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17-Apr-2014

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 x2156 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, April 17, 2014The development of stem cell therapies to cure a variety of diseases depends on the ability to characterize stem cell populations based on cell surface markers. Researchers from the Finnish Red Cross have discovered a new marker that is highly expressed in a type of stem cells derived from human umbilical cord blood, which they describe in an article in BioResearch Open Access, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available free on the BioResearch Open Access website.

Heli Suila and colleagues, Finnish Red Cross Blood Service, Helsinki, Finland present evidence to show that the glycan O-GLcNAc, is present on the surface of stem cells and is part of a stem cell-specific surface signature. In the article "Extracellular O-Linked N-Acetylglucosamine Is Enriched in Stem Cells Derived from Human Umbilical Cord Blood" the authors suggest that the glycan plays a crucial role in a cell signaling pathway that regulates embryonic development.

"This work is particularly interesting as epidermal growth factor domains are found on the Notch receptors, suggesting that these novel glycans may be involved in Notch receptor signaling pathways in stem cells," says BioResearch Open Access Editor Jane Taylor, PhD, MRC Centre for Regenerative Medicine, University of Edinburgh, Scotland.

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About the Journal

BioResearch Open Access is a bimonthly peer-reviewed open access journal led by Editor-in-Chief Robert Lanza, MD, Chief Scientific Officer, Advanced Cell Technology, Inc. and Editor Jane Taylor, PhD. The Journal provides a new rapid-publication forum for a broad range of scientific topics including molecular and cellular biology, tissue engineering and biomaterials, bioengineering, regenerative medicine, stem cells, gene therapy, systems biology, genetics, biochemistry, virology, microbiology, and neuroscience. All articles are published within 4 weeks of acceptance and are fully open access and posted on PubMedCentral. All journal content is available on the BioResearch Open Access website.

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Novel marker discovered for stem cells derived from human umbilical cord blood

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Could not connect to DB: 1040: Too many connectionsCould not execute 'UPDATE pressrelease SET r_hits = r_hits+ 1, r_total_hits = r_total_hits+ 1, r_pub_hits = r_pub_hits+ 1, r_total_pub_hits = r_total_pub_hits+ 1 WHERE r_id = 265098' on database eurekalert: 2002: Can't connect to local MySQL server through socket '/tmp/mysql.sock' (2)

PUBLIC RELEASE DATE:

17-Apr-2014

Contact: Jane C. Figueiredo janefigu@usc.edu PLOS

A common genetic variant that affects one in three people appears to significantly increase the risk of colorectal cancer from the consumption of processed meat, according to study published today in PLOS Genetics. The study of over 18,000 people from the U.S., Canada, Australia and Europe represents the first large-scale genome-wide analysis of genetic variants and dietary patterns that may help explain more of the risk factors for colorectal cancer. Dr Jane Figueiredo at the Keck School of Medicine of the University of Southern California, explained that eating processed meat is associated with an increased risk of colorectal cancer and for about a third of the general population who carry this genetic variant, the risk of eating processed meat is even higher compared to those who do not. "Our results, if replicated by other studies, may provide us with a greater understanding of the biology into colorectal carcinogenesis," said Dr Ulrike Peters of the Fred Hutchinson Cancer Research Center's Public Health Sciences Division.

The study population totaled 9,287 patients with colorectal cancer and a control group of 9,117 individuals without cancer, all participants in 10 observational studies that were pooled in the largest meta-analysis sponsored by the National Institutes of Health-funded Genetics and Epidemiology of Colorectal Cancer Consortium (GECCO) and Colorectal Cancer Family Registry. Scientists systematically searched 2.7 million variants to identify those that are associated with the consumption of meat, fiber, fruits and vegetables. A significant interaction between the genetic variant rs4143094 and processed meat consumption was detected. This variant is located on the same chromosome 10 region that includes GATA3, a transcription factor gene previously linked to several forms of cancer. The transcription factor encoded by this gene plays a role in the immune system. Dr Figueiredo hypothesized that the genetic locus found to interact with processed meat may have interesting biological significance given its location in the genome, but further functional analyses are required.

