Archive for the ‘Gene Therapy Research’ Category

Dublin - Research and Markets (http://www.researchandmarkets.com/research/e0c7cab9/nanotechnology_in) has announced the addition of the "Nanotechnology in Health Care" book to their offering.

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Research and Markets: Nanotechnology in Health Care. An In-Depth Investigation of Nanotechnology-Based Therapy

Featured Article Academic Journal Main Category: Genetics Also Included In: Flu / Cold / SARS;Swine Flu Article Date: 26 Mar 2012 - 3:00 PDT

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People who do not have the rare variant of IFITM3 only have mild reactions to the influenza virus, said the researchers who found the gene codes for a protein that is important for helping the body defend itself against the virus.

It appears that when there is plenty of IFITM3 protein in the body, the flu virus can't penetrate deep into the lungs.

The 2009 H1N1 "swine flu" pandemic showed how quickly a new virus can spread, and how a generally mild infection can become serious and even kill a small subset of the population, the authors write in their background information.

The antiviral role of IFITM3 in humans was first suggested by studies that showed the protein blocked the growth of influenza virus and dengue virus in cultured cells.

So they decided to take this further by examining the effect of this protein family in lab mice.

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Gene Explains Why Flu Can Be Serious

We already know that during sexual reproduction, offsprings get 50 percent of the genes from the father and the other half from its mother. While the parents' genes determine the offsprings' traits, some of these genes are switched on only on the paternal side while others are switched on only on the maternal side. This influences certain traits, such as the number of piglets born.

In genetics, this means that there is a difference between two DNA classes: BA (in which B is maternal and switched on and A is paternal and switched off) and AB (the exact opposite). This is called 'genetic imprinting'. The switches which turn the genes 'on' and 'off' are present in specific parts of the genome, as was already discovered in earlier research on humans. Researchers Albart Coster and Ole Masen used genetic markers to examine the pig genome to find the genes which regulate fertility. Their search brought them to the DIO3 gene. Subsequent research showed that if the breeding pig gets a strain of this gene from the mother, it gives birth to 12.7 piglets on the average. If the DIO3 strain originates from the father, only 11.9 piglets are born. It is remarkable that just one gene can bring about such a considerable difference.

'Other genes can also influence the sow's fertility,' says Bovenhuis, 'but the DIO gene alone is responsible for 15 percent of the genetic variation in offsprings.' This gene can therefore be a major selection criterion in the pig breeding sector. But Bovenhuis says that their research is significant because it offers fundamental knowledge on the epigenetics of, for example, humans and mice. This is also why their article has been published in the Plos One journal at the end of February.

Geneticists do not yet know exactly whether imprinting affects embryo development or fertility. This can only be discovered if there is a big difference in the offsprings' traits. 'If the effect of the DIO3 gene on fertility had only been a few percent, we would never have discovered this gene,' says Bovenhuis.

Provided by Wageningen University

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Maternal gene causes more piglets to be born

An international team of researchers has discovered a human genetic flaw that could explain why influenza makes some people more sick than others.

Reporting in the journal Nature, British and American researchers, led by the Wellcome Trust Sanger Institute (WTSI) in the UK, said the variant of the IFITM3 gene was much more common in people hospitalized for the flu than in those who were able to fight the disease at home.

The researchers said this could explain why during the 2009/10 H1N1 swine flu pandemic most people had mild symptoms, while others got seriously ill and died. They said they scoured genetic databases covering thousands of people and found evidence that around one in 400 people may have the flawed genetic variant.

IFITM3 is an important protein that protects cells against infection and is believed to play a crucial role in the immune systems response against viruses such as H1N1. When the protein is abundant in the body, the spread of the virus in the lungs is hindered, but if the protein is defective or absent, the virus can spread rapidly, causing greater illness and perhaps death.

Aaron Everitt, lead researcher from WTSI, said although the IFITM3 protein is known to play an important role in limiting the spread of viruses in cells, little is known about how it works in lungs. Our new research helps to explain how both the gene and protein are linked to viral susceptibility, he added.

