Back pain or discomfort is common during pregnancy and should beexpected to some degree by most women.Back pain may be experiencedduring any point of your pregnancy; however, it most commonly occurslater in pregnancy as baby grows.

Back paincan disrupt your daily routine or interfere with a good night of sleep. The good news is there are steps you can take to manage the back painthat you experience.

You are not alone if you experience back pain during your pregnancy. The prevalence varies with reports showing between 50 to 70 percentof pregnant women experiencing back pain.

Back pain during pregnancy is related to a number of factors.Somewomen begin to have lower back pain with the onset of pregnancy. Women who are most at risk for back pain are those who are overweightor had back pain prior to pregnancy.

Here is a list of potential causesof back pain or discomfort during pregnancy:

Back pain may not be prevented completely, but there are things thatyou can do to reduce the severity or frequency.

Here are a few steps you can take to help reduce the back pain you are experiencing:

There are a number of things you can do to treat back pain duringpregnancy.Some of the steps you take to avoid back pain may alsobe used to treat current back pain.

Here are some other common interventions:

Experiencing back pain is usually not a reason to contactyour health care provider, but there are situations where contactingyour provider is necessary.

Read this article:
Back Pain During Pregnancy: Causes, Treatment & Prevention

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The UCLA Program is a combined program caring for patients with Hematologic Malignancies receiving chemotherapy and those patients for whom Stem Cell Transplantation is the therapy of choice. The treatmentof blood and marrow cancers includecurrently available therapies, investigational drugs and treatments, as well as stem cell transplantation. Our physicians meet weekly to discussindividual treatment approachesas part of developing a coordinated treatment recommendation.

Bone Marrow Transplantation was first performed at UCLA in 1968 using a related allogeneic transplant to treat an 18 month old child with severe combined immunodeficiency syndrome. The UCLA Marrow Transplantation Program was formally initiated in 1973. Unrelated donor marrow transplants have been carried out at UCLA since 1987, and Cord Blood Transplants have been performed at UCLA since 1996. Autologous transplants have been performed at our program since 1977. Since 1992 most of the Autologous Transplants have utilized Peripheral Blood Stem Cells. Since 1998 an increasing number of the Allogenic Transplants have utilized Peripheral Blood Stem Cells. From inception to the completion of 2007 we have performed 3726 transplants (3080 transplants in the adult population and 646 in the pediatric population).

For decades, this comprehensive program has provided a full range of services as a local, regional, national, and international referral center for transplantations for selected malignancies:

Our goals include finding new and innovative treatments for malignancies and expanding the effectiveness and applicability of bone marrow transplantation through such means as biologic response modifiers, growth factors, and chemotherapeutic agents.

Protocols involving chemotherapy with or without radiation therapy for patients in remission or relapse are available using bone marrow or peripheral blood stem cells from allogeneic, autologous and unrelated donors.

A bone marrow transplant is a procedure that transplant healthy bone marrow into a patient whose bone marrow is not working properly. A bone marrow transplant may be done for several conditions including hereditary blood diseases, hereditary metabolic diseases, hereditary immune deficiencies, and various forms of cancer.

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Bone MarrowTransplant

How to Schedule Your Evaluation Appointment at UCLA

The United Network for Organ Sharing (UNOS) provides a toll-free patient services lines to help transplant candidates, recipients, and family members understand organ allocation practices and transplantation data. You may also call this number to discuss problems you may be experiencing with your transplant center or the transplantation system in general. The toll-free patient services line number is 1-888-894-6361

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Bone Marrow/Stem Cell Transplant | UCLA Transplantation ...

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Dr.DorisTayloris involved in both laboratory and clinical studies using cell therapy to treat disease. Almost5 million Americans are living with heart failure and more than half a million new cases are diagnosed annually. Almost 50,000 people die each year while awaiting a heart transplant and, for a decade or more, only about 2,200 heart transplants have been performed in the entire United States. The need is dwarfed by the availability of donor organs.

This is one of the reasons there is such hope placed in the promising field of regenerative medicine. The groundbreaking work of Dr. Taylor and her team has demonstrated the ability in the lab to strip organs, including the heart, of their cellular make-up leaving a decellularized "scaffold." The heartcan then be re-seeded with cells that, when supplied with blood and oxygen, regenerate the scaffold into a functioning heart. Dr. Taylor calls this using nature's platform to create a bioartificial heart.

The hope is that this research is an early step toward being able to grow a fully functional human heart in the laboratory. Dr. Taylor has demonstrated that the process works for other organs as well, such as kidney, pancreas, lung, and liver where she has already tested the same approachopening a door in the field of organ transplantation.

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About Regenerative Medicine Research at the Texas Heart ...

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Introduction

[Note: Many of the medical and scientific terms used in this summary are found in the NCI Dictionary of Genetics Terms. When a linked term is clicked, the definition will appear in a separate window.]

[Note: Many of the genes described in this summary are found in the Online Mendelian Inheritance in Man (OMIM) database. When OMIM appears after a gene name or the name of a condition, click on OMIM for a link to more information.]

Colorectal cancer (CRC) is the third most commonly diagnosed cancer in both men and women.

Estimated new cases and deaths from CRC in 2015:[1]

About 75% of patients with CRC have sporadic disease with no apparent evidence of having inherited the disorder. The remaining 25% of patients have a family history of CRC that suggests a hereditary contribution, common exposures among family members, or a combination of both. Genetic mutations have been identified as the cause of inherited cancer risk in some colon cancerprone families; these mutations are estimated to account for only 5% to 6% of CRC cases overall. It is likely that other undiscovered genes and background genetic factors contribute to the development of familial CRC in conjunction with nongenetic risk factors.

(Refer to the PDQ summaries on Colorectal Cancer Screening; Colorectal Cancer Prevention; Colon Cancer Treatment; and Rectal Cancer Treatment for more information about sporadic CRC.)

Colorectal tumors present with a broad spectrum of neoplasms, ranging from benign growths to invasive cancer and are predominantly epithelial-derived tumors (i.e., adenomas or adenocarcinomas).

Pathologists have classified the lesions into the following three groups:

Research, however, suggests increased CRC risk in some families who have multiple members affected with juvenile polyposis, Peutz-Jeghers syndrome, and hyperplastic polyposis.[2-4]

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Genetics of Colorectal Cancer - National Cancer Institute

Recommendation and review posted by Bethany Smith

Mesenchymal stem cells, or MSCs, are multipotent stromal cells that can differentiate into a variety of cell types,[1] including: osteoblasts (bone cells),[2]chondrocytes (cartilage cells),[3]myocytes (muscle cells)[4] and adipocytes (fat cells). This phenomenon has been documented in specific cells and tissues in living animals and their counterparts growing in tissue culture.