Colorectal cancer is a multi-factorial disease attributed to both genetic causes and lifestyle factors; including diet. About 30 known genetic susceptibility alleles for colorectal cancer have been pinpointed throughout the genome. How specific foods affect the activities of genes has not been established but represents an important area of research for prevention. "The possibility that genetic variants may modify an individual's risk for disease based on diet has not been thoroughly investigated but represents an important new insight into disease development," said Dr Li Hsu, the lead statistician on the study. "Diet is a modifiable risk factor for colorectal cancer. Our study is the first to understand whether some individuals are at higher or lower risk based on their genomic profile. This information can help us better understand the biology and maybe in the future lead to targeted prevention strategies," said Dr Figueiredo.

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New gene variant found increases the risk of colorectal cancer from eating processed meat

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17-Apr-2014

Contact: Helen Dodson helen.dodson@yale.edu 203-436-3984 Yale University

New Haven, Conn. Researchers from Yale School of Medicine and Celera Diagnostics have confirmed the significance of a genetic variant that substantially increases the risk of a frequently fatal thoracic aortic dissection or full rupture. The study appears online in PLOS ONE.

Thoracic aortic aneurysms, or bulges in the artery wall, can develop without pain or other symptoms. If they lead to a tear dissection or full rupture, the patient will often die without immediate treatment. Therefore, better identification of patients at risk for aortic aneurysm and dissection is considered essential.

The research team, following up on a previous genome-wide association study by researchers at Baylor College of Medicine, investigated genetic variations in a protein called FBN-1, which is essential for a strong arterial wall. After studying hundreds of patients at Yale, they confirmed what was found in the Baylor study: that one variation, known as rs2118181, put patients at significantly increased risk of aortic tear and rupture.

"Although surgical therapy is remarkable and effective, it is incumbent on us to move to a higher genetic level of understanding of these diseases," said senior author John Elefteriades, M.D., the William W. L. Glenn Professor of Surgery (Section of Cardiac Surgery) at Yale School of Medicine, and director of the Aortic Institute at Yale-New Haven Hospital. "Such studies represent important steps along that path."

The researchers hope their confirmation of the earlier study may help lead to better clinical care of patients who may be at high risk of this fatal condition. "Patients with this mutation may merit earlier surgical therapy, before aortic dissection has a chance to occur," Elefteriades says. Yale cardiothoracic surgeons will now begin assessing this gene in clinical patients with aneurysm disease.

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NewLink Genetics Presents Data at the AACR 2014 Annual Meeting
AMES, IA, via eTeligis, 4/9/2014 11:00:00 AM NewLink Genetics Presents Data at the AACR 2014 Annual Meeting Data Demonstrate Synergistic Anti-Tumor Activity ...

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Simons Institute Open Lecture: Evolutionary Genetics in the Crush of Genomics
Charles H. Langley, UC Davis http://simons.berkeley.edu/events/openlectures2014-spring-3.

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Keyword Genetics Review - How to use it?
Click here for details: http://rogerminh.com/keyword-genetics-review-bonus/

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Genetics and Inheritance
Download the Show Notes: http://www.mindset.co.za/learn/sites/files/LXL2014/LXL_Gr12LifeSciences_09_Genetics Inheritance_09Apr2014.pdf In this live Gr 12 Lif...

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The Future of Genetics in Our Everyday Lives - SXSW Interactive 2014 (Full Session)
Is DNA the programming language of the future? What role do genetics and personalized medicine play in the healthcare revolution? Can big data and community ...

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The Harvard-MIT genomic science institute stays mute on how it will assert control over the tools expected to speed cures and change gene therapy.

One of the most important genetic technologies developed in recent years is now patented, and researchers are wondering what they will and wont be allowed to do with the powerful method for editing the genome.

On Tuesday, the Broad Institute of MIT and Harvard announced that it had been granted a patent covering the components and methodology for CRISPRa new way of making precise, targeted changes to the genome of a cell or an organism. CRISPR could revolutionize biomedical research by giving scientists a more efficient way of re-creating disease-related mutations in lab animals and cultured cells; it may also yield an unprecedented way of treating disease (see Genome Surgery).

The patent, issued just six months after its application was filed, covers a modified version of the CRISPR-Cas9 system found naturally in bacteria, which microbes use to defend themselves against viruses. The patent also covers methods for designing and using CRISPRs molecular components.