The role of IFITM3 in humans was first suggested by studies using a genetic screen, which showed the protein blocked the growth of the flu and dengue in cells. This finding led the team to further investigate how the gene works in both humans and mice.

For the study, the researchers removed the gene from mice and found when they developed flu, their symptoms were much worse than the mice that still had the gene. They found that the loss of this single gene in mice can turn a mild case of influenza into a potentially fatal infection.

Armed with this knowledge, the researchers sequenced the IFITM3 genes of 53 patients hospitalized with the flu and found three (one in 18) have a genetic mutation of this gene, which is rare in normal people.

Since IFITM3 appears to be a first line defender against infection, our efforts suggest that individuals and populations with less IFITM3 activity may be at increased risk during a pandemic and that IFITM3 could be vital for defending human populations against other viruses such as avian influenza virus and dengue virus, said Dr. Abraham Brass, an Assistant Professor at the Ragon Institute and Gastrointestinal Unit of Massachusetts General Hospital, and co-lead author of the study.

The team said these findings need to be replicated in bigger studies before they can positively rule that the IFITM3 gene mutation is the key factor for causing serious illness.

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Gene Can Transform Mild Flu Into A Life-threatening Disease

Public release date: 26-Mar-2012 [ | E-mail | Share ]

Contact: Peggy Calicchia calicchi@cshl.edu 516-422-4012 Cold Spring Harbor Laboratory

March 27, 2012 Large numbers of people moved between Africa and Europe during recent and well-documented time periods such as the Roman Empire, the Arab conquest, and the slave trade, and genetic evidence of these migrations lives on in Europeans today. But were there more ancient migrations? In a study published online today in Genome Research, researchers present the first genetic evidence for prehistoric gene flow between Africa and Europe, dating back as far as 11,000 years ago.

To trace the evolution and ancestry of humans, scientists study the DNA sequence of the mitochondria, a specialized cellular structure that produces energy for the cell and carries genetic information that is separate from the rest of the genome that resides in the nucleus. While the nuclear genome is a mix of genetic information from both mother and father, the mitochondrial DNA (mtDNA) is passed directly from mother to child without any contribution of DNA from the father. But not everyone's mtDNA is exactly alike: over long periods of time, small changes in the mtDNA sequence have arisen in different populations. Geneticists can use these changes as markers that indicate the movements and migrations of humans in the past, and classify them into specific "haplogroups."

In this study, an international team of researchers performed the largest analysis of complete mtDNA genomes belonging to haplogroup L (a lineage of sub-Saharan Africa origin) in Europe to date, aiming to untangle the history of genetic links between the two contents. By comparing the sequences of mtDNA genomes from various regions of Europe with mitochondrial genomes from around the world, they made a very surprising observation regarding when sub-Saharan lineages appeared in Europe.

"It was very surprising to find that more than 35 percent of the sub-Saharan lineages in Europe arrived during a period that ranged from more than 11,000 years ago to the Roman Empire times," said Dr. Antonio Salas of the University of Santiago de Compostela and senior author of the study. The other 65% of European haplogroup L lineages arrived in more recent times.

The authors explain that these contacts likely connected sub-Saharan Africa to Europe not only via North Africa, but also directly by coastal routes. Salas said that it still remains unknown why there was genetic flow between the Africa and Europe in prehistoric times, but one possible scenario is that some bidirectional flow was promoted when the last glaciation pushed some Europeans southward, until the glacier receded and populations returned north.

In addition to tracing the genetic links of Africa and Europe back to prehistoric times, Salas expects that their work will also help those individuals who want to learn more about their own ancestry. "There is a growing interest in direct-to-consumer genetic testing, including those aimed to serve a public interested in reconstructing their ancestry," Salas said. "Studies like the one presented here will help to unravel inferences made in these studies."

Scientists from the University of Santiago de Compostela (Galicia, Spain), the University of Perugia (Perugia, Italy), the University of Pavia (Pavia, Italy), the Sorenson Molecular Genealogy Foundation (Salt Lake City, UT), the University of Oxford (Oxford, UK), and the National Institute of Toxicology and Forensic Science (Sevilla, Spain) contributed to this study.