While the terms mesenchymal stem cell and marrow stromal cell have been used interchangeably, neither term is sufficiently descriptive:

The youngest, most primitive MSCs can be obtained from the umbilical cord tissue, namely Wharton's jelly and the umbilical cord blood. However the MSCs are found in much higher concentration in the Whartons jelly compared to the umbilical cord blood, which is a rich source of hematopoietic stem cells. The umbilical cord is easily obtained after the birth of the newborn, is normally thrown away, and poses no risk for collection. The umbilical cord MSCs have more primitive properties than other adult MSCs obtained later in life, which might make them a useful source of MSCs for clinical applications.

An extremely rich source for mesenchymal stem cells is the developing tooth bud of the mandibular third molar. While considered multipotent, they may prove to be pluripotent. The stem cells eventually form enamel, dentin, blood vessels, dental pulp, and nervous tissues, including a minimum of 29 different unique end organs. Because of extreme ease in collection at 810 years of age before calcification, and minimal to no morbidity, they will probably constitute a major source for personal banking, research, and multiple therapies. These stem cells have been shown capable of producing hepatocytes.

Additionally, amniotic fluid has been shown to be a rich source of stem cells. As many as 1 in 100 cells collected during amniocentesis has been shown to be a pluripotent mesenchymal stem cell.[9]

Adipose tissue is one of the richest sources of MSCs. There are more than 500 times more stem cells in 1 gram of fat than in 1 gram of aspirated bone marrow. Adipose stem cells are actively being researched in clinical trials for treatment of a variety of diseases.

The presence of MSCs in peripheral blood has been controversial. However, a few groups have successfully isolated MSCs from human peripheral blood and been able to expand them in culture.[10] Australian company Cynata also claims the ability to mass-produce MSCs from induced pluripotent stem cells obtained from blood cells using the method of K. Hu et al.[11][12]

Mesenchymal stem cells are characterized morphologically by a small cell body with a few cell processes that are long and thin. The cell body contains a large, round nucleus with a prominent nucleolus, which is surrounded by finely dispersed chromatin particles, giving the nucleus a clear appearance. The remainder of the cell body contains a small amount of Golgi apparatus, rough endoplasmic reticulum, mitochondria, and polyribosomes. The cells, which are long and thin, are widely dispersed and the adjacent extracellular matrix is populated by a few reticular fibrils but is devoid of the other types of collagen fibrils.[13][14]

The International Society for Cellular Therapy (ISCT) has proposed a set of standards to define MSCs. A cell can be classified as an MSC if it shows plastic adherent properties under normal culture conditions and has a fibroblast-like morphology. In fact, some argue that MSCs and fibroblasts are functionally identical.[15] Furthermore, MSCs can undergo osteogenic, adipogenic and chondrogenic differentiation ex-vivo. The cultured MSCs also express on their surface CD73, CD90 and CD105, while lacking the expression of CD11b, CD14, CD19, CD34, CD45, CD79a and HLA-DR surface markers.[16]

MSCs have a great capacity for self-renewal while maintaining their multipotency. Beyond that, there is little that can be definitively said. The standard test to confirm multipotency is differentiation of the cells into osteoblasts, adipocytes, and chondrocytes as well as myocytes and neurons. MSCs have been seen to even differentiate into neuron-like cells,[17][18] but there is lingering doubt whether the MSC-derived neurons are functional.[19] The degree to which the culture will differentiate varies among individuals and how differentiation is induced, e.g., chemical vs. mechanical;[20] and it is not clear whether this variation is due to a different amount of "true" progenitor cells in the culture or variable differentiation capacities of individuals' progenitors. The capacity of cells to proliferate and differentiate is known to decrease with the age of the donor, as well as the time in culture. Likewise, whether this is due to a decrease in the number of MSCs or a change to the existing MSCs is not known.[citation needed]

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Mesenchymal stem cell - Wikipedia, the free encyclopedia

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High levels of active TGF- in the bone marrow and abnormalities in bone remodeling are associated with multiple skeletal disorders. Genetic mutations in the TGF- signaling pathway cause premature activation of matrix latent TGF- and may manifest with various skeletal defects. There are additional diseases that result in high levels of active TGF-, which may contribute to the pathology. Here, we discuss how abnormal TGF- signaling results in uncoupled bone remodeling, mainly by loss of site-directed recruitment of MSCs that causes aberrant bone formation. Direct or indirect inhibition of TGF- signaling may provide potential therapeutic options for these disorders.

Genetic disorders. The critical role of TGF-1 in the reversal phase of bone remodeling is demonstrated by the range of skeletal disorders resulting from mutations in genes involved in TGF-1 signaling. Camurati-Engelmann disease (CED), characterized by a fusiform thickening of the diaphysis of the long bones and skull, is caused by mutations in TGFB1 that result in premature activation of TGF-1 (7174). Approximately 11 different TGFB1 mutations have been identified from families affected by CED (75, 76). All of the mutations are located in the region encoding LAP, either destabilizing LAP disulfide bridging or affecting secretion of the protein, both of which increase TGF-1 signaling, as confirmed by in vitro cell cultures and mouse models. Bone histology sections from patients with CED show decreased trabecular connectivity despite normal bone histomorphometric parameters with respect to osteoblast and osteoclast numbers (76, 77), suggestive of uncoupled bone remodeling. In vitro, the ratio of active to total TGF-1 in conditioned medium from cells expressing the CED mutant TGF-1 is significantly higher and enhances MSC migration (18). Targeted recruitment of MSCs to the bone-remodeling site is likely disrupted, secondary to loss of a TGF- gradient.

Elevations in TGF- signaling have also been observed in many genetic connective tissue disorders with craniofacial, skeletal, skin, and cardiovascular manifestations, including Marfan syndrome (MFS), Loeys-Dietz syndrome (LDS), and Shprintzen-Goldberg syndrome (SGS). MFS is caused by mutations in fibrillin and often results in aortic dilation, myopia, bone overgrowth, and joint laxity. Fibrillin is deposited in the ECM and normally binds TGF-, rendering it inactive. In MFS, the decreased level of fibrillin enhances TGF- activity (78). LDS is caused by inactivating mutations in genes encoding TRI and TRII (79). Physical manifestations include arterial aneurysms, hypertelorism, bifid uvula/cleft palate, and bone overgrowth resulting in arachnodactyly, joint laxity, and scoliosis. Pathologic analyses of affected tissue suggest chronically elevated TGF- signaling, despite the inactivating mutation (79). The mechanism of enhanced TGF- signaling remains under investigation. SGS is caused by mutations in the v-ski avian sarcoma viral oncogene homolog (SKI; refs. 80, 81) and causes physical features similar to those of MFS plus craniosynostosis. SKI negatively regulates SMAD-dependent TGF- signaling by impeding SMAD2 and SMAD3 activation, preventing nuclear translocation of the SMAD4 complex, and inhibiting TGF- target gene output by competing with p300/CBP for SMAD binding and recruiting transcriptional repressor proteins, such as mSin3A and HDACs (8284).