The inventor listed on the patent is Feng Zhang, an MIT researcher and core faculty member of the Broad. Zhang was an MIT Technology Review Innovator Under 35 in 2013.

The patent describes how the tools could be used to treat diseases, and lists many specific conditions from epilepsy, to Huntingtons, to autism, and macular degeneration. One of the most exciting possibilities for CRISPR is its potential to treat genetic disorders by directly correcting mutations on a patients chromosomes. That would enable doctors to treat diseases that cannot be addressed by more traditional methods, a goal already set by a startup cofounded by Zhang called Editas Medicine (see New Genome-Editing Method Could Make Gene Therapy More Precise and Effective).

Another founder of Editas, Jennifer Doudna, and her institute, the University of California, have a pending patent application for CRISPR technology. How that west coast application will be affected is not yet clear. Its also unclear what impact the Broads claims on the technology will have on its commercial use and on basic research.

Chelsea Loughran, an intellectual property litigation lawyer who has been following CRISPR over the last year, says that lots of people are already using CRISPR and its not clear if it will now become harder for them to do that. All of that is in the hands of MIT and the Broad, she says.

While MIT, Harvard, and the Broad all jointly own the CRISPR patents announced yesterday, the Broads technology licensing office is managing decisions about who will get licenses to use the technology, says Lita Nelsen, director of the MIT Technology Licensing Office. (Licenses areformal permissions to use a patented technology, often in exchange for money.)

A spokesperson for the Broad says that specific details around licensing arent available at this time, but the Broad does intend to make this technology broadly available to scientists.

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Broad Institute Gets Patent on Revolutionary Gene-Editing Method

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PUBLIC RELEASE DATE:

16-Apr-2014

Contact: Tom Vasich tmvasich@uci.edu 949-824-6455 University of California - Irvine

Irvine, Calif., April 16, 2014 A class of drugs developed to treat immune-related conditions and cancer including one currently in clinical trials for glioblastoma and other tumors eliminates neural inflammation associated with dementia-linked diseases and brain injuries, according to UC Irvine researchers.

In their study, assistant professor of neurobiology & behavior Kim Green and colleagues discovered that the drugs, which can be delivered orally, eradicated microglia, the primary immune cells of the brain. These cells exacerbate many neural diseases, including Alzheimer's and Parkinson's, as well as brain injury.

"Because microglia are implicated in most brain disorders, we feel we've found a novel and broadly applicable therapeutic approach," Green said. "This study presents a new way to not just modulate inflammation in the brain but eliminate it completely, making this a breakthrough option for a range of neuroinflammatory diseases."

The researchers focused on the impact of a class of drugs called CSF1R inhibitors on microglial function. In mouse models, they learned that inhibition led to the removal of virtually all microglia from the adult central nervous system with no ill effects or deficits in behavior or cognition. Because these cells contribute to most brain diseases and can harm or kill neurons the ability to eradicate them is a powerful advance in the treatment of neuroinflammation-linked disorders.

Green said his group tested several selective CSF1R inhibitors that are under investigation as cancer treatments and immune system modulators. Of these compounds, they found the most effective to be a drug called PLX3397, created by Plexxikon Inc., a Berkeley, Calif.-based biotechnology company and member of the Daiichi Sankyo Group. PLX3397 is currently being evaluated in phase one and two clinical trials for multiple cancers, including glioblastoma, melanoma, breast cancer and leukemia.

Crucially, microglial elimination lasted only as long as treatment continued. Withdrawal of inhibitors produced a rapid repopulation of cells that then grew into new microglia, said Green, who's a member of UC Irvine's Institute for Memory Impairments and Neurological Disorders.

This means that eradication of these immune cells is fully reversible, allowing researchers to bring microglia back when desired. Green added that this work is the first to describe a new progenitor/potential stem cell in the central nervous system outside of neurogenesis, a discovery that points to novel opportunities for manipulating microglial populations during disease.

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Cancer drugs block dementia-linked brain inflammation, UCI study finds

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A class of drugs developed to treat immune-related conditions and cancer -- including one currently in clinical trials for glioblastoma and other tumors -- eliminates neural inflammation associated with dementia-linked diseases and brain injuries, according to UC Irvine researchers.

