Finished heart switches stem cells off

Transcription factor Ajuba regulates stem cell activity in the heart during embryonic development

July 12, 2012

It is not unusual for babies to be born with congenital heart defects. This is because the development of the heart in the embryo is a process which is not only extremely complex, but also error-prone. Scientists from the Max Planck Institute for Heart and Lung Research in Bad Nauheim have now identified a key molecule that plays a central role in regulating the function of stem cells in the heart. As a result, not only could congenital heart defects be avoided in future, but new ways of stimulating the regeneration of damaged hearts in adults may be opened up.

Cardiac development out of control: Absence of the transcription factor Ajuba during cardiac development, as is the case in the right-hand photo due to genetic intervention, disrupts development of the heart in the fish embryo. In addition to an increased number of cardiac muscle cells (green with red-stained nuclei), the heart is additionally deformed during development.

Max Planck Institute for Heart and Lung Research

Max Planck Institute for Heart and Lung Research

It's a long road from a cluster of cells to a finished heart. Cell division transforms what starts out as a collection of only a few cardiac stem cells into an ever-larger structure from which the various parts of the heart, such as ventricles, atria, valves and coronary vessels, develop. This involves the stem and precursor cells undergoing a complex process which, in addition to tightly regulated cell division, also includes cell migration, differentiation and specialisation. Once the heart is complete, the stem cells are finally switched off.

Scientists from the Max Planck Institute for Heart and Lung Research in Bad Nauheim have now discovered how major parts of this development process are regulated. Their search initially focused on finding binding partners for transcription factor Isl1. Isl1 is characteristic of a specific group of cardiac stem cells which are consequently also known as Isl1+ cells. During their search, the researchers came across Ajuba, a transcription factor from the group of LIM proteins. "We then took a closer a look at the interaction between these two molecules and came to the conclusion that Ajuba must be an important switch", says Gergana Dobreva, head of the "Origin of Cardiac Cell Lineages" Research Group at the Bad Nauheim-based Max Planck Institute.

Using an animal model, the scientists then investigated the effects of a defective switch on cardiac development. Embryonic development can be investigated particularly effectively in the zebrafish. The Bad Nauheim-based researchers therefore produced a genetically modified fish that lacked a functioning Ajuba protein. Cardiac development in these fishes was in fact severely disrupted. In addition to deformation of the heart, caused by twisting of the cardiac axis, what particularly struck the researchers was a difference in size in comparison with control animals. "In almost all the investigated fish we observed a dramatic enlargement of the heart. If Ajuba is absent, there is clearly no other switch that finally silences the Isl1-controlled part of cardiac development", says Dobreva.

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Dr. Hans-Willem Snoeck and colleagues at Columbia University Medical Center reported the first successful development of functional human lung tissue from stem cells in the Dec. 1, 2013, edition of the journal Nature Biotechnology.

The development is an extension of Snoecks previous work in producing human induced pluripotent stem cells from skin cells. Human induced pluripotent stem cells perform exactly like human embryonic stem cells. The benefits of human induced pluripotent stem cells from include the avoidance of potential rejection and legal complications.

The researchers were able to create the six most necessary lung tissues from induced pluripotent stem cells. The work included the development of type 2 alveolar epithelial cells that are necessary to produce surfactants that facilitate the exchange of oxygen and carbon dioxide in the lungs.

The development indicates that lung transplants from donors will eventually become a thing of the past as skin cells from a person with a lung disease can be turned into stem cells that can develop an entire new lung. This method avoids any chance of rejection because the lungs developed from the skin cells are the same as lung cells that a person was born with.

The development also will enable selected cell regeneration of lung cells to treat specific diseases that only involve certain parts of the lung.

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In addition, study results show clinical event rates in gene therapy patients are significantly lower three years later compared to those patients receiving placebo. Also, patients experienced no negative side effects following gene therapy delivery at three-year follow-up.

"This study shows AAV1/SERCA2a gene therapy has long-lasting and beneficial effects for congestive heart failure patients allowing us to block the downward spiral of patients with severe heart failure, " says principal investigator Roger J. Hajjar, MD, Director of the Cardiovascular Research Center and the Arthur & Janet C. Ross Professor of Medicine at Icahn School of Medicine at Mount Sinai, who developed the gene therapy approach.

The gene therapy uses a modified adeno-associated viral-vector derived from a parvovirus. The one-time gene therapy is injected through the coronary arteries of heart failure patients using catheters. It works by introducing healthy SERCA2a genes into cells. The delivery of the SERCA2a gene produces SERCA2a enzymes, which helps heart cells restore their proper use of calcium.

SERCA2a is an enzyme critical for proper pumping of calcium in calcium compartments within cells. SERCA2a dysfunction or reduced expression occurs in patients with heart failure. When SERCA2a is down-regulated, calcium stays longer in the cells than it should, and it induces pathways that lead to overgrowth of new and enlarged cells. This contributes to an enlarged heart in heart failure patients.

Previously, CUPID 1 study results showed the gene therapy to be clinically safe and effective for over 12 months with improved heart function status and left ventricular function, along with a significant decrease in recurrent cardiovascular events. CUPID 1 was the first-in human clinical gene therapy randomized, double-blind study which enrolled 39 patients with advanced heart failure.

