Archive for the ‘Gene Therapy Research’ Category

SAN DIEGO--(BUSINESS WIRE)--

Cytori Therapeutics (CYTX) announced this morning that a peer-reviewed case series using Cytoris cell therapy to treat patients suffering from complex cryptoglandular fistula has been published in the current issue of the British Medical Journal: Case Reports. The patients were treated by Dr. David Borowski and Dr. Pud Bhaskar, Consultant Surgeons at the University Hospital of North Tees, a National Health Service (NHS) hospital in the United Kingdom.

In this case series, three patients suffering from long-standing complex cryptoglandular fistula-in-ano were treated using fat grafts enriched with their own adipose-derived stem and regenerative cells (ADRCs), processed using Cytoris Celution system. The ADRC-enriched graft was injected directly into the tissue surrounding the fistula to close the fistula track. The interior opening of the fistula was closed with a mucosal advancement flap. All three patients remain fully healed at two to three year follow-up, with one patient undergoing colostomy reversal to restore bowel continuity.

These three patients are the initial cases treated within a phase I feasibility study; all three had been suffering from the symptoms of their fistulae with considerable reduction in their ability to lead a normal life, said Dr. Borowski. Other treatments had failed, and the successful treatment with ADRC-enriched lipofilling has helped them to resume a normal lifestyle. With these encouraging results, we are currently collaborating with several other centers in the UK and Europe to explore the efficacy of this treatment in a greater number of patients, and for other indications, in the setting of clinical trials.

This successful case series at a respected NHS hospital in the UK illustrates the breadth of Cytoris soft tissue business and the potential of Cytoris cell therapy to help patients who have few, if any, alternative treatment options. The data, showing that ADRC-enriched fat grafting appears to be safe and feasible for cryptoglandular fistula patients, validates the expansion of Cytoris CE Mark claims to include cryptoglandular fistula and other soft tissue and wound indications in August of this year.

Based on a report of the American College of Surgeons, there are between 43,000 and 140,000 fistula cases per year in Europe, of which cryptoglandular fistula are a subset. Cryptoglandular fistula is the most common cause of persistent perianal infection, causing abnormal fecal contamination and potentially incontinence.

About Cytori

Cytori Therapeutics, Inc. is developing cell therapies based on autologous adipose-derived regenerative cells (ADRCs) to treat cardiovascular disease and repair soft tissue defects. Our scientific data suggest ADRCs improve blood flow, moderate the immune response and keep tissue at risk of dying alive. As a result, we believe these cells can be applied across multiple ischemic conditions. These therapies are made available to the physician and patient at the point-of-care by Cytoris proprietary technologies and products, including the Celution system product family. http://www.cytori.com

Cautionary Statement Regarding Forward-Looking Statements

This communication includes forward-looking statements regarding events, trends and business prospects, which may affect our future operating results and financial position. Such statements, including, but not limited to, those regarding the potential of Cytoris cell therapy to help no-option patients, and statements regarding the safety and feasibility of this procedure for cryptoglandular fistula patients, are subject to risks and uncertainties that could cause our actual results and financial position to differ materially. Some of these risks and uncertainties include the uncertainties regarding the collection and results of clinical data, as well as our history of operating losses, regulatory uncertainties, dependence on third party performance, and other risks and uncertainties described under the "Risk Factors" section in Cytori's Securities and Exchange Commission Filings on Form 10-K and Form 10-Q. Cytori assumes no responsibility to update or revise any forward-looking statements contained in this press release to reflect events, trends or circumstances after the date of this press release.

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Cryptoglandular Fistula Repair Case Series Using Cytori Cell Therapy Published in the British Medical Journal: Case ...

JERUSALEM--(BUSINESS WIRE)--

Gamida Cell Ltd., a world leader in stem cell population expansion technologies and stem cell therapy products for transplantation and regenerative medicine, announced today that the first patient, enrolled in its pilot study of NiCord as an investigational treatment for sickle cell disease (SCD), has been transplanted at Duke University in North Carolina.

Gamida Cell CEO Dr. Yael Margolin said, The NiCord study is a first step in broadening Gamida Cells pipeline of cell therapies to treat patients who suffer from severe non-malignant diseases with a very large unmet clinical need.

SCD is a group of inherited red blood cell disorders where red blood cells become hard and sticky and look like a C-shaped farm tool called a sickle. According to statistics, SCD affects 90,000 to 100,000 in the US alone, mainly African-Americans and Hispanic-Americans. Symptoms range in type and severity. SCD can be fatal and to date, the only cure for SCD is stem cell transplantation from a family related matched donor.

Dr. Margolin continued, Sickle cell disease can be cured with a successful bone marrow transplantation, especially from a family related fully matched donor. Most patients do not pursue this option, since they do not have the suitable donor. NiCord is intended to reverse this situation and provide a readily available cure.

NiCord is an expanded cell graft derived from an entire unit of umbilical cord blood and enriched with stem cells. NiCord was developed based on Gamida Cells proprietary NAM technology.

The official name of the study is Allogeneic Stem Cell Transplantation of NiCord, Umbilical Cord Blood-Derived Ex Vivo Expanded Stem and Progenitor Cells, in Combination With a Second, Unmanipulated Cord Blood Unit in Patients With Sickle Cell Disease. http://www.clinicaltrials.gov/ct2/show/NCT01590628?term=nicord&rank=1. A total of 10 patients, ages 2 21, will be enrolled in the NiCord study, a single center, single arm trial evaluating the safety and efficacy of transplanting NiCord together with a second un-manipulated cord blood unit in patients with SCD following myeloablative therapy. The study will also assess transplant-related mortality, event-free survival and overall survival at 100, 180 and 365 days, respectively.

About Gamida Cell

Gamida Cell is a world leader in stem cell population expansion technologies and stem cell therapy products for transplantation and regenerative medicine. The companys pipeline of stem cell therapy products are in development to treat a wide range of conditions including blood cancers, solid tumors, non-malignant hematological diseases such as hemoglobinopathies, neutropenia and acute radiation syndrome, autoimmune diseases and metabolic diseases as well as conditions that can be helped by regenerative medicine. Gamida Cells therapeutic candidates contain populations of adult stem cells, selected from non-controversial sources such as umbilical cord blood, bone marrow and peripheral blood, which are expanded in culture. Gamida Cells current shareholders include: Elbit Imaging (EMITF), Clal Biotechnology Industries (CBI.TA), Israel Healthcare Venture, Teva Pharmaceutical Industries (TEVA), Amgen, Denali Ventures and Auriga Ventures. For more information, please visit: http://www.gamida-cell.com.

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First Pediatric Sickle Cell Disease Patient Receives NiCord® Stem Cell Transplantation in Gamida Cell Pilot Study at ...