In their study, assistant professor of neurobiology & behavior Kim Green and colleagues discovered that the drugs, which can be delivered orally, eradicated microglia, the primary immune cells of the brain. These cells exacerbate many neural diseases, including Alzheimer's and Parkinson's, as well as brain injury.

"Because microglia are implicated in most brain disorders, we feel we've found a novel and broadly applicable therapeutic approach," Green said. "This study presents a new way to not just modulate inflammation in the brain but eliminate it completely, making this a breakthrough option for a range of neuroinflammatory diseases."

The researchers focused on the impact of a class of drugs called CSF1R inhibitors on microglial function. In mouse models, they learned that inhibition led to the removal of virtually all microglia from the adult central nervous system with no ill effects or deficits in behavior or cognition. Because these cells contribute to most brain diseases -- and can harm or kill neurons -- the ability to eradicate them is a powerful advance in the treatment of neuroinflammation-linked disorders.

Green said his group tested several selective CSF1R inhibitors that are under investigation as cancer treatments and immune system modulators. Of these compounds, they found the most effective to be a drug called PLX3397, created by Plexxikon Inc., a Berkeley, Calif.-based biotechnology company and member of the Daiichi Sankyo Group. PLX3397 is currently being evaluated in phase one and two clinical trials for multiple cancers, including glioblastoma, melanoma, breast cancer and leukemia.

Crucially, microglial elimination lasted only as long as treatment continued. Withdrawal of inhibitors produced a rapid repopulation of cells that then grew into new microglia, said Green, who's a member of UC Irvine's Institute for Memory Impairments and Neurological Disorders.

This means that eradication of these immune cells is fully reversible, allowing researchers to bring microglia back when desired. Green added that this work is the first to describe a new progenitor/potential stem cell in the central nervous system outside of neurogenesis, a discovery that points to novel opportunities for manipulating microglial populations during disease.

Study results appear in today's issue of Neuron.

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The above story is based on materials provided by University of California - Irvine. Note: Materials may be edited for content and length.

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Cancer drugs block dementia-linked brain inflammation, study finds

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Stem cell scientist Mahendra Rao, former director of the now-defunct Center For Regenerative Medicine at the National Institutes of Health. Photo taken in December, 2013 during a speech by Rao at the World Stem Cell Summit in San Diego.

One of the nation's top stem cell scientists has become an adviser to San Diego's Stemedica, a developer of stem cell-based therapies.

Dr. Mahendra Rao joined Stemedica's scientific and medical advisory board, and will help guide the company's strategy, said Maynard Howe, chief executive of the privately held company. Rao's career as a scientist who has also worked for companies and federal agencies makes him particularly useful, Howe said.

Rao is a medical doctor with a PhD in developmental neurobiology from CalTech. He headed the neurosciences division of the National Institute on Aging. He also led the stem cell division of Carlsbad-based Life Technologies, now a unit of Thermo Fisher Scientific. The two companies are on good terms: Life Technologies sells two kinds of stem cells made by Stemedica, used for research purposes, Howe said.

Rao was most recently founding director of the Center for Regenerative Medicine at the National Institutes of Health, which has been shut down. Rao, who resigned at the end of March, said he was disappointed at the slow pace of funding studies with artificial embryonic stem cells, called induced pluripotent stem cells. Stemedica announced his appointment April 8.

Rao said Wednesday that his goal now is to advance stem cell therapies through the private sector. Stemedica drew his attention because it had developed a method of reliably generating "clinically compliant" stem cells suitable for use in therapy.

In addition, Rao said he likes that Stemedica is developing combination stem cell therapies, using a variety called mesenchymal stem cells. This variety of stem cell generates chemicals that promote short-term regrowth and seems to enhance the survival of other transplanted stem cells. For example, mesenchymal stem cells could help transplanted neural stem cells integrate into the brain.

"That's a high-risk process and it's a much more difficult road, but they seem to be willing to do that," Rao said.

He has also rejoined the board of Q Therapeutics, a Salt Lake City company developing treatments for spinal cord injuries and other neurological disorders. Rao is the company's scientific founder, but had to leave the company when he joined the NIH.

