Archive for the ‘Gene Therapy Research’ Category

Public release date: 24-Jul-2013 [ | E-mail | Share ]

Contact: Meng Zhao eic@nrren.org 86-138-049-98773 Neural Regeneration Research

Synaptic remodeling is one of the most common pathological changes after epileptic seizures. Ectopic synaptic reconstruction in the hippocampus is considered to be closely related with temporal lobe epilepsy. Mossy fiber sprouting may trigger synaptic connections or synaptic remodeling in hippocampal CA3 pyramidal cells, which could lead to the formation of excitatory synaptic circuits, thereby increasing epileptic susceptibility. Exogenous neuropeptide Y has antiepileptic effects; however, the underlying mechanism and optimal administration method for neuropeptide Y are still unresolved. Previous studies have used intracerebroventricular injection of neuropeptide Y into animal models of epilepsy. Dr. Fan Zhang and team from Hebei Medical University published a relevant study in the Neural Regeneration Research (Vol. 8, No. 17, 2013) entitled "Neuropeptide Y gene transfection inhibits post-epileptic hippocampal synaptic reconstruction". These researchers found that after intracerebroventricular injection of neuropeptide Y gene, mossy fiber sprouting in the hippocampal CA3 region of epileptic rats was significantly suppressed, hippocampal synaptophysin (p38) mRNA and protein expression were inhibited, and epileptic seizures were reduced. These findings suggest that a recombinant adeno-associated virus expression vector carrying the neuropeptide Y gene reduces mossy fiber sprouting and inhibits abnormal synaptophysin expression, thereby suppressing post-epileptic synaptic reconstruction.

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Article: " Neuropeptide Y gene transfection inhibits post-epileptic hippocampal synaptic reconstruction," by Fan Zhang1, 2, Wenqing Zhao1, Wenling Li3, Changzheng Dong3, Xinying Zhang3, Jiang Wu3, Na Li3, Chuandong Liang3 (1 Graduate School, Hebei Medical University, Shijiazhuang 050011, Hebei Province, China; 2 Hebei General Hospital, Shijiazhuang 050071, Hebei Province, China; 3 Department of Neurosurgery, People's Hospital of Hebei Province, Shijiazhuang 050071, Hebei Province, China)

Zhang F, Zhao WQ, Li WL, Dong CZ, Zhang XY, Wu J, Li N, Liang CD. Neuropeptide Y gene transfection inhibits post-epileptic hippocampal synaptic reconstruction. Neural Regen Res. 2013;8(17):1597-1605.

Contact: Meng Zhao eic@nrren.org 86-138-049-98773 Neural Regeneration Research http://www.nrronline.org/

Full text: http://www.sjzsyj.org:8080/Jweb_sjzs/CN/article/downloadArticleFile.do?attachType=PDF&id=628

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Gene transduction inhibits post-epileptic hippocampal synaptic reconstruction

The stand-off between the Madurai Kamaraj University administration and one of its professors has intensified with the varsity issuing a press statement on Tuesday against S. Krishnaswamy, who was removed as the head of Department of Genetic Engineering (DGE) in March.

The Registrar (in-charge) S.V. Hariharan issued a statement accusing Mr. Krishnaswamy of indulging in a mud slinging campaign against the university authorities in gross violation of code of conduct and legal ethics and requested the media to publish the statement in the interest of a public institution which was (being) subjected to attack out of mala fide intention.

According to the press communiqu, Mr. Krishnaswamy was relieved from the DGE and shifted to the Centre of Excellence in Bio-informatics (CEB) as he was ineligible to hold the post of Head of DGE, a statutory department. It claimed that he joined as an Information Scientist in the bio-informatics project of the School of Biological Sciences on a temporary basis in 1990.

In 1997, he was placed as an Information Scientist in CEB in the Professors scale of pay in violation of norms laid down by the University Grants Commission, the university as well as the State government. In 2001, he was re-designated as a Reader with effect from 1990 and as Professor with effect from 1997, again in violation of norms applicable for such re-designation.

He was elevated as a Senior Professor in 2007 and erroneously nominated as Head of the Department of Genetic Engineering in 2009, the statement claimed. Dr. S. Krishnaswamy has been bringing discredit in a habitual manner to the university by launching an online misinformation campaign through his old students and association friends which is a gross violation of all service rules, it read.

It also pointed out that the Madras High Court Bench here had last month dismissed a case filed by him challenging his removal from DGE.

Im kept out

Reacting to the press release, Mr. Krishnaswamy said that he had been shifted from a statutory department to a less significant centre of excellence with the motive of keeping him away from the universitys Academic Council and Senate meetings. The authorities do not want any one to raise questions at such meetings and therefore the entire exercise of shunting me out is an attempt to curtail the voice of dissent, he said.

Claiming that he had been rightly appointed in DGE, he said: After shifting me out, the university has appointed another female professor as the head. But the irony remains that the incumbent was promoted as a Professor in 2010 on the basis of clearance given by a committee comprising me. If I am ineligible to be the HOD, then she too is ineligible because her professorship itself becomes questionable.

Mr. Krishnaswamy also said that he received a communication from the university on March 15, informing him that he had been relieved from the headship of DGE.

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An individual versus institution

Public release date: 25-Jul-2013 [ | E-mail | Share ]

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

New Rochelle, NY, July 25, 2013While ovary removal during hysterectomy protects against future risk of ovarian cancer, the decision to conserve the ovaries and the hormones they produce may have advantages for preventing heart disease, hip fracture, sexual dysfunction, and cognitive decline. Other than a woman's cancer risk, the most important factor that should determine ovarian conservation vs. removal is her agewhether she is older or younger than 50according to a Review article published in Journal of Women's Health, a peer-reviewed publication from Mary Ann Liebert, Inc., publishers. The article is available free on the Journal of Women's Health website at http://www.liebertpub.com/jwh.

Catherine Matthews, MD, University of North Carolina, Chapel Hill, emphasizes the difficult choice women must often make in the article "A Critical Evaluation of the Evidence for Ovarian Conservation Versus Removal at the Time of Hysterectomy for Benign Disease."