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Genetic study unravels ancient links between African and European populations

- Human genome and mouse studies identify new precise genetic links

Newswise Working with genetically engineered mice and the genomes of thousands of people with schizophrenia, researchers at Johns Hopkins say they now better understand how both nature and nurture can affect ones risks for schizophrenia and abnormal brain development in general.

The researchers reported in the March 2 issue of Cell that defects in a schizophrenia-risk genes and environmental stress right after birth together can lead to abnormal brain development and raise the likelihood of developing schizophrenia by nearly one and half times.

Our study suggests that if people have a single genetic risk factor alone or a traumatic environment in very early childhood alone, they may not develop mental disorders like schizophrenia, says Guo-li Ming, M.D., Ph.D., professor of neurology and member of the Institute for Cell Engineering at the Johns Hopkins University School of Medicine. But the findings also suggest that someone who carries the genetic risk factor and experiences certain kinds of stress early in life may be more likely to develop the disease.

Pinpointing the cause or causes of schizophrenia has been notoriously difficult, owing to the likely interplay of multiple genes and environmental triggers, Ming says. Searching for clues at the molecular level, the Johns Hopkins team focused on the interaction of two factors long implicated in the disease: Disrupted-in-Schizophrenia 1 (DISC1) protein, which is important for brain development, and GABA, a brain chemical needed for normal brain function.

To find how these factors impact brain development and disease susceptibility, the researchers first engineered mice to have reduced levels of DISC1 protein in one type of neuron in the hippocampus, a region of the brain involved in learning, memory and mood regulation. Through a microscope, they saw that newborn mouse brain cells with reduced levels of DISC1 protein had similar sized and shaped neurons as those from mice with normal levels of DISC1 protein. To change the function of the chemical messenger GABA, the researchers engineered the same neurons in mice to have more effective GABA. Those brain cells looked much different than normal neurons, with longer appendages or projections. Newborn mice engineered with both the more effective GABA and reduced levels of DISC1 showed the longest projections, suggesting, Ming said, that defects in both DISC1 and GABA together could change the physiology of developing neurons for the worse.

Meanwhile, other researchers at University of Calgary and at the National Institute of Physiological Sciences in Japan had shown in newborn mice that changes in environment and routine stress can impede GABA from working properly during development. In the next set of experiments, the investigators paired reducing DISC1 levels and stress in mice to see if it could also lead to developmental defects. To stress the mice, the team separated newborns from their mothers for three hours a day for ten days, then examined neurons from the stressed newborns and saw no differences in their size, shape and organization compared with unstressed mice. But when they similarly stressed newborn mice with reduced DISC1 levels, the neurons they saw were larger, more disorganized and had more projections than the unstressed mouse neurons. The projections, in fact, went to the wrong places in the brain.

Next, to see if their results in mice correlated to suspected human schizophrenia risk factors, the researchers compared the genetic sequences of 2,961 schizophrenia patients and healthy people from Scotland, Germany and the United States. Specifically, they determined if specific variations of DNA letters found in two genes, DISC1 and a gene for another protein, NKCC1, which controls the effect of GABA, were more likely to be found in schizophrenia patients than in healthy individuals. They paired 36 DNA letter changes in DISC1 and two DNA letter variations in NKCC1 one DNA letter change per gene in all possible combinations. Results showed that if a persons genome contained one specific combination of single DNA letter changes, then that person is 1.4 times more likely than people without these DNA changes to develop schizophrenia. Having these single DNA letter changes in either one of these genes alone did not increase risk.

Now that we have identified the precise genetic risks, we can rationally search for drugs that correct these defects, says Hongjun Song, Ph.D., co-author, professor of neurology and director of the Stem Cell Program at the Institute for Cell Engineering.