Stemedica and its affiliated companies are undertaking multiple clinical trials of stem cell therapies. One of the most advanced is for stroke, Howe said. See utsandiego.com/stemedicastroke1 for detailed information.

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Top stem cell scientist joins Stemedica

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Two Central Pennsylvania dogs are receiving a regenerative therapy for arthritis thats unprecedented for this area and less expensive than standard surgery. Stem Cell therapy is a way to repair damaged tissue and treat injury. When dealing with dogs, veterinarians say its the future of treatments and its becoming less costly.

Gunny is a 7-year-old German Shepard. He underwent the revolutionary stem cell therapy at the Palmyra Animal Clinic. Vets say the stem cell therapy is a way to combat Gunnys arthritis in his hips. Doctors collected fatty tissue from his shoulder, processed the stem cells in the lab and injected the cells back into his hips. This happens all in one day for around $1500. Prior to this, surgery could cost around $3,000.

Dr. Calvin Clements of the Palmyra Animal Clinic says, Injected in a damaged joint or ligament, these cells will take on that characteristic and differentiate into the cartilage or tissue were dealing with and help to regenerate it.

Dr. Clements says results are noticeable in about a month. On average, animals improve 85%.

For more information, contact the Palmyra Animal Clinic at 717-838-5451.

To learn more click here.

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Personalized Medicine for Women - Dr. Deborah Money
A preview of Dr. Deborah Money #39;s talk at UBC Robson Square in Vancouver BC Event Details: http://gynintheknow.com/Resources/%EF%BF%BC%EF%BF%BC-personalized-m...

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Scottish Rugby supporting spinal cord injury research at Aberdeen University

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Dr. Lathrop spinal cord injury restoration (English)
An amazing injury treatment case with SCENAR manufactured by RITM OKB ZAO (Taganrog, Russia). More details on SCENAR capabilities at http://scenar.com.ru/ind...

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Living and Aging with Spinal Cord Injury : Session 1 Part A
Session 1 Part A. The longitudinal SCI life histories study. Dr Martin Sullivan, Ass Prof Sarah Derrett, Prof Charlotte Paul Sessions from a Mini Symposium c...

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Diff bw Surgical Hair Transplantaion Stem Cell Therapy - Health file
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April 16, 2014

Brett Smith for redOrbit.com Your Universe Online

New research from scientists at Stanford University has revealed a genetic variant that raises the risk of developing Alzheimers disease in women, but not in men.

After analyzing information on numerous older individuals who were followed over time, the scientists recognized a genetic variant called ApoE4 that conveyed the sex-specific elevated risk level, according to their report in the Annals of Neurology.

While more women suffer from Alzheimers than men, women also tend to live longer increasing their odds of developing the cognitive disorder. However, the study researchers found the risk from the genetic variant remained even after considering age.

Even after correcting for age, women appear to be at greater risk, said Dr. Michael Greicius, study author and assistant professor of neurology at Stanford.

In the study, researchers considered records that had been stored in two large, openly available databases. In one repository, the scientists reviewed clinical assessments of 5,000 people whose cognitive test outcome was normal at the start and 2,200 people who had originally showed indications of mild cognitive impairment.

Within both groups, being an ApoE4 carrier showed higher probability of Alzheimers disease. Additionally, the team also saw that for those who began with normal cognitive function, the greater risk was only minimal for men, while women who had the ApoE4 variant had near double the odds of moving on to mild cognitive impairment or Alzheimers disease as people who didnt.

Our study showed that, among healthy older controls, having one copy of the ApoE4 variant confers a substantial Alzheimers disease risk in women, but not in men, Greicius said.

From the second database, researchers examined imaging information and measurements of a number of biomarkers from spinal fluid that signal mild cognitive impairment and ultimately Alzheimers disease. Evaluation of 1,000 patients files from this collection not only validated ApoE4s sex-specific effect, but it also produced evidence that may assist investigators in exploring, and potentially explaining, the molecular components connecting ApoE4 to Alzheimers disease, Greicius said.

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Gene Variant Confers Higher Alzheimer's Risk For Women

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PUBLIC RELEASE DATE:

16-Apr-2014

Contact: Tom Abate tabate@stanford.edu 650-736-2245 Stanford University Medical Center

STANFORD, Calif. Consider the marvel of the embryo. It begins as a glob of identical cells that change shape and function as they multiply to become the cells of our lungs, muscles, nerves and all the other specialized tissues of the body.

