOS). PCOS is characterized by a hormonal imbalance that can lead to irregular menstruation, acne, excess hair elsewhere on the body (hirsutism), and weight gain.

Androgenetic alopecia is a frequent cause of hair loss in both men and women. This form of hair loss affects an estimated 50 million men and 30 million women in the United States. Androgenetic alopecia can start as early as a person's teens and risk increases with age; more than 50 percent of men over age 50 have some degree of hair loss. In women, hair loss is most likely after menopause.

A variety of genetic and environmental factors likely play a role in causing androgenetic alopecia. Although researchers are studying risk factors that may contribute to this condition, most of these factors remain unknown. Researchers have determined that this form of hair loss is related to hormones called androgens, particularly an androgen called dihydrotestosterone. Androgens are important for normal male sexual development before birth and during puberty. Androgens also have other important functions in both males and females, such as regulating hair growth and sex drive.

Hair growth begins under the skin in structures called follicles. Each strand of hair normally grows for 2 to 6 years, goes into a resting phase for several months, and then falls out. The cycle starts over when the follicle begins growing a new hair. Increased levels of androgens in hair follicles can lead to a shorter cycle of hair growth and the growth of shorter and thinner strands of hair. Additionally, there is a delay in the growth of new hair to replace strands that are shed.

Although researchers suspect that several genes play a role in androgenetic alopecia, variations in only one gene, AR, have been confirmed in scientific studies. The AR gene provides instructions for making a protein called an androgen receptor. Androgen receptors allow the body to respond appropriately to dihydrotestosterone and other androgens. Studies suggest that variations in the AR gene lead to increased activity of androgen receptors in hair follicles. It remains unclear, however, how these genetic changes increase the risk of hair loss in men and women with androgenetic alopecia.

Researchers continue to investigate the connection between androgenetic alopecia and other medical conditions, such as coronary heart disease and prostate cancer in men and polycystic ovary syndrome in women. They believe that some of these disorders may be associated with elevated androgen levels, which may help explain why they tend to occur with androgen-related hair loss. Other hormonal, environmental, and genetic factors that have not been identified also may be involved.

Read more about the AR gene.

The inheritance pattern of androgenetic alopecia is unclear because many genetic and environmental factors are likely to be involved. This condition tends to cluster in families, however, and having a close relative with patterned hair loss appears to be a risk factor for developing the condition.

You may find the following resources about androgenetic alopecia helpful. These materials are written for the general public.

You may also be interested in these resources, which are designed for healthcare professionals and researchers.

The resources on this site should not be used as a substitute for professional medical care or advice. Users seeking information about a personal genetic disease, syndrome, or condition should consult with a qualified healthcare professional. See How can I find a genetics professional in my area? in the Handbook.

See the article here:
Androgenetic alopecia - Genetics Home Reference

In mammals, sex is determined by two sex chromosomes, known as the X and the Y chromosomes. Genes located on either the X or the Y chromosome are known as "sex-linked" genes. Genes on any chromosomes other than the X or Y are known as autosomal genes. The Karyotype: A Visualization of the Chromosomes Normal female mammals have two X chromosomes. Normal males have one X and one Y chromosome. This can be seen in this human male karyotype: The X and Y chromosomes appear at the bottom right corner of the image. If this were a female, the two sex chromosomes would both be relatively larger X chromosomes. As you can see, compared to the X chromosome, the Y chromosome is small and carries fewer genes.

The exact genes carried on the X chromosome varies among species. In humans, for example, the gene coding for normal clotting factors and the gene coding for normal cone photoreceptor pigment are located on the X chromosome. Abnormal mutant forms of these genes can result in hemophilia (a potentially fatal disorder in which the blood fails to clot) in the former case, and red-green color blindness in the latter.

There are two possible (normal) male genotypes:

At a certain point in the embryonic development of every female mammal (including cats), one of the two X chromosomes in each cell inactivates by supercoiling into a structure known as a Barr Body. This irreversible process is known as Lyonization; it leaves only ONE active X chromosome in each cell of the female embryo. Only the alleles on the active (uncoiled) X chromosome are expressed.

