Archive for the ‘Gene Therapy Research’ Category

STAMFORD, Conn.--(BUSINESS WIRE)--

The 2012 "Young Investigator" grant recipients have been announced by Alliance for Cancer Gene Therapy, Inc. (ACGT), including its first international awardee.

ACGT (www.acgtfoundation.org) is the nations only not-for-profit exclusively dedicated to cancer cell and gene therapy treatments for all types of cancer. 100% of contributions go directly to research, and fund grants with leading scientists in the U.S. and Canada. ACGT has funded 41 grants since its founding in 2001 by Barbara Netter and her late husband, Edward, to conduct and accelerate critically needed innovative research for all types of cancer.

The ACGT Young Investigator Award funds assistant professors on the tenure track who are conducting independent and innovative cell and gene therapy for cancer research in their own dedicated lab. ACGT grants are typically the first they have received, which later attract additional funding and are critical in helping Young Investigators establish their independence.

ACGT's Board approved two 2012 Young Investigator Awards, pending final contract approval. The award to Alexander Stegh, PhD, Assistant Professor, Neurology, at Northwestern University, Feinberg School of Medicine, will fund a research study into a potential new treatment for brain cancer. Stegh's study seeks to better understand metabolic vulnerabilities to the most common and aggressive malignant primary brain tumor in humans, glioblastoma (GBM), and aims to establish more effective methods of attacking and destroying a cancer that has been particularly treatment resistant.

Douglas Mahoney, PhD, Assistant Professor, Department of Microbiology, Immunology and Infectious Disease, at the University of Calgary, Canada, is ACGTs first international grantee. His study focuses on oncolytic virus therapy, which, unlike conventional drugs, orchestrates tumor cell death in multiple ways, simultaneously. Virus-based treatment is considered among the most promising gene therapy techniques. Dr. Mahoney and his team will work to engineer next-generation and virus combinations to break through treatment barriers. Although Dr. Mahoneys initial research was on breast cancer, the technique can be used against many cancers.

"It is discouraging to see federal cutbacks in cancer research funding," said Barbara Netter, ACGTs President. "ACGT is stepping into the breach to boost funding for promising research that can deliver cancer cell and gene therapy discoveries like the recently announced breakthrough leukemia treatments pioneered by Dr. Carl June at the University of Pennsylvania, one of ACGTs first Clinical Translation grantees."

ACGT has awarded 27 grants to Young Investigators and 14 grants to Clinical Investigators totaling $23.7 million funding innovative basic research and clinical translation. ACGTs Scientific Advisory Council comprised of 16 renowned physicians and researchers, conducts the rigorous review process. Young Investigator Grants range from $250,000 to $500,000 over a 2-3 year period. Clinical Translational Grants range from $500,000 to $1,000,000. Seventeen ACGT funded research projects have been approved for human clinical trials; 11 of which are underway. To donate, please visit http://www.acgtfoundation.org or call 203.358.8000.

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2012 "Young Investigator" Grant Recipients Announced; Funding Cutting-Edge Cell and Gene Therapy Research for Cancer

RICHMOND, Calif. (TheStreet) -- Sangamo BioSciences (SGMO) is a gene therapy company with a single product in human clinical studies and a market value of more than $500 million. The rest of the company's pipeline is still preclinical, meaning the only testing being done is in test tubes and rats.

Preclinical-stage drug companies don't typically carry market values of $500 million, which makes Sangamo's SB-728 HIV therapy -- the product in phase II studies -- really important. Sangamo won't trade at $10 per share, like it does today, if SB-728 blows up. Without any drugs in human studies, Sangamo's market cap might easily be cut in half or more, which would be appropriate, particularly for a company trying to develop something as challenging as gene therapies.

Keep this perspective in mind when you hear Sangamo executives talk about the potential for SB-728 to be a "functional cure" for HIV. Throwing the words "cure" and "HIV" into the same sentence generates serious buzz -- and rightly so -- because there is no current curative treatment for HIV. Unfortunately, the data presented on SB-728 to date, including Wednesday, do not match the hype.

See if (SGMO) is in our portfolio

It is unrealistic to believe SB-728 will ever become a "functional cure" for HIV because the scientific and regulatory bar for any drug to warrant that label is extremely high. Current HIV medicines aren't curative, but they do drop viral loads to undetectable levels and keep them there basically forever. HIV patients can take a single pill each morning and basically never have to worry about their disease getting worse. These patients will grow old and die of something else before they succumb to AIDS. That's an amazing achievement in a disease that was a certain death sentence 30 years ago.

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Sangamo's HIV Gene Therapy Is A Valuation Prop, Nothing More

Mice were given an antibiotic in their drinking water which activated a mutant gene known as Omomyc, and this in turn blocked the production of Myc.

Previous studies had already established this procedure for inhibiting Myc, but there were concerns it could have serious sideeffects.

In the new experiment, described in the Genes and Development journal, Mice with up to 200 lung tumours were given the therapy for four weeks, followed by four-week rest periods for more than a year.

After the first treatment all the mice's tumours disappeared, but 63 per cent then relapsed. Following the second treatment, only 11 per cent of the original tumours resurfaced. After eight therapy cycles, only two tumours could be identified.

Dr Soucek said: "The most important finding was that there were no signs of resistance to treatment. This is one of the biggest disadvantages of many anticancer therapies: the disease develops resistance and can return even more aggressively.

"The fact that the results are maintained over time, that there is no tumour relapse and no resistance, suggests that Myc-targeted therapy may offer an unprecedented way forward."

Francesco Pezzella, Professor of Tumour Pathology at Oxford University, who was not involved in the study, said it was a promising proof of concept but cautioned that the approach was not directly applicable to humans.