"AAV1/SERCA2a gene therapy has been proven to be a safe and effective therapeutic intervention for advanced heart failure," says Dr. Hajjar. "Our long-term results support the potential use of AAV1/SERCA2a gene therapy as a new important additional tool for treating and managing advanced heart failure patients."

This study was presented as an Oral Session (Abstract 10667): Long Term Follow-up of Patients with Advanced Heart Failure Following a Single Intracoronary Infusion of AAV1/SERCA2a.

In addition, on Nov. 19 Dr. Hajjar also presented at the AHA Scientific Sessions 2013 a Plenary talk entitled, "How the Postgenome Era Will Change the Practice of Cardiology" and discussed his work on targeted gene therapy for human heart failure.

In his Plenary talk, Dr Hajjar presented his new findings just published in the journal Science Translational Medicine on Nov. 13 that show delivery of small ubiquitin-related modifier 1 (SUMO-1), an important regulator of SERCA2a, in preclinical heart failure models improves cardiac contractility and prevents left ventricular dilatation two major aspects of heart failure. According to Dr. Hajjar, the transition of this SUMO-1 gene therapy from pigs to humans seems likely in the short-term. Also, Dr. Hajjar revealed that development of novel cardiotropic vectors may render cardiovascular gene therapy easier and less-invasive in the near future.

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When cases of illegal trading in endangered species drew public attention a few years ago, the Eijkman Institute for Molecular Biology became a bridge between genetic research and law enforcement.

The institute received samples of animal body parts that the Forestry Ministry had seized from poachers. Later, the institute identified them using forensic DNA tests.

Through molecular analysis, the institute could identify the body parts of the protected endangered species to be used as evidence to prosecute the poachers.

The advanced molecular biology technique really overcame difficulties we faced in providing evidence for law enforcement, Herawati Sudoyo, the Eijkman Institute for Molecular Biologys deputy chairman, said recently.

Speaking at a discussion titled Capacity Building in Wildlife Conservation and Forensic Genetics held jointly by the institute and the Research and Technology Ministry, Herawati said forensic genetics for investigation into wildlife-related crimes was one of the most outstanding achievements of the Eijkman Institute in the last few years.

A string of activities in barcoding animals such as fish, larvae, birds, insects and marine organisms using special markers including the mitochondrial DNA and Y STR are part of early initiatives taken by the institute on the wildlife conservation using forensic genetics.

This is the role of the Eijkman Institute to develop molecular genetic markers for species and sub-species identification by scrutinizing genetic patterns among geographically isolated populations, defining sub-species level for conservation management purposes, and revising traditional species and sub-species designation, said Herawati.

Ross McEwing, the TRACE Wildlife Forensics Networks technical director, said forensic genetics was the key to wildlife investigation as it could identify both species and the population origin of species or their parts as well as establishing a database of individuals for enforcement purposes. We have seen a growing awareness among countries of the need for forensic genetics to save wildlife, he said.

Citing examples, McEwing said wildlife forensic DNA testing in Malaysia had increased by 80 percent with 1,205 forensic samples processed. Vietnam has requested training courses for wildlife enforcement officers. All captive tigers in the country have been sampled for a DNA sampling/database. It also has requested assistance in establishing wildlife DNA forensics.

Noviar Andayani, a scientist from the Wildlife Conservation Society (WCS) Indonesia Program, also said her institution had been looking more into genetic management of endangered species. (Published June 28, 2012)

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Genetic testing, also known as DNA testing, allows the genetic diagnosis of vulnerabilities to inherited diseases, and can also be used to determine a child's parentage (genetic mother and father) or in general a person's ancestry. Normally, every person carries two copies of every gene (with the exception of genes related to sex-linked traits, which are only inherited from the mother by males), one inherited from their mother, one inherited from their father. The human genome is believed to contain around 20,00025,000 genes. In addition to studying chromosomes to the level of individual genes, genetic testing in a broader sense includes biochemical tests for the possible presence of genetic diseases, or mutant forms of genes associated with increased risk of developing genetic disorders. Genetic testing identifies changes in chromosomes, genes, or proteins.[1] Most of the time, testing is used to find changes that are associated with inherited disorders. The results of a genetic test can confirm or rule out a suspected genetic condition or help determine a person's chance of developing or passing on a genetic disorder. Several hundred genetic tests are currently in use, and more are being developed.[2][3]

Since genetic testing may open up ethical or psychological problems, genetic testing is often accompanied by genetic counseling.[citation needed]

Because genetic mutations can directly affect the structure of the proteins they code for, testing for specific genetic diseases can also be accomplished by looking at those proteins or their metabolites, or looking at stained or fluorescent chromosomes under a microscope.[4]

This article focuses on genetic testing for medical purposes. DNA sequencing, which actually produces a sequences of As, Cs, Gs, and Ts, is used in molecular biology, evolutionary biology, metagenomics, epidemiology, ecology, and microbiome research.