The neurocutaneous syndrome neurofibromatosis type 1 (NF1) has been noted to have skeletal features similar to those of CED, MFS, and LDS, including kyphoscoliosis, osteoporosis, and tibial pseudoarthrosis. Hyperactive TGF-1 signaling has been implicated as the primary factor underlying the pathophysiology of the osseous defects in Nf1fl/Col2.3Cre mice, a model of NF1 that closely recapitulates the skeletal abnormalities found in human disease (85). The exact mechanisms mediating mutant neurofibrominassociated enhancement of TGF- production and signaling remain unknown.

Osteoarthritis. While genetic disorders are rare, they have provided critical insight into the pathophysiology of more common disorders. Uncoupled bone remodeling accompanies the onset of osteoarthritis. TGF-1 is activated in subchondral bone in response to altered mechanical loading in an anterior cruciate ligament transection (ACLT) mouse model of osteoarthritis (86). High levels of active TGF-1 induced formation of nestin+ MSC clusters via activation of ALK5-SMAD2/3. MSCs underwent osteoblast differentiation in these clusters, leading to formation of marrow osteoid islets. Transgenic expression of active TGF-1 in osteoblastic cells alone was sufficient to induce osteoarthritis, whereas direct inhibition of TGF- activity in subchondral bone attenuated the degeneration of articular cartilage. Knockout of Tgfbr2 in nestin+ MSCs reduced osteoarthritis development after ACLT compared with wild-type mice, which confirmed that MSCs are the target cell population of TGF- signaling. High levels of active TGF-1 in subchondral bone likely disrupt the TGF- gradient and interfere with targeted migration of MSCs. Furthermore, mutations of ECM proteins that bind to latent TGF-s, such as small leucine-rich proteoglycans (87) and fibrillin (88), or mutations in genes involved in activation of TGF-, such as in CED (76) and LDS (89), are associated with high osteoarthritis incidence. Osteoblast differentiation of MSCs in aberrant locations appears histologically as subchondral bone osteoid islets and alters the thickness of the subchondral plate and calcified cartilage zone, changes known to be associated with osteoarthritis (90, 91). A computer-simulated model found that a minor increase in the size of the subchondral bone (1%2%) causes significant changes in the mechanical load properties on articular cartilage, which likely leads to degeneration (86). Importantly, inhibition of the TGF- signaling pathway delayed the development of osteoarthritis in both mouse and rat models (86).

MSCs in bone loss. Aging leads to deterioration of tissue and organ function. Skeletal aging is especially dramatic: bone loss in both women and men begins as early as the third decade, immediately after peak bone mass. Aging bone loss occurs when bone formation does not adequately compensate for osteoclast bone resorption during remodeling. Age-associated osteoporosis was previously believed to be due to a decline in survival and function of osteoblasts and osteoprogenitors; however, recent work by Park and colleagues found that mature osteoblasts and osteoprogenitors are actually nonreplicative cells and require constant replenishment from bone marrow MSCs (92). When MSCs fail to migrate to bone-resorptive sites or are unable to commit and differentiate into osteoblasts, new bone formation is impaired. Therefore, insufficient recruitment of MSCs, or their differentiation to osteoblasts, at the bone remodeling surface may contribute to the decline in bone formation in the elderly.

There are multiple hypotheses regarding the decreased osteogenic potential of MSCs during aging. For example, during aging, the bone marrow environment has an increased concentration of ROS and lipid oxidation that may decrease osteoblast differentiation, yet increase osteoclast activity (93, 94). MSCs also undergo senescence, which decreases proliferative capacity and contributes to decreased bone formation (95, 96). Cellular senescence involves the secretion of a plethora of factors, including TGF-, which induces expression of cyclin-dependent kinase inhibitors 2A and 2B (p16INK4A and p15INK4B, respectively; refs. 97).

Microgravity experienced by astronauts during spaceflight causes severe physiological alterations in the human body, including a 1%2% loss of bone mass every month during spaceflight (98). Several studies have shown decreases in osteoblastic markers of bone formation and increases in bone resorption (99101). The underlying molecular mechanisms responsible for the apparent concurrent decrease in bone formation and increase in bone resorption remain under investigation. Work by the McDonald group suggests that bone remodeling may become uncoupled under zero-gravity conditions secondary to decreased RhoA activity and resultant changes in actin stress fiber formation (102). In modeled microgravity, cultured human MSCs exhibit disruption of F-actin stress fibers within three hours of initiation of microgravity; the fibers are completely absent after seven days. RhoA activity is significantly reduced, and introduction of an adenoviral construct expressing constitutively active RhoA can reverse the elimination of stress fibers, significantly increasing markers of osteoblast differentiation (102). Under zero-gravity conditions, RhoA is unable to bind to its receptor, and a sufficient number of MSCs may not be able to migrate correctly to the bone-resorptive site for osteoblast differentiation, ultimately leading to bone loss with every cycle of remodeling.

Bone metastases are a frequent complication of cancer and often have both osteolytic and osteoblastic features, indicative of dysregulated bone remodeling. The importance of the bone marrow microenvironment contributing to the spread of cancer was first described in 1889 (103), postulating that tumor cells can grow only if they are in a conducive environment. Activation of matrix TGF- during bone remodeling plays a central role in the initiation of bone metastases and tumor expansion by regulating osteolytic and prometastatic factors (reviewed in refs. 104110). For example, TGF- can induce osteoclastic bone destruction by upregulating tumor cell expression of PTHrP and IL-11. Additionally, upregulation of CXCR4 by TGF- may home cancer cells to bones.

Link:
JCI - Bone marrow mesenchymal stem cells and TGF- ...

Recommendation and review posted by Bethany Smith

An immune disorder is a dysfunction of the immune system. These disorders can be characterized in several different ways:

According to the International Union of Immunological Societies, more than 150 primary immunodeficiency diseases (PIDs) have been characterized.[1] However, the number of acquired immunodeficiencies exceeds the number of PIDs.[2]

It has been suggested that most people have at least one primary immunodeficiency.[3] Due to redundancies in the immune system, though, many of these are never detected.