Now, in a feat of reverse tissue engineering, Stanford University researchers have begun to unravel the complex genetic coding that allows embryonic cells to proliferate and transform into all of the specialized cells that perform myriad biological tasks.

A team of interdisciplinary researchers took lung cells from the embryos of mice, choosing samples at different points in the development cycle. Using the new technique of single-cell genomic analysis, they recorded what genes were active in each cell at each point. Though they studied lung cells, their technique is applicable to any type of cell.

"This lays out a playbook for how to do reverse tissue engineering," said Stephen Quake, PhD, the Lee Otterson Professor in the School of Engineering and a Howard Hughes Medical Institute investigator.

The researchers' findings are described in a paper published online April 13 in Nature. Quake, who also is a professor of bioengineering and of applied physics, is the senior author. The lead authors are postdoctoral scholars Barbara Treutlein, PhD, and Doug Brownfield, PhD.

The researchers used the reverse-engineering technique to study the cells in the alveoli, the small, balloon-like structures at the tips of the airways in the lungs. The alveoli serve as docking stations where blood vessels receive oxygen and deliver carbon dioxide.

Treutlein and Brownfield isolated 198 lung cells from mouse embryos at three stages of gestation: 14.5 days, 16.5 days and 18.5 days (mice are usually born at 20 days). They also took some lung cells from adult mice.

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When his tomato plants were just a week old, technicians manually punched a hole in each seedling to get leaf tissue that was taken to a nearby lab, converted into a chemical soup and then scanned for genetic markers linked to desired traits.

Krivanek uses the information to keep just 3percent of the seedlings and grow them until they fruit this spring, when he can evaluate fully grown plants, keep a few hundred, sow their seeds and then screen those plants.

Im improving my odds. Maybe I can introduce to market a real super-hybrid in five years, Krivanek said. A predecessor might take a whole career.

The technology called marker-assisted or molecular breeding is far removed from the better-known and more controversial field of genetic engineering, in which a plant or animal can receive genes from a different organism.

Marker-assisted breeding, by contrast, lays bare the inherent genetic potential of an individual plant to allow breeders to find the most promising seedling among thousands for further breeding. Because the plants natural genetic boundaries are not crossed, the resulting commercial hybrid is spared the regulatory gantlet and the public opposition focused on such plants as genetically modified Roundup Ready corn or soybeans, which are engineered to withstand herbicide sprays.

Marker-assisted breeding has been embraced not only by the multinational biotech companies here in Californias Central Valley but also by plant scientists in government, research universities and nongovernmental organizations fervently seeking new, overachieving crops. The goal is to sustainably feed an expanding global population while dealing with the extremes of climate change.

But critics of Big Agriculture worry about the needs of small-scale farmers and breeders. Low-tech conventional breeding judging plants by how they look and perform, not by their DNA has been the lifeblood of small seed companies and local growers, often in conjunction with breeding programs at land-grant universities. But those programs have shrunk by a third in recent years, and the remaining ones are increasingly gravitating to the trendy sphere of molecular breeding.

Organic farmers, who need crop varieties designed for specific regions and less-intensive growing methods, are not being served by the new applied science, said John Navazio, a senior scientist with the Organic Seed Alliance.

There used to be a significant winter spinach production area in southern Virginia and Delmarva, and thats completely gone, he said. The spinach-growing industry has moved to megagrowers in California and Arizona.

Progress comes sooner

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Trait by trait, plant scientists swiftly weed out bad seeds through marker-assisted breeding

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PHILADELPHIA Daniel J. Rader, MD, a widely recognized international leader in the human genetics of lipoprotein biology and cardiovascular disease, has been named the new chair of the Department of Genetics in the Perelman School of Medicine at the University of Pennsylvania. He has been a faculty member at Penn for 20 years and is currently the chief of the Division of Translational Medicine and Human Genetics and the Edward S. Cooper, MD/Norman Roosevelt and Elizabeth Meriwether McLure Professor of Medicine.