Genetic testing is "the analysis of, chromosomes (DNA), proteins, and certain metabolites in order to detect heritable disease-related genotypes, mutations, phenotypes, or karyotypes for clinical purposes."[5] It can provide information about a person's genes and chromosomes throughout life. Available types of testing include:

Non-diagnostic testing includes:

Many diseases have a genetic component with tests already available.

over-absorption of iron; accumulation of iron in vital organs (heart, liver, pancreas); organ damage; heart disease; cancer; liver disease; arthritis; diabetes; infertility; impotence[7]

Obstructive lung disease in adults; liver cirrhosis during childhood; when a newborn or infant has jaundice that lasts for an extended period of time (more than a week or two), an enlarged spleen, ascites (fluid accumulation in the abdominal cavity), pruritus (itching), and other signs of liver injury; persons under 40 years of age that develops wheezing, a chronic cough or bronchitis, is short of breath after exertion and/or shows other signs of emphysema (especially when the patient is not a smoker, has not been exposed to known lung irritants, and when the lung damage appears to be located low in the lungs); when you have a close relative with alpha-1 antitrypsin deficiency; when a patient has a decreased level of A1AT.

Elevation of both serum cholesterol and triglycerides; accelerated atherosclerosis, coronary heart disease; cutaneous xanthomas; peripheral vascular disease; diabetes mellitus, obesity or hypothyroidism

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Genetic testing - Wikipedia, the free encyclopedia

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Frederick, MD (PRWEB) November 28, 2013

Dr. Jon Rowley and Dr. Uplaksh Kumar, Co-Founders of RoosterBio, Inc., a newly formed biotech startup located in Frederick, are paving the way for even more innovation in the rapidly growing fields of Synthetic Biology and Regenerative Medicine. Synthetic Biology combines engineering principles with basic science to build biological products, including regenerative medicines and cellular therapies. Regenerative medicine is a broad definition for innovative medical therapies that will enable the body to repair, replace, restore and regenerate damaged or diseased cells, tissues and organs. Regenerative therapies that are in clinical trials today may enable repair of damaged heart muscle following heart attack, replacement of skin for burn victims, restoration of movement after spinal cord injury, regeneration of pancreatic tissue for insulin production in diabetics and provide new treatments for Parkinsons and Alzheimers diseases, to name just a few applications.

While the potential of the field is promising, the pace of development has been slow. One main reason for this is that the living cells required for these therapies are cost-prohibitive and not supplied at volumes that support many research and product development efforts. RoosterBio will manufacture large quantities of standardized primary cells at high quality and low cost, which will quicken the pace of scientific discovery and translation to the clinic. Our goal is to accelerate the development of products that incorporate living cells by providing abundant, affordable and high quality materials to researchers that are developing and commercializing these regenerative technologies says Dr. Rowley.

RoosterBios current focus is to supply high volume research-grade cells manufactured with processes consistent with current Good Manufacturing Practices (cGMP). These cells will be used for tissue engineering research and cell-based product development. This will position RoosterBio to quickly move on to producing clinical-grade cells to be used in translational R&D and clinical studies.

We have spent almost 20 years as cell and tissue technologists and have lived with the pain of needing to generate large amounts of cells for experiments this whole time. RoosterBio was founded to address this problem for cell and tissue engineers, saving them time and money, and accelerating their path to the clinic, says Dr. Rowley. RoosterBio will supply cells, starting with adult human bone marrow-derived stem cells, at volumes that will allow for a more rapid pace of experimentation in the lab.

We will also offer paired media that has been engineered to quickly and efficiently expand the supplied cells to hundreds of millions or billions of cells within 1-2 weeks, something that would take 4-8 weeks using cell and media systems currently on the market, adds Dr. Kumar. We aim to usher in a new era of productivity to the field, and we believe that our products will at least triple the efficiency of the average laboratory.

RoosterBio, Inc. is located in the Frederick Innovative Technology Center on Metropolitan Court in Frederick. Dr. Rowley entered into the incubation program in October of this year, and already gained four full time employees, and has several academic and industrial collaborators lined up. This team has made remarkable progress and are already poised for their official product launch for their human bone marrow-derived Mesenchymal Stem Cells (hBM-MSC), anticipated in March 2014.

RoosterBios product formats have been extraordinarily well received by the market, and RoosterBio has already secured customers who are anxiously awaiting their product launch. "I am excited to see that someone is taking on the challenge of providing a sufficient number of MSCs to immediately start experiments upon their receipt. This saves us several weeks of time upfront waiting for cells to expand to volumes that allow us to begin experiments, says Todd McDevitt, Director of the Stem Cell Engineering Center at the Georgia Institute of Technology. For tissue engineering folks like myself, this means we can focus our time on high priority research questions and not spend the majority of our time performing routine cell culture."

The Tissue Engineering and Regenerative Medicine industry is one of the fastest growing in the life science sector with the total expenditure in 2011 at $17.1 billion. This number is expected to increase in 2020 to $40.5 billion. The sales of stem cell products accounted for $1.38 billion in 2010 and is expected to reach $3.9 billion by the year 2014 and $8 billion in annual revenues by 2020.

About RoosterBio

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Stem Cell Therapy Injections
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[International version] Linda van Laake: "We want to work together to improve stem cell treatment"
Dr Linda van Laake is assistant professor and specialist registrar in Cardiology at the University Medical Center Utrecht and Hubrecht Institute. She carries...

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One year long recovery after polytrauma and spinal cord injury (paraplegia)
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[International version] Linda van Laake: "We want to work together to improve stem cell treatment"
Dr Linda van Laake is assistant professor and specialist registrar in Cardiology at the University Medical Center Utrecht and Hubrecht Institute. She carries...

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Skin Doctors YouthCell Range Sophie Falkiner TVC
YouthCell contains the latest plant stem cell technology (PhytoCellTec) to help delay the appearance of chronological ageing of the skin. These plant stem ...