Other authors of the paper from Johns Hopkins are Ju Young Kim, Cindy Y. Liu, Fengyu Zhang, Xin Duan, Zhexing Wen, Juan Song, Kimberly Christian and Daniel R. Weinberger. Emer Feighery, Bai Lu and Joseph H. Callicott from the National Institute of Mental Health, Dan Rujescu of Ludwig-Maximilians-University, and David St Clair of the University of Aberdeen Royal Cornhill Hospital are additional authors.

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Genetic Risk and Stressful Early Infancy Join to Increase Risk for Schizophrenia

Public release date: 26-Mar-2012 [ | E-mail | Share ]

Contact: Karen N. Peart karen.peart@yale.edu 203-432-1326 Yale University

Obese youths with particular genetic variants may be more prone to fatty liver disease, a leading cause of chronic liver disease in children and adolescents in industrialized countries, according to new findings by Yale School of Medicine researchers.

The study, which focused on three ethnic groups, is published in the March issue of the journal Hepatology.

Led by Nicola Santoro, M.D., associate research scientist in the Department of Pediatrics at Yale School of Medicine, the authors measured the hepatic, or liver, fat content of children using magnetic resonance imaging. The study included 181 Caucasian, 139 African-American and 135 Hispanic children who were, on average, age 13.

"We observed that a common genetic variant known as Patatin-like phospholipase domain containing protein-3 (PNPLA3) working with a regulatory protein called glucokinase (GCKR), was associated with increased triglycerides, very low-density lipoproteins levels, and fatty liver," said Santoro.

Santoro explained that his observations could help unravel the genetic mechanisms that contribute to liver fat metabolism. "This may drive the decisions about future drug targets to treat hypertriglyceridemia and non-alcoholic fatty liver disease," he said.

Childhood obesity is a global health concern. Experts say nonalcoholic fatty liver disease is now the leading cause of chronic liver disease in children and adolescents in industrialized countries.

"Our findings confirm that obese youths with genetic variants in the GCKR and PNPLA3 genes may be more susceptible to fatty liver disease," said Santoro, who is cautious about automatically extending this observation to the overall population.

"Our data refer to a population of obese children and adolescents," he said. "I think that further studies in a larger sample size involving lean subjects and adults may help to further define in more details these associations."

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Researchers unravel genetic mechanism of fatty liver disease in obese children

By George Winslow -- Broadcasting & Cable, 3/26/2012 5:41:01 PM Pixeldust Studios has produced around eight minutes of original animation sequences that will be used in a one-hour episode of PBS's Nova series called "Cracking Your Genetic Code" that will air on March 28.

The PBS special will explore the medical benefits of the genetic revolution and some of the ethical questions raised by these new technologies. To help tell that story, Pixeldust created animated sequences showing the science behind genes, chromosomes and DNA as well as how certain medications and drugs work in the human body.

"Pixeldust did an amazing job coming up with creative ways to visualize the human genome," noted Sarah Holt, producer for Nova/PBS & Holt Productions in a statement. "Their animators skillfully took the audience inside a human cell, past human chromosomes, and into DNA that is coiled inside the nucleus. The animation was sophisticated and artistically gorgeous to look at, but also helped the audience grasp difficult concepts in genomics [while laboring]...to ensure the accuracy of the scientific details."

Ricardo Andrade, founder and executive creative director at Pixeldust added in a statement that they used "warm colors" to give the "work a more organic look." The studio also consulted with a noted cell biologist to ensure the scientific accuracy of the images.

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PBS' 'Nova' Applies Pixeldust to Genetics

(RTTNews.com) - Myriad Genetics Inc. (MYGN) announced that the Supreme Court of the United States remanded the case of The Association for Molecular Pathology, et al., v. Myriad Genetics Inc., et al to the Federal Circuit Court of Appeals.

The company said that as a result of this decision by the Supreme Court, the United States Court of Appeals for the Federal Circuit will reconsider their decision dated July 29, 2011, which upheld Myriad's gene patents.

In that decision, the Federal Circuit declared that the composition of matter claims covering isolated DNA of the BRCA 1 and BRCA 2 genes are patent-eligible under Section 101 of the United States Patent Act.