For Immediate Release Sunday, November 11, 2012 1 p.m. EST

An international group of scientists has identified three genetic regions that predispose Asian women who have never smoked to lung cancer. The finding provides further evidence that risk of lung cancer among never-smokers, especially Asian women, may be associated with certain unique inherited genetic characteristics that distinguishes it from lung cancer in smokers.

Lung cancer in never-smokers is the seventh leading cause of cancer deaths worldwide, and the majority of lung cancers diagnosed historically among women in Eastern Asia have been in women who never smoked. The specific genetic variations found in this study had not been associated with lung cancer risk in other populations.

Although environmental factors, such as secondhand smoke (also known as environmental tobacco smoke) or exhaust from indoor cooking are likely account for some cases of lung cancer among Asian women who have never smoked, they explain only a small proportion of the disease. To gain a better understanding of lung cancer in Asian female never-smokers, researchers from the National Cancer Institute (NCI), part of the National Institutes of Health, partnered with researchers from several other countries to create the Female Lung Cancer Consortium in Asia to conduct one of the largest genome-wide association studies (GWAS) in female never-smokers to date. GWAS compares DNA markers across the genome between people with a disease or trait to people without the disease or trait.

"This study is the first large-scale genome-wide association study of lung cancer among never-smoking females anywhere in the world," said Qing Lan, M.D., Ph.D. , a senior investigator in NCIs Division of Cancer Epidemiology and Genetics, and the leader of the study.

The consortium, whose findings were reported Nov.11, 2012, online in Nature Genetics , conducted a GWAS that combined data from 14 studies that included a total of approximately 14,000 Asian women (6,600 with lung cancer and 7,500 without lung cancer). The studies included data on environmental factors, including exposure to secondhand smoke.

The consortium found that variations at three locations in the genome two on chromosome 6 and one on chromosome 10 were associated with lung cancer in Asian female never-smokers. The discovery on chromosome 10 was particularly significant because it has not been found in any other GWAS of lung cancer in white or Asian populations.

Our study provides strong evidence that common inherited genetic variants contribute to an increased risk of lung cancer among Asian women who have never smoked, said Nathaniel Rothman, M.D., a senior investigator in NCI's Division of Cancer Epidemiology and Genetics and coauthor of the study. "These variants may also increase lung cancer risk associated with environmental factors, such as environmental tobacco smoke."

The researchers did not detect an association with variations at a location on chromosome 15 that has been associated with lung cancer risk in many previous GWAS of lung cancer in smokers. The absence of this association provides further support for the suggestion that the genetic variation on chromosome 15 may be smoking-related.

The researchers found some evidence that Asian women with one of the newly identified genetic variants may be more susceptible to the effects of environmental tobacco smoke. However, the authors note that more research is needed to draw definitive conclusions from this observation.

Originally posted here:
Gene variations linked to lung cancer susceptibility in Asian women

By Randy Dotinga HealthDay Reporter

FRIDAY, Nov. 9 (HealthDay News) -- In middle-aged people, a link may exist between weakened memory and genetic traits associated with obesity, raising the possibility that extra pounds change how our brains work, a new study suggests.

Researchers found the link between genes and memory in whites but not in blacks.

The research "could be useful in identifying people who may need more help with declining cognition," said John Speakman, a professor at the Institute of Biological and Environmental Sciences at the University of Aberdeen in Scotland, who is familiar with the findings.

Although some people believe obesity is purely a failure of individual will, scientists think genetic makeup has a lot to do with the propensity to gain extra pounds. Studies of twins and families suggest that genes account for about 65 percent of variance in body weight, Speakman said.

The new study focuses on four genetic traits related to a gene that's thought to play a role in obesity. Researchers looked for signs of the traits among nearly 8,400 white and 2,100 black people aged 45 to 64.

They found signs of a link between problems being able to remember words and two of the genetic traits. The connection held up even after the researchers adjusted their results so they wouldn't be thrown off by factors like large or small numbers of people who were of certain ages, genders, levels of obesity and education levels.

What's going on? It's not clear. Speakman said it's possible that the gene may affect both weight and memory.

"On the other hand, they could be linked because of negative impacts of obesity on memory function, or vice versa," he said. "The data don't allow us to see if that might be the case."

Dr. Michael Schwartz, director of the Diabetes and Obesity Center of Excellence at the University of Washington, in Seattle, pointed out that the connection held up even when the researchers tried to remove any influence of weight levels.

Continued here:
Study Ties Obesity-Related Gene to Weaker Memory

While I was at Spencer Wells poster at ASHG I was primarily curious about bar plots. Hes got really good spatial coverage, so Im moderately excited about the paper (though I didnt see much explicit testing of phylogenetic hypotheses, which I think this sort of paper has to do now; were beyond PCA and bar plots only papers). That being said, Spencer was more interested in me promoting the Scientific Grants Program. Heres some more information:

The Genographic Projects Scientific Grants Program awards grants on a rolling basis for projects that focus on studying the history of the human species utilizing innovative anthropological genetic tools. The variety of projects supported by the scientific grants will aim to construct our ancient migratory and demographic history while developing a better understanding of the phylogeographic structure of world populations. Sample research topics could include subjects like the origin and spread of the Indo-European languages, genetic insights into Papua New Guineas high linguistic diversity, the number and routes of migrations out of Africa, the origin of the Inca, or the genetic impact of the spread of maize agriculture in the Americas.

Recipients will typically be population geneticists, students, linguists, and other researchers or scientists interested in pursuing questions relevant to the Genographic Projects broad goal of exploring our migratory history. Recipients of Genographic scientific grant funds will become members of the Genographic Consortium, and will be expected to act as agents of the greater Genographic mission, participating in and reporting on multiple aspects of Genographic fieldwork, in addition to their own proposed and missionaligned pilot projects. Openness and transparency within the Consortium are the key values of the projects research team, and grantees will be expected to abide by this code of conduct.

If you poke through their material they say that the grant will be $25 to $50 thousand dollars. Thats 125 to 250 Geno 2.0 chips. Speaking of which, I sent in a chip about a month ago now. The results should be back soon.

So why was Spencer so keen on me pushing this again? (Ive mentioned it before) After being at ASHG 2012 Im shocked in the small sample space of people interested in these sorts of historical genetic questions. I say this because Ive reviewed/read most of the papers which were present as posters. I wonder on occasion if Im missing out on something, but these results indicate no, theres only so many labs doing this sort of work. The last is the key question. This is where bottom up non-academic science can do wonders. An Indian group presented a poster at ASHG, and when they told me of the similarities between Iyers and Bengali Brahmins I couldnt help but admit that Yes, I know that already, my friend Zack Ajmal came to that conclusion. If you are an academic you need to go beyond tools and methods and analytic insights which someone with a spare computer and some marginal free time can generate. Academic monopolies on these data are going to be short-lived at best. And all for the good. Im sick & tired of intellectual rents.

Excerpt from:
The Genographic Project’s Scientific Grants Program | Gene Expression

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An article by SciDev.Net.