Conflicting data regarding the potential benefits of removing a woman's healthy ovaries at the time of a hysterectomy have led to confusion. When there is no acute reason to remove a woman's ovaries at the time of hysterectomy and she has no increased genetic risk for ovarian cancer, the accumulated data indicate that elective bilateral ovary removal should be discouraged in women younger than 50 years. The withdrawal of ovarian hormones can have negative health consequences in this population. However, in postmenopausal women, it is advisable to remove the ovaries to protect against ovarian cancer, as the medical literature shows that elective ovary removal is not likely to have an adverse effect on heart disease, hip fracture, sexual dysfunction, or cognitive function at this stage of a woman's life.

"As 600,000 hysterectomies for benign disease are performed annually in the U.S. alone, it is imperative that we have clear guidelines for retaining versus removing normal ovaries," says Susan G. Kornstein, MD, Editor-in-Chief of Journal of Women's Health, Executive Director of the Virginia Commonwealth University Institute for Women's Health, Richmond, VA, and President of the Academy of Women's Health.

###

About the Journal

Journal of Women's Health, published monthly, is a core multidisciplinary journal dedicated to the diseases and conditions that hold greater risk for or are more prevalent among women, as well as diseases that present differently in women. The Journal covers the latest advances and clinical applications of new diagnostic procedures and therapeutic protocols for the prevention and management of women's healthcare issues. Complete tables of content and a sample issue may be viewed on the Journal of Women's Health website at http://www.liebertpub.com/jwh. Journal of Women's Health is the Official Journal of the Academy of Women's Health and the Society for Women's Health Research.

About the Academy

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Should a woman's ovaries be removed during a hysterectomy for noncancerous disease?

Scientists have long known that asthma and allergies, which are on the rise in children in the developed world, are caused by a combination of genetic and environmental factors.

What has stumped them, though, is which genes are responsible.

Now, in what is thought to be a scientific first, researchers at Johns Hopkins Childrens Center and the Johns Hopkins Institute of Genetic Medicine in Maryland have identified a genetic glitch they believe is at the root of a range of allergic disorders, from peanuts to pollen to bee stings.

As a result, the team is now investigating whether common drugs already widely prescribed for other conditions can halt or reverse allergic symptoms, including asthma, in animals.

This is a really huge breakthrough because we are finally getting at the root causes of these diseases, lead investigator Dr. Pamela Frischmeyer-Guerrerio, an immunologist at Johns Hopkins Childrens Center, said in an interview. That gives us a huge handle on how to develop new treatments.

According to researchers, the culprit is aberrant signalling abnormal communication between cells in a protein called transforming growth factor-beta. The protein, also known as TGF-beta, has widespread effects on the body, including the maturation of infants stomachs in a way that develops tolerances to common foods that might otherwise induce an allergic reaction, and prevents allergies in later life.

Disruptions in TGF-beta signalling does not simply nudge immune cells to misbehave, but appears to single-handedly unlock the very chain reaction that eventually leads to allergic disease, said Dr. Harry Dietz, a cardiologist at Johns Hopkins Childrens Center and senior investigator for the study.

The findings were published Wednesday in Science Translational Medicine.

Researchers became curious about the effects of TGF-beta over several years after noticing that patients with Loeys-Dietz Syndrome (named in part after the Johns Hopkins cardiologist) were more prone to allergies than most people. Loeys-Dietz is a rare condition marked by flimsy blood vessels and a dangerous stretching of the aorta that is caused in part by abnormal TGF-beta signalling.

Their study involved 58 children with Loeys-Dietz between the ages of seven and 20 with a history of allergies such as food allergies, rhinitis, eczema, asthma and gastrointestinal and esophageal allergic disease.

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Scientists discover a genetic glitch at the root of allergies

Public release date: 24-Jul-2013 [ | E-mail | Share ]

Contact: Ekaterina Pesheva epeshev1@jhmi.edu 410-502-9433 Johns Hopkins Medicine

Newly published research by investigators at Johns Hopkins Children's Center and the Johns Hopkins Institute of Genetic Medicine reveals that a faulty genetic pathway already known for its role in some connective tissue disorders is also a potent player in many types of allergies.

Scientists have long understood that allergies are the result of a complex interplay between environment and genes, but now, in what investigators believe is a scientific first, a single genetic pathway has been implicated in an array of allergic disorders.

A report on the study's findings, published July 24 in Science Translational Medicine, shows that aberrant signaling by a protein called transforming growth factor-beta, or TGF-beta, may be responsible for disrupting the way immune cells respond to common foods and environmental allergens, leading to a wide range of allergic disorders.

TGF-beta is well known for its widespread effects in the body, from controlling how cells in a various organs grow and develop to overseeing how they communicate with one another. Mutations in the genes that lead to abnormal TGF-beta signaling are also keys to Marfan and Loeys-Dietz syndromes, genetic conditions marked by blood vessel laxity and dangerous stretching of the aorta, the body's largest blood vessel.

"We have evidence that the same glitch in TGF-beta that is responsible for some of the clinical manifestations seen in Marfan and Loeys-Dietz diseases also lies behind the cascade of events that culminates in the development of conditions like asthma, food allergies and eczema," says lead investigator Pamela Frischmeyer-Guerrerio, M.D., Ph.D., an immunologist at Johns Hopkins Children's Center.

Notably, the researchers add, their experiments suggest TGF-beta is more than a mere contributor in the disease process.

"Disruption in TGF-beta signaling does not simply nudge immune cells to misbehave but appears to singlehandedly unlock the very chain reaction that eventually leads to allergic disease," says senior investigator Harry "Hal" Dietz, M.D., a cardiologist at Johns Hopkins Children's Center, professor in the McKusick-Nathans Institute of Genetic Medicine at Hopkins and director of the William S. Smilow Center for Marfan Research.

The researchers' curiosity about a wider role for TGF-beta was ignited years ago when they first noticed that patients with Loeys-Dietz syndrome (LDS) had higher than normal rates of allergies.