Lyonization is random in each cell: there's no way to predict which of the two X chromosomes will become inactivated. Hence, any given cell of a heterozygous female could end up as either of the following:

A heterozygous cat will be a patchwork of these two types of cells. Lyonization takes place relatively early in development, when the cat is still a blastula, and all the cells descended from a blastomere with a particular X chromosome inactivated as a Barr Body will also have the same Barr Body inactivated. That means that all the skin tissues that arise from a cell like the left one will express black fur, and all the skin tissue that arise from a cell like the right one will express orange fur. Hence:

Here's an overview:

This is why calico cats are almost invariably female.

A calico cat is a tortoiseshell expressing an additional genetic condition known as piebalding. A piebald animal has patches of white (i.e., unpigmented) skin/fur. This is controlled by a different locus (S) than the black/orange fur colors.

The patches may be relatively large, or rather small and interwoven:

Larger patches may be caused by:

See more here:
The Genetics of Calico Cats - Department of Biology

Tortoiseshell describes a coat coloring found almost exclusively in female cats,[1][2] so called because of the similarity to the tortoiseshell material. Also called Torties for short, these cats combine two colors other than white, either closely mixed or in large patches.[2] The colors are often described as red and black, but "red" can instead be orange, yellow, or cream[2] and "black" can instead be chocolate, grey, tabby, or blue.[2] A tortoiseshell cat with the tabby pattern as one of its colors is a Torbie.

"Tortoiseshell" is typically reserved for cats with relatively small or no white markings. Those that are largely white with tortoiseshell patches are described as tricolor,[2] tortoiseshell-and-white (in the United Kingdom), or calico (in Canada and the United States). Tortoiseshell markings appear in many different breeds as well as in non-purebred domestic cats.[3] This pattern is especially preferred in the Japanese Bobtail breed.[4]

Tortoiseshell cats have coats with patches of various shades of red and black, as well as white. The size of the patches can vary from a fine speckled pattern to large areas of color. Typically, the more white a cat has, the more solid the patches of color. Dilution genes may modify the coloring, lightening the fur to a mix of cream and blue, lilac or fawn. The markings on tortoiseshell cats are usually asymmetrical. Occasionally tabby patterns of black and brown (eumelanistic) and red (phaeomelanistic) colors are also seen. These patched tabbies are often called tortie-tabby, torbie or, with large white areas, caliby.[5] Tortoiseshell can also be expressed in the point pattern.

Frequently there will be a "split face" pattern with black on one side of the face and orange on the other, with the dividing line running down the bridge of the nose.

Tortoiseshell and calico coats result from an interaction between genetic and developmental factors. The primary gene for coat color (B) for the colors brown, chocolate, cinnamon, etc., can be masked by the co-dominant gene for the orange color (O) which is on the X Chromosome and has two alleles, the Orange (XO) and not-Orange (Xo), that produce orange phaeomelanin and black eumelanin pigments, respectively. (NOTE: Typically, the X for the chromosome is assumed from context and the alleles are referred to by just the uppercase O for the orange, or lower case o for the not-orange.) The Tortoiseshell and Calico cats are indicated: Oo to indicate they are heterozygous on the O gene. The (B) and (O) genes can be further modified by a recessive dilute gene (dd) which softens the colors. Orange becomes Cream, Black becomes Gray, etc. Various terms are used for specific colors, for example, Gray is also called Blue, Orange is also called Ginger. Therefore a Tortoiseshell cat may be a Chocolate Tortoiseshell or a Blue/Cream Tortoiseshell or the like, based on the alleles for the (B) and (D) genes.

The cells of female cats, which like other mammalian females have two X chromosomes (XX), undergo the phenomenon of X-inactivation,[6][7] in which one or the other of the X-chromosomes is turned off at random in each cell in very early development. The inactivated X becomes a Barr body. Cells in which the chromosome carrying the Orange (O) allele is inactivated express the alternative non-Orange (o) allele, determined by the (B) gene. Cells in which the non-Orange (o) allele is inactivated express the Orange (O) allele. Pigment genes are expressed in melanocytes that migrate to the skin surface later in development. In bi-colored tortoiseshell cats, the melanocytes arrive relatively early, and the two cell types become intermingled, producing the characteristic brindled appearance consisting of an intimate mixture of orange and black cells, with occasional small diffuse spots of orange and black.