The international collection of the South Pacific's coconut palm species, held at a field gene bank in Papua New Guinea (PNG), is under threat from a disease outbreak close to the gene bank.

The warning came at a meeting on the Pacific coconut research and development (R&D) strategy in Samoa last week (31 October1 November), convened by the Australian Centre for International Agricultural Research and the Secretariat of the Pacific Community.

The deadly disease, Bogia Coconut Syndrome, is threatening the survival of a gene bank of region's most important tree, the coconut, a number of which are endemic. Named after the town of Bogia on the north coast of mainland PNG, the disease appears to be caused by bacteria similar to, but distinct from, the bacteria that cause the better known Lethal Yellowing disease that attacks palm species.

Ironically, PNG was selected as the site for the gene bank in the 1990s because the country was relatively free of coconut pests and diseases.

In an attempt to contain the disease, movement of coconuts and coconut palms, both from the gene bank and for commercial reasons, out of the affected region has been banned, with roadblocks in place to help enforce this.

But these restrictions are preventing the gene bank from fulfilling one of its key roles: distributing useful varieties in support of R&D efforts.

The gene bank holds 3,200 coconut palms, representing 57 different varieties of Cocos nucifera, and is one of five international coconut collections around the world.

Roland Bourdeix, coordinator of the International Coconut Genetic Resources Network, is arranging an urgent mission to PNG to assess the situation.

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South Pacific coconut gene bank under threat

ScienceDaily (Nov. 13, 2012) Why do we get older? When do we die and why? Is there a life without aging? For centuries, science has been fascinated by these questions. Now researchers from Kiel (Germany) have examined why the polyp Hydra is immortal -- and unexpectedly discovered a link to aging in humans.

The study carried out by Kiel University together with the University Medical Center Schleswig-Holstein (UKSH) will be published this week in the Proceedings of the National Academy of Sciences (PNAS).

Hydra -- mysteriously immortal

The tiny freshwater polyp Hydra does not show any signs of aging and is potentially immortal. There is a rather simple biological explanation for this: these animals exclusively reproduce by budding rather than by mating. A prerequisite for such vegetative-only reproduction is that each polyp contains stem cells capable of continuous proliferation. Without these stem cells, the animals could not reproduce any more. Due to its immortality, Hydra has been the subject of many studies regarding aging processes for several years.

Aging in humans

When people get older, more and more of their stem cells lose the ability to proliferate and thus to form new cells. aging tissue cannot regenerate any more, which is why for example muscles decline. Elderly people tend to feel weaker because their heart muscles are affected by this aging process as well. If it were possible to influence these aging processes, humans could feel physically better for much longer. Studying animal tissue such as those of Hydra -- an animal full of active stem cells during all its life -- may deliver valuable insight into stem cell aging as such.

Human longevity gene discovered in Hydra

"Surprisingly, our search for the gene that causes Hydra to be immortal led us to the so-called FoxO gene," says Anna-Marei Bhm, PhD student and first author of the study. The FoxO gene exists in all animals and humans and has been known for years. However, until now it was not known why human stem cells become fewer and inactive with increasing age, which biochemical mechanisms are involved and if FoxO played a role in aging. In order to find the gene, the research group isolated Hydra's stem cells and then screened all of their genes.

Immortality mechanism of Hydra revealed

The Kiel research team examined FoxO in several genetically modified polyps: Hydra with normal FoxO, with inactive FoxO and with enhanced FoxO. The scientists were able to show that animals without FoxO possess significantly fewer stem cells. Interestingly, the immune system in animals with inactive FoxO also changes drastically. "Drastic changes of the immune system similar to those observed in Hydra are also known from elderly humans," explains Philip Rosenstiel of the Institute of Clinical Molecular Biology at UKSH, whose research group contributed to the study.

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Solving the mystery of aging: Longevity gene makes Hydra immortal and humans grow older

New Delhi, Nov. 12: Scientists have identified a novel candidate gene for diabetes that they say appears to put Indians at a higher risk of the disease than any of the 56 diabetes genes discovered earlier.

A consortium of Indian researchers announced today that the new gene also seems to establish a link between the brain and diabetes, hinting at previously unknown disease mechanisms that scientists hope will eventually lead to new treatment strategies.

The gene called TMEM163, identified by the Indian Diabetes Consortium, makes a protein that plays a role in the transfer of signals between brain cells. Most of the earlier diabetes genes influence either the behaviour of insulin-producing cells in the pancreas or mechanisms of insulin resistance.

"We now have a new hypothesis about diabetes," said Dwaipayan Bharadwaj, a scientist at the Institute of Genomics and Integrative Biology in New Delhi and a member of the consortium. "People with one version of this gene are at risk of developing defective insulin secretion ' we're now trying to validate this idea through laboratory and animal experiments."

Bharadwaj and his colleagues identified the gene through India's largest genome study for diabetes that looked for genetic differences between 6700 patients with diabetes and 5700 persons without the disease. Their findings are scheduled for publication in the international journal Diabetes.

The study has also found that 49 among the 56 genes previously reported as associated with diabetes in other populations ' mainly white Caucasians are also observed in the Indian population.

But TMEM163, among all the candidate genes, appears to confer the highest risk of diabetes ' a person with a disease-associated variant of TMEM163 has 1.56 times higher risk of diabetes than a person without this variant.

A gene called TCF7L2 has until now shown the strongest association ' people with one variant of this gene have 1.51-fold higher risk of diabetes than people without that variant.

A senior endocrinologist who's a member of the consortium said that the new candidate gene and all the other known genes for diabetes explain only about eight per cent of the extra risk of diabetes among Indians.

"Diet and lifestyle appear to contribute far more to the risk of diabetes than genes ' so diet and exercise still remain a key to diabetes control," said Nikhil Tandon, professor of endocrinology at the All India Institute of Medical Sciences in New Delhi. "But the new gene is interesting because it opens a new avenue for research to understand underlying mechanisms of the disease."

Excerpt from:
Scientists unravel new diabetes gene

MEMPHIS, Tenn., Nov. 12, 2012 /PRNewswire/ -- Research led by the St. Jude Children's Research Hospital Washington University Pediatric Cancer Genome Project has identified a fusion gene responsible for almost 30 percent of a rare subtype of childhood leukemia with an extremely poor prognosis.

To view the multimedia assets associated with this release, please click: http://www.multivu.com/mnr/58586-st-jude-children-s-research-hospital-gene-sequencing-childhood-leukemia

The finding offers the first evidence of a mistake that gives rise to a significant percentage of acute megakaryoblastic leukemia (AMKL) cases in children. AMKL accounts for about 10 percent of pediatric acute myeloid leukemia (AML). The discovery paves the way for desperately needed treatment advances.