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Johns Hopkins researchers reveal genetic glitch at the root of allergies

PHILADELPHIA A researcher from the Perelman School of Medicine at the University of Pennsylvania and colleagues have identified the genetic mutation in Africans with HIV that puts them at a much higher risk for tuberculosis (TB) infections.

Africans have some of the highest rates of TB in the world, and it has long been suspected that genetic susceptibility plays a role. However, establishing candidate genes across populations to gauge risk has remained a challenge.

Now, a new study, published this week in the online Early Edition of the Proceedings of the National Academy of Sciences, found that a commonly occurring polymorphism in an immune response gene called macrophage migration inhibitory factor (MIF) confers almost a two-and-a-half fold increased risk for severe TB in patients from Uganda who were co-infected with HIV.

Low-expressers of MIF were almost twice as common among people of African ancestry as Caucasians.

These results help explain the increased incidence of TB among this group, said Rituparna Das, MD, PhD, an instructor in the division of Infectious Diseases at Penn Medicine. Moreover, this is especially important in people co-infected with HIV, who have a compromised immune system and also constitute the major public health challenge of controlling TB.

TBs prevalence is rising because of drug resistance and an increasing number of patients who are co-infected with HIV. People with HIV and latent TB infection are at a much higher risk for progressing to active TB disease, so identifying patients earlier and getting them in preventative TB treatments is a priority.

Therapies to augment MIF action are under development, and may provide a new tool to combat the global TB epidemic, said Dr. Das.

Recently, Dr. Das received funding from the Penn Center for AIDS Research to further examine MIF in Botswana. The pilot project will examine the distribution of MIF genetic polymorphisms among HIV co-infected patients with pulmonary TB from the Botswana-UPenn Partnership site.

With the high degree of TB exposure in that community, we hope to identify which patients are more likely to go on to develop active TB disease, and in the future, target these patients for preventive therapies, said Dr. Das.

The research published in PNAS was supported by the National Institutes of Health and the Burrough Wellcome Fund. A release on the PNAS study can also be found here.

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Study Explains Why Africans May be More Susceptible to Tuberculosis

BROOMFIELD, Colo.--(BUSINESS WIRE)--

ARCA biopharma, Inc. (ABIO), a biopharmaceutical company developing genetically-targeted therapies for cardiovascular diseases, today announced the Steering Committee for GENETIC-AF, the Companys Phase 2B/3 trial evaluating GencaroTM (bucindolol hydrochloride) as a potential treatment for atrial fibrillation. The Steering Committee is comprised of experts in the field of cardiology and electrophysiology, particularly in clinical development.

Stuart Connolly, MD, Director of the Division of Cardiology at McMaster University in Hamilton, Ontario, has been appointed Chairman of the Steering Committee. William T. Abraham, MD, Director of the Division of Cardiovascular Medicine at The Ohio State University Wexner Medical Center, has been appointed co-Chair of the Steering Committee.

The Steering Committee of GENETIC-AF provides a balance of atrial fibrillation and heart failure clinical trials expertise, with each member being an expert in one or the other or both, said Dr. Michael R. Bristow, President and Chief Executive Officer of ARCA. We are delighted to have Dr. Connolly chair the Steering Committee. He brings a wealth of experience over a distinguished career in the field of electrophysiology, particularly in clinical trials in atrial fibrillation, which makes him a natural fit to help guide the development of Gencaro. Dr. Abraham is also an expert in heart failure clinical investigation and brings a background of leadership in both drug and device trials in chronic heart failure populations. Thus, GENETIC-AF will have the benefit of trial leadership that is at the forefront of both atrial fibrillation and heart failure outcome trials."

I am honored to participate in the GENETIC-AF trial, an innovative approach to evaluating the potential efficacy of Gencaro as a treatment for atrial fibrillation, said Dr. Connolly. "Atrial fibrillation is a growing problem where current medical therapy does not provide adequate treatment, particularly in heart failure populations. I look forward to working with the teams at ARCA and Medtronic to advance a potential new treatment for patients at high risk for developing, or living with, atrial fibrillation.

Dr. Abraham said, "I am pleased to be closely involved with the GENETIC-AF trial, which explores new territory on two important fronts: prospective identification of a genetic subpopulation potentially more responsive to a cardiovascular drug, and demonstration that a drug, in this case Gencaro, may be safe and effective in preventing atrial fibrillation in the unmet need population of heart failure with reduced left ventricular ejection fraction."

Additional Steering Committee members are:

The Steering Committee will provide scientific oversight for the GENETIC-AF trial as well as communicate its recommendations regarding trial conduct with the trials Data Safety Monitoring Board.

GENETIC-AF Clinical Trial

GENETIC-AF is planned as a Phase 2B/3, multi-center, randomized, double-blind clinical trial comparing Gencaro to metoprolol CR/XL for prevention of AF in patients with heart failure and reduced left ventricular ejection fraction (HFREF). ARCA plans to enroll only patients with the genetic variant of the beta-1 cardiac receptor which the Company believes responds most favorably to Gencaro. GENETIC-AF has an adaptive design, under which the Company plans to initiate it as a Phase 2B study in approximately 200 patients and then, depending on the results of an interim analysis by the trial Data Safety Monitoring Board (DSMB), expand the trial to a Phase 3 study by enrolling an estimated additional 420 patients. The Company anticipates that patient enrollment in GENETIC-AF will begin in the first quarter of 2014.

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ARCA biopharma Announces Steering Committee for GENETIC-AF Trial

Newswise Newly published research by investigators at the Johns Hopkins Children's Center and the Johns Hopkins Institute of Genetic Medicine reveals that a faulty genetic pathway already known for its role in some connective tissue disorders is also a potent player in many types of allergies.

Scientists have long understood that allergies are the result of a complex interplay between environment and genes, but now, in what investigators believe is a scientific first, a single genetic pathway has been implicated in an array of allergic disorders.

A report on the study's findings, published July 24 in Science Translational Medicine, shows that aberrant signaling by a protein called transforming growth factor-beta, or TGF-beta, may be responsible for disrupting the way immune cells respond to common foods and environmental allergens, leading to a wide range of allergic disorders.