"While, this case should not have any direct impact to Myriad and its operations because of our extensive patent estate, it has great importance to the medical, pharmaceutical, biotechnology and other commercial industries, as well as the hundreds of millions of people whose lives are bettered by the products these industries develop based on the promise of strong patent protection," said Peter Meldrum, President and CEO of Myriad Genetics.

"Thus, we are prepared to vigorously defend the patent claims granted to Myriad by the U.S. Patent and Trademark Office and believe that we will be successful," said Peter Meldrum.

For comments and feedback: contact editorial@rttnews.com

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Myriad Genetics Says Supreme Court Of United States Remands Gene Patenting Case

LOS ANGELES--(BUSINESS WIRE)--

Response Genetics, Inc. (Nasdaq:RGDX - News), a company focused on the development and commercialization of molecular diagnostic tests for cancer, announced today the addition of Stephanie H. Astrow, Ph.D., as the Companys Vice President for Research and Development. In her role, Dr. Astrow will be responsible for leading the companys research and development programs, as well as identifying and incorporating new technologies into the services that the Company provides to the medical community.

With her strong background in the oncology molecular diagnostics industry we believe Stephanie is the perfect fit to lead our R&D efforts, said Thomas Bologna, Chairman and Chief Executive Officer of Response Genetics. Stephanies track record of identifying and developing biomarker assays and driving scientific innovation to expand business will be a tremendous asset to us and we are looking forward to her contributions.

Dr. Astrow brings extensive experience in molecular diagnostics research and development as well as operational experience to her role at Response Genetics. Most recently, Dr. Astrow was Scientific Director for Oncology at Quest Diagnostics, the largest global provider of diagnostic testing. At Quest, she played a key role in expanding business by introducing new assays and services, as well as coordinating development strategy for companion diagnostics with key pharmaceutical companies. Prior to her work at Quest, Dr. Astrow served as Vice President and Director of Oncology at Pathway Diagnostics, and Vice President, Scientific Director of Impath, Inc. Dr. Astrow received a Bachelor of Arts in Biology and Medicine at Brown University, and her Ph.D. in Molecular and Cell Biology from the University of California, Berkeley. She also holds a Masters of Business Administration from Pepperdine University.

Dr. Astrow, commenting on her appointment said, I couldnt be more excited to be joining Response Genetics, a company that matches my background and interests very well. I look forward to putting my skills and experience to work in helping people with cancer, and being part of a company that is both patient-centric and well suited to prosper in the exciting field of personalized diagnostics.

About Response Genetics, Inc.

Response Genetics Inc. (RGI) is a CLIA-certified clinical laboratory focused on the development and sale of molecular diagnostic tests for cancer. RGIs principal customers include oncologist, pathologists and hospitals. In addition to diagnostic testing services, the Company generates revenue from the sales of its analytical testing services of clinical trial specimens to the pharmaceutical industry. RGI was founded in 1999 and its principal headquarters are located in Los Angeles, California. For additional information, please visit http://www.responsegenetics.com.

Forward-Looking Statement Notice

Except for the historical information contained herein, this press release and the statements of representatives of RGI related thereto contain or may contain, among other things, certain forward-looking statements, within the meaning of the Private Securities Litigation Reform Act of 1995.

Such forward-looking statements involve significant risks and uncertainties. Such statements may include, without limitation, statements with respect to the Companys plans, objectives, projections, expectations and intentions, such as the ability of the Company to continue to execute on its business strategy and operations, the ability to expand our test panels, the ability , and other statements identified by words such as projects, may, could, would, should, believes, expects, anticipates, estimates, intends, plans or similar expressions.

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Response Genetics, Inc. Announces Appointment of Stephanie Astrow, Ph.D., as Vice President, Research and Development

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Seattle Genetics Announces Pivotal ADCETRIS™ (Brentuximab Vedotin) Hodgkin Lymphoma Study Published in Journal of ...