Primary immune deficiency diseases are those caused by inherited genetic mutations. Secondary or acquired immune deficiencies are caused by something outside the body such as a virus or immune suppressing drugs.[4]

Primary immune diseases are at risk to an increased susceptibility to, and often recurrent ear infections, pneumonia, bronchitis, sinusitis or skin infections. Immunodeficient patients may less frequently develop abscesses of their internal organs, autoimmune or rheumatologic and gastrointestinal problems.[5]

An allergy is an abnormal immune reaction to a harmless antigen.

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Immune disorder - Wikipedia, the free encyclopedia

Recommendation and review posted by simmons

Indications Fine lines and wrinkles associated with expression lines that occur of time as well as environmental factors such as sun damage and smoking. Hyperpigmentation and/or uneven skin tone. Loss of elasticity and firmness. Spider veins. Lack of proper hydration.

Ingredients Proprietary Aloe/Vitamin/Mineral Blend (AVM), Tamarind Extract, Gotu Kola, Essential Oil Blend*, Palmitoyl Hexapeptide (Argireline), Palmitoyl Pentapeptide (Matrixyl), Hyaluronic Acid, Pomegranate extract, Olive leaf Extract, ALA, DMAE, Allantoin, DevaBrightT **, Herbal infusion Blend:*** Soy extract, EGF (Epidermal Growth Factor), Vitamin E Oil, Vitamins A and B2, CoQ10; guar gum and gum Arabic; Certified kosher and vegan xanthan gum & potassium sorbate; essential oil of lemongrass. * Essential Oil Blend:(Sunflower, Hemp seed, Jojoba, Borage, Evening Primrose, Sesame, Sea Buckthorn, Almond & grapeseed) ** DevaBright: (proprietary herbal blend of Licorice root, Kojic acid & Uva ursi) *** Botanical Actives (herbal infusion): Bladderwrack, Eyebright, Slippery Elm, Fennel seed, Chickweed, Neem leaf, Skullcap, Echinacea, Calendula flowers, Bilberry (vitamin C bioflavanoids), Ginko leaf, Hawthorne berry, Green Tea, Marshmallow root, St. Johns Wort, Rosemary leaf & Alfalfa

Directions Twice a day, after cleansing skin, pat dry and apply small quantity evenly to face, neck and exposed'V' of chest. Concentrate on expression lines and areas most affected by sun damage and dryness, as well as areas of uneven pigment and loss of firmness.

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Aryu-Deva BioScience Renewal Complex

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Organisms of many species are specialized into male and female varieties, each known as a sex.[1]Sexual reproduction involves the combining and mixing of genetic traits: specialized cells known as gametes combine to form offspring that inherit traits from each parent. Gametes can be identical in form and function (known as isogamy), but in many cases an asymmetry has evolved such that two sex-specific types of gametes (heterogametes) exist (known as anisogamy). By definition, male gametes are small, motile, and optimized to transport their genetic information over a distance, while female gametes are large, non-motile and contain the nutrients necessary for the early development of the young organism. Among humans and other mammals, males typically carry XY chromosomes, whereas females typically carry XX chromosomes, which are a part of the XY sex-determination system.

The gametes produced by an organism determine its sex: males produce male gametes (spermatozoa, or sperm, in animals; pollen in plants) while females produce female gametes (ova, or egg cells); individual organisms which produce both male and female gametes are termed hermaphroditic. Frequently, physical differences are associated with the different sexes of an organism; these sexual dimorphisms can reflect the different reproductive pressures[clarification needed] the sexes experience.

Sexual reproduction first probably evolved about a billion years ago within ancestral single-celled eukaryotes.[2] The reason for the evolution of sex, and the reason(s) it has survived to the present, are still matters of debate. Some of the many plausible theories include: that sex creates variation among offspring, sex helps in the spread of advantageous traits, and that sex helps in the removal of disadvantageous traits.

Sexual reproduction is a process specific to eukaryotes, organisms whose cells contain a nucleus and mitochondria. In addition to animals, plants, and fungi, other eukaryotes (e.g. the malaria parasite) also engage in sexual reproduction. Some bacteria use conjugation to transfer genetic material between cells; while not the same as sexual reproduction, this also results in the mixture of genetic traits.

The defining characteristic of sexual reproduction in eukaryotes is the difference between the gametes and the binary nature of fertilization. Multiplicity of gamete types within a species would still be considered a form of sexual reproduction. However, no third gamete is known in multicellular animals.[3][4][5]

While the evolution of sex dates to the prokaryote or early eukaryote stage,[citation needed] the origin of chromosomal sex determination may have been fairly early in eukaryotes.[citation needed] The ZW sex-determination system is shared by birds, some fish and some crustaceans. Most mammals, but also some insects (Drosophila) and plants (Ginkgo) use XY sex-determination.[citation needed]X0 sex-determination is found in certain insects.

No genes are shared between the avian ZW and mammal XY chromosomes,[6] and from a comparison between chicken and human, the Z chromosome appeared similar to the autosomal chromosome 9 in human, rather than X or Y, suggesting that the ZW and XY sex-determination systems do not share an origin, but that the sex chromosomes are derived from autosomal chromosomes of the common ancestor of birds and mammals. A paper from 2004 compared the chicken Z chromosome with platypus X chromosomes and suggested that the two systems are related.[7]

Sexual reproduction in eukaryotes is a process whereby organisms form offspring that combine genetic traits from both parents. Chromosomes are passed on from one generation to the next in this process. Each cell in the offspring has half the chromosomes of the mother and half of the father.[8] Genetic traits are contained within the deoxyribonucleic acid (DNA) of chromosomesby combining one of each type of chromosomes from each parent, an organism is formed containing a doubled set of chromosomes. This double-chromosome stage is called "diploid", while the single-chromosome stage is "haploid". Diploid organisms can, in turn, form haploid cells (gametes) that randomly contain one of each of the chromosome pairs, via meiosis.[9] Meiosis also involves a stage of chromosomal crossover, in which regions of DNA are exchanged between matched types of chromosomes, to form a new pair of mixed chromosomes. Crossing over and fertilization (the recombining of single sets of chromosomes to make a new diploid) result in the new organism containing a different set of genetic traits from either parent.