Investigators traced the genetic misstep to the rearrangement of chromosome 16, which brings together pieces of two genes and sets the stage for production of an abnormal protein. The fusion protein features the front end of CBFA2T3, a blood protein, and the back of GLIS2, a protein that is normally produced only in the kidney. Work that appears in the November 13 edition of the journal Cancer Cell reports that in a variety of laboratory models the CBFA2T3-GLIS2 protein switched on genes that drive immature blood cells to keep dividing long after normal cells had died. This alteration directly contributes to leukemia.

AMKL patients with the fusion gene were also found to be at high risk of failing therapy. Researchers checked long-term survival of 40 AMKL patients treated at multiple medical centers around the world and found about 28 percent of patients with the fusion gene became long-term survivors, compared to 42 percent for patients without CBFA2T3-GLIS2. Overall long-term survival for pediatric AML patients in the U.S. is now 71 percent.

"The discovery of the CBFA2T3-GLIS2 fusion gene in a subset of patients with AMKL paves the way for improved diagnostic testing, better risk stratification to help guide treatment and more effective therapeutic interventions for this aggressive childhood cancer," said James Downing, M.D., St. Jude scientific director and the paper's corresponding author. The first author is Tanja Gruber, M.D., Ph.D., an assistant member in the St. Jude Department of Oncology.

Co-author Richard Wilson, Ph.D., director of The Genome Institute at Washington University School of Medicine in St. Louis, noted: "We identified this unusual gene fusion by comparing the genome of children's healthy cells with the genome of their cancer cells. This type of in-depth exploration and analysis is crucial to finding unexpected structural rearrangements in the DNA that can lead to cancer. With this discovery, we now can search for more effective treatment options that target this precise defect."

The study is part of the Pediatric Cancer Genome Project, a three-year collaboration between St. Jude and Washington University to sequence the complete normal and cancer genomes of 600 children and adolescents with some of the most aggressive and least understood cancers. The human genome is the instruction book for assembling and sustaining a person. The instructions are packaged in the DNA molecule. Sequencing the genome involves determining the exact order of the four chemical bases that make up DNA. Human DNA is organized into 46 chromosomes.

"We focused on AMKL because no one had any idea of what caused this leukemia in most patients," Gruber said. The study excluded AMKL patients who were infants or children with Down syndrome because earlier research had linked their disease to other chromosomal rearrangements.

When researchers in this study sequenced just the genes that were switched on in the AMKL cells of 14 young patients, the scientists discovered half carried the CBFA2T3-GLIS2 fusion. Additional fusion genes were identified in five of the other patients. Each of those fusion genes occurred in a single patient. The genes involved included HOXA9 and MN1, both previously linked to leukemia, and GATA2 and FLII, which play roles in normal development of the megakaryocytic blood cells that are targeted in AMKL. Megakaryocytes produce the platelets that help blood clot.

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Gene sequencing project identifies abnormal gene that launches rare childhood leukemia

Black Sheep Part 1 Full Movie
full movie : tinyurl.com Black Sheep Part 1 Full Movie, Black Sheep Part 1 Movie, Black Sheep Movie Part 1, Black Sheep Part 1 The Movie, Black Sheep Part 2 Full Movie, Black Sheep Movie Full Movie, Black Sheep (2006) Movie Part 1 English Full, Black Sheep Movie HD trailer. An experiment in genetic engineering turns harmless sheep into blood-thirsty killers that terrorize a sprawling New Zealand farm.From:talcean teriViews:0 0ratingsTime:06:10More inFilm Animation

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Black Sheep Part 1 Full Movie - Video

Millions Spent Defeating Prop 37-GMO #39;s: Why They Don #39;t Want Us To Know What We #39;re Eating
Howard Vlieger began studying GMO crops in 1994 and is fortunate to work with some of the lead scientists in the world on research projects involving GMO crops. The real life experience that he has from being a farmer and working with farmers all across the US gives him a unique perspective on GMOs. Howard has been giving presentations to educate people about GMOs for more than 6 years in 13 states. Howard serves on the board of directors for the Farm and Ranch Freedom Alliance (FARFA) and the Food Freedom Foundation. Show Highlights: Howard Vlieger and his organization Verity Farms have been researching the affects of genetically engineered crops on the soil, animals and humans since 1992. What they have learned and see every day in 2012 is beyond spooky. -The gut ecology is impaired when animals and humans consume GM organisms, at one tenth of a part per million -BT Corn linked to poor conception rates, immune and digestive issues -There are three top issues with genetic engineering of crops: the ecology of the soil, immune and digestive disruption and super weeds requiring more and more glyphosates. -The birds and the bees are affected -The story behind Roundup Ready Alfalfa, and it #39;s not pretty -These foreign proteins with GMO #39;s are not digestible. Period -Are you eating eggs fed GMO corn and Soy? -The Germans are saying No to GMO #39;s -A strong immune system and our own garden are our best defense here. -In 2010, 170 million acres of corn and soy were planted -- 92% GMO ...From:Patrick TimponeViews:1531 13ratingsTime:09:56More inScience Technology

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Millions Spent Defeating Prop 37-GMO's: Why They Don't Want Us To Know What We're Eating - Video

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/vvb7t7/bioprocess) has announced the addition of Elsevier Science and Technology's new book "Bioprocess Engineering" to their offering.

Bioprocess Engineering involves the design and development of equipment and processes for the manufacturing of products such as food, feed, pharmaceuticals, nutraceuticals, chemicals, and polymers and paper from biological materials. It also deals with studying various biotechnological processes.

"Bioprocess Kinetics and Systems Engineering" first of its kind contains systematic and comprehensive content on bioprocess kinetics, bioprocess systems, sustainability and reaction engineering.

Dr. Shijie Liu reviews the relevant fundamentals of chemical kinetics-including batch and continuous reactors, biochemistry, microbiology, molecular biology, reaction engineering, and bioprocess systems engineering- introducing key principles that enable bioprocess engineers to engage in the analysis, optimization, design and consistent control over biological and chemical transformations.

The quantitative treatment of bioprocesses is the central theme of this book, while more advanced techniques and applications are covered with some depth. Many theoretical derivations and simplifications are used to demonstrate how empirical kinetic models are applicable to complicated bioprocess systems.

Key Features

- Contains extensive illustrative drawings which make the understanding of the subject easy

- Contains worked examples of the various process parameters, their significance and their specific practical use

- Provides the theory of bioprocess kinetics from simple concepts to complex metabolic pathways

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Research and Markets: Bioprocess Engineering

Public release date: 12-Nov-2012 [ | E-mail | Share ]

Contact: Zoe Tzanev ztzanev@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, November 12, 2012Mary Ann Liebert, Inc., publishers is proud to launch the Liebert Author Advocacy Program (LAAP), an innovative membership program for academic, corporate, and funding institutions designed to support Open Access (OA) and enhance the visibility and share-ability of academic research. The LAAP and associated AuthorCite portal provide a cost-effective way to support OA publishing for affiliated researchers, as well as a dedicated platform to archive, promote, and share OA articles published in any Liebert journal.