TGF-beta is well known for its widespread effects in the body, from controlling how cells in various organs grow and develop to overseeing how they communicate with one another. Mutations in the genes that lead to abnormal TGF-beta signaling are also keys to Marfan and Loeys-Dietz syndromes, genetic conditions marked by blood vessel laxity and dangerous stretching of the aorta, the body's largest blood vessel.

"We have evidence that the same glitch in TGF-beta that is responsible for some of the clinical manifestations seen in Marfan and Loeys-Dietz diseases also lies behind the cascade of events that culminates in the development of conditions like asthma, food allergies and eczema," says lead investigator Pamela Frischmeyer-Guerrerio, M.D., Ph.D., an immunologist at Johns Hopkins Children's Center.

Notably, the researchers add, their experiments suggest TGF-beta is more than a mere contributor in the disease process.

"Disruption in TGF-beta signaling does not simply nudge immune cells to misbehave but appears to singlehandedly unlock the very chain reaction that eventually leads to allergic disease," says senior investigator Harry "Hal" Dietz, M.D., a cardiologist at Johns Hopkins Children's Center, professor in the McKusick-Nathans Institute of Genetic Medicine at Johns Hopkins and director of the William S. Smilow Center for Marfan Research.

The researchers' curiosity about a wider role for TGF-beta was ignited years ago when they first noticed that patients with Loeys-Dietz syndrome (LDS) had higher than normal rates of allergies.

The present study involved 58 children with LDS, ages 7 to 20, followed at Johns Hopkins. Most of them had either a history of allergic disease or active allergies, like allergic rhinitis, eczema, food allergies, asthma, and gastrointestinal and esophageal allergic disease. Not surprisingly, these patients also had abnormally high levels of several traditional markers of allergic disease, including IgE -- an antibody that drives life-threatening allergic responses -- and high numbers of eosinophils, white blood cells involved in allergic reactions.

Because TGF-beta is known to control immune cell maturation, the researchers homed in on a group of cells known as regulatory T cells, which keep tabs on other immune cells to ensure that they don't go into overdrive. LDS patients had unusually high levels of regulatory T cells, but the real surprise came when researchers noticed that instead of acting in their regular role as inflammation tamers, the regulatory T cells were doing the opposite -- secreting allergy-promoting signaling molecules called cytokines. Regulatory T cells obtained from patients with known allergies but without LDS were misbehaving in much the same way, a finding that suggests TGF-beta may induce immune cell malfunction even in the absence of LDS, the researchers say.

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Researchers Reveal Genetic Glitch at the Root of Allergies

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Single Genetic Glitch May Explain Most Allergies and Asthma

July 24, 2013 Newly published research by investigators at Johns Hopkins Children's Center and the Johns Hopkins Institute of Genetic Medicine reveals that a faulty genetic pathway already known for its role in some connective tissue disorders is also a potent player in many types of allergies.

Scientists have long understood that allergies are the result of a complex interplay between environment and genes, but now, in what investigators believe is a scientific first, a single genetic pathway has been implicated in an array of allergic disorders.

A report on the study's findings, published July 24 in Science Translational Medicine, shows that aberrant signaling by a protein called transforming growth factor-beta, or TGF-beta, may be responsible for disrupting the way immune cells respond to common foods and environmental allergens, leading to a wide range of allergic disorders.

TGF-beta is well known for its widespread effects in the body, from controlling how cells in a various organs grow and develop to overseeing how they communicate with one another. Mutations in the genes that lead to abnormal TGF-beta signaling are also keys to Marfan and Loeys-Dietz syndromes, genetic conditions marked by blood vessel laxity and dangerous stretching of the aorta, the body's largest blood vessel.

"We have evidence that the same glitch in TGF-beta that is responsible for some of the clinical manifestations seen in Marfan and Loeys-Dietz diseases also lies behind the cascade of events that culminates in the development of conditions like asthma, food allergies and eczema," says lead investigator Pamela Frischmeyer-Guerrerio, M.D., Ph.D., an immunologist at Johns Hopkins Children's Center.

Notably, the researchers add, their experiments suggest TGF-beta is more than a mere contributor in the disease process.

"Disruption in TGF-beta signaling does not simply nudge immune cells to misbehave but appears to singlehandedly unlock the very chain reaction that eventually leads to allergic disease," says senior investigator Harry "Hal" Dietz, M.D., a cardiologist at Johns Hopkins Children's Center, professor in the McKusick-Nathans Institute of Genetic Medicine at Hopkins and director of the William S. Smilow Center for Marfan Research.

The researchers' curiosity about a wider role for TGF-beta was ignited years ago when they first noticed that patients with Loeys-Dietz syndrome (LDS) had higher than normal rates of allergies.

The present study involved 58 children with LDS, ages 7 to 20, followed at Johns Hopkins. Most of them had either a history of allergic disease or active allergies, like allergic rhinitis, eczema, food allergies, asthma, and gastrointestinal and esophageal allergic disease. Not surprisingly, these patients also had abnormally high levels of several traditional markers of allergic disease, including IgE -- an antibody that drives life-threatening allergic responses -- and high numbers of eosinophils, white blood cells involved in allergic reactions.

Because TGF-beta is known to control immune cell maturation, the researchers homed in on a group of cells known as regulatory T cells, which keep tabs on other immune cells to ensure that they don't go into overdrive. LDS patients had unusually high levels of regulatory T cells, but the real surprise came when researchers noticed that instead of acting in their regular role as inflammation tamers, the regulatory T cells were doing the opposite -- secreting allergy-promoting signaling molecules called cytokines. Regulatory T cells obtained from patients with known allergies but without LDS were misbehaving in much the same way, a finding that suggests TGF-beta may induce immune cell malfunction even in the absence of LDS, the researchers say.

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Genetic glitch at the root of allergies revealed

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RUTHERFORD, N.J.--(BUSINESS WIRE)--

Cancer Genetics, Inc. (CGIX) ("CGI" or the "Company"), an emerging leader in DNA-based cancer diagnostics, today announced that its board of directors has increased the board to eight directors and appointed Keith L. Brownlie to serve on the board and its audit committee.