In many organisms, the haploid stage has been reduced to just gametes specialized to recombine and form a new diploid organism; in others, the gametes are capable of undergoing cell division to produce multicellular haploid organisms. In either case, gametes may be externally similar, particularly in size (isogamy), or may have evolved an asymmetry such that the gametes are different in size and other aspects (anisogamy).[10] By convention, the larger gamete (called an ovum, or egg cell) is considered female, while the smaller gamete (called a spermatozoon, or sperm cell) is considered male. An individual that produces exclusively large gametes is female, and one that produces exclusively small gametes is male. An individual that produces both types of gametes is a hermaphrodite; in some cases hermaphrodites are able to self-fertilize and produce offspring on their own, without a second organism.[11]

Most sexually reproducing animals spend their lives as diploid organisms, with the haploid stage reduced to single cell gametes.[12] The gametes of animals have male and female formsspermatozoa and egg cells. These gametes combine to form embryos which develop into a new organism.

Original post:
Sex - Wikipedia, the free encyclopedia

Recommendation and review posted by Bethany Smith

This WHO classification covers the female and male breast, ovaries, fallopian tumors, uterine cervix, uterine corpus, vulva, vagina and inherited tumor syndromes. It includes a comprehensive classification of benign and malignant neoplasms. Targeted readership includes pathologists, gynaecologists, surgeons, oncologists, and basic scientists. Similar to the previous volumes of the series, the book includes numerous color photographs, magnetic resonance images, CT scans and charts. In addition to its pathology and genetics, each lesion is described with its epidemiology, etiology, clinical features, as well as prognosis and predictive factors.

This book is in the series commonly referred to as the "Blue Book" series. Pathology and Genetics of Tumors of the Breast and Female Genital Organs

Contributors::Dr Vera M. Abeler, Dr Jorge Albores-Saavedra, Dr Isabel Alvarado-Cabrero, Dr Erik Sgaard Andersen, Dr Alan Ashworth, Dr Jean-Pierre Bellocq, Dr Christine Bergeron, Dr Ross S. Berkowitz, Dr Werner Bcker, Dr Anne-Lise Brresen-Dale, Dr Annegien Broeks, Dr C. Hilary Buckley, Dr Gianni Bussolati,Dr Rosmarie Caduff,Dr Maria-Luisa Carcangiu, Dr Silvestro Carinelli, Dr Annie N. Cheung, Dr Anne-Marie Cleton-Jansen, Dr Cees J. Cornelisse, Dr Christopher P. Crum, Dr Bruno Cutuli, Dr Peter Devilee, Dr Mojgan Devouassoux-Shisheboran, Dr Manfred Dietel, Dr Stephen Dobbs, Dr Maria Drijkoningen, Dr Douglas Easton, Dr Rosalind Eeles, Dr Ian O. Ellis, Dr Charis Eng, Dr Vincenzo Eusebi, Dr Mathias Fehr, Dr Rosemary A. Fisher, Dr Riccardo Fodde, Dr Silvia Franceschi, Dr Shingo Fujii, Dr David R. Genest, Dr Deborah J. Gersell, Dr Blake Gilks, Dr David E. Goldgar,Dr Annekathryn Goodman,Dr Pierre Hainaut, Dr Janet Hall, Dr Urs Haller, Dr Antonius G.J.M. Hanselaar, Dr Steffen Hauptmann, Dr Michael R. Hendrickson, Dr Sylvia H. Heywang-Kbrunner, Dr Heinz Hfler, Dr Roland Holland, Dr Jocelyne Jacquemier, Dr Rudolf Kaaks, Dr Apollon I. Karseladze, Dr Richard L. Kempson, Dr Takako Kiyokawa, Dr Ikuo Konishi, Dr Rahel Kubik-Huch, Dr Robert J. Kurman, Dr Sunil R. Lakhani, Dr Janez Lamovec, Dr Salvatore Lanzafame, Dr Sigurd Lax, Dr Kenneth R. Lee, Dr Fabio Levi, Dr Gatan Macgrogan, Dr Gaetano Magro, Dr Kien T. Mai, Dr W. Glenn Mccluggage, Dr Hanne Meijers-Heijboer, Dr Rosemary R. Millis, Dr Farid Moinfar, Dr Samuel C. Mok, Dr Alvaro N. Monteiro, Dr Eoghan E. Mooney, Dr Philippe Morice, Dr Hans Morreau, Dr Kiyoshi Mukai, Dr Mary Murnaghan, Dr George L. Mutter, Dr Steven Narod, Dr Jahn M. Nesland, Dr Edward S. Newlands, Dr Bernt B. Nielsen, Dr Francisco F. Nogales, Dr Hiroko Ohgaki, Dr Magali Olivier, Dr Andrew G. str, Dr Jorma Paavonen, Dr Paivi Peltomak, Dr Johannes L. Peterse, Dr Jurgen J.M. Piek, Dr Paola Pisani, Dr Steven Piver, Dr Jaime Prat, Dr Klaus Prechtel, Dr Dieter Prechtel, Dr Usha Raju, Dr Juan Rosai, Dr Lawrence M. Roth, Dr Peter Russell, Dr Joanne K.L. Rutgers, Dr Rengaswamy Sankaranarayanan, Dr Anna Sapino, Dr Annie J. Sasco, Dr Xavier Sastre-Garau, Dr Stuart J. Schnitt, Dr John O. Schorge, Dr Peter E. Schwartz, Dr Robert E. Scully, Dr Hideto Senzaki, Dr Elvio G. Silva, Dr Steven G. Silverberg, Dr Jorge Soares, Dr Leslie H. Sobin, Ms Nayanta Sodha Msc, Dr Mike R. Stratton, Dr Csilla Szabo, Dr Lszl Tabr, Dr Aleksander Talerman, Dr Colette Taranger-Charpin, Dr Fattaneh A. Tavassoli, Dr. Antonio Bernardino Almeida, Dr Massimo Tommasino, Dr Airo Tsubura, Dr Paul J. Van Diest, Dr Laura J. Vant Veer, Dr Russell S. Vang, Dr Hans F.A. Vasen, Dr A.R. Venkitaraman, Dr Ren H.M. Verheijen, Dr William R. Welch, Dr Michael Wells, Dr Edward J. Wilkinson, Dr Andrew Wotherspoon,

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Pathology and Genetics of Tumours of the Breast and Female ...

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If you're making plans for summer fun and vacations, keep in mind that the sun, while the source of life for our planet, has potentially dangerous effects that should not be overlooked.

Below, we'll explain the basics for helping to keep you and your family safe and healthy in the summer months.

Every man, woman, and child ought to be applying UVA and UVB-filtering sunscreen prior to outdoor ventures that involve exposure to sunlight, especially between the hours of 10:00 a.m. and 2:00 p.m., when the sun's rays are at their strongest.

People living near the equator and at high altitudes need to be particularly vigilant concerning protection. Parents should consider not only themselves, but their children as well, since blistering sunburns early in life have been associated with the development of skin cancers in adulthood.