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In computer-based text processing and digital typesetting, a non-breaking space, no-break space or non-breakable space (NBSP) is a variant of the space character that prevents an automatic line break (line wrap) at its position. In certain formats (such as HTML), it also prevents the collapsing of multiple consecutive whitespace characters into a single space. The non-breaking space is also known as a hard space or fixed space. In Unicode, it is encoded at U+00A0 no-break space (HTML:    ).

Text-processing software typically assumes that an automatic line break may be inserted anywhere a space character occurs; a non-breaking space prevents this from happening (provided the software recognizes the character). For example, if the text 100 km will not quite fit at the end of a line, the software may insert a line break between 100 and km. To avoid this undesirable behaviour, the editor may choose to use a non-breaking space between 100 and km. This guarantees that the text 100km will not be broken: if it does not fit at the end of a line it is moved in its entirety to the next line.

A second common application of non-breaking spaces is in plain text file formats such as SGML, HTML, TeX, and LaTeX, which sometimes treat sequences of whitespace characters (space, newline, tab, form feed, etc.) as if they were a single white-space character. Such collapsing of white-space allows the author to neatly arrange the source text using line breaks, indentation and other forms of spacing without affecting the final typeset result.[1][2]

In contrast, non-breaking spaces are not merged with neighboring whitespace characters, and can therefore be used by an author to insert additional visible space in the formatted text. For example, in HTML, non-breaking spaces may be used in conjunction with a fixed-width font to create tabular alignment (courier new font family used):

Column 1Column 2 ---------------- 1.22.3

(note that the use of the pre tag, the whitespace:pre CSS rule, or a table are alternative, if not necessarily better, ways to achieve the same result in HTML)

If ordinary spaces are used instead then the spaces are collapsed when the HTML is rendered and the layout is broken:

Column 1 Column 2 -------- -------- 1.2 2.3

Non-breaking space can also be used to automatically change formatting in a document. This is useful for things like class plans and recipe files where the description of a cell or line may be different from the actual text or title.

Unicode defines several other non-break space characters[3] that differ from the regular space in width:

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Nov. 27, 2013 A team of researchers has brought new clarity to the picture of how gene-environmental interactions can kill nerve cells that make dopamine. Dopamine is the neurotransmitter that sends messages to the part of the brain that controls movement and coordination. Their discoveries, described in a paper published online today in Cell, include identification of a molecule that protects neurons from pesticide damage.

"For the first time, we have used human stem cells derived from Parkinson's disease patients to show that a genetic mutation combined with exposure to pesticides creates a 'double hit' scenario, producing free radicals in neurons that disable specific molecular pathways that cause nerve-cell death," says Stuart Lipton, M.D., Ph.D., professor and director of Sanford-Burnham's Del E. Webb Center for Neuroscience, Aging, and Stem Cell Research and senior author of the study.

Until now, the link between pesticides and Parkinson's disease was based mainly on animal studies and epidemiological research that demonstrated an increased risk of disease among farmers, rural populations, and others exposed to agricultural chemicals.

In the new study, Lipton, along with Rajesh Ambasudhan, Ph.D., research assistant professor in the Del E. Webb Center, and Rudolf Jaenisch, M.D., founding member of Whitehead Institute for Biomedical Research and professor of biology at the Massachusetts Institute of Technology (MIT), used skin cells from Parkinson's patients that had a mutation in the gene encoding a protein called alpha-synuclein. Alpha-synuclein is the primary protein found in Lewy bodies -- protein clumps that are the pathological hallmark of Parkinson's disease.

Using patient skin cells, the researchers created human induced pluripotent stem cells (hiPSCs) containing the mutation, and then "corrected" the alpha-synuclein mutation in other cells. Next, they reprogrammed all of these cells to become the specific type of nerve cell that is damaged in Parkinson's disease, called A9 dopamine-containing neurons -- thus creating two sets of neurons -- identical in every respect except for the alpha-synuclein mutation.

"Exposing both normal and mutant neurons to pesticides -- including paraquat, maneb, or rotenone -- created excessive free radicals in cells with the mutation, causing damage to dopamine-containing neurons that led to cell death," said Frank Soldner, M.D., research scientist in Jaenisch's lab and co-author of the study.

"In fact, we observed the detrimental effects of these pesticides with short exposures to doses well below EPA-accepted levels," said Scott Ryan, Ph.D., researcher in the Del E. Webb Center and lead author of the paper.

Having access to genetically matched neurons with the exception of a single mutation simplified the interpretation of the genetic contribution to pesticide-induced neuronal death. In this case, the researchers were able to pinpoint how cells with the mutation, when exposed to pesticides, disrupt a key mitochondrial pathway -- called MEF2C-PGC1alpha -- that normally protects neurons that contain dopamine. The free radicals attacked the MEF2C protein, leading to the loss of function of this pathway that would otherwise have protected the nerve cells from the pesticides.

"Once we understood the pathway and the molecules that were altered by the pesticides, we used high-throughput screening to identify molecules that could inhibit the effect of free radicals on the pathway," said Ambasudhan. "One molecule we identified was isoxazole, which protected mutant neurons from cell death induced by the tested pesticides. Since several FDA-approved drugs contain derivatives of isoxazole, our findings may have potential clinical implications for repurposing these drugs to treat Parkinson's."