As a prominent physician-scientist, Dr. Rader will bring his robust knowledge of genetic approaches to improving health to guide the department of Genetics into an era where genes play a role in our strategies to prevent and treat a broad array of diseases, said J. Larry Jameson, MD, PhD, Executive Vice President for the Health System and Dean of the Perelman School of Medicine. His long record of leadership in the classroom, the exam room, and the lab will be invaluable to the department and overall genetics research at Penn.

Dr. Rader holds multiple leadership roles at Penn Medicine. In addition to heading the Division of Translational Medicine and Human Genetics within the Department of Medicine, he also serves as Associate Director of the Institute for Translational Medicine and Therapeutics (ITMAT).

He co-directs the new Penn Medicine BioBank, an integrated, centralized resource for consenting, collecting, processing, and storing DNA, plasma/serum, and tissue for human genetics and translational research. This venture is a cornerstone of Penn Medicines efforts in human genetics and translational and personalized medicine. Dr. Rader also has key relationships with Penns Cardiovascular Institute (CVI) and Institute for Diabetes, Obesity, and Metabolism (IDOM).

In his research program, Dr. Rader has used human genetics and model systems to elucidate novel biological pathways in lipoprotein metabolism and atherosclerosis. His lab discovered and characterized the enzyme endothelial lipase, demonstrated its effects on high density lipoproteins (HDL) in mice, and then found that loss-of-function mutations in the gene cause high levels of HDL in humans. He is among the worlds leaders in using both humans and model systems to dissect the functional genomics of human genetic variants associated with plasma lipid traits as well as coronary heart disease.

He has had a long interest in Mendelian disorders of lipoprotein metabolism and has a strong translational interest in development of novel therapies for these disorders. He was involved in the identification of the molecular defect in a rare genetic disorder causing very low levels of low density lipoproteins (LDL), which spurred the development of inhibitors of this protein to reduce levels of LDL. Indeed, when one such drug was abandoned by a pharmaceutical firm, he went on to oversee its development for the orphan disease homozygous familial hypercholesterolemia (HoFH), characterized by extremely high levels of LDL and heart disease in childhood. This decade-long endeavor led to FDA and European approval of lomitapide, the first effective medication for the treatment of HoFH.

Dr. Rader has received numerous awards as a physician-scientist, including the Burroughs Wellcome Fund Clinical Scientist Award in Translational Research, the Bristol Myers Squibb Cardiovascular Research Award, the Doris Duke Charitable Foundation Distinguished Clinical Investigator Award, the Jeffrey M. Hoeg Award for Basic Science and Clinical Research from the American Heart Association, the American Heart Associations Clinical Research Prize, and the Clinical Research Forums Distinguished Clinical Research Award. He has been elected to the American Society of Clinical Investigation and to the Association of American Physicians. In 2011, he received one of the nations highest honors in biomedicine when he was elected to the Institute of Medicine.

Dr. Rader has also received many awards for his outstanding teaching activities. At the Perelman School of Medicine, he has received the William Osler Patient Oriented Research Award, as well as the Donald B. Martin Outstanding Teacher Award and the Outstanding Faculty Award from the Department of Medicine. Along with these accolades, Dr. Rader has been honored by Philadelphia magazine, which has named him to its Top Docs honor roll every year since 2002.

Dr. Rader earned his medical degree at the Medical College of Pennsylvania, followed by an internship and a residency at Yale-New Haven Hospital. Next, he served as a post-doctoral fellow at the National Institutes of Health, where he developed skills in basic science as well as translational research involving patients with genetic lipid disorders.

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Group C 42 Huntington #39;s Genetics Revealed
Biology Project: GaTech BIOL 1510- Huntington #39;s Disease.

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Group C 42 Huntington's Genetics Revealed - Video

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Keyword Genetics Review | Watch Video Keyword Genetics Demo
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By: Junl Lee

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Keyword Genetics Review | Watch Video Keyword Genetics Demo - Video

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Gerbil Colors And Genetics
Thanks for watching! Hope you enjoyed. Please comment, rate, subscribe, and request! If you have any questions about gerbils, just ask me! Is it an emergency...

By: GerbNerdLolz

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Gerbil Colors And Genetics - Video

Recommendation and review posted by Bethany Smith