In tri-colored calico cats, a separate gene interacts developmentally with the coat color gene. This spotting gene produces white, unpigmented patches by delaying the migration of the melanocytes to the skin surface. There are a number of alleles of this gene that produce greater or lesser delays. The amount of white is artificially divided into mitted, bicolor, harlequin, and van, going from almost no white to almost completely white. In the extreme case, no melanocytes make it to the skin and the cat is entirely white (but not an albino). In intermediate cases, melanocyte migration is slowed, so that the pigment cells arrive late in development and have less time to intermingle. Observation of tri-color cats will show that, with a little white color, the orange and black patches become more defined, and with still more white, the patches become completely distinct. Each patch represents a clone of cells derived from one original cell in the early embryo.[8]

A male cat, like males of other therian mammals, has only one X and one Y chromosome (XY). That X chromosome does not undergo X-inactivation, and coat color is determined by which allele is present on the X. Accordingly the cat's coat will be either entirely orange or non-orange. Very rarely (approximately 1 in 3,000[9]) a male tortoiseshell or calico is born. These animals typically have an extra X chromosome (XXY), a condition known in humans as Klinefelter syndrome, and their cells undergo an X-inactivation process like that in females. As in humans, these cats often are sterile because of the imbalance in sex chromosomes. Some male calico or tortoiseshell cats may be chimeras, which result from the fusion in early development of two embryos with different color genotypes. Others are mosaics, in which the XXY condition arises after conception and the cat is a mixture of cells with different numbers of X chromosomes.

Cats of this coloration are believed to bring good luck in the folklore of many cultures.[10] In the United States, these are sometimes referred to as money cats.[11]

According to cat expert Jackson Galaxy, tortoiseshell cats tend to have a much more distinct personality.[12] The magazine of the Smithsonian Institution has reported that studies suggest many tortoiseshell owners believe their cats have increased attitude and they call it "tortitude" but science does not support this.[13]

Continued here:
Tortoiseshell cat - Wikipedia, the free encyclopedia

James K. Adams, Professor of Biology, Dalton State College

Andrew D. Warren, Yale Peabody Museum of Natural History

mybutterflybugs

mybutterflybugs

Kim Davis, Mike Stangeland, and Andrew Warren, Butterflies of America

In the realm of genetic anomalies found in living organisms perhaps none is more visually striking than bilateral gynandromorphism, a condition where an animal or insect contains both male and female characteristics, evenly split, right down the middle. While cases have been reported in lobsters, crabs and even in birds, it seems butterflies and moths lucked out with the visual splendor of having both male and female wings as a result of the anomaly. For those interested in the science, heres a bit from Elise over at IFLScience:

In insects the mechanism is fairly well understood. A fly with XX chromosomes will be a female. However, an embryo that loses a Y chromosome still develops into what looks like an adult male, although it will be sterile. Its thought that bilateral gynandromorphism occurs when two sperm enter an egg. One of those sperm fuses with the nucleus of the egg and a female insect develops. The other sperm develops without another set of chromosomes within the same egg. Both a male and a female insect develop within the same body.

Above are some great examples of bilateral gynandromorphism, but follow the links above and below for many more. (via Live Science, The Endless Airshow, Butterflies of America, IFLScience)

See related posts on Colossal about butterflies, genetics.

Link:
Spectacular Genetic Anomaly Results in Butterflies with ...

Many women are unable to conceive and deliver a healthy baby due to genetic factors. Sometimes this is due to an inherited chromosome abnormality. Other times it is because of a single-gene defect passed from parent to child.

In addition, if other women in your family have had problems conceiving due to premature menopause, endometriosis or other factors, you may be at increased risk of the same problems.

Chromosomally abnormal embryos have a low rate of implantation in the mothers uterus, often leading to miscarriages. If an abnormal embryo does implant, the pregnancy may still result in miscarriage or the birth of a baby with physical problems, developmental delay, or mental retardation.

There are several kinds of chromosome abnormalities:

Translocation is the most common of these. Although a parent who carries a translocation is frequently normal, his or her embryo may receive too much or too little genetic material, and a miscarriage often results.

Couples with specific chromosome defects may benefit from pre-implantation genetic diagnosis (PGD) in conjunction with in vitro fertilization (IVF).

Down syndrome is usually associated with advanced maternal age and is a common example of aneuploidy. Down syndrome is caused by having an extra number-21 chromosome (three instead of two). It is also referred to as trisomy 21.