LAAP member institutions receive a 25% discount on OA article processing charges (APC) for research published in any Liebert journal; a customized microsite to highlight published OA articles; immediate global access to peer-reviewed OA articles on major indexing services; and complimentary access to the AuthorCite platform for OA authors publishing in Liebert journals. AuthorCite is a robust online marketing platform that enables authors to build professional visibility and enhance the impact of their research. Participating LAAP institutions are also eligible for a 10% discount on the subscription list price of any Liebert journal purchased directly from the publisher. LAAP participants pay a flat annual membership fee based on the number of full-time faculty and/or researchers at their institution.

"We are committed to flexible, innovative publishing services that facilitate Open Access to original research articles, alongside value-added premium journal content," says Mary Ann Liebert, president of Mary Ann Liebert, Inc., publishers. "The launch of our Liebert Author Advocacy Program serves to advance research discovery, scholarly exchange, and, ultimately, the impact of original research contributions."

###

For more information on LAAP membership, visit the website at http://www.authoradvocacy.com or contact laap@liebertpub.com.

About the Publisher

Mary Ann Liebert, Inc., publishers is a privately held, fully integrated media company universally acknowledged for publishing authoritative peer-reviewed journals in the most promising areas of biomedical research, the life sciences, medicine, surgery, and public health. Mary Ann Liebert, Inc. publications continue to make critical contributions in advancing research and facilitating collaboration throughout the world in academia, industry, and government, and are also highly respected resources for legislators, policy makers, and educators. The firm publishes more than 70 journals, books, and newsmagazines. A complete list is available on our website at http://www.liebertpub.com.

Mary Ann Liebert, Inc. 140 Huguenot St., New Rochelle, NY 10801-5215 Phone: (914) 740-2100 (800) M-LIEBERT Fax: (914) 740-2101 http://www.liebertpub.com

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New Liebert Author Advocacy Program (LAAP) promotes scholarly publishing

If you could know whether your unborn child was going to be born with a genetic defect, would you want that information? Thatisthe basis of a quad test, offered to every pregnant woman, the first in a series of detection tools to determine if something is off with the fetus.

In part one of this three part series on genetic selection, 7News looks into how this test works and the conflict between nature and science.

When Melanie and Rick Sarro of Lake Charlesdecided to start a family later in life, they knew it carried a risk for pregnancy problems, but that did notdeter their plans. "We knew that we wanted to have children and that we were gonna have to not waste any time to do it," said Melanie.

Before the Sarros celebrated their third anniversary, Zachary was here and baby number two was on the way. "The pregnancywent very smoothly, it was uneventful," said Rick, "so it was a joyous event for both of them."

Because of Melanie's age, 37, her doctor offered a standard quad test, something she did.

Dr. Marshall St. Amant is the Director of Maternal Fetal Medicine at Woman's Hospital in Baton Rouge and his team of physicians travels to Lake Charles a few times a week to treat local women with high risk pregnancies. He says asimple blood test canshow a woman's risk for genetic defects. "Itnever tells you for sure that the baby has a problem or does not have the problem you're looking for," he said, "it just says the risk is greater than or less than her predetermined risk by her age."

If the quad test does show that the mother is at risk of having a child with a genetic abnormality, then an amniocentesis is offered under the guidance of ultrasound technology with athin needle. "The fluid is removed over a period of a couple of minutes and then it's sent to a laboratory for a very specialized analysis,"said Dr. St. Amant.

Amniocentesis is the gold standard for diagnosing genetic disorders, analyzing every chromosome. "It will identify any numerical abnormality of the chromosomes, being a whole extra copy of a chromosome. It will also identify broken chromosomes," said Dr.St. Amant.

Defects are reported on a caryotype with nearly 100 percent accuracy.

The most common findings are on chromosome 18, known as Edwards syndrome and on 21, Down syndrome. "The patient would be offered the ability to continue the pregnancy," said Dr. St.Amant, "a secondary alternative would be the patient would be offered the ability to end the pregnancy."

Link:
Genetic testing of a fetus offered for pregnant women

Washington, November 13 (ANI): A new study has found a genetic link between chronic pancreatitis and alcohol consumption.

Researchers from the University of Pittsburgh School of Medicine and more than 25 other health centers across the United States found a genetic variant on chromosome X near the claudin-2 gene (CLDN2) that predicts which men who are heavy drinkers are at high risk of developing chronic pancreatitis.

"The discovery that chronic pancreatitis has a genetic basis solves a major mystery about why some people develop chronic pancreatitis and others do not," said David C. Whitcomb, M.D., professor of medicine, cell biology and physiology, and human genetics at the University of Pittsburgh School of Medicine and lead author of the report.

"We also knew there was an unexpected higher risk of men developing pancreatitis with alcohol consumption, but until now we weren't sure why. Our discovery of this new genetic variant on chromosome X helps explain this mystery as well," he stated.

Chronic pancreatitis is a progressive inflammatory disease characterized by abdominal pain and permanent damage to the pancreas.

Most studies report excessive alcohol consumption as the major risk factor for adult-onset chronic pancreatitis. However, according to Dr. Whitcomb, who also is chief of the Division of Gastroenterology, Hepatology and Nutrition, only 3 percent of individuals who are alcoholics develop chronic pancreatitis, suggesting a pancreas-specific risk factor.

The study was conducted over 10 years and involved more than 2,000 patients, all of whom underwent DNA testing in a study funded by the National Institutes of Health. Researchers discovered that there was a common DNA variant on the X chromosome that is present in 26 percent of men without pancreatitis, but jumps to nearly 50 percent of men diagnosed with alcoholic pancreatitis.

Women have two X chromosomes, so most women with the high-risk DNA variant on one X chromosome appear to be protected from alcoholic chronic pancreatitis by the other X chromosome, if it is normal. Men have one X chromosome and one Y chromosome, so if they inherit a high-risk X chromosome, there is no protection.

The factor on chromosome X does not appear to cause pancreatitis, but if pancreatic injury occurs for any reason such as gallstone pancreatitis or abdominal trauma, it is more likely that the person will develop chronic pancreatitis - especially if they also drink alcohol.

"This information is important because the high-risk chromosome can be identified in patients who drink and have early signs of pancreatic injury," said Dhiraj Yadav, M.D., M.P.H., associate professor of medicine, Division of Gastroenterology, Hepatology and Nutrition at Pitt, and a co-investigator on the study.

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How alcohol consumption ups risk of chronic pancreatitis

The Institute of Medicine of the National Academy of Sciences has elected 70 new members including Lynda Chin, Stephen Quake, and Daniel Kastner. Chin is currently a professor and chair of genomic medicine and scientific director of the Institute for Applied Cancer Science at the University of Texas MD Anderson Cancer Center. Quake is a professor of bioengineering at Stanford University and an investigator at the Howard Hughes Medical Institute. Kastner is the scientific director of the National Human Genome Research Institute, where, among other duties, he leads the inflammatory disease section of the medical genetics branch.