"It would be a good idea in humans to try and find a way to block that gene," he said. "But the way they have done it is not possible in humans because it requires a modified gene which is inserted inside the [mice's] cells.

"It gives the green light for pharmaceutical studies to try to find a compound that can block this gene...but whether it would be possible to block it in humans is still completely unknown."

Originally posted here:
Mice 'cured' of lung cancer with gene therapy

Public release date: 5-Mar-2013 [ | E-mail | Share ]

Contact: David Kelly 303-315-6374 University of Colorado Denver

AURORA, Colo. (March 5, 2013) Researchers have discovered that deleting a specific gene in mice prevents them from becoming obese even on a high fat diet, a finding they believe may be replicated in humans.

"When fed a diet that induces obesity these mice don't get fat," said Prof. James McManaman, Ph.D., lead author of the study and vice-chairman of research for Obstetrics and Gynecology at the University of Colorado School of Medicine. "It may be possible to duplicate this in humans using existing technology that targets this specific gene."

The two-year study, funded by the National Institutes of Health and the U.S. Department of Agriculture, was published last month in the Journal of Lipid Research.

The research team created a strain of mice without the Plin2 gene which produces a protein that regulates fat storage and metabolism. They immediately found that the mice were resistant to obesity.

Usually, mice fed a high fat diet will eat voraciously, yet these showed an unusual restraint. Not only did they eat less, they were more active.

Their fat cells were also 20 percent smaller than typical mice and did not show the kind of inflammation usually associated with obesity, the study said. Obesity-associated fatty liver disease, common in obese humans and rodents, was absent in the mice without the Plin2 gene.

"The mice were healthier," McManaman said. "They had lower triglyceride levels, they were more insulin-sensitive, they had no incidents of fatty liver disease and there was less inflammation in the fat cells."

The absence of the gene may cause fat to be metabolized faster, he said.

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Researchers discover gene that causes obesity in mice

Removing Plin2 gene made mice resistant to obesity Fat cells were 20% smaller and rodents also ate less Scientists think the effect could be duplicated in humans

By Claire Bates

PUBLISHED: 07:53 EST, 6 March 2013 | UPDATED: 09:02 EST, 6 March 2013

Switching off a certain gene could stop junk food eaters from gaining weight

Switching off a 'fat' gene could prevent you from piling on the pound even if you stick to a high-fat diet, say researchers.

A two-year study found that removing this gene in mice made them resistant to obesity. The animals showed unusual restraint when fed a high-calorie diet and were more active as well.

'When fed a diet that induces obesity these mice dont get fat,' said study author Professor James McManaman from the University of Colorado.

'It may be possible to duplicate this in humans using existing technology that targets this specific gene.'

The absence of the gene may cause fat to be broken down faster by the body, he said.

The research team created a strain of mice without the Plin2 gene, which humans also possess. It produces a protein that regulates fat storage and metabolism.

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Switching off obesity gene found to prevent weight-gain EVEN if eating a high-fat diet

Washington, March 6 (ANI): University of Colorado School of Medicine researchers say that deleting a specific gene in mice prevents them from gaining weight, even on a high fat diet.

"When fed a diet that induces obesity these mice don't get fat," said Prof. James McManaman, Ph.D., lead author of the study and vice-chairman of research for Obstetrics and Gynecology at the University of Colorado School of Medicine.

"It may be possible to duplicate this in humans using existing technology that targets this specific gene."

The research team created a strain of mice without the Plin2 gene which produces a protein that regulates fat storage and metabolism. They immediately found that the mice were resistant to obesity.

Usually, mice fed a high fat diet will eat voraciously, yet these showed an unusual restraint. Not only did they eat less, they were more active.

Their fat cells were also 20 percent smaller than typical mice and did not show the kind of inflammation usually associated with obesity, the study said. Obesity-associated fatty liver disease, common in obese humans and rodents, was absent in the mice without the Plin2 gene.

"The mice were healthier," McManaman said. "They had lower triglyceride levels, they were more insulin-sensitive, they had no incidents of fatty liver disease and there was less inflammation in the fat cells."

The absence of the gene may cause fat to be metabolized faster, he said.

"Now we want to know why this works physiologically," McManaman said. "We want to better understand how this affects food consumption."

According to the study, understanding how Plin2 is involved in the control of energy balance will provide new insights into "the mechanisms by which nutrition overload is detected, and how individuals adapt to, or fail to adapt to, dietary challenges."

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Disabling gene eliminates obesity in mice

Public release date: 5-Mar-2013 [ | E-mail | Share ]

Contact: Tara Wilcox-Ghanoonparvar twilcox-ghanoonparvar@jdrf.org 212-479-7524 JDRF

New York, NY, March 5, 2013 A JDRF-funded study out of Switzerland has shown that a single gene called SIRT1 may be involved in the development of type 1 diabetes (T1D) and other autoimmune diseases. The study, "Identification of a SIRT1 Mutation in a Family with Type 1 Diabetes," was published today in Cell Metabolism and represents the first demonstration of a monogenetic defect leading to the onset of T1D.

The research began when Marc Donath, M.D., endocrinologist and researcher at the University Hospital Basel in Switzerland, discovered an interesting pattern of autoimmune disease within the family of one of his patients, a 26-year-old male who had recently been diagnosed with T1D. The patient showed an uncommonly strong family history of T1D; his sister, father, and paternal cousin had also been diagnosed earlier in their lives. Additionally, another family member had developed ulcerative colitis, also an autoimmune disease.

"This pattern of inheritance was indicative of dominant genetic mutation, and we therefore decided to attempt to identify it," Dr. Donath said.