More information about genetics and chromosomes is available at the Web page Genetics Made Simple.

More rare is the existence of an inherited genetic disease due to abnormal genes or mutations. Chromosome analysis of the parents blood identifies such an inherited genetic cause in less than 5 percent of couples.

Single-gene abnormalities are mutations caused by changes in the DNA sequence of a gene, which produce proteins that allow cells to work properly. Gene mutations alter the functioning of cells due to a lack of a protein.

Single-gene disorders usually indicate a family history of a specific genetic disease such as cystic fibrosis (CF) an incurable and fatal disease affecting the mucous glands of vital organs and Tay Sachs, also a fatal disorder, in which harmful quantities of a fatty substance build up in tissues and nerve cells in the brain.

Though generally rare, these diseases are usually devastating to a family. Fortunately, much progress has been made in detection through pre-implantation genetic diagnosis (PGD) in conjunction with in vitro fertilization (IVF).

Although a couple may otherwise have no fertility problems, IVF and PGD can work together to spare mother and father from heartache in cases where there is a known single-gene family history.

Learn more about Genetics

Read more here:
Female Infertility Genetic Causes | RSC New Jersey

http://www.baumanmedical.com - Hair loss affects tens of millions of American women, but new diagnostic procedures, effective treatments and tracking methods are available.

LaserCap delivers an effective, clinical dose of laser therapy anywhere, anytime because it is the first cordless, rechargeable, portable laser that has 224 separate laser diodes (not LEDs) that fits conveniently under a standard baseball hat. Laser treatments with LaserCap are 30 minutes, every other day. 650nm wavelength, 5mW per laser diode. Laser therapy does not regrow dead hair follicles, but it makes weaker hair follicles produce thicker, stronger and longer hair fibers. All laser patients should be measured in three areas using a HairCheck(TM) Cross sectional hair bundle measurement tool.

Female Androgen Sensitivity Genetic Testing is performed to determine if a women is likely to experience severe female hereditary hair loss and predict a post-menopausal woman's response to the off-label treatment finasteride (propecia). The female Androgen Sensitivity test is performed in minutes in the doctor's office using a cheek swab.

For more information on LaserCap, visit http://www.lasercap.info

To learn more about Hair Restoration Physician, Dr. Alan J. Bauman, M.D. visit http://www.baumanmedical.com

Read more from the original source:
Female Hereditary Hair Loss Treatment & Genetic Testing ...

The following is a guest post by Amber Larsen of Massage and Health by Amber Kim:

My body, my face, my features will never be repeated. How I look is not going to mimic the girl next to me in the gym. My body shape will not be the same as another female that I may be slightly jealous of because shes thinner than me. My ass is going to be bigger and there is nothing I can do about it.

My genetics did it.

It's amazing - on average, most women will have about thirteen negative thoughts about their appearance per day. If you break it down, it means that every waking hour we think negatively about ourselves. I cant lie; I know I have done the same. My ass is too big, my abs stick out, my latissimus dorsi is getting a bit too big because my bras are cutting into my skin (CrossFit did it).

According to cognitive behavioral psychology, the self-hate is called withdrawal emotions. These emotions make us want to withdraw from situations or things that are linked to the emotions that are causing us to feel this way. Essentially, you can say you can be withdrawing from yourself. This can cause us to either make drastic decisions, such as not to eat, or do things that can do us harm, or do the opposite - not take care of ourselves because we ask whats the use? I hope in writing this it can shed some light as to why you body looks the way it does, and how to embrace that you are unique and to work with your genetics.

What exactly is genetics? Genetics is a wide domain, but in short it is the study of heredity, more specifically the characteristics we inherit from our parents. Our appearance, abilities, susceptibility to disease, and even life span is influenced by heredity. That is just skimming the surface of genetics, but an overall view is that your body shape and your abilities in the gym are inherited from your parents. So what does that say about my personal body? My lower half will always be bigger because it is inherited from my father side. My upper body will always be a wee bit smaller because its inherited from my mothers side. The bottom line is, ladies, I will never weigh 110 pounds. Its not in my genetics, and you know what? Im okay with that.

Many times the media portrays an ideal size for a woman, but you know what? For a healthy woman who eats correctly and exercises on a regular basis there is no ideal size. The reason is because genetically we are all different. There is nothing wrong with a woman who has a leaner, thinner body, because she may be genetically predisposed to having a leaner frame. There is also nothing wrong with a woman who tends to be stronger looking with a larger frame for the same reason. Both body images are different, but both are ideal based on each individual womans inherited genetics.