While the study clearly shows the relationship between a mutation, the environment, and the damage done to dopamine-containing neurons, it does not exclude other mutations and pathways from being important as well. The team plans to explore additional molecular mechanisms that demonstrate how genes and the environment interact to contribute to Parkinson's and other neurodegenerative diseases, such as Alzheimer's and ALS.

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Researchers from the UK have found something that can actually drive mice to drinkand no, it isnt stress induced by narrowly dodging mousetraps on a daily basis.

A joint research project conducted on mice by students from five UK universitiesImperial College London, Newcastle University, UCL, University of Dundee, and University of Sussexhighlighted the effects of a gene called Gabrb1 on regulating alcohol consumption. The study revealed that a mutation in the gene caused mice to drink enough alcohol in 1 hour to render them intoxicated and unable to move properly.

Gabrb1, the alcohol-regulating gene

Perhaps unsurprisingly, the researchers found that ordinary mice had no special interest in alcoholic beverages, opting to go for a bottle of normal water over a bottle of diluted alcohol.

However, mice with a mutated Gabrb1 gene showed a strong preference for alcoholic beverages, even going as far as to consume about 85% of their daily fluid intake in the form of alcohol.

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This morning (November 28, 2013) National Geographic Wild (NGW) broadcasted a documentary on TV showing the Sacramento-Davis area scientist from the University of California - Davis, Leslie A. Lyons, School of Veterinary Medicine, and her research team traveling abroad a few years ago to find out where cats originated by testing their DNA in various countries. Was it Egypt or Turkey where the cat was first domesticated, most likely to keep the stored grain safe from mice? The answer is Egypt. You can check out the study, published in the January 2008 issue of Genomics, "The ascent of cat breeds: Genetic evaluations of breeds and worldwide random-bred populations."

The house cats' family tree is rooted in Fertile Crescent, starting with Egypt, the study confirmed as it covered the diaspora of the modern cat. Cats roaming the temples in Southern Egypt were found to be bigger than housecats in other parts of the world, as if they had more recently begun to be domesticated.

Thousands of years ago in Egypt, cats protected the grain bins from being eaten by rodents. From there, cats spread over most of the world. You also can check out the site, The Lyons' Den - UC Davis School of Veterinary Medicine.

The feline genetics laboratory of Professor Leslie Lyons at UC Davis is located in the Center for Companion Animal Health (CCAH). Research focuses on the genetics of the domestic cat and the development of genetic tools and resources that assist gene mapping in the cat and other companion animals.

Feline research is focused on the discovery of mutations that cause inherited diseases and phenotypic traits and in the population dynamics of breed development and domestic cat evolution. See, "Feline Research Projects" and "How to Participate." All cats can participate, and all contributions are confidential, the website notes.

There are a variety of ways to assist genetic research of the domestic cat - any cat owner can be of assistant. Listed below are the different ways you can help. Please also see the Feline Research Projects for additional information.

The Fertile Crescent of the Middle East has long been identified as a cradle of civilization for humans. In a new genetic study, researchers at the University of California, Davis, have concluded that all ancestral roads for the modern day domestic cat also lead back to the same locale.

Findings of the study, according to the January 28, 2008 news release, "Cats' family tree rooted in Fertile Crescent, study confirms," involving more than 11,000 cats, are reported in the cover article of the January 2008 issue of the journal Genomics. This study confirms earlier research suggesting that the domestication of the cat started in the Fertile Crescent region. It also provides a warning for modern cat fanciers to make sure they maintain a broad genetic base as they further develop their breeds, said Monika Lipinski, according to the news release. Lipinski (at the time of the 2008 news release) is noted in the news release as a lead researcher on the study and a doctoral candidate in the School of Veterinary Medicine.

Leslie Lyons, an authority on cat genetics and principal investigator on this study, said, according to the news release: More than 200 genetic disorders have been identified in modern cats, and many are found in pure breeds. We hope that cat breeders will use the genetic information uncovered by this study to develop efficient breed-management plans and avoid introducing genetically linked health problems into their breeds.

History of the Modern Cat

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Genetic engineering (GE) is the modification of an organisms genetic composition by artificial means, often involving the transfer of specific traits, or genes, from one organism into a plant or animal of an entirely different species. When gene transfer occurs, the resulting organism is called transgenic or a GMO (genetically modified organism).

Genetic engineering is different from traditional cross breeding, where genes can only be exchanged between closely related species. With genetic engineering, genes from completely different species can be inserted into one another. For example, scientists in Taiwan have successfully inserted jellyfish genes into pigs in order to make them glow in the dark.

All life is made up of one or more cells. Each cell contains a nucleus, and inside each nucleus are strings of molecules called DNA (deoxyribonucleic acid). Each strand of DNA is divided into small sections called genes. These genes contain a unique set of instructions that determine how the organism grows, develops, looks, and lives.

During genetic engineering processes, specific genes are removed from one organism and inserted into another plant or animal, thus transferring specific traits.

Nearly 400 million acres of farmland worldwide are now used to grow GE crops such as cotton, corn, soybeans and rice. In the United States, GE soybeans, corn and cotton make up 93%, 88% and 94% of the total acreage of the respective crops. The majority of genetically engineered crops grown today are engineered to be resistant to pesticides and/or herbicides so that they can withstand being sprayed with weed killer while the rest of the plants in the field die.