Four years of analysis using three different genotyping and sequencing techniques pointed to a mutation on the SIRT1 gene as the common indicator of autoimmune disease within the family. The SIRT1 gene plays a role in regulating metabolism and protecting against age-related disease. To gain more understanding of how this genetic change in SIRT1 leads to T1D, Dr. Donath and his team performed additional studies with animal models of T1D. When the mutant SIRT1 gene found in the families was expressed in beta cells, those beta cells generated more mediators that were destructive to them. Furthermore, knocking out the normal SIRT1 gene in mice resulted in their becoming more susceptible to diabetes with greatly increased islet destruction. Dr. Donath speculates that the beta cell impairment and death due to the SIRT1 mutation subsequently activates the immune system toward T1D.

"The identification of a gene leading to type 1 diabetes could allow us to understand the mechanism responsible for the disease and may open up new treatment options," Dr. Donath explained.

Patricia Kilian, Ph.D., director of the Beta Cell Regeneration Program at JDRF, concurred, and said that the development is exciting for many reasons: "While the change in the genetic makeup within this family with type 1 diabetes is rare, the discovery of the role of the SIRT1 pathway in affecting beta cells could help scientists find ways to enhance beta cell survival and function in more common forms of the disease. This study also reinforces increasing evidence that abnormal beta cell function has a role in the development of type 1 diabetes, and that blocking or reversing early stages of beta cell dysfunction may help prevent or significantly delay the disease's onset. Drug companies are already in the process of developing SIRT1 activators, which could eventually speed our ability to translate these new research findings into meaningful therapies for patients."

JDRF is continuing to fund research by Dr. Donath that builds off of these latest findings.

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First single gene mutation shown to result in type 1 diabetes

Mar. 5, 2013 Researchers have discovered that deleting a specific gene in mice prevents them from becoming obese even on a high fat diet, a finding they believe may be replicated in humans.

"When fed a diet that induces obesity these mice don't get fat," said Prof. James McManaman, Ph.D., lead author of the study and vice-chairman of research for Obstetrics and Gynecology at the University of Colorado School of Medicine. "It may be possible to duplicate this in humans using existing technology that targets this specific gene."

The two-year study, funded by the National Institutes of Health and the U.S. Department of Agriculture, was published last month in the Journal of Lipid Research.

The research team created a strain of mice without the Plin2 gene which produces a protein that regulates fat storage and metabolism. They immediately found that the mice were resistant to obesity.

Usually, mice fed a high fat diet will eat voraciously, yet these showed an unusual restraint. Not only did they eat less, they were more active.

Their fat cells were also 20 percent smaller than typical mice and did not show the kind of inflammation usually associated with obesity, the study said. Obesity-associated fatty liver disease, common in obese humans and rodents, was absent in the mice without the Plin2 gene.

"The mice were healthier," McManaman said. "They had lower triglyceride levels, they were more insulin-sensitive, they had no incidents of fatty liver disease and there was less inflammation in the fat cells."

The absence of the gene may cause fat to be metabolized faster, he said.

"Now we want to know why this works physiologically," McManaman said. "We want to better understand how this affects food consumption."

According to the study, understanding how Plin2 is involved in the control of energy balance will provide new insights into "the mechanisms by which nutrition overload is detected, and how individuals adapt to, or fail to adapt to, dietary challenges."

See the article here:
Gene identified that causes obesity in mice: Deleting gene eliminates obesity, could work for humans

Scientists at Duke and Johns Hopkins found mutations in two genes that could become therapeutic targets in malignant glioma. Could this be the research breakthrough in the type of pediatric brain stem tumor that children must face?

(PRWEB) March 05, 2013

Scientists at Duke University Medical Center in Durham, N.C. and Johns Hopkins University in Baltimore, Md. have discovered a gene that could be a prime target in malignant glioma, a dangerous class of brain tumors.

The Rory David Deutsch Foundation partners with the Preston Robert Tisch Brain Tumor Center at Duke. Ross and Mindy Deutschs 7-year-old son, Rory, died from a brainstem glioma in 1998.

Specifically, the scientists at Duke and Johns Hopkins found mutations in two genes that could become therapeutic targets in malignant glioma. Could this be the research breakthrough in the type of pediatric brain stem tumor that Rory was diagnosed with and other children must face?

I can say this is potentially one of the most important discoveries in genetic studies on malignant gliomas, in the low-grade to high-grade forms of the tumor, Hai Yan, MD, PhD, lead author, an assistant in the Duke Department of Pathology, said in an article on the Tisch Brain Tumor Centers website. The findings are published in the Feb. 19 issue of the New England Journal of Medicine.

The fact that the defective genes code for metabolic enzymes found only in malignant glioma, and not in normal tissue, could make the gene products therapeutic targets, Yan said.

These genetic flaws might also help distinguish between primary and secondary glioblastoma multiforme (GBM), two subtypes of especially deadly malignant gliomas, with survival of only months after their diagnosis. Patients that have mutation of the genes, isocitrate dehydrogenase 1, gene 1 and 2 (IDH1 and IDH2), also had a longer survival time.

Yan called the results clear cut, and added that he had never seen gene gene mutations as striking as in this study in the six years he has done intensive genetic studies in brain cancer.

The Rory David Deutsch Foundation wants to raise public awareness about brain tumors and other childhood diseases through research that its funding at the Tisch Brain Tumor Center and Lurie Childrens Hospital of Chicago. There are endowed research programs at both facilities.

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Rory David Deutsch Foundation: Brain Tumor Cancer Research Uncovers New Gene

Editor's Choice Main Category: Melanoma / Skin Cancer Also Included In: Obesity / Weight Loss / Fitness;Genetics Article Date: 05 Mar 2013 - 0:00 PST

Current ratings for: Obesity Gene Linked To Skin Cancer

5 (1 votes)

The finding came from a new study conducted by Cancer Research UK experts at the University of Leeds, England, and was published in Nature Genetics.