SILVER SPRING, Md.--(BUSINESS WIRE)--

Nuvilex, Inc. (OTCQB:NVLX), an emerging international biotechnology provider of cell and gene therapy solutions through its associate SG Austria, announced today a significant advance in gene therapy with a new, unique, and specialized system for induction of gene expression in encapsulated cells.

In a recent publication in the Journal of Controlled Release, SG Austria and its research partners described a new system for induction of gene expression, or the means for stimulating a gene to be expressed within cells, including those that have been encapsulated and implanted in the body.

The process described in the publication involves the stimulation of pre-programmed living cells, encapsulated using the Cell-in-a-Box technology, to express therapeutic genes under the control of a heat shock protein inducible promoter. This is done by simultaneously co-encapsulating pre-programmed cells and magnetic nanoparticles, which are much smaller than the cells. When subjected to an alternating magnetic field, the magnetic nanoparticles inside the capsules vibrate, producing heat. This results in a localized, temporary increase in temperature inside the capsules. This heat causes specialized heat shock proteins in the cells to induce expression of the therapeutic gene(s).

Although both cell and gene therapies have an enormous range of potential applications, a critical issue in modern molecular biology has been to be able to regulate and control gene expression. Therefore, many systems have been created to regulate gene expression. Those gene expression systems currently available mostly rely on small molecules such as hormones or antibiotics as inducers. Unfortunately, administration of some of these inducers is difficult to control, the effects on gene regulation are typically slow, and they do not easily shut off once turned on. The new system developed by SG Austria and its partners will allow doctors in the future to more accurately control both dosage and the synthesis of specific proteins for treating a disease.

Dr. Robert Ryan, CEO of Nuvilex, said: "We are excited by this latest development, since fine-tuned heating of the encapsulated cells by nanoparticles by a localized magnetic field will allow carefully regulated gene expression within a short time. All of this can be done from outside the body they have been placed in. This system has great versatility and potential for advancing cell and gene therapy approaches, substantially increasing the value and dramatically expanding the capabilities of our live cell encapsulation technology."

About Nuvilex

Nuvilex, Inc. (OTCQB:NVLX) is an emerging international biotechnology provider of live, clinically useful, therapeutically valuable, encapsulated cells as well as services for encapsulating live cells for the research and medical communities. Through substantial effort, the aspects of our corporate activities alone and in concert with SG Austria continue to move toward agreement completion and ultimately a strong future together. Our companys ultimate clinical offerings will include cancer, diabetes and other treatments using the companys industry-leading cell and gene therapy expertise and cutting-edge, live-cell encapsulation technology.

Safe Harbor Statement

This press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995 involving risks and uncertainties including product demand, market competition, and Nuvilexs ability to meet current or future plans which may cause actual results, events, and performances, expressed or implied, to vary and/or differ from those contemplated or predicted. Investors should study and understand all risks before making an investment decision. Readers are recommended not to place undue reliance on forward-looking statements or information. Nuvilex is not obliged to publicly release revisions to any forward-looking statement to reflect events or circumstances afterward, or to disclose unanticipated occurrences, except as required under applicable laws.

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Nuvilex Announces Advance in Gene Therapy for Encapsulated Living Cells Using Magnetic Nanoparticles

24-03-2012 07:46 This is the harvest of adipose tissue for combination with bone marrow aspirate concentrate for stem cell therapy

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Adipose harvest for stem cell therapy by Dr Adelson - Video

25-03-2012 10:22 Dr Adelson aspirates bone marrow for concentration for stem cell therapy for musculoskeletal pain conditions

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bone marrow aspiration for stem cell therapy by Dr Adelson - Video

(RTTNews.com) - An important clinical trial, which evaluated the use of autologous bone-marrow-cell therapy in patients with chronic ischemic heart failure, has failed to meet the prespecified end points of improvement in most measures of heart function, according to the results presented at the American College of Cardiology 2012 Scientific Sessions.