Mr. Brownlie worked with the accounting firm of Ernst & Young LLP, from 1974 to 2010, where he served as audit partner for numerous public companies and was the Life Science Industry Leader for the New York Metro Area, where he was involved with over 100 public and private financings and M&A transactions. He received a B.S. in Accounting from Lehigh University and is a Certified Public Accountant in the state of New Jersey.

Mr. Brownlie co-founded the New Jersey Entrepreneur of the Year Program and was Vice President and Trustee of the New Jersey Society of CPAs. In addition, he served as accounting advisor to the board of the Biotechnology Council of New Jersey. Mr. Brownlie currently serves as a member of the Board of Directors of Soligenix, Inc., a publicly-traded biopharmaceutical company, Epicet Corporation, a publicly-traded specialty pharmaceutical company and RXi Pharmaceuticals Corporation, a publicly-traded biotechnology company.

About Cancer Genetics, Inc.

Cancer Genetics, Inc. (CGI) is an emerging leader in DNA-based cancer diagnostics and servicessome of the most prestigious medical institutions in the world. Our tests target cancers that are difficult to diagnose and predict treatment outcomes. These cancers include hematological, urogenital and HPV-associated cancers. We also offer a comprehensive range of non-proprietary oncology-focused tests and laboratory services that provide critical genomic information to healthcare professionals as well as biopharma and biotech. Our state-of-the-art reference lab is focused entirely on maintaining clinical excellence and is both CLIA certified and CAP accredited and has licensure from several states including New York State. CGI has established strong research collaborations with major cancer centers such as Memorial Sloan-Kettering, The Cleveland Clinic, Mayo Clinic and the National Cancer Institute. For further information, please seewww.cancergenetics.com.

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Cancer Genetics Appoints New Member to Board of Directors

Let #39;s Play Metal Gear Solid - Part 3 Darpa Chief
During a training mission on Shadow Moses Island in February 2005, at a nuclear weapons facility on a remote island off the coast of Alaska, FOXHOUND and the...

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Let #39;s Play Metal Gear Solid - Part 4 Genome Soldiers invasion
During a training mission on Shadow Moses Island in February 2005, at a nuclear weapons facility on a remote island off the coast of Alaska, FOXHOUND and the...

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Let's Play Metal Gear Solid - Part 4 Genome Soldiers invasion - Video

Public release date: 24-Jul-2013 [ | E-mail | Share ]

Contact: Alison Barbuti alison.barbuti@manchester.ac.uk 44-016-127-58383 University of Manchester

Scientists from The University of Manchester have used stem cell gene therapy to treat a fatal genetic brain disease in mice for the first time.

The method was used to treat Sanfilippo a fatal inherited condition which causes progressive dementia in children but could also benefit several neurological, genetic diseases.

Researchers behind the study, published in the journal Molecular Therapy this month, are now hoping to bring a treatment to trial in patients within two years.

Sanfilippo, a currently untreatable mucopolysaccharide (MPS) disease, affects one in 89,000 children in the United Kingdom, with sufferers usually dying in their mid-twenties. It is caused by the lack of SGSH enzyme in the body which helps to breakdown and recycle long chain sugars, such as heparan sulphate (HS). Children with the condition build up and store excess HS throughout their body from birth which affects their brain and results in progressive dementia and hyperactivity, followed by losing the ability to walk and swallow.

Dr Brian Bigger, from the University of Manchester's Institute of Human Development who led the research, said bone marrow transplants had been used to correct similar HS storage diseases, such as Hurler syndrome, by transplanting normal cells with the missing enzyme but the technique did not work with Sanfilippo disease. This is because monocytes, a type of white blood cell, from the bone marrow, did not produce enough enzyme to correct the levels in the brain.

Dr Bigger said: "To increase SGSH enzyme from bone marrow transplants, and to target it to the cells that traffic into the brain, we have developed a stem cell gene therapy which overproduces the SGSH enzyme specifically in bone marrow white blood cells.

"We have shown that mice treated by this method produce five times the normal SGSH enzyme levels in the bone marrow and 11 per cent of normal levels in the brain.

"The enzyme is taken up by affected brain cells and is enough to correct brain HS storage and neuro inflammation to near normal levels and completely corrects the hyperactive behaviour in mice with Sanfilippo.

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New stem cell gene therapy gives hope to prevent inherited neurological disease

Published: Wednesday, July 24, 2013 at 4:59 p.m. Last Modified: Wednesday, July 24, 2013 at 4:59 p.m.

The University of Floridas ophthalmology department, together with gene therapy company AGTC in Alachua, received an $8.4 million grant from the National Eye Institute at the National Institutes of Health to study gene therapy for achromatopsia, a genetic condition that severely impairs peoples vision.

The NEI gives out few grants each year, and this one lasts five years.

Its a very significant grant. Its a great validation of the team that we put together, said Sue Washer, president and CEO of AGTC.

According to Dr. William Hauswirth, the UF professor who will be leading the UF portion of the trial, Barring any real unforeseen and unfortunate challenges, well be trying it on patients in three years.

Hauswirth has been working on gene therapy for blindness for the past 30 years, using recombinant viruses to generate copies of faulty or missing genes affecting vision.

Achromatopsia, which affects the cones on the retina called fovea, makes it very difficult for people to read, navigate and recognize others. Patients are also very sensitive to bright room light, and most are legally blind, Hauswirth explained.

Its a relatively common disease, even though its still considered an orphan disease, but there are lots of patients out there, Hauswirth said, adding that the condition affects about 22,000 people in the United States and Europe.

They would all love to do (the trial), but well have to start carefully with a few patients in each site.

Washer said the therapy being studied in this trial could potentially help about half those patients, those who carry the faulty gene.

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Researchers see gene-therapy grant improving vision

July 23, 2013 In cancer, the spread of tumor cells from the primary site to other parts of the body is called metastasis and is a major cause of death, especially in patients with breast cancer. A new study by Kiran Chada, PhD, professor of biochemistry and molecular biology at Robert Wood Johnson Medical School, part of Rutgers, The State University of New Jersey, shows that metastasis in breast cancer and the risk of death are reduced when the function of the gene HGMA2, is limited.