Individuals with certain variations in a stretch of DNA within the FTO gene, known as intron 8, may have a higher chance of developing melanoma, according to the results.

Scientists have known that the most critical genetic risk factor for obesity and overeating are variations in a different part of the FTO gene, referred to as intron 1.

In 2010, researchers at the Medical Research Council (MRC), UK, demonstrated that overactivity of the gene FTO leads to overeating and obesity.

These variants are associated with BMI (body mass index), which calculates a person's shape by using their height and weight. People with high BMIs may have a raised risk of a range of diseases, such as kidney disease, type 2 diabetes, womb (endometrial) cancer and a host of other problems.

The current study, however, is the first to demonstrate that the gene plays a role in the development of melanoma, a disease which is not associated with obesity and BMI.

The report implies that FTO plays a more wide-ranging part than experts believed in the past, with different areas of the gene being linked to a range of diseases.

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Obesity Gene Linked To Skin Cancer

March 6, 2013

April Flowers for redOrbit.com Your Universe Online

A research team from the University of Colorado School of Medicine and The Obesity and Metabolism Laboratory at Tufts University has discovered that deleting a specific gene in mice prevents them from becoming obese, even if they are fed a high fat diet.The team believes this finding has the potential to be replicated in humans.

When fed a diet that induces obesity these mice dont get fat, said James McManaman, Ph.D., vice-chairman of research for Obstetrics and Gynecology at the University of Colorado School of Medicine. It may be possible to duplicate this in humans using existing technology that targets this specific gene.

The National Institutes of Health (NIH) and the US Department of Agriculture funded the study, which lasted two years.The findings were published in a recent issue of the Journal of Lipid Research.

The researchers created a strain of mice missing the Plin2 gene.Plin2 produces a protein that regulates fat storage and metabolism.It was immediately apparent that the mice were resistant to obesity.

Normal mice that are fed a high fat diet will usually eat voraciously, taking in as many calories as they can.The mice that were missing the Plin2 gene, however, showed an unusual restraint and ate considerably less.The researchers found that they were also more physically active.

The researchers found that the fat cells in these mice were 20 percent smaller than the average mouse as well.The cells also did not show the kind of inflammation of tissue typically associated with obesity.The mice missing the Plin2 gene also displayed a lack of obesity-associated fatty liver disease, common in obese humans and rodents.

The mice were healthier, McManaman said. They had lower triglyceride levels, they were more insulin-sensitive, they had no incidents of fatty liver disease and there was less inflammation in the fat cells. He also suggested that the absence of the gene may cause fat to be metabolized faster.

Now we want to know why this works physiologically, McManaman said. We want to better understand how this affects food consumption.

The rest is here:
By Simply Deleting A Gene , Researchers Eliminate Obesity In Mice

John Harris on Enhancing Evolution (Interview)
In this interview John Harris talks about the arguments of his book Enhancing Evolution. In the book Enhancing Evolution, John Harris, dismantles objections to genetic engineering, stem-cell research, designer babies, and cloning and makes an ethical case for biotechnology that is both forthright and rigorous.

By: ISEI scienceethics

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John Harris on Enhancing Evolution (Interview) - Video

David Pearce - Interview
en.wikipedia.org David Pearce is a British utilitarian philosopher. He believes and promotes the idea that there exists a strong ethical imperative for humans to work towards the abolition of suffering in all sentient life. His book-length internet manifesto The Hedonistic Imperative[3] outlines how technologies such as genetic engineering, nanotechnology, pharmacology, and neurosurgery could potentially converge to eliminate all forms of unpleasant experience among human and non-human animals, replacing suffering with gradients of well-being, a project he refers to as "paradise engineering". A transhumanist and a vegan, Pearce believes that we (or our future posthuman descendants) have a responsibility not only to avoid cruelty to animals within human society but also to alleviate the suffering of animals in the wild. ==The Naturalisation of Heaven== ==Sabotage at the Mill==

By: Adam Ford

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David Pearce - Interview - Video

BLADE RUNNER ( filming location video ) Harrison Ford Ridley Scott
FOLLOW ME ON FACEBOOK http://www.facebook.com Visit the blog : ontheset-bladerunner.blogspot.com This video was posted exactly 27 years after the Blade Runner release date on June 25, 1982. That date was chosen by producer Alan Ladd, Jr. because his previous highest-grossing films (Star Wars and Alien) had a similar opening date in 1977 and 1979. Blade Runner is a 1982 American science fiction film, directed by Ridley Scott and starring Harrison Ford, Rutger Hauer, and Sean Young. The film depicts a dystopian Los Angeles in November 2019 in which genetically manufactured beings called replicants visually indistinguishable from adult humans are used for dangerous or menial work on Earth #39;s "off-world colonies". Following a replicant uprising, replicants become illegal on Earth and specialist police called "blade runners" are trained to hunt down and "retire" escaped replicants on Earth. The plot focuses on a brutal and cunning group of recently-escaped replicants hiding in Los Angeles and the semi-retired blade runner, Rick Deckard (Harrison Ford), who reluctantly agrees to take on one more assignment. Blade Runner is based on the novel Do Androids Dream of Electric Sheep? by Philip K. Dick. Blade Runner is a literate science fiction film, thematically enfolding the philosophy of religion and moral implications of human mastery of genetic engineering in the context of classical Greek drama and hubris, and draws on Biblical images, such as Noah #39;s flood, and literary sources, such ...

By: Herve Attia

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BLADE RUNNER ( filming location video ) Harrison Ford Ridley Scott - Video

Public release date: 5-Mar-2013 [ | E-mail | Share ]

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

New Rochelle, NY, March 5, 2013Reducing preventable hospital readmissions is a cornerstone of emerging healthcare policy. The U.S. government has developed payment policies that will decrease payments to hospitals with excess patient readmission levels, for example. Early lessons learned from these current policy initiatives hint at their likelihood for success and are examined in an insightful article in Population Health Management, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The article is available free on the Population Health Management website at http://www.liebertpub.com/pop.