GE proponents claim genetically engineered crops use fewer pesticides than non-GE crops, when in reality GE plants can require even more chemicals. This is because weeds become resistant to pesticides, leading farmers to spray even more on their crops. This pollutes the environment, exposes food to higher levels of toxins, and creates greater safety concerns for farmers and farm workers.

Some GE crops are actually classified as pesticides. For instance, the New Leaf potato, which has since been taken off grocery shelves, was genetically engineered to produce the Bt (Bacillus thuringiensis) toxin in order to kill any pests that attempted to eat it. The actual potato was designated as a pesticide and was therefore regulated by the Environmental Protection Agency (EPA), instead of the Food & Drug Administration (FDA), which regulates food. Because of this, safety testing for these potatoes was not as rigorous as with food, since the EPA regulations had never anticipated that people would intentionally consume pesticides as food.

Adequate research has not yet been carried out to identify the effects of eating animals that have been fed genetically engineered grain, nor have sufficient studies been conducted on the effects of directly consuming genetically engineered crops like corn and soy. Yet despite our lack of knowledge, GE crops are widely used throughout the world as both human and animal food.

Scientists are currently working on ways to genetically engineer farm animals. Atlantic salmon have been engineered to grow to market size twice as fast as wild salmon, chickens have been engineered so that they cannot spread H5N1 avian flu to other birds, and research is being conducted to create cattle that cannot develop the infectious prions that can cause bovine spongiform encephalopathy (aka mad cow disease). At this point, no GE animals have been approved by the FDA to enter the food supply. Genetic engineering experiments on animals do, however, pose potential risks to food safety and the environment.

In 2003, scientists at the University of Illinois were conducting an experiment that involved inserting cow genes into female pigs in order to increase their milk production. They also inserted a synthetic gene to make milk digestion easier for the piglets. Although the experimental pigs were supposed to be destroyed, as instructed by the FDA, 386 offspring of the experimental pigs were sold to slaughterhouses, where they were processed and sent to grocery stores as pork chops, sausage, and bacon.

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Genetics Interview

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BBC Genetics Discussed by Two Pro Bodybuilders
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Hardly a day passes without stories in the news concerning human genetics. Whether it is about new research into the genetic causes for illness, obesity, or even editorials concerning the use of stem cells in genetic research, the average American is bombarded with news about genetics. Someone who teaches about the marvels, latest discoveries and controversies surrounding genetics is Amy Hubert, an assistant professor in the department of biological sciences at Southern Illinois University Edwardsville. Despite the popularity of the subject, Hubert had a very personal reason why entered the field.

My undergraduate genetics class was really interesting, Hubert said. I actually started out my undergraduate career as chemistry major, but I realized about halfway through that I really enjoyed my biology classes that I was taking as electives more than I enjoyed the chemistry classes. So I took genetics class and really enjoyed it and the lab that went with it. A native of Concordia, Kan., she obtained her bachelors degree in biology from the University of Kansas and her doctorate in genetics from the University of Wisconsin- Madison. After switching majors, she became more and more interested in molecular biology, which is key for understanding the workings of heredity.

One of the emphasis options was genetics and since I enjoyed the class so much thats the one I chose, she said. Thats what I got my degree in and just went on from there. These days she is working on a rapidly evolving field: the regeneration of the nervous system. This is research that is really entering a new frontier of science. In her work she studies microscopic organisms. One question many people ask is if they can regenerate the nervous system of a worm, why not a human?

Its a little more complicated than that, explained Hubert. The worms are actually a few millimeters long. While you can see them with the naked eye, we study them with a microscope. And they have this amazing ability to regenerate any of their body parts, including their nervous system. That is due to this population of stem cells that they maintain throughout their lifetime that lets them make new cells, including nervous system cells.

Although humans are quite a bit more complicated, Hubert said that scientists are hoping that some of what they learn from the worms is applicable, particularly in relation to stem cells.

Stem cells are cells that have the ability to replace themselves, she explained. So they can divide and make another stem cell. Or they can divide and create a cell that goes on to differentiate, a process in which it takes on characteristics of other cell types. Examples of those cells are the ones we find in the muscle, heart, or skin tissues.

The characteristics of stem cells are that they have those abilities to both replace themselves and create more stem cells so they can proliferate, or they can differentiate and make other types of cells. So they are capable of producing other cells that are necessary for other functions. Another concept one commonly hears in the media is that there is a gene that controls everything, but what about environmental influences?

Identical twins have the same exact genes. So if you see differences between identical twins reared in different environments, or even in the same environment, then you can use that to calculate what percentage of that trait or behavior or whatever you are measuring is controlled by genetic influences versus what percentage is controlled by environmental influences, she explained.

What we see is that any complex trait is going to be a combination of both the genetic and environmental components, she added. Also using fraternal twins, who share half of their genes, we can compare the differences in the similarities in identical twins and the similarity between fraternal twins. We can start to get at what parts of the traits involve genetics and what parts involve the environment.

Despite the fact that each offspring has 50 percent of the genes of each parent, not all genes are the same when it comes to dominance in the characteristics they express. That is why siblings can be very different from each other. Its all a random mixture, and sometimes it turns out that you look more like one parent than the other, Hubert said.

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Genetics answers questions and raises more - The Edwardsville ...