This finding, published in Cancer Research, a journal of the American Association for Cancer Research (AACR), may be used to develop therapeutic treatments for patients.

"Our research has shown that HGMA2 plays a part in regulating the spread of cancer and could be considered a driver of the process," said Dr. Chada, who was principal investigator of the study. "Further studies could result in the development of therapeutic treatments for patients with breast cancer which could prevent HGMA2's function, reduce the spread of cancer and extend a patient's life."

According to Dr. Chada, only a subset of cancer cells in the primary tumor is potentially metastatic and these cells are found at the edge of the tumor in a region known as the invasive front. Dr. Chada's laboratory showed that normal cells do not express HMGA2, and the expression of this gene product converts normal cells into metastatic cells. Furthermore, the majority of cells which express HMGA2 in human breast cancer tissue were found to be at the invasive front. In additional studies, the researchers showed mice that could not express the HMGA2 gene were found to have a substantially reduced incidence of breast cancer.

Dr. Chada's laboratory conducted the research along with the laboratory of Jeanine D' Armiento, MD, PhD, assistant professor of medicine at Columbia University Funding for the study was provided by grants from the Columbia University LAM Center and the National Heart, Lung and Blood Institute of the National Institutes of Health.

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The above story is based on materials provided by Rutgers Robert Wood Johnson Medical School, via Newswise.

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Gene that may stop the spread of breast cancer identified

Newswise In cancer, the spread of tumor cells from the primary site to other parts of the body is called metastasis and is a major cause of death, especially in patients with breast cancer. A new study by Kiran Chada, PhD, professor of biochemistry and molecular biology at Robert Wood Johnson Medical School, part of Rutgers, The State University of New Jersey, shows that metastasis in breast cancer and the risk of death are reduced when the function of the gene HGMA2, is limited. This finding, published in Cancer Research, a journal of the American Association for Cancer Research (AACR), may be used to develop therapeutic treatments for patients.

Our research has shown that HGMA2 plays a part in regulating the spread of cancer and could be considered a driver of the process, said Dr. Chada, who was principal investigator of the study. Further studies could result in the development of therapeutic treatments for patients with breast cancer which could prevent HGMA2s function, reduce the spread of cancer and extend a patients life.

According to Dr. Chada, only a subset of cancer cells in the primary tumor is potentially metastatic and these cells are found at the edge of the tumor in a region known as the invasive front. Dr. Chadas laboratory showed that normal cells do not express HMGA2, and the expression of this gene product converts normal cells into metastatic cells. Furthermore, the majority of cells which express HMGA2 in human breast cancer tissue were found to be at the invasive front. In additional studies, the researchers showed mice that could not express the HMGA2 gene were found to have a substantially reduced incidence of breast cancer.

Dr. Chadas laboratory conducted the research along with the laboratory of Jeanine D Armiento, MD, PhD, assistant professor of medicine at Columbia University Funding for the study was provided by grants from the Columbia University LAM Center and the National Heart, Lung and Blood Institute of the National Institutes of Health.

About Rutgers Robert Wood Johnson Medical School As one of the nation's leading comprehensive medical schools, Robert Wood Johnson Medical School, part of Rutgers, The State University of New Jersey, is dedicated to the pursuit of excellence in education, research, health care delivery, and the promotion of community health. In cooperation with Robert Wood Johnson University Hospital, the medical school's principal affiliate, they comprise New Jersey's premier academic medical center. In addition, Robert Wood Johnson Medical School has 34 other hospital affiliates and ambulatory care sites throughout the region.

Robert Wood Johnson Medical School encompasses 20 basic science and clinical departments, and hosts centers and institutes including The Cardiovascular Institute, the Child Health Institute of New Jersey, the Center for Advanced Biotechnology and Medicine, the Environmental and Occupational Health Sciences Institute, and the Stem Cell Institute of New Jersey. The medical school maintains educational programs at the undergraduate, graduate, and postgraduate levels for more than 1,500 students on its campuses in New Brunswick and Piscataway, and provides continuing education courses for health care professionals and community education programs. To learn more about Robert Wood Johnson Medical School, visit rwjms.rutgers.edu. Find us online at http://www.Facebook.com/RWJMS and http://www.twitter.com/UMDNJ_RWJMS.

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Gene that May Stop the Spread of Breast Cancer is Identified

caption: Nnimmo Bassey

Nature has the right responses to changing climate and holds the ace to the survival of species on the planet. Humans simply have to be humble enough to accept that we do not understand everything about the intricacies of natural processes. The time has indeed come when the world has to accept that working with nature is immeasurably more beneficial than working against her. Agricultural genetic engineering (GE) over the past few decades has strived to upturn nature and box her for profit, but as it has consistently turned out, nature continues to trump the manipulators.

The power of the biotech industry has been more successful in restraining and constraining governments to do their bidding than in overcoming the power of nature. Their grip on governments has worked to the extent that when they commit crimes like genetic contamination all governments do is to legalise the misdeed so that it may become entrenched and so that the polluter profits from their crimes. And nature pays. And humans and other species pay.

Those who plead caution with regard to the planting and eating of genetically engineered (GE) crops are vilified as anti-science, whereas a close scrutiny shows that it is actually the biotech industries who are anti-science and who pretend that their approximate experimentations are precise in any serious way. Usually speaking from the position of power, proponents discount calls for reason and pleas that we have just one planet and that it is the diversity in nature that is the bedrock of resilience to variable climatic and other conditions.

The Financial Times in an editorial titled Seeds of Doubt and published on 21 July 2013 raises very deep issues. It's subtitle, "Europe is right to be cautious over GM crops" captures the essence of the timely warning. The editorial informs that most GE crops are engineered to resist harmful insects or pests and to withstand glysophate, a type of herbicide. These engineering feats are expected to protect crops from target insects and to relief the farmer of the need to weed - a task that places a lot of stress on small-scale farmers. However, the application of the technology requires that farmers adopt monoculture as the norm and avoid mixed cropping and crop rotation as well.