Ultraviolet-blocking sunglasses and protective hats and clothing offer significant protection and, unlike sunscreen, don't have to be reapplied throughout the day.

Vitamin D supplements are inexpensive, less time-consuming than sunbathing, and confer no health risk if consumed in a reasonable dose.

If you are unsure of the right amount of the vitamin to use, arrange to have your blood tested for serum 25-hydroxyvitamin D and adjust your vitamin dose accordingly.

Heatstroke symptoms include a body temperature of 104 degrees Fahrenheit or higher, altered mental state, dry skin (unless vigorously exercising), skin flushing, nausea and vomiting, headache and rapid breathing or heart rate.

Heat stroke most often afflicts older individuals due to a reduction in their blood vessels' ability to dilate in response to heat, which is caused by a decrease in nitric oxide production. This also increases the risk for heart-related problems.

Recent studies show folic acid increases vasodilation by increasing nitric oxide production. This is valuable for aging men and women to protect against the cardiac risks associated with hot weather.1

Originally posted here:
The Life Extension Blog

Recommendation and review posted by Bethany Smith

General Information About Adult Non-Hodgkin Lymphoma (NHL)

The NHLs are a heterogeneous group of lymphoproliferative malignancies with differing patterns of behavior and responses to treatment.[1]

Like Hodgkin lymphoma, NHL usually originates in lymphoid tissues and can spread to other organs. NHL, however, is much less predictable than Hodgkin lymphoma and has a far greater predilection to disseminate to extranodal sites. The prognosis depends on the histologic type, stage, and treatment.

Estimated new cases and deaths from NHL in the United States in 2015:[2]

NHL usually originates in lymphoid tissues.

Anatomy of the lymph system.

The NHLs can be divided into two prognostic groups: the indolent lymphomas and the aggressive lymphomas.

Indolent NHL types have a relatively good prognosis with a median survival as long as 20 years, but they usually are not curable in advanced clinical stages.[3] Early-stage (stage I and stage II) indolent NHL can be effectively treated with radiation therapy alone. Most of the indolent types are nodular (or follicular) in morphology.

The aggressive type of NHL has a shorter natural history, but a significant number of these patients can be cured with intensive combination chemotherapy regimens.

In general, with modern treatment of patients with NHL, overall survival at 5 years is over 60%. Of patients with aggressive NHL, more than 50% can be cured. The vast majority of relapses occur in the first 2 years after therapy. The risk of late relapse is higher in patients who manifest both indolent and aggressive histologies.[4]

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Adult Non-Hodgkin Lymphoma Treatment - National Cancer ...

Recommendation and review posted by Bethany Smith

Psoriasis is a skin condition that causes red, flaky, crusty patches of skin covered with silvery scales.

These patches normally appear on your elbows, knees, scalp and lower back, but can appear anywhere on your body.Most people are only affected with small patches. In some cases, the patches can be itchy or sore.

Psoriasis affects around 2% of people in the UK. It can start at any age, but most often develops in adults under 35 years old. The condition affects men and women equally.

The severity of psoriasis varies greatly from person to person. For some people it's just a minor irritation, but for others it can havea major impact on their quality of life.

Psoriasis is a long-lasting (chronic) disease that usually involves periods when you have no symptoms ormild symptoms, followed by periods when symptoms are more severe.

Read more about the symptoms of psoriasis.

People with psoriasis have anincreased production of skin cells.

Skin cells are normallymade and replaced every three to four weeks, but in psoriasis this process only lasts about three to seven days. The resulting build-up of skin cells is what creates the patches associated with psoriasis.

Although the process isn't fully understood, it's thoughtto be related to a problem with the immune system. The immune systemis your body's defence against disease and infection, but for people with psoriasis, it attacks healthy skin cells by mistake.

Psoriasis can run in families,although the exact role that genetics plays in causing psoriasis is unclear.

Read the rest here:
Psoriasis - NHS Choices

Recommendation and review posted by simmons

Updated March 2015

According to the National Spinal Cord Injury Association, as many as 450,000 people in the U.S. are living with a spinal cord injury (SCI). Other organizations conservatively estimate this figure to be about 250,000.

Every year, an estimated 11,000 SCIs occur in the U.S. Most of these are caused by trauma to the vertebral column, thereby affecting the spinal cord's ability to send and receive messages from the brain to the body's systems that control sensory, motor and autonomic function below the level of injury.

According to the Centers for Diseases Control and Prevention (CDC), SCI costs the nation an estimated $9.7 billion each year. Pressure sores alone, a common secondary condition among people with SCI, cost an estimated $1.2 billion.

Incidence

The Spinal Column/Cord

The spinal cord is about 18 inches long, extending from the base of the brain to near the waist. Many of the bundles of nerve fibers that make up the spinal cord itself contain upper motor neurons (UMNs). Spinal nerves that branch off the spinal cord at regular intervals in the neck and back contain lower motor neurons (LMNs).

The spine itself is divided into four sections, not including the tailbone:

Cervical vertebrae (C1-7) located in the neck;

Thoracic vertebrae (T1-12), in the upper back (attached to the ribcage);

Original post:
AANS - Spinal Cord Injury

Recommendation and review posted by sam

This site is a free and informative resource for those living with a spinal cord injury or other disabling injuries or diseases of the spine. It is meant to be a "best of the web" site for SCI health and caregiver information. Visit regularly for updated resources, news and more. If you know of something that should be added, such as a good resource site, news, clinical trials, pictures, etc., please contact me.

This site was originally created as my own personal resource. As it grew I decided to share it with others like me (C5/6 Quadriplegic per a diving accident in 1999). Please note that only quality websites and related information are listed here. So, there is no need to bookmark a bunch of sites as the best resources are right here for you.

Be sure to check out the spinal cord injury news blog. It's updated on a regular basis featuring current SCI news. If you know of any encouraging news, a new SCI resource, a new daily living aid or just something noteworthy drop me a line and I'll try to post it.

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Spinal Cord Injury Information Pages

Recommendation and review posted by sam

Introduction

Multiple sclerosis is a progressive autoimmune disease and the most common neurological disease diagnosed in young adults. It is believed that multiple sclerosis occurs when the bodys own immune system attacks the central nervous system. Commonly called MS, the disease generally gets worse with time and can cause significant nerve damage.

The progression and severity of multiple sclerosis varies greatly among individuals. The severity of multiple sclerosis ranges from mild to severe and disabling, and it can result in muscle weakness, loss of balance, and difficulty walking.