Recommendation and review posted by Bethany Smith

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Stem Cell Treatment and Stem Cell Therapy | Vista Stem Cell

Recommendation and review posted by simmons

Charles A. Goldthwaite, Jr., Ph.D.

Cardiovascular disease (CVD), which includes hypertension, coronary heart disease (CHD), stroke, and congestive heart failure (CHF), has ranked as the number one cause of death in the United States every year since 1900 except 1918, when the nation struggled with an influenza epidemic.1 In 2002, CVD claimed roughly as many lives as cancer, chronic lower respiratory diseases, accidents, diabetes mellitus, influenza, and pneumonia combined. According to data from the 19992002 National Health and Nutrition Examination Survey (NHANES), CVD caused approximately 1.4 million deaths (38.0 percent of all deaths) in the U.S. in 2002. Nearly 2600 Americans die of CVD each day, roughly one death every 34 seconds. Moreover, within a year of diagnosis, one in five patients with CHF will die. CVD also creates a growing economic burden; the total health care cost of CVD in 2005 was estimated at $393.5 billion dollars.

Given the aging of the U.S. population and the relatively dramatic recent increases in the prevalence of cardiovascular risk factors such as obesity and type 2 diabetes,2,3 CVD will continue to be a significant health concern well into the 21st century. However, improvements in the acute treatment of heart attacks and an increasing arsenal of drugs have facilitated survival. In the U.S. alone, an estimated 7.1 million people have survived a heart attack, while 4.9 million live with CHF.1 These trends suggest an unmet need for therapies to regenerate or repair damaged cardiac tissue.

Ischemic heart failure occurs when cardiac tissue is deprived of oxygen. When the ischemic insult is severe enough to cause the loss of critical amounts of cardiac muscle cells (cardiomyocytes), this loss initiates a cascade of detrimental events, including formation of a non-contractile scar, ventricular wall thinning (see Figure 6.1), an overload of blood flow and pressure, ventricular remodeling (the overstretching of viable cardiac cells to sustain cardiac output), heart failure, and eventual death.4 Restoring damaged heart muscle tissue, through repair or regeneration, therefore represents a fundamental mechanistic strategy to treat heart failure. However, endogenous repair mechanisms, including the proliferation of cardiomyocytes under conditions of severe blood vessel stress or vessel formation and tissue generation via the migration of bone-marrow-derived stem cells to the site of damage, are in themselves insufficient to restore lost heart muscle tissue (myocardium) or cardiac function.5 Current pharmacologic interventions for heart disease, including beta-blockers, diuretics, and angiotensin-converting enzyme (ACE) inhibitors, and surgical treatment options, such as changing the shape of the left ventricle and implanting assistive devices such as pacemakers or defibrillators, do not restore function to damaged tissue. Moreover, while implantation of mechanical ventricular assist devices can provide long-term improvement in heart function, complications such as infection and blood clots remain problematic.6 Although heart transplantation offers a viable option to replace damaged myocardium in selected individuals, organ availability and transplant rejection complications limit the widespread practical use of this approach.

Figure 6.1. Normal vs. Infarcted Heart. The left ventricle has a thick muscular wall, shown in cross-section in A. After a myocardial infarction (heart attack), heart muscle cells in the left ventricle are deprived of oxygen and die (B), eventually causing the ventricular wall to become thinner (C).

2007 Terese Winslow

The difficulty in regenerating damaged myocardial tissue has led researchers to explore the application of embryonic and adult-derived stem cells for cardiac repair. A number of stem cell types, including embryonic stem (ES) cells, cardiac stem cells that naturally reside within the heart, myoblasts (muscle stem cells), adult bone marrow-derived cells, mesenchymal cells (bone marrow-derived cells that give rise to tissues such as muscle, bone, tendons, ligaments, and adipose tissue), endothelial progenitor cells (cells that give rise to the endothelium, the interior lining of blood vessels), and umbilical cord blood cells, have been investigated to varying extents as possible sources for regenerating damaged myocardium. All have been tested in mouse or rat models, and some have been tested in large animal models such as pigs. Preliminary clinical data for many of these cell types have also been gathered in selected patient populations.

However, clinical trials to date using stem cells to repair damaged cardiac tissue vary in terms of the condition being treated, the method of cell delivery, and the primary outcome measured by the study, thus hampering direct comparisons between trials.7 Some patients who have received stem cells for myocardial repair have reduced cardiac blood flow (myocardial ischemia), while others have more pronounced congestive heart failure and still others are recovering from heart attacks. In some cases, the patient's underlying condition influences the way that the stem cells are delivered to his/her heart (see the section, quot;Methods of Cell Deliveryquot; for details). Even among patients undergoing comparable procedures, the clinical study design can affect the reporting of results. Some studies have focused on safety issues and adverse effects of the transplantation procedures; others have assessed improvements in ventricular function or the delivery of arterial blood. Furthermore, no published trial has directly compared two or more stem cell types, and the transplanted cells may be autologous (i.e., derived from the person on whom they are used) or allogeneic (i.e., originating from another person) in origin. Finally, most of these trials use unlabeled cells, making it difficult for investigators to follow the cells' course through the body after transplantation (see the section quot;Considerations for Using These Stem Cells in the Clinical Settingquot; at the end of this article for more details).