Caprotec Bioanalytics has appointed Jonathan Turner to be CEO and managing director. Turner will take over the CEO spot from company founder Hubert Koester, who will continue to work with the company as acting chief scientific officer and chairman of the scientific advisory board. Turner formerly was senior VP at XL Techgroup, a technology developer and equity firm, and he held senior management posts at Boehringer Ingelheim, Astrazeneca, and Schering.

Bill Bowen has been appointed by Sequenom SVP and general counsel. He will report directly to Chairman and CEO Harry Hixson and will be responsible for the company's legal and patent issues. Bowen was previously with Gen-Probe, where he was SVP and general counsel. Before that he was a business litigation partner at Luce Forward Hamilton & Scripps.

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Foundation Medicine, AstraZeneca to ID Genetic Mutations for Cancer Drug Development

SAN DIEGO, Nov. 12, 2012 /PRNewswire/ --Sequenom, Inc. (SQNM), a life sciences company providing innovative diagnostic testing and genetic analysis solutions, today announced its wholly-owned subsidiary, Sequenom Center for Molecular Medicine (Sequenom CMM), presented results from a study of its RetnaGene AMD laboratory-developed test to predict risk of disease progression during the 2012 Joint Meeting of the American Academy of Ophthalmology and the Asia-Pacific Academy of Ophthalmology in Chicago.

This Sequenom CMM laboratory-developed genetic test (LDT) combines patient disease stage with patient genetic variation to evaluate the risk of a patient with early or intermediate AMD to progress to advanced choroidal neovascularization (CNV) disease within 2, 5, and 10 years. CNV is the most common form of 'wet' advanced age-related macular degeneration (AMD), in which new blood vessels in the eye leak fluid, compromising central vision. Advanced disease impacts approximately 10 percent of AMD patients, but is associated with 90 percent of vision loss in AMD.

The clinical validation of the laboratory test predicting progression to CNV was conducted using patient DNA samples made available through the National Eye Institute's Age-Related Eye Disease Study (AREDS). More than 2,000 patients were genotyped for 13 single nucleotide gene polymorphisms (SNPs) in genes previously shown to be associated with CNV. Sequenom CMM compared the predictive value of a phenotype model, based on the assessment of disease grade currently used in clinical practice. The predictive model that combined genotype with phenotype was found to be more accurate in predicting CNV progression (AUC=0.96) than the phenotype model alone based on disease grade (AUC=0.89), concluding that inclusion of the genotype assessment is more effective in predicting CNV progression compared with phenotype alone.

"Physicians today rely on an assessment of patient disease stage to predict the risk of progressing to CNV, and this genetic laboratory developed test will help improve the accuracy of prediction by assessing individual risk based on the genetic predisposition of the patient," said Allan T. Bombard, M.D., Sequenom's Chief Medical Officer.

The study was conducted in compliance with the Coriell Cell Repositories Institutional Review Board, in accordance with Department of Health and Human Services (45 CFR Part 46). The dataset used for the analysis was obtained from the National Eye Institute-Age-Related Eye Disease Study (NEI-AREDS) Genetic Repository. Funding support for AREDS was provided by the National Eye Institute grant N01-EY-0-2127, National Institutes of Health, Bethesda, Maryland.

At the meeting: Paper 30031594: Combining Genotype and Phenotype to Predict Progression to Choroidal Neovascularization (CNV) in Patients with AMD (Presented Monday, November 12, 3:42 PM in S406B)

About SequenomSequenom, Inc. (SQNM) is a life sciences company committed to improving healthcare through revolutionary genetic analysis solutions. Sequenom develops innovative technology, products and diagnostic tests that target and serve discovery and clinical research, and molecular diagnostics markets. The company was founded in 1994 and is headquartered in San Diego, California. Sequenom maintains a Web site at http://www.sequenom.com to which Sequenom regularly posts copies of its press releases as well as additional information about Sequenom. Interested persons can subscribe on the Sequenom Web site to email alerts or RSS feeds that are sent automatically when Sequenom issues press releases, files its reports with the Securities and Exchange Commission or posts certain other information to the Web site.

Sequenom CMM, LLCSequenom Center for Molecular Medicine (Sequenom CMM), a CAP accredited and CLIA-certified molecular diagnostics laboratory, is developing a broad range of laboratory-developed tests with a focus on prenatal and ophthalmic diseases and conditions. These laboratory-developed tests provide beneficial patient management options for obstetricians, geneticists, maternal fetal medicine specialists, retinal specialists and ophthalmologists. Sequenom CMM is changing the landscape in genetic disorder diagnostics using proprietary cutting edge technologies.

Forward-Looking Statements Except for the historical information contained herein, the matters set forth in this press release are forward-looking statements within the meaning of the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995, including statements regarding the benefits or expectations of Sequenom CMM's genetic AMD test including the test's ability to help improve the accuracy of predicting the risk of a patient progressing to CNV by assessing individual risk based on the genetic predisposition of the patient, Sequenom's commitment to improving healthcare through revolutionary genetic analysis solutions, and Sequenom CMM changing the landscape in genetic disorder diagnostics. These forward-looking statements are subject to risks and uncertainties that may cause actual results to differ materially, including the risks and uncertainties associated with Sequenom's ability to develop and commercialize new technologies and products and to scale up its operations to meet increased product demand, particularly for new technologies and products such as Sequenom CMM's prenatal and other diagnostics testing services, Sequenom's ability to manage its existing cash resources or raise additional cash resources, customer demand, Sequenom's ability to obtain payor reimbursement and payment collection and the timing thereof, for Sequenom CMM's diagnostic test services including the MaterniT21 PLUS LDT, Sequenom's ability to convert to accrual accounting for its diagnostic test services including the MaterniT21 PLUS LDT, competition, intellectual property protection and intellectual property rights of others, government regulation particularly with respect to diagnostic products and laboratory developed tests, obtaining or maintaining regulatory approvals, ongoing litigation, including patent litigation asserting infringement by our products or challenging the validity of our patents, and other risks detailed from time to time in Sequenom, Inc.'s most recent Quarterly Report on Securities and Exchange Commission Form 10-Q and Annual Report on Securities and Exchange Commission Form 10-K and other documents subsequently filed with or furnished to the Securities and Exchange Commission. These forward-looking statements are based on current information that may change and you are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date of this press release. All forward-looking statements are qualified in their entirety by this cautionary statement, and Sequenom, Inc. undertakes no obligation to revise or update any forward-looking statement to reflect events or circumstances after the issuance of this press release.

(Logo: http://photos.prnewswire.com/prnh/20040415/SQNMLOGO)

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Study Shows Sequenom CMM's RetnaGene LDT Accurately Predicts Risk of Progression to Wet Form of AMD

Public release date: 12-Nov-2012 [ | E-mail | Share ]

Contact: Sarah Avery sarah.avery@duke.edu 919-660-1306 Duke University Medical Center

DURHAM, N.C. In the first broad genetic landscape mapped of a Burkitt lymphoma tumor, scientists at Duke Medicine and their collaborators identified 70 mutations, including several that had not previously been associated with cancer and a new one that was unique to the disease.