The editorial notes the truth that critical farmers and scientists have long said, that target pests develop ways of overcoming the engineered defences while weeds have simply become super weeds, tough to hold down and tough to kill. Consequent upon these realities the biotech industry has had to continue to produce more toxic defences and chemicals in bids to overcome the resistance. Unfortunately for the industry, it has turned out that "the harder they come, the harder they fall", as the reggae musicians sing. Those superbugs and super weeds would make even Spider Man jealous.

The FT editorial urges, "regulators should take a broad view of the ecological change triggered when new species are released." It adds that "Narrow fixation on the biochemical properties of a crop risks missing the wood for the trees." The editorial concludes that if Europe has saved her environment and forgone gains enjoyed for some time by farmers in the USA since the 1990s " it will have been a small price to pay."

One wonders why most African governments are not paying attention to the truth that natural resilience is the only way to secure our environment. We cannot afford to go the way of farmers who do not see their crops as food but as commodities to be processed into products for the market. This is the logic of the so-called value-added agricultural production mantra. While there is nothing wrong with value-addition, food crops need to be seen primarily as food crops to avoid needless and harmful tinkering by those who only see market shelves when they look at farms.

Coming on the same day as the FT editorial is another article, this time in the New York Times, that lays bare the tragic consequences of dependence on GE crops in a region of the USA. The article titled Our Coming Food Crisis and written by Gary Paul Nabhan, talks of the risks faced by farmers in a town in California as a metaphor for climate induced food crisis that could hit the USA and by extension impact the world through spiked food prices.

Nabhan draws attention to the higher temperatures being recorded in the area and stresses that when this persists it necessitates the use of more water for irrigation. This does not only place a demand on available surface and ground water, but also leads to higher energy need to pump the water over longer distances. Passing these costs to the consumer translates directly to increased food prices.

Continued here:
Standing Against GMOs By Nnimmo Bassey

The Government of the Russian Federation approved a "roadmap" for the development of biotechnology and genetic engineering, to increase the production of GMOs. The move will be done to catch up with the rest of the world in this segment of the market. The document, posted on the website of the government, says that the global biotechnology market has been developing rapidly and is expected to reach two trillion dollars by 2025. Russia's share in the global biotechnology market accounts for less than 0.1 percent. Moreover, Russia does not manufacture genetically modified products in several segments of the market.

The Russian Ministry for Economic Development has developed an action plan in the field of biopharmaceuticals, biomedical, industrial biotechnology, bio-energy, agri-food biotechnology, forest biotechnology, environmental biotechnology and genetic engineering to develop research, production and cooperation, as well as improve state regulation and personnel training.

By 2018, Russia is to achieve the following volumes of biotechnological products: in the sphere of consumption - 300 billion rubles; in production - 200 billion rubles; export - 50 billion rubles.

The plan is expected to be realized, despite the fact that scientists are still undecided, how the consumption of GM food affects the human body.

Read more from the original source:
Russia to increase production of GMO despite scientific uncertainty

Public release date: 23-Jul-2013 [ | E-mail | Share ]

Contact: Tracie White traciew@stanford.edu 650-723-7628 Stanford University Medical Center

STANFORD, Calif. Students who had their genome tested as part of a groundbreaking medical school course on personalized medicine improved their knowledge of the class materials by an average of 31 percent compared with those who didn't undergo the testing, according to a study by researchers at the Stanford University School of Medicine.

While the sample size was small 23 students sent their saliva to a commercial genetics testing company; eight did not the results may encourage educators to consider this approach in the future, the authors said.

"These results indicate that learning principles of human genetics is more powerful, and learning is more sustained, when exploring your own data," said Keyan Salari, MD, PhD, a former Stanford student who initially proposed the course, called "Genomics and Personalized Medicine." Salari, who is the lead author of the study, is now a urology resident at the Massachusetts General Hospital in Boston. The study will be published July 23 in PLOS ONE.

The eight-week elective course was the first in the country to give students in advanced-degree programs the option of personal genotyping as part of the curriculum. It was designed to teach them how the explosion of knowledge about genetics over the past 10 years could affect the treatment of patients. Since the course was first offered in 2010, the use of genetic testing in clinical care has grown.

The course, which is still being taught, was designed as a way to train future doctors and scientists in the skills necessary to use this new tool. The study, which was based on a pre- and post-course survey taken voluntarily by the majority of the students in the class, also showed that personal testing and the use of personal genotype data in the classroom did not appear to cause significant anxiety.

"This was a novel teaching approach," said Kelly Ormond, co-author of the study and associate professor of genetics. "There is always a lot of interest in whether personalized learning can influence education. ... What our study shows is that it might have benefits for some self-selected students, and is worthy of cautious consideration."

Initially controversial, the course was only approved after a campus task force met regularly for a year to debate the pros and cons of students undergoing genetic testing as part of a class. A number of concerns were raised, including the possible anxiety of learning they could be more susceptible to certain diseases, such as diabetes or Parkinson's. A number of safeguards were subsequently included as part of the course plan, including complete anonymity as to which students chose to undergo testing.

Salari conceived of the idea for the course in 2009 as a PhD student in genetics. He was working as a teaching assistant in the first-year human genetics course for medical students. At the time, the course curriculum consisted primarily of traditional genetics and didn't reflect the genomics revolution of the past 10 years. Salari had also recently undergone his own genetic testing, and saw the educational benefits.

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Genetic testing improved student learning in personalized medicine class, Stanford study finds

July 23, 2013 Students who had their genome tested as part of a groundbreaking medical school course on personalized medicine improved their knowledge of the class materials by an average of 31 percent compared with those who didn't undergo the testing, according to a study by researchers at the Stanford University School of Medicine.

While the sample size was small -- 23 students sent their saliva to a commercial genetics testing company; eight did not -- the results may encourage educators to consider this approach in the future, the authors said.

"These results indicate that learning principles of human genetics is more powerful, and learning is more sustained, when exploring your own data," said Keyan Salari, MD, PhD, a former Stanford student who initially proposed the course, called "Genomics and Personalized Medicine." Salari, who is the lead author of the study, is now a urology resident at the Massachusetts General Hospital in Boston. The study was published July 23 in PLOS ONE.