Is your view on your body slowly changing?

So take a good look at my body (yes this is more difficult for me then you think). This photo is from 2012 and this is me at 140 pounds. If you see, my body is a bit stocky, bulky, and (since I am 53) technically overweight. By the way, you can see some of my cellulite and, yes, I did throw away my scale! My abs stick out and so does my ass.

You can see my body is made up of mostly fast-twitch muscle fibers, or type II muscle fibers. My muscles are different in that they contain a higher number of glycolytic enzymes, which means my muscles do very well anaerobically. Also, my body can be viewed as a bit of a subtype of fast twitch muscles in that I am efficient in strength movements and halfway decent at aerobic movements (not the best though). My body is adaptable with endurance training, but it will not be my strongest area of fitness. Bottom line, the body you see is genetically predisposed to strength work.

Now, a slow-twitch body will not look exactly like this. A slow-twitch body will be leaner because the muscle fibers tend to be longer. These muscles contain larger amounts of mitochondria and higher concentrations of myoglobin than my own body. Again, slow twitch muscle tissue is an inherited trait.

I am not super skinny (as you can see above), but its important to realize that each body is unique and has strengths and weaknesses. Each body is beautiful in its own right, and its important for all of you to embrace what makes you an individual. There is no ideal weight or look for any woman. Women look different based off of their genetic make up, and thats truly a beautiful thing. Just think - no one will ever look exactly like you. And you have automatically inherited strengths that will help you in your fitness goals.

Embrace the person you are. I know it can be difficult to stop the negative self talk that your body does not look like the skinny Victorias Secret model, but you know what? Maybe you were never meant to look that way based off of your genetic heredity. Maybe you were meant to look strong and maybe you were built for strength, which is beautiful. Even if you are a leaner person who wishes to look stronger, well you can, even with a leaner frame, and you can also embrace that your body allows you to work efficiently aerobically based on your genetic make-up.

The image you have of your body should be positive. No one can be you, and no one can look exactly like you because you are genetically different. There is so much beauty in that. Embrace the genetic make up that make your body unique to those around you. I hope you will not be afraid to wear that bikini this summer or to workout without a shirt on. Your body is beautiful because its uniquely you.

This is my body. I have learned to embrace the body that allows me to do amazing things. I hope you will do the same.

Read more from the original source:
The Female Form: Embrace Your Genetics and Find Beauty in ...

The XY sex-determination system is the sex-determination system found in humans, most other mammals, some insects (Drosophila), and some plants (Ginkgo). In this system, the sex of an individual is determined by a pair of sex chromosomes (gonosomes). Females have two of the same kind of sex chromosome (XX), and are called the homogametic sex. Males have two distinct sex chromosomes (XY), and are called the heterogametic sex.

This system is in contrast with the ZW sex-determination system found in birds, some insects, many reptiles, and other animals, in which the heterogametic sex is female.

A temperature-dependent sex determination system is found in some reptiles.

All animals have a set of DNA coding for genes present on chromosomes. In humans, most mammals, and some other species, two of the chromosomes, called the X chromosome and Y chromosome, code for sex. In these species, one or more genes present on their Y-chromosome that determine maleness. In this process, an X chromosome and a Y chromosome act to determine the sex of offspring, often due to genes located on the Y chromosome that code for maleness. Offspring have two sex chromosomes: an offspring with two X chromosomes will develop female characteristics, and an offspring with an X and a Y chromosome will develop male characteristics.

In humans, a single gene (SRY) present on the Y chromosome acts as a signal to set the developmental pathway towards maleness. Presence of this gene starts off the process of virilization. This and other factors result in the sex differences in humans.[1] The cells in females, with two X chromosomes, undergo X-inactivation, in which one of the two X chromosomes is inactivated. The inactivated X chromosome remains within a cell as a Barr body.

Humans, as well as some other organisms, can have a chromosomal arrangement that is contrary to their phenotypic sex; for example, XX males or XY females (see androgen insensitivity syndrome). Additionally, an abnormal number of sex chromosomes (aneuploidy) may be present, such as Turner's syndrome, in which a single X chromosome is present, and Klinefelter's syndrome, in which two X chromosomes and a Y chromosome are present, XYY syndrome and XXYY syndrome.[1] Other less common chromosomal arrangements include: triple X syndrome, 48, XXXX, and 49, XXXXX.