Findings from the genetic sequencing of Burkitt lymphoma, an aggressive form of lymphoma, could be used to develop new drugs or aim existing therapies at mutations known to be susceptible. The researchers published their findings online Sunday, Nov. 11, 2012, in the journal Nature Genetics.

"This study lays out the most common genetic alterations in the disease, and allows us to understand the biology of the disease so we can design better therapies," said Sandeep S. Dave, M.D., MBA, MS, associate professor at Duke and senior author of the study.

Dave and colleagues sequenced the first complete Burkitt lymphoma genome, plus the genes from 59 additional Burkitt cases and 94 diffuse large B cell lymphomas, which share many of the same characteristics of Burkitt lymphoma. Similarities between the malignancies can often lead to mistaken diagnoses and failed treatments.

The researchers reported striking differences in the gene mutation patterns of Burkitt lymphomas vs. the diffuse large B cell lymphomas.

"It's important that doctors make the right diagnosis for Burkitt lymphoma, which can be cured with the correct therapies," Dave said. "But if misdiagnosed and given the standard chemotherapy regimes for diffuse large B cell lymphomas, Burkitt lymphoma patients invariably relapse."

The analysis identified 70 genes that were frequently mutated in the Burkitt lymphomas, including a number of genes that were identified in cancer for the first time. One of the newly identified gene mutations, ID3, appeared in 34 percent of the Burkitt cases, but was not evident in any of the diffuse large B cell lymphomas. The mutation has a silencing effect on a gene that suppresses cell growth, enabling cells to multiply.

Dave said this alteration alone may not cause cancer, but when it occurs along with the MYC gene mutations that are common in Burkitt lymphoma and other malignancies, it works like an accelerant to fuel tumor growth. That finding could prove helpful for developing a new drug to function like a normal ID3 gene and suppress cancer cell proliferation in lymphomas as well as numerous other cancers.

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Duke Medicine news -- Genome sequencing of Burkitt Lymphoma reveals unique mutation

ScienceDaily (Nov. 12, 2012) A new study published online November 12 in Nature Genetics reveals a genetic link between chronic pancreatitis and alcohol consumption. Researchers from the University of Pittsburgh School of Medicine and more than 25 other health centers across the United States found a genetic variant on chromosome X near the claudin-2 gene (CLDN2) that predicts which men who are heavy drinkers are at high risk of developing chronic pancreatitis.

This finding enables doctors to identify people with early signs of pancreatitis or an attack of acute pancreatitis who are at very high risk for progressing to chronic pancreatitis, allowing them to take preventative action to slow the development of the disease, and give the pancreas a chance to heal. Once an individual develops pancreatitis it takes several years for the pancreas to deteriorate.

"The discovery that chronic pancreatitis has a genetic basis solves a major mystery about why some people develop chronic pancreatitis and others do not," said David C. Whitcomb, M.D., professor of medicine, cell biology and physiology, and human genetics at the University of Pittsburgh School of Medicine and lead author of the report. "We also knew there was an unexpected higher risk of men developing pancreatitis with alcohol consumption, but until now we weren't sure why. Our discovery of this new genetic variant on chromosome X helps explain this mystery as well."

Over 100,000 Americans suffer from chronic pancreatitis, a progressive inflammatory disease characterized by abdominal pain and permanent damage to the pancreas. Most studies report excessive alcohol consumption as the major risk factor for adult-onset chronic pancreatitis. However, according to Dr. Whitcomb, who also is chief of the Division of Gastroenterology, Hepatology and Nutrition, only 3 percent of individuals who are alcoholics develop chronic pancreatitis, suggesting a pancreas-specific risk factor.

The study was conducted over 10 years and involved more than 2,000 patients, all of whom underwent DNA testing in a study funded by the National Institutes of Health. Researchers discovered that there was a common DNA variant on the X chromosome that is present in 26 percent of men without pancreatitis, but jumps to nearly 50 percent of men diagnosed with alcoholic pancreatitis. Women have two X chromosomes, so most women with the high-risk DNA variant on one X chromosome appear to be protected from alcoholic chronic pancreatitis by the other X chromosome, if it is normal. Men have one X chromosome and one Y chromosome, so if they inherit a high-risk X chromosome, there is no protection.

The factor on chromosome X does not appear to cause pancreatitis, but if pancreatic injury occurs for any reason such as gallstone pancreatitis or abdominal trauma, it is more likely that the person will develop chronic pancreatitis -- especially if they also drink alcohol.

"This information is important because the high-risk chromosome can be identified in patients who drink and have early signs of pancreatic injury," said Dhiraj Yadav, M.D., M.P.H., associate professor of medicine, Division of Gastroenterology, Hepatology and Nutrition at Pitt, and a co-investigator on the study. "If pancreatic injury and acute pancreatitis occur, patients must stop drinking immediately."

Nationally, 16 percent of men drink alcohol at levels defined by the National Institute on Alcohol Abuse and Alcoholism as high risk. Twenty-six percent of these men who drink heavily are at high risk of chronic pancreatitis following pancreas injury. Only 10 percent of women drink alcohol at dangerous levels, and of these only 6 percent have the X chromosome variant on both X chromosomes.

"Previous discoveries show that chronic pancreatitis without alcohol involvement has a strong genetic link. This helps to eliminate the previous stigma that patients with chronic pancreatitis must also be heavy drinkers," added Dr. Whitcomb. "This study proves that there is a genetic element to the disease."

Referrals of at-risk patients are welcome at UPMC and other large academic centers. The Pancreas Clinic within the UPMC Digestive Disorder Center is designed to evaluate patients using genetic and other data to provide treatment that is individualized to each patient. In addition to clinical care, the physician-scientists who staff this clinic are actively involved in teaching physicians and trainees the art and science of personalized medicine for chronic pancreatitis.

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Genetic link between pancreatitis and alcohol consumption

Public release date: 12-Nov-2012 [ | E-mail | Share ]

Contact: Cristina Mestre MestreCA@upmc.edu 412-586-9776 University of Pittsburgh Schools of the Health Sciences

PITTSBURGH, Nov. 12, 2012 A new study published online today in Nature Genetics reveals a genetic link between chronic pancreatitis and alcohol consumption. Researchers from the University of Pittsburgh School of Medicine and more than 25 other health centers across the United States found a genetic variant on chromosome X near the claudin-2 gene (CLDN2) that predicts which men who are heavy drinkers are at high risk of developing chronic pancreatitis. This finding enables doctors to identify people with early signs of pancreatitis or an attack of acute pancreatitis who are at very high risk for progressing to chronic pancreatitis, allowing them to take preventative action to slow the development of the disease, and give the pancreas a chance to heal. Once an individual develops pancreatitis it takes several years for the pancreas to deteriorate.