In "Turning Readmission Reduction Policies into Results: Some Lessons from a Multistate Initiative to Reduce Readmissions," Jessica Mittler, PhD and coauthors from The Pennsylvania State University (University Park, PA), Weill Cornell Medical College (New York, NY), and University of Pennsylvania School of Medicine (Philadelphia, PA) present findings to suggest that current readmissions policies will produce "uncertain success."

Mittler et al. identify three critical challenges that stand in the way of the success of current policies, and propose specific strategies and interventions based on the development of collaborative relationships within the medical community and more coordinated care, more evidence-based policy decisions, and the importance of targeting improvement and incentives to individual institutions.

"Medicare has wisely moved away from the traditional fee-for-service model. The future belongs to those providers who work to establish collaborative relationships across the care community and invest in programs that keep patients out of the hospital," says Population Health Management Editor-in-Chief David B. Nash, MD, MBA, Dean and Dr. Raymond C. and Doris N. Grandon Professor, Jefferson School of Population Health, Philadelphia, PA.

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About the Journal

Population Health Management is an authoritative peer-reviewed journal published bimonthly in print and online that reflects the expanding scope of health care management and quality. The Journal delivers a comprehensive, integrated approach to the field of population health and provides information designed to improve the systems and policies that affect health care quality, access, and outcomes. Comprised of peer-reviewed original research papers, clinical research, and case studies, the content encompasses a broad range of chronic diseases (such as cardiovascular disease, cancer, chronic pain, diabetes, depression, and obesity) in addition to focusing on various aspects of prevention and wellness. Tables of content and a sample issue may be viewed on the Population Health Management website at http://www.liebertpub.com/pop. Population Health Management is the Official Journal of the Care Continuum Alliance.

About the Publisher

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Are new national policies designed to reduce hospital readmissions working?

Published Wednesday, March 6, 2013, 8:10 AM

Updated Wednesday, March 6, 2013, 10:08 AM

Ireland's four courts: Judge makes landmark ruling calling for 1937 Constitution of Ireland to be reviewed to reflect on modern fertility methods

Photo by Google Images

The genetic mother of twins born through a surrogate pregnancy has won her court battle to be declared the legal mother on the childrens birth certificates.

In this landmark case the genetic mother defeated the Irish government. In the past Ireland had refused the mothers demands to be recorded as a parent on the childrens birth certs. The Irish States defense for their stance had been the 1937 constitution, which states that the woman who gives birth to the baby is recorded as the mother.

On Tuesday Dublin High Court Justice Henry Abbott said that these 1937 laws governing birth certificates and parentage needed to be updated to reflect the growing use of artificial insemination, embryo implantation, and other fertility techniques.

The genetic mother in question, whose identity is withheld under Irish law, had been declared medically unable to carry her child. Her sister volunteered to serve as a surrogate mother.

Marion Campbell, lawyer for the parents, told RTE, Irelands State broadcaster, that they are delighted with the outcome.

Campbell said, It has been a very long, hard and emotional time for them and they would like to express their thanks for the support shown to them by their family, friends and legal representatives.

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Genetic mother of twins wins historic Irish surrogacy case

Sam Wood, PHILLY.COM Posted: Wednesday, March 6, 2013, 6:00 AM

There's a genetic testing revolution underway at your local hospital. And it's causing doctors and medical students to confront some very thorny issues.

"Personalized medicine" uses genetic information derived from tests to predict a patient's chances of coming down with diseases and offers ways of tailoring some cures.

Could testing on a fetus show that the person has the potential to be autistic? Gay? If so, what will parents do with the information?

A product of a $30 billion effort to sequence the human genome, the tests until recently have been limited to those wealthy enough to pay up to $10,000. But the tests have dropped to about $1,000.

Dr. Art Caplan, a professor of medical ethics at New York University, brought a host of provocative questions raised by the tests and their use in new treatments to Cooper University Medical School in Camden on Tuesday.

The inaugural speaker of the Berkowitz Family Foundation Lecture, Caplan dismissed most of the consumer-targeted versions of the genetic tests - those that claim to match diet and lifestyle to personal DNA - as "ethically worrisome" and "nonsense added to ridiculousness." Others, including 23andMe and DeCodeMe, are "more legitimate," he said.

Caplan, gregarious with a white mop of hair, also spoke about the developing field of pharmacogenomics, the study of prescribing drugs for patients based on their personal DNA.

"It's great, but it's still the early days," Caplan said.

Prenatal testing will drive most of the upcoming controversy, Caplan said.

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Promise and perils of ‘personalized’ medicine

Updated day 21
five by five cannabis grow room. Agent Orange, TGA Genetics, Subcool. Mystery Strain. Hortilux.

By: majorcasteven1

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Updated day 21 - Video

FOR SALE ~ LUGER Daughter FHF Z380
2/10 Full Blood Doe ~ FERN HOLLOW FARM Z380. An own daughter of LUGER *Ennobled. A BINGO STAR *Ennobled RUGER *Ennobled Gdaughter. If You Are Looking For a Show Or Donor Doe With 2DOX Genetics You #39;ve Found Her! She Sells Exposed To A Dappled RIPPER Gson. BINGO STAR *Ennobled RUGER *Ennobled On The TopSide - COLLATERAL DAMAGE *Ennobled, 2DOX SOURCERER Bottomside.