XY system in mammals: Sex is determined by presence of Y. "Female" is the default sex; due to the absence of the Y.[2] In the 1930s, Alfred Jost determined that the presence of testosterone was required for Wolffian duct development in the male rabbit.[3]

SRY is an intronless sex-determining gene on the Y chromosome in the therians (placental mammals and marsupials).[4] Non-human mammals use several genes on the Y-chromosome. Not all male-specific genes are located on the Y-chromosome. Other species (including most Drosophila species) use the presence of two X chromosomes to determine femaleness. One X chromosome gives putative maleness. The presence of Y-chromosome genes is required for normal male development.

Birds and many insects have a similar system of sex determination (ZW sex-determination system), in which it is the females that are heterogametic (ZW), while males are homogametic (ZZ).

Many insects of the order Hymenoptera instead have a system (the haplo-diploid sex-determination system), where the males are haploid individuals (which just one chromosome of each type), while the females are diploid (with chromosomes appearing in pairs). Some other insects have the X0 sex-determination system, where just one chromosome type appears in pairs for the female but alone in the males, while all other chromosomes appear in pairs in both sexes.

See the rest here:
XY sex-determination system - Wikipedia, the free encyclopedia

Sexual differentiation

Differentiation of the male and female reproductive systems does not occur until the fetal period of development.

Sexual differentiation is the process of development of the differences between males and females from an undifferentiated zygote. As male and female individuals develop from zygotes into fetuses, into infants, children, adolescents, and eventually into adults, sex and gender differences at many levels develop: genes, chromosomes, gonads, hormones, anatomy, and psyche.

Sex differences range greatly and include physiologically differentiating. Sex-dichotomous differences are developments which are wholly characteristic of one sex only. Examples of sex-dichotomous differences include aspects of the sex-specific genital organs such as ovaries, a uterus or a phallic urethra. In contrast, sex-dimorphic differences are matters of degree (e.g., size of phallus). Some of these (e.g., stature, behaviors) are mainly statistical, with much overlap between male and female populations.

Nevertheless, even the sex-dichotomous differences are not absolute in the human population, and there are individuals who are exceptions (e.g., males with a uterus, or females with an XY karyotype), or who exhibit biological and/or behavioral characteristics of both sexes.

Sex differences may be induced by specific genes, by hormones, by anatomy, or by social learning. Some of the differences are entirely physical (e.g., presence of a uterus) and some differences are just as obviously purely a matter of social learning and custom (e.g., relative hair length). Many differences, though, such as gender identity, appear to be influenced by both biological and social factors ("nature" and "nurture").

The early stages of human differentiation appear to be quite similar to the same biological processes in other mammals and the interaction of genes, hormones and body structures is fairly well understood. In the first weeks of life, a fetus has no anatomic or hormonal sex, and only a karyotype distinguishes male from female. Specific genes induce gonadal differences, which produce hormonal differences, which cause anatomic differences, leading to psychological and behavioral differences, some of which are innate and some induced by the social environment.

Humans, many mammals, insects and other animals have an XY sex-determination system. Humans have forty-six chromosomes, including two sex chromosomes, XX in females and XY in males. It is obvious that the Y chromosome must carry at least one essential gene which determines testicular formation (originally termed TDF). A gene in the sex-determining region of the short arm of the Y, now referred to as SRY, has been found to direct production of a protein, testis determining factor, which binds to DNA, inducing differentiation of cells derived from the genital ridges into testes. In transgenic XX mice (and some human XX males), SRY alone is sufficient to induce male differentiation.

Various processes are involved in the development of sex differences in humans. Sexual differentiation in humans includes development of different genitalia and the internal genital tracts, breasts, body hair, and plays a role in gender identification.[1]

The development of sexual differences begins with the XY sex-determination system that is present in humans, and complex mechanisms are responsible for the development of the phenotypic differences between male and female humans from an undifferentiated zygote.[2] Atypical sexual development, and ambiguous genitalia, can be a result of genetic and hormonal factors.[3]

Read more:
Sexual differentiation - Wikipedia, the free encyclopedia