"The discovery that chronic pancreatitis has a genetic basis solves a major mystery about why some people develop chronic pancreatitis and others do not," said David C. Whitcomb, M.D., professor of medicine, cell biology and physiology, and human genetics at the University of Pittsburgh School of Medicine and lead author of the report. "We also knew there was an unexpected higher risk of men developing pancreatitis with alcohol consumption, but until now we weren't sure why. Our discovery of this new genetic variant on chromosome X helps explain this mystery as well."

Over 100,000 Americans suffer from chronic pancreatitis, a progressive inflammatory disease characterized by abdominal pain and permanent damage to the pancreas. Most studies report excessive alcohol consumption as the major risk factor for adult-onset chronic pancreatitis. However, according to Dr. Whitcomb, who also is chief of the Division of Gastroenterology, Hepatology and Nutrition, only 3 percent of individuals who are alcoholics develop chronic pancreatitis, suggesting a pancreas-specific risk factor.

The study was conducted over 10 years and involved more than 2,000 patients, all of whom underwent DNA testing in a study funded by the National Institutes of Health. Researchers discovered that there was a common DNA variant on the X chromosome that is present in 26 percent of men without pancreatitis, but jumps to nearly 50 percent of men diagnosed with alcoholic pancreatitis. Women have two X chromosomes, so most women with the high-risk DNA variant on one X chromosome appear to be protected from alcoholic chronic pancreatitis by the other X chromosome, if it is normal. Men have one X chromosome and one Y chromosome, so if they inherit a high-risk X chromosome, there is no protection.

The factor on chromosome X does not appear to cause pancreatitis, but if pancreatic injury occurs for any reason such as gallstone pancreatitis or abdominal trauma, it is more likely that the person will develop chronic pancreatitis especially if they also drink alcohol.

"This information is important because the high-risk chromosome can be identified in patients who drink and have early signs of pancreatic injury," said Dhiraj Yadav, M.D., M.P.H., associate professor of medicine, Division of Gastroenterology, Hepatology and Nutrition at Pitt, and a co-investigator on the study. "If pancreatic injury and acute pancreatitis occur, patients must stop drinking immediately."

Nationally, 16 percent of men drink alcohol at levels defined by the National Institute on Alcohol Abuse and Alcoholism as high risk. Twenty-six percent of these men who drink heavily are at high risk of chronic pancreatitis following pancreas injury. Only 10 percent of women drink alcohol at dangerous levels, and of these only 6 percent have the X chromosome variant on both X chromosomes.

"Previous discoveries show that chronic pancreatitis without alcohol involvement has a strong genetic link. This helps to eliminate the previous stigma that patients with chronic pancreatitis must also be heavy drinkers," added Dr. Whitcomb. "This study proves that there is a genetic element to the disease."

Excerpt from:
Genetic link between pancreatitis and alcohol consumption, says Pitt team

The Truth About Loose Skin - Is It Loose Skin or Fat?
Like / Share / Subscribe! It #39;s all greatly appreciated! Loose Skin Vs. Body Fat The cause of loose skin may change from person to person and its ability to go back to normal will be based on a variety of factors. This often happens after a drastic change in weight, commonly when weight is lost to quickly. Is it possible to non-surgically reduce loose skin? Well that is going to depend on genetics, age, amount of weight lost etc. This video will cover a few of those topics and my experience! Facebook: http://www.facebook.com Twitter: twitter.com Instagram: @mattyfusaro FusaroFitness Mailing Address: Matty Fusaro PO BOX 1746 Rocky Point, NY 11778 ***Message about monetization: This is an original video made by me and I own rights to all the content. I created this video with my own camera and used the editing software by Apple Final Cut Pro X. It contains no movies or tv visuals. I own all the pictures in it. There are no video games or performances. Outro Music *Message about Music from LDUK About LDUK Music LDUK Youtube Channel - http://www.youtube.com Song Title - Triangle DreamsFrom:Matty FusaroViews:1374 114ratingsTime:05:21More inSports

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Steveo #39;s Ultimate Genetics Pack
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Creatures 4 - GangNorn Style (PC, MAC, iPad, iPhone)
http://www.creatures4-thegame.co.uk What is Creatures 4? All of us have heard of artificial intelligence... Well, Creatures is artificial life. Since its release in 1996, the saga has charmed and amazed adults and children alike with its believable and lifelike characters and open-ended and in-depth gameplay. Ten years and over two million games sold later, Fishing Cactus and Bigben Interactive work together to produce a brand new game based on this amazing license. The idea is to keep what made the success of the previous games, while opening it to a wider audience. The new opus will be a Free-to-Play, available on PC / Mac, iOS (iPhone, iPad, iPod Touch) and Android systems. A collector #39;s edition full of surprises will also be available. Creatures 4 is a life simulation game featuring the most adorable creatures: the Norns. Thanks to its one of a kind Artificial Intelligence, they come with their own fully complete DNA, making them unique and allowing them to evolve, learn, interact and even reproduce! Their physical appearance and behaviors are all influenced by their genetics (but not gene manipulation!) and experience. Nature or nurture, the possibilities in Creatures 4 are absolutely infinite! Creatures 4 has a number of tools for raising Norns, such as a diagnostic system that is simple, clear, and complete. And don #39;t forget that in Creatures 4, you are not just in charge of an animal: your Norns are born, live, learn, reproduce, and die, leaving the world to the ones ...From:SmoogleViews:0 4ratingsTime:00:52More inGaming

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Creatures 4 - GangNorn Style (PC, MAC, iPad, iPhone) - Video

Laser Genetics
Get a great deal here redirect.viglink.com?key=1f0527e04637dcdb26bf99b11836bfbf out=http%3A%2F%2Fwww%2Eamazon%2Ecom%2Fdp%2FB004SY2L06 Product Description Laser Genetics The ND-3X40 Laser Designator is a precision optical lighting instrument using advanced green laser technology. The patented Rotary Optical Collimator allows full adjustment and control of beam diameter and intensity to focus ligh where you need it most. Rotating the collimator provides enough illumination to ligh a trail at nigh or paint a target at up to 400 yards*. Two CR123 3V batteries provide over 8 hours of continuous use (4 hours of continuous at 0 Farhenheit) *Distance will vary depending on weather and terrain. Optics used on 3.5-10X50 Rifle ScopeFrom:celine hendricksViews:0 0ratingsTime:00:53More inScience Technology

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ACCESS News: Benjamin Gregg, Author, Professor of Government at UT
Tamara and Professor Benjamin Gregg from the University of Texas discuss the role of politics, science, and genetics; the difference between human rights and civil rights; and "Life, Liberty, and the Pursuit of Happiness".From:ACCESSNewsUSViews:3 0ratingsTime:27:00More inNews Politics

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