The eight-week elective course was the first in the country to give students in advanced-degree programs the option of personal genotyping as part of the curriculum. It was designed to teach them how the explosion of knowledge about genetics over the past 10 years could affect the treatment of patients. Since the course was first offered in 2010, the use of genetic testing in clinical care has grown.

The course, which is still being taught, was designed as a way to train future doctors and scientists in the skills necessary to use this new tool. The study, which was based on a pre- and post-course survey taken voluntarily by the majority of the students in the class, also showed that personal testing and the use of personal genotype data in the classroom did not appear to cause significant anxiety.

"This was a novel teaching approach," said Kelly Ormond, co-author of the study and associate professor of genetics. "There is always a lot of interest in whether personalized learning can influence education. ... What our study shows is that it might have benefits for some self-selected students, and is worthy of cautious consideration."

Initially controversial, the course was only approved after a campus task force met regularly for a year to debate the pros and cons of students undergoing genetic testing as part of a class. A number of concerns were raised, including the possible anxiety of learning they could be more susceptible to certain diseases, such as diabetes or Parkinson's. A number of safeguards were subsequently included as part of the course plan, including complete anonymity as to which students chose to undergo testing.

Salari conceived of the idea for the course in 2009 as a PhD student in genetics. He was working as a teaching assistant in the first-year human genetics course for medical students. At the time, the course curriculum consisted primarily of traditional genetics and didn't reflect the genomics revolution of the past 10 years. Salari had also recently undergone his own genetic testing, and saw the educational benefits.

"I was curious about what stories were hidden in my genome, what health risks, what responses to drugs that might be predicted," Salari said. "For instance, I learned I might have a higher risk for age-related macular degeneration. That led me to read and learn a lot more about the genetics of that disease than I probably would have otherwise."

He added: "I wanted to find a way to translate my passion for genomics to all these medical students."

Read more from the original source:
Genetic testing improved student learning in personalized medicine class

The Future of Beef Cattle Breeding and Genetics
As the genomic tools are being integrated into the National site evaluations and the calculations of EPDs, increased accuracy of the EPDs helps the producers...

By: SDSUiGrow

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The Future of Beef Cattle Breeding and Genetics - Video

RUTHERFORD, N.J.--(BUSINESS WIRE)--

Cancer Genetics, Inc. (CGIX) ("CGI" or the "Company"), an emerging leader in DNA-based cancer diagnostics, launched its proprietary cervical cancer test and is marketing the molecular product globally through its network of distribution partners. Cervical cancer is the second most common cancer in women worldwide, with 500,000 new cases annually and almost 80% of cases occurring in developing countries.

CGIs FISH-based HPV-Associated Cancer Test (FHACT) uses a unique combination of genetic markers to detect genetic abnormalities located at 3q, 5p, 20q and chromosome 7. A recent study concluded that these four biomarkers are associated with the severity of cervical lesions. The findings of the study, published in the July issue of Gynecologic Oncology, http://dx.doi.org/10.1016/j.ygyno.2013.06.005, support the use of FHACT as an aid in the screening of women with HPV-positive abnormal cervical lesions. By identifying lesions that will progress to a higher grade versus those that will regress, FHACT can allow for a better triage of patients before referral for colposcopy and consequently reduce the associated healthcare burden.

The test can be performed directly on Pap smear or liquid based-cytology and does not require any resampling. It is therefore an ideal fit in countries where women have reduced access to routine screening. We think that FHACT will be a new tool to help identify women with high risk of progressing to cervical cancer, says Dr. Q. Annie Hasan, Ph.D., F.N.A.Sc., Head of Department and Senior Consultant, Department of Genetics and Molecular Medicine, Kamineni Hospitals, Hyderabad, India. This is particularly important in India due to the rising incidence of cervical cancer caused by difficulty in implementation of cervical screening programs, which require repeated evaluation in large number of women. In partnership with its distributors and collaborators, CGI will conduct workshops in India and Mexico to accelerate adoption of FHACT amongst the clinical community.

In industrialized countries, it is estimated that about one million women undergo colposcopy procedures each year, while only 3,700 cancer cases are actually diagnosed. The Company expects FHACT to aid in lowering healthcare costs and reducing the number of unwarranted colposcopies by providing genomic information of the lesion not available until now. CGI plans to make FHACT available in the U.S. later this year and will be working closely with several laboratories and hospitals to implement an early adoption of the test.

The design and development of FHACT was supported in part by a Small Business Innovation Research (SBIR) grant. In addition to cervical cancer, FHACT is applicable to other HPV-associated cancers. CGI is currently conducting ongoing validations with key thought leaders for head and neck cancer and anal cancer. Results from these studies are expected to be available by year end.

About Cancer Genetics, Inc.

Cancer Genetics, Inc. (CGI) is an emerging leader in DNA-based cancer diagnostics and servicessome of the most prestigious medical institutions in the world. Our tests target cancers that are difficult to diagnose and predict treatment outcomes. These cancers include hematological, urogenital and HPV-associated cancers. We also offer a comprehensive range of non-proprietary oncology-focused tests and laboratory services that provide critical genomic information to healthcare professionals as well as biopharma and biotech. Our state-of-the-art reference lab is focused entirely on maintaining clinical excellence and is both CLIA certified and CAP accredited and has licensure from several states including New York State. CGI has established strong research collaborations with major cancer centers such as Memorial Sloan-Kettering, The Cleveland Clinic, Mayo Clinic and the National Cancer Institute. For further information, please seewww.cancergenetics.com.

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Cancer Genetics Launches New Genetic Test For Cervical Cancer Management

HIV/AIDS Stem Cell Clinical Trial: Introduction by Jeff Sheehy
For more information, see the CIRM HIV/AIDS fact sheet at: http://www.cirm.ca.gov/about-stem-cells/hivaids-fact-sheet On July 9th 2013, Calimmune announced t...

By: California Institute for Regenerative Medicine

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HIV/AIDS Stem Cell Clinical Trial: Introduction by Jeff Sheehy - Video