In some cases, multiple sclerosis can lead to serious complications, such as choking and paralysis. Early diagnosis and medical care can help manage and control symptoms and minimize complications of multiple sclerosis.

2015 Healthgrades Operating Company, Inc. All rights reserved. May not be reproduced or reprinted without permission from Healthgrades Operating Company, Inc. Use of this information is governed by the Healthgrades User Agreement.

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Multiple Sclerosis - Symptoms, Causes, Treatments

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Haematopoietic stem cells and early lymphoid progenitors ...

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BCH Division of Genetics and Genomics Seminar

Generating Cartilage from Human Pluripotent Stem Cells: A Developmental Approach.

Special Seminar

How Neurons Talk to the Blood: Sensory Regulation of Hematopoiesis in the Drosophila Model

Genetics Seminar Series

Neural Reprogramming of Germline Cells and Trans-Generational Memory in Drosophila

BCH Division of Genetics and Genomics Seminar

Genetics Seminar Series - Focused Seminars

Reflecting the breadth of the field itself, the Department of Genetics at Harvard Medical School houses a faculty working on diverse problems, using a variety of approaches and model organisms, unified in their focus on the genome as an organizing principle for understanding biological phenomena. Genetics is not perceived simply as a subject, but rather as a way of viewing and approaching biological phenomena.

While the range of current efforts can best be appreciated by reading the research interests of individual faculty, the scope of the work conducted in the Department includes (but is by no means limited to) human genetics of both single gene disorders and complex traits, development of genomic technology, cancer biology, developmental biology, signal transduction, cell biological problems, stem cell biology, computational genetics, immunology, synthetic biology, epigenetics, evolutionary biology and plant biology.

More here:
Home | HMS Department of Genetics

Recommendation and review posted by Bethany Smith

Back pain is a common problem that affects most people at some point in their life.

It may be triggered by bad posture while sitting or standing, bending awkwardly, or lifting incorrectly. Its not generally caused by a serious condition. Find out more about thecauses of back pain.

In most cases, back pain will improve in a few weeks or months, although some people experience long-term pain or pain that keeps coming back.

Backache is most common in the lower back ('lumbago'), although it can be felt anywhere along your spine, from your neck down to your hips. Read information onneck pain andshoulder pain, which are covered separately.

Sometimes, back pain can be caused by an injury or disease, such as:

The rest of this information will focus on back pain that doesnt have an obvious cause. Doctors call this non-specific back pain.

Most cases of back pain get better on their own and you may not need to see a doctor.

If youve only had back pain for a few days or weeks, the following advice may help relieve your symptoms and speed up your recovery:

Although it can be difficult to be cheerful or optimistic if you are in pain, its important to stay positive because this can help you recover faster.

Read more about treatments for short-term back pain.

Original post:
Back pain - NHS Choices

Recommendation and review posted by simmons

Description

An in-depth report on the causes, diagnosis, treatment, and prevention of back pain, including sciatica.

Herniated disk; Sciatica

Overview:

Treatment:

Back pain is one of the most common reasons people visit their doctor. According to the National Institute of Arthritis and Musculoskeletal and Skin Diseases, 25% of adults have at least a day of back pain during a typical 3 month period.

Back pain can be acute, subacute, or chronic.

Back pain can occur in any area of the back, but it most often strikes the lower back, which supports most of the body's weight.

The back is highly complex. Pain may result from damage or injury to any of its various bones, nerves, muscles, ligaments, and other structures. Still, despite sophisticated techniques, which provide detailed anatomical images of the spine and other tissues, the cause of most cases of back pain remains unknown.

Vertebrae. The spine is a column of small bones, or vertebrae, that support the entire upper body. The column is grouped into three sections:

See the original post here:
Back pain and sciatica | University of Maryland Medical Center

Recommendation and review posted by simmons

Bio-Technology is a research oriented science, a combination of Biology and Technology. It covers a wide variety of subjects like Genetics, Biochemistry, Microbiology, Immunology, Virology, Chemistry and Engineering and is also concerned with many other subjectslike Health and Medicine, Agriculture and Animal Husbandry, Cropping system and Crop Management, Ecology, Cell Biology, Soil science and Soil Conservation, Bio-statistics, Plant Physiology, Seed Technology etc. Bio-Technology is the use of living things, especially cells and bacteria in industrial process. There is a great scope in this field as the demand for biotechnologist are growing in India as well as abroad.

There are many applications of biotechnology such as developing various medicines, vaccines and diagnostics, increasing productivity, improving energy production and conservation. Biotechnology's intervention in the area of animal husbandry has improved animal breeding. It also helps to improve the quality of seeds, insecticides and fertilizers. Environmental biotechnology helps for pollution control and waste management.

Most of the information that has led to the emergence of biotechnology in the present form has been generated during the last five decades. The setting up of a separate Department of Biotechnology (DBT) (www.dbtindia.nic.in ) under the Ministry of Science and Technology in 1986 gave a new impetus to the development of the field of modern biology and biotechnology in India. More than 6000 biotechnologists of higher skill are required in India as per the report from the Human Resource Development Ministry. To overcome this vast requirement the department of Biotechnology (DBT) has highlighted the need to set up a regulatory body for the maintenance of standard education under the name of 'All- India Board of Biotechnology Education and Training' under the AICTE .

Read more:
Biotechnology Careers in India : How to become a ...

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Contact A Well Regarded Leaking Taps Plumber For Your Northern Suburbs Pipe Relining Job

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Biotechnology

Recommendation and review posted by sam

You will have a low white blood cell count after your treatment. This means you are more at risk of getting an infection. You are likely to get an infection from the normally harmless bacteria we all have in our digestive systems and on our skin.

To stop this from happening your nurse may give you tablets called gut sterilisers (antibiotics) and mouthwashes. And they will encourage you to have a shower each day.

You are also at risk of infection from food. The nurses on the ward will tell you and your relatives about the food you can and can't eat. The rules vary from hospital to hospital but you may be told that

Your room will be thoroughly cleaned every day. Your visitors will be asked to wash their hands before they come into your room. They may also have to wear disposable gloves and aprons. Visitors with coughs and colds are not allowed. Some hospitals don't allow you to have plants or flowers in your room because bacteria and fungi can grow in the soil or water, and may cause infection.

Even with all these precautions, most people do get an infection at some point and need to have antibiotics. You can help yourself by trying to do your mouth care properly and getting up to shower and have your bed changed even on the days you don't feel too good.

After a transplant you will have lost immunity to diseases you were vaccinated against as a child. The team caring for you will advise you about the immunisations you need and when. You should only have inactivated immunisations and not live ones. To lower the risk of you getting any of these infections it is important that all your family have the flu vaccine and any children have all their immunisations.