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FOR SALE ~ LUGER Daughter FHF Z380 - Video

Spannabis 2013 DNA Genetics and Rare Dankness
We talk with Scott from Rare Dankness Seeds and Don from DNA Genetics...www.urbangroweronline.com

By: urbanremo

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Spannabis 2013 DNA Genetics and Rare Dankness - Video

BETHESDA, Md., March 6, 2013 /PRNewswire-USNewswire/ -- The ACMG Foundation for Genetic and Genomic Medicine and genetics professionals from around the world will be on hand to present bicycles to local Phoenix-area children from the Muscular Dystrophy Association (MDA) as part of the ACMG's 2013 Annual Clinical Genetics Meeting and Conference in Exhibit Hall BCD of the Phoenix Convention Center, Friday, March 22 at 10 a.m.

This is the third annual ACMG Foundation Day of Caring and is sponsored by the ACMG Foundation for Genetic and Genomic Medicine, a prominent nonprofit genetics foundation based in Bethesda, MD.

Phoenix-area MDA Director of Health Care Services Maureen Salloom thanked the Foundation for the gift, "Thank you so much to the ACMG Foundation for providing bicycles to children with neuromuscular diseases. Our families are very grateful for this generous donation, as buying a customized bicycle would not be feasible due to high medical bills and other financial obligations. Without this donation, some children would never have had the experience of riding a bike," she said. "The Association's research, health care services, advocacy and education programs provide help and hope to more than 1 million Americans affected by more than 40 progressive neuromuscular diseases."

The medical genetics community, including physicians, genetic counselors, and other genetics health professionals are dedicated to improving the lives of children and adults with genetic conditions," said Bruce R. Korf, MD, Ph.D., FACMG, President of the ACMG Foundation. "We are delighted that we can play a role in helping children with neuromuscular disorders enjoy the pleasure of owning a new bike like so many other children their age."

"What better way to demonstrate caring than by supporting children affected by genetic disorders with a special surprise. Having and riding a bike is right of passage in a kid's life -- we're happy we can make that possible."

The ACMG Foundation for Genetic and Genomic Medicine, whose theme is Better Health Through Genetics, supports education, research and a variety of other programs to translate genetic research into better health for all individuals.

The ACMG Foundation 2013 Day of Caring is supported by PerkinElmer, Shire, members of the American College of Medical Genetics and Genomics and the ACMG Foundation for Genetic and Genomic Medicine.

To view television coverage of last year's Day of Caring visit TheACMGChannel on Youtube at: http://www.youtube.com/theacmgchannel.

The ACMG Foundation for Genetic and Genomic Medicine (www.acmgfoundation.org), a 501(c)(3) nonprofit organization, is a community of supporters and contributors who understand the importance of medical genetics and genomics and genetic counseling in healthcare. Established in 1992, the ACMG Foundation supports the American College of Medical Genetics and Genomics' mission to "translate genes into health" by raising funds to promote the profession of medical genetics and genomics to medical students, to fund the training of future medical geneticists, to support best-practices and tools for practicing physicians and laboratory directors, to promote awareness and understanding of our work in the general public, and much more.

SOURCE ACMG Foundation for Genetic and Genomic Medicine

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Prominent Genetics Foundation to Present Adapted Bikes to Children from Muscular Dystrophy Association at Heartwarming ...

Newswise Bethesda, MDMarch 5, 2013 Listed below are the selected highlights for the March 2013 issue of the Genetics Society of Americas journal, GENETICS. The March issue is available online at http://www.genetics.org/content/current. Please credit GENETICS, Vol. 193, MARCH 2013, Copyright 2013.

Please feel free to forward to colleagues who may be interested in these articles on cellular genetics; population and evolutionary genetics; genome integrity and transmission; and genome and systems biology.

ISSUE HIGHLIGHTS Cellular Genetics Systems genetics implicates cytoskeletal genes in oocyte control of cloned embryo quality, pp. 877896 Yong Cheng, John Gaughan, Uros Midic, Zhiming Han, Cheng-Guang Liang, Bela G. Patel, and Keith E. Latham Cloning by somatic cell nuclear transfer is a powerful technology that offers a unique means of dissecting developmental processes. This article reveals oocyte-expressed genes that support early cloned embryo development. The major category of genes encodes proteins associated with the subcortical cytoskeleton and cytoskeletal elements such as the spindle. Discovery that cytoskeleton-associated proteins are key determinants of early clone development provides new insight into the pathways that support cloning.

Population and Evolutionary Genetics Molecular characterization and evolution of self- incompatibility genes in Arabidopsis thaliana: The case of the Sc haplotype, pp. 985994 Kathleen G. Dwyer, Martin T. Berger, Rimsha Ahmed, Molly K. Hritzo, Amanda A. McCulloch, Michael J. Price, Nicholas J. Serniak,Leonard T. Walsh, June B. Nasrallah, and Mikhail E. Nasrallah The switch from cross-pollination to self-pollination in Arabidospis thaliana was accompanied by inactivation of the two S-locus self recognition genes that determine self-incompatibility. This article reports a structural and functional analysis of an S haplotype belonging to the one group of A. thaliana S haplotypes that had remained largely uncharacterized. The results reveal the various ways the S locus was inactivated during or after the multiple independent switches to self-fertility that occurred in A. thaliana.

Population and Evolutionary Genetics Detecting signatures of selection through haplotype differentiation among hierarchically structured populations, pp. 929941 Mara Ins Fariello, Simon Boitard, Hugo Naya, Magali SanCristobal, and Bertrand Servin One strategy to identify genes underlying traits influenced by adaptation is to look for genomic regions with outstanding differences between populations, typically using the FST statistic. But FST accounts neither for relatedness between populations nor for correlation between neighboring loci. These authors present a new approach that incorporates both features and show it provides increased power to detect selection events. Their approach promises a better understanding of the genetic mechanisms underlying adaptation.