Despite the relative infancy of this field, initial results from the application of stem cells to restore cardiac function have been promising. This article will review the research supporting each of the aforementioned cell types as potential source materials for myocardial regeneration and will conclude with a discussion of general issues that relate to their clinical application.

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6. Mending a Broken Heart: Stem Cells and Cardiac Repair [Stem ...

Recommendation and review posted by Bethany Smith

Nov. 28, 2013 Up until a few years ago, the common school of thought held that the mammalian heart had very little regenerative capacity. However, scientists now know that heart muscle cells constantly regenerate, albeit at a very low rate. Researchers at the Max Planck Institute for Heart and Lung Research in Bad Nauheim, have identified a stem cell population responsible for this regeneration. Hopes are growing that it will be possible in future to stimulate the self-healing powers of patients with diseases and disorders of the heart muscle, and thus develop new potential treatments.

Some vertebrates seem to have found the fountain of youth, the source of eternal youth, at least when it comes to their heart. In many amphibians and fish, for example, this important organ has a marked capacity for regeneration and self-healing. Some species in the two animal groups have even perfected this capability and can completely repair damage caused to heart tissue, thus maintaining the organ's full functionality.

The situation is different for mammals, whose hearts have a very low regenerative capacity. According to the common school of thought that has prevailed until recently, the reason for this deficit is that the heart muscle cells in mammals cease dividing shortly after birth. It was also assumed that the mammalian heart did not have any stem cells that could be used to form new heart muscle cells. On the contrary: new studies show that aged muscle cells are also replaced in mammalian hearts. Experts estimate, however, that between just one and four percent of heart muscle cells are replaced every year.

Scientists in Thomas Braun's Research Group at the Max Planck Institute for Heart and Lung Research have succeeded in identifying a stem cell population in mice that plays a key role in this regeneration of heart muscle cells. Experiments conducted by the researchers in Bad Nauheim on genetically modified mice show that the Sca1 stem cells in a healthy heart are involved in the ongoing replacement of heart muscle cells. The Sca-1 cells increase their activity if the heart is damaged, with the result that significantly more new heart muscle cells are formed.

Since, in comparison to the large amount of heart muscle cells, Sca-1 stem cells account for just a tiny proportion of the cells in the heart muscle, searching for them is like searching for a needle in a haystack. "We also faced the problem that Sca-1 is no longer available in the cells as a marker protein for stem cells after they have been changed into heart muscle cells. To prove this, we had to be inventive," says project leader Shizuka Uchida. The Max Planck researchers genetically modified the stem cells to such an extent that, in addition to the Sca-1, they produced another visible marker. Even if Sca-1 was subsequently no longer visible, the marker could still be detected permanently.

"In this way, we were able to establish that the proportion of heart muscle cells originating from Sca-1 stem cells increased continuously in healthy mice. Around five percent of the heart muscle cells regenerated themselves within 18 months," says Uchida. Moreover, mice suffering from heart disease triggered by the experiment had up to three times more of these newly formed heart muscle cells.

"The data shows that, in principle, the mammalian heart is able to trigger regeneration and renewal processes. Under normal circumstances, however, these processes are not enough to ultimately repair cardiac damage," says Braun. The aim is to find ways in which the formation of new heart muscle cells from heart stem cells can be improved and thereby strengthen the heart's self-healing powers.

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The heart's own stem cells play their part in regeneration

Recommendation and review posted by Bethany Smith

November 28, 2013

By LAURAN NEERGAARD AP Medical Writer

WASHINGTON (AP) -- Could paying for bone marrow cells really boost the number of donors? The Obama administration is taking steps to block a federal court ruling that had opened a way to find out.

Buying or selling organs has long been illegal, punishable by five years in jail. The 1984 National Organ Transplantation Act that set the payment ban didn't just refer to solid organs -- it included bone marrow transplants, too.

Thousands of people with leukemia and other blood diseases are saved each year by bone marrow transplants. Thousands more, particularly minorities, still have trouble finding a genetically compatible match even though millions of volunteers have registered as potential donors under the current altruistic system.

A few years ago, the libertarian Institute for Justice sued the government to challenge that system. It argued that more people with rare marrow types might register to donate -- and not back out later if they're found to be a match -- if they had a financial incentive such as a scholarship paid by a nonprofit group.

Ultimately, a panel of the 9th U.S. Circuit Court of Appeals ruled that some, not all, marrow donors could be compensated -- citing a technological reason. Years ago, the only way to get marrow cells was to extract them from inside bone. Today, a majority of donors give marrow-producing cells through a blood-filtering process that's similar to donating blood plasma. Because it's legal to pay plasma donors, the December 2011 court ruling said marrow donors could be paid, too, as long as they give in that newer way.

"They're not even transplanting your bone marrow. They're transplanting these baby blood cells," said Jeff Rowes, an attorney with the Institute for Justice. It represented some families who'd had trouble finding donors, and was pushing for a study of compensation as a next step.

Not so fast, says the Obama administration. The government now has proposed a regulation to keep the ban intact by rewriting some legal definitions to clarify that it covers marrow-producing stem cells no matter how they're derived.

"It is not a matter of how you obtain it," said Shelley Grant of the Health Resources and Services Administration's transplant division. "Whether we obtain them through the marrow or the circulatory system, it is those stem cells that provide a potential cure."

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Gov't to keep ban on paying bone marrow donors | Minnesota ...

Recommendation and review posted by Bethany Smith