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General Information About Non-Small Cell Lung Cancer (NSCLC)

NSCLC is any type of epithelial lung cancer other than small cell lung cancer (SCLC). The most common types of NSCLC are squamous cell carcinoma, large cell carcinoma, and adenocarcinoma, but there are several other types that occur less frequently, and all types can occur in unusual histologic variants. Although NSCLCs are associated with cigarette smoke, adenocarcinomas may be found in patients who have never smoked. As a class, NSCLCs are relatively insensitive to chemotherapy and radiation therapy compared with SCLC. Patients with resectable disease may be cured by surgery or surgery followed by chemotherapy. Local control can be achieved with radiation therapy in a large number of patients with unresectable disease, but cure is seen only in a small number of patients. Patients with locally advanced unresectable disease may achieve long-term survival with radiation therapy combined with chemotherapy. Patients with advanced metastatic disease may achieve improved survival and palliation of symptoms with chemotherapy, targeted agents, and other supportive measures.

Estimated new cases and deaths from lung cancer (NSCLC and SCLC combined) in the United States in 2014:[1]

Lung cancer is the leading cause of cancer-related mortality in the United States.[1] The 5-year relative survival rate from 1995 to 2001 for patients with lung cancer was 15.7%. The 5-year relative survival rate varies markedly depending on the stage at diagnosis, from 49% to 16% to 2% for patients with local, regional, and distant stage disease, respectively.[2]

NSCLC arises from the epithelial cells of the lung of the central bronchi to terminal alveoli. The histological type of NSCLC correlates with site of origin, reflecting the variation in respiratory tract epithelium of the bronchi to alveoli. Squamous cell carcinoma usually starts near a central bronchus. Adenocarcinoma and bronchioloalveolar carcinoma usually originate in peripheral lung tissue.

Anatomy of the respiratory system.

Smoking-related lung carcinogenesis is a multistep process. Squamous cell carcinoma and adenocarcinoma have defined premalignant precursor lesions. Before becoming invasive, lung epithelium may undergo morphological changes that include the following:

Dysplasia and carcinoma in situ are considered the principal premalignant lesions because they are more likely to progress to invasive cancer and less likely to spontaneously regress.

In addition, after resection of a lung cancer, there is a 1% to 2% risk per patient per year that a second lung cancer will occur.[3]

NSCLC is a heterogeneous aggregate of histologies. The most common histologies include the following:

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Non-Small Cell Lung Cancer Treatment - National Cancer ...

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Sickle-cell disease (SCD), also known as sickle-cell anaemia (SCA) and drepanocytosis, is a hereditary blood disorder, characterized by an abnormality in the oxygen-carrying haemoglobin molecule in red blood cells. This leads to a propensity for the cells to assume an abnormal, rigid, sickle-like shape under certain circumstances. Sickle-cell disease is associated with a number of acute and chronic health problems, such as severe infections, attacks of severe pain ("sickle-cell crisis"), and stroke, and there is an increased risk of death.

Sickle-cell disease occurs when a person inherits two abnormal copies of the haemoglobin gene, one from each parent. Several subtypes exist, depending on the exact mutation in each haemoglobin gene. A person with a single abnormal copy does not experience symptoms and is said to have sickle-cell trait. Such people are also referred to as carriers.

The complications of sickle-cell disease can be prevented to a large extent with vaccination, preventive antibiotics, blood transfusion, and the drug hydroxyurea/hydroxycarbamide. A small proportion requires a transplant of bone marrow cells.

Almost 300,000 children are born with a form of sickle-cell disease every year, mostly in sub-Saharan Africa, but also in other parts of the world such as the West Indies and in people of African origin elsewhere in the world. In 2013 it resulted in 176,000 deaths up from 113,000 deaths in 1990.[1] The condition was first described in the medical literature by the American physician James B. Herrick in 1910, and in the 1940s and 1950s contributions by Nobel prize-winner Linus Pauling made it the first disease where the exact genetic and molecular defect was elucidated.

Sickle-cell disease may lead to various acute and chronic complications, several of which have a high mortality rate.[2]

The terms "sickle-cell crisis" or "sickling crisis" may be used to describe several independent acute conditions occurring in patients with SCD. SCD results in anemia and crises that could be of many types including the vaso-occlusive crisis, aplastic crisis, sequestration crisis, haemolytic crisis, and others. Most episodes of sickle-cell crises last between five and seven days.[3] "Although infection, dehydration, and acidosis (all of which favor sickling) can act as triggers, in most instances, no predisposing cause is identified."[4]

The vaso-occlusive crisis is caused by sickle-shaped red blood cells that obstruct capillaries and restrict blood flow to an organ resulting in ischaemia, pain, necrosis, and often organ damage. The frequency, severity, and duration of these crises vary considerably. Painful crises are treated with hydration, analgesics, and blood transfusion; pain management requires opioid administration at regular intervals until the crisis has settled. For milder crises, a subgroup of patients manage on NSAIDs (such as diclofenac or naproxen). For more severe crises, most patients require inpatient management for intravenous opioids; patient-controlled analgesia devices are commonly used in this setting. Vaso-occlusive crisis involving organs such as the penis[5] or lungs are considered an emergency and treated with red-blood cell transfusions. Incentive spirometry, a technique to encourage deep breathing to minimise the development of atelectasis, is recommended.[6]

Because of its narrow vessels and function in clearing defective red blood cells, the spleen is frequently affected.[7] It is usually infarcted before the end of childhood in individuals suffering from sickle-cell anemia. This spleen damage increases the risk of infection from encapsulated organisms;[8][9] preventive antibiotics and vaccinations are recommended for those lacking proper spleen function.

Splenic sequestration crises are acute, painful enlargements of the spleen, caused by intrasplenic trapping of red cells and resulting in a precipitous fall in hemoglobin levels with the potential for hypovolemic shock. Sequestration crises are considered an emergency. If not treated, patients may die within 12 hours due to circulatory failure. Management is supportive, sometimes with blood transfusion. These crises are transient, they continue for 34 hours and may last for one day.[10]

Acute chest syndrome (ACS) is defined by at least two of the following signs or symptoms: chest pain, fever, pulmonary infiltrate or focal abnormality, respiratory symptoms, or hypoxemia.[11] It is the second-most common complication and it accounts for about 25% of deaths in patients with SCD, majority of cases present with vaso-occlusive crises then they develop ACS.[12][13] Nevertheless, about 80% of patients have vaso-occlusive crises during ACS.

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Sickle-cell disease - Wikipedia, the free encyclopedia

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