Genome Integrity and Transmission Mutations to the piRNA pathway component aubergine enhance meiotic drive of segregation distorter in Drosophila melanogaster, pp. 771784 Selena L. Gell and Robert A. Reenan How Segregation Distorter (SD) in Drosophila melanogaster violates Mendels laws by enhancing its own transmission in meiosis remains a mystery, despite 60 years of study. Gell and Reenan discovered a novel role for the Piwi-interacting RNA (piRNA) pathway in this phenomenon. The fact that defects in the piRNA pathway, which is thought to defend against transposon invasion of the germline, enhances segregation distortion of SD suggests that the piRNA pathway also suppresses this unusual selfish genetic element.

Review Long noncoding RNAs: Past, present, and future, pp. 651669 Johnny T. Y. Kung, David Colognori, and Jeannie T. Lee Long noncoding RNAs are emerging as potential key players in all aspects of biology. However, the claim that much of the genome is transcribed into a complex regulatory machinery is controversial. The authors frame the debate in its historical context and offer general lessons distilled from current knowledge of the functions of these RNAs, providing an incisive snapshot of this rapidly moving field.

Population and Evolutionary Genetics Synchronous waves of failed soft sweeps in the laboratory: Remarkably rampant clonal interference of alleles at a single locus, pp. 943952 Ming-Chun Lee and Christopher J. Marx From populations of microbes evolving in the laboratory to human genomic diversity, it is increasingly clear that adaptation often involves multiple beneficial alleles at the same locus that rise in frequency together as a soft sweep. This article reports a dramatic example of this during experimental evolution of Methylobacterium, where up to 17 similar alleles were simultaneously present in a single population. Their frequencies rose and fell at different times across populations but synchronously within each population as a single wave of genotypes of nearly equivalently fit genotypes.

Genome and Systems Biology Modeling causality for pairs of phenotypes in system genetics, pp. 10031013 Elias Chaibub Neto, Aimee T. Broman, Mark P. Keller, Alan D. Attie, Bin Zhang, Jun Zhu, and Brian S. Yandell To disentangle causal relationships among phenotypes in segregating populations, these investigators modeled causality for pairs of phenotypes. Their resulting tests enable biologists to choose for investigation a few gene pairs from a short rank-ordered list of candidates. The authors provide software tools and show their utility with yeast datasets.

Cellular Genetics A novel interaction between aging and ER overload in a protein conformational dementia, pp. 865876 Angela Schipanski, Sascha Lange, Alexandra Segref, Aljona Gutschmidt, David A. Lomas, Elena Miranda, Michaela Schweizer, Thorsten Hoppe, and Markus Glatzel This article describes a novel interaction between aging and ER overload. The authors studied a dementia disease in Caenorhabdidis elegans and mice to learn how disturbed protein homeostasis contributes to disease development. They show that induction of the unfolded protein response is critical for age-related disease progression. Their results suggest that the unfolded protein response may offer a therapeutic target for dementias.

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GENETICS Journal Highlights for March 2013

Public release date: 5-Mar-2013 [ | E-mail | Share ]

Contact: Phyllis Edelman pedelman@genetics-gsa.org 301-634-7302 Genetics Society of America

Bethesda, MDMarch 5, 2013 Listed below are the selected highlights for the March 2013 issue of the Genetics Society of America's journal, Genetics. The March issue is available online at http://www.genetics.org/content/current. Please credit Genetics, Vol. 193, MARCH 2013, Copyright 2013.

Please feel free to forward to colleagues who may be interested in these articles on cellular genetics; population and evolutionary genetics; genome integrity and transmission; and genome and systems biology.

ISSUE HIGHLIGHTS

Cellular Genetics: Systems genetics implicates cytoskeletal genes in oocyte control of cloned embryo quality, pp. 877-896 Yong Cheng, John Gaughan, Uros Midic, Zhiming Han, Cheng-Guang Liang, Bela G. Patel, and Keith E. Latham

Cloning by somatic cell nuclear transfer is a powerful technology that offers a unique means of dissecting developmental processes. This article reveals oocyte-expressed genes that support early cloned embryo development. The major category of genes encodes proteins associated with the subcortical cytoskeleton and cytoskeletal elements such as the spindle. Discovery that cytoskeleton-associated proteins are key determinants of early clone development provides new insight into the pathways that support cloning.

Population and Evolutionary Genetics: Molecular characterization and evolution of self- incompatibility genes in Arabidopsis thaliana: The case of the Sc haplotype, pp. 985-994 Kathleen G. Dwyer, Martin T. Berger, Rimsha Ahmed, Molly K. Hritzo, Amanda A. McCulloch, Michael J. Price, Nicholas J. Serniak,Leonard T. Walsh, June B. Nasrallah, and Mikhail E. Nasrallah

The switch from cross-pollination to self-pollination in Arabidospis thaliana was accompanied by inactivation of the two S-locus "self " recognition genes that determine self-incompatibility. This article reports a structural and functional analysis of an S haplotype belonging to the one group of A. thaliana S haplotypes that had remained largely uncharacterized. The results reveal the various ways the S locus was inactivated during or after the multiple independent switches to self-fertility that occurred in A. thaliana.

Population and Evolutionary Genetics: Detecting signatures of selection through haplotype differentiation among hierarchically structured populations, pp. 929-941 Mara Ins Fariello, Simon Boitard, Hugo Naya, Magali SanCristobal, and Bertrand Servin

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Genetics Society of America's Genetics journal highlights for March 2013

ALISO VIEJO, Calif.--(BUSINESS WIRE)--

Ambry Genetics, a global leader in clinical diagnostics and genomic services, announced today that they have officially reached a new milestone in Next-Gen sequencing.

We have reached an incredible milestone in next-generation sequencing (NGS)," said Ardy Arianpour, Vice President of Business Development at Ambry Genetics. Ever since NGS was launched, we have worked diligently to build a customer-centric business to provide our clients with the tools and resources they need to successfully reach their goals. Our clients have shown us loyalty that is reflected in the numbers.

Ambry invested in NGS in 2007 when it was first commercially available and soon after launched their genomic services division running large academic, biotech and government projects. Building on years of experience, Ambry was first to offer an NGS based diagnostic test in April 2010, with the introduction of an 81-gene panel for X-Linked intellectual disability. NGS is ideal for analyzing large sets of genes involved in molecularly heterogeneous disorders, reducing both cost and turn-around-time over traditional Sanger sequencing.

These aspects are crucial where test results can have a direct affect on medical management or family planning. With that in mind, in 2011 Ambry launched the Clinical Diagnostic ExomeTM, making them the first CLIA-certified laboratory to offer whole-exome sequencing clinically. These successes were followed by Marfan syndrome and the Primary Ciliary Dyskinesia NGS panels. Last year, Ambry continued its release of innovative NGS panels with its widely adopted hereditary cancer syndrome product line and most recently its hereditary cardiovascular disease panels.

Ambry remains at the forefront of technology and diagnostics. Incorporating feedback from clients, scientists and market research analysis, Ambry continues to develop and enhance their comprehensive testing menu. Significant laboratory automation investments, enhancements and restructuring has allowed Ambry to focus on reducing test turn-around-time (TAT). Accordingly, Ambry has reduced its full CFTR sequencing plus deletion and duplication analysis TAT in half to five-to-thirteen days. This is the fastest turn-around-time in the world for CFTR sequencing and marks only the beginning of improvements to come.

"As a company, Ambry Genetics is fully committed to providing answers through cutting-edge science and operational improvements," said Charles Dunlop, Chief Executive Officer at Ambry Genetics. Watching the company grow has been sensational, but something tells me the coming years will be the best to come."

About Ambry Genetics

Ambry Genetics is a CAP-accredited and CLIA-certified commercial clinical laboratory with headquarters in Aliso Viejo, California. Since the company's inception in 1999, it has become a leader in providing genetic services focused on clinical diagnostics and genomic services, particularly sequencing and array services. Ambry has established a solid reputation for unparalleled service and has been at the forefront of applying new technologies to the clinical molecular diagnostics market and to the advancement of disease research. To learn more about testing and services available through Ambry Genetics, visit http://www.ambrygen.com.

Continued here:
Ambry Genetics Achieves Company Milestone, Surpasses 10,000 Diagnostic and 100,000 Genomics Next Generation Sequencing ...

SEATTLE, WA--(Marketwire - Mar 6, 2013) - Atossa Genetics, Inc. ( NASDAQ : ATOS ), The Breast Health Company, announced today that Steven C. Quay, M.D., Ph.D., FCAP, chairman, CEO & president, and Kyle Guse, CFO and general counsel, will present the Company's business model, growth strategy and products and services at the 25th Annual ROTH Conference at the Ritz-Carlton Laguna Niguel in Dana Point, California, on Tuesday, March 19, 2013, at 3:30 pm Pacific Time.

Dr. Quay commented, "This is Atossa's first time presenting at this much anticipated event. We appreciate the opportunity afforded to us to discuss our growth strategy and provide an update on the national rollout of our ForeCYTE Breast Health Test, which is a highly significant development that positions Atossa for accelerated growth in 2013 and beyond. In addition, the rollout of the ArgusCYTE Breast Health Test and launch of the FullCYTE and NextCYTE breast health tests, as well as securing a partner for clinical development of our intraductal therapy this year, each represent significant upside potential in 2013."

About Atossa Genetics, Inc.

Atossa Genetics, Inc. ( NASDAQ : ATOS ), The Breast Health Company, is based in Seattle, WA, and is focused on preventing breast cancer through the commercialization of patented, FDA-cleared diagnostic medical devices and patented, laboratory developed tests (LDT) that can detect precursors to breast cancer up to eight years before mammography, and through research and development that will permit it to commercialize treatments for pre-cancerous lesions.

The National Reference Laboratory for Breast Health (NRLBH), a wholly owned subsidiary of Atossa Genetics, Inc., is a CLIA-certified high-complexity molecular diagnostic laboratory located in Seattle, WA, that provides the patented ForeCYTE Breast Health Test, a risk assessment test for women 18 to 73 years of age akin to the Pap Smear, and the ArgusCYTE Breast Health Test, a blood test for recurrence in breast cancer survivors that provides a "liquid biopsy" for circulating cancer cells and a tailored treatment plan for patients and their caregivers.

Forward-Looking Statements

Except for the historical information contained herein, the matters set forth in this press release, including statements regarding Atossa's plans, regulatory actions, Atossa's responses to regulatory actions, expectations, projections, potential opportunities, goals and objectives are forward-looking statements within the meaning of the "safe harbor" provisions of the Private Securities Litigation Reform Act of 1995. These forward-looking statements are subject to risks and uncertainties that may cause actual results to differ materially from the anticipated or estimated future results, including the risks and uncertainties associated with actions by the FDA, regulatory clearances, responses to regulatory matters, Atossa's ability to continue to manufacture and sell its products, the efficacy of Atossa's products and services, the market demand for and acceptance of Atossa's products and services and other risks detailed from time to time in the Atossa's, filings including its registration statement form S-1 filed January 28, 2013, as amended and supplemented from time to time. All forward-looking statements are qualified in their entirety by this cautionary statement, and Atossa undertakes no obligation to revise or update any forward-looking statement to reflect events or circumstances after the issuance of this press release.

Originally posted here:
Atossa Genetics to Present at the 25th Annual ROTH Conference