The trial dubbed, FOCUS - a phase II study, is the largest study to date to investigate if a patient's own bone marrow cells improved myocardial perfusion, reduced left ventricular end-systolic volume or enhanced maximal oxygen consumption in patients with coronary artery disease or LV dysfunction, and limiting heart failure or angina. The FOCUS trial was undertaken by the National Heart, Lung, and Blood Institute-sponsored Cardiovascular Cell Therapy Research Network.

Ninety two patients with chronic ischemic heart disease , having a left ventricular ejection fraction of 45% or less, a perfusion defect by single-photon emission tomography, or SPECT, who were no longer candidates for revascularization, were enrolled in the trial. Sixty one patients in the study were administered bone marrow cells through transendocardial injections while thirty one patients were administered placebo.

An assessment of primary endpoints at 6 months has revealed that there is no statistically significant difference between the treatment group and placebo arm in left ventricular end-systolic volume assessed by echocardiography, maximal oxygen consumption, and reversibility on SPECT. The secondary outcomes, including percent myocardial defect, total defect size, fixed defect size, regional wall motion, and clinical improvement, also has not exhibited any difference between the two arms.

However, according to the study authors, exploratory analyses have revealed that left ventricular ejection fraction improved in the treatment group compared with the placebo group by 2.7%.

The authors, led by Emerson Perin, concluded that the findings provide evidence for further studies to determine the relationship between the composition and function of bone marrow product and clinical end points. Understanding these relationships will improve the design and interpretation of future studies of cardiac cell therapy, the authors noted.

The results were published online March 24 in the Journal of the American Medical Association.

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Bone Marrow Stem Cell Therapy Trial - Clues, But No Answers

3/25/2012 10:50 AM ET (RTTNews) - An important clinical trial, which evaluated the use of autologous bone-marrow-cell therapy in patients with chronic ischemic heart failure, has failed to meet the prespecified end points of improvement in most measures of heart function, according to the results presented at the American College of Cardiology 2012 Scientific Sessions.

The trial dubbed, FOCUS - a phase II study, is the largest study to date to investigate if a patient's own bone marrow cells improved myocardial perfusion, reduced left ventricular end-systolic volume or enhanced maximal oxygen consumption in patients with coronary artery disease or LV dysfunction, and limiting heart failure or angina. The FOCUS trial was undertaken by the National Heart, Lung, and Blood Institute-sponsored Cardiovascular Cell Therapy Research Network.

Ninety two patients with chronic ischemic heart disease , having a left ventricular ejection fraction of 45% or less, a perfusion defect by single-photon emission tomography, or SPECT, who were no longer candidates for revascularization, were enrolled in the trial. Sixty one patients in the study were administered bone marrow cells through transendocardial injections while thirty one patients were administered placebo.

An assessment of primary endpoints at 6 months has revealed that there is no statistically significant difference between the treatment group and placebo arm in left ventricular end-systolic volume assessed by echocardiography, maximal oxygen consumption, and reversibility on SPECT. The secondary outcomes, including percent myocardial defect, total defect size, fixed defect size, regional wall motion, and clinical improvement, also has not exhibited any difference between the two arms.

However, according to the study authors, exploratory analyses have revealed that left ventricular ejection fraction improved in the treatment group compared with the placebo group by 2.7%.

The authors, led by Emerson Perin, concluded that the findings provide evidence for further studies to determine the relationship between the composition and function of bone marrow product and clinical end points. Understanding these relationships will improve the design and interpretation of future studies of cardiac cell therapy, the authors noted.

The results were published online March 24 in the Journal of the American Medical Association.

by RTT Staff Writer

For comments and feedback: editorial@rttnews.com

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FOCUS : Bone Marrow Cell Therapy Trial Fails To Meet Goals

25 March 2012 Last updated at 13:00 ET By Eleanor Bradford BBC Scotland Health Correspondent

Scientists have discovered a gene which may make some people more susceptible to flu.

The gene was found by Edinburgh University researchers working with the Wellcome Trust Sanger Institute near Cambridge.

It may explain why apparently healthy people have needed intensive care after contracting swine flu, while others were unaware they had been infected.

The findings have been published in the journal Nature.

An analysis of the DNA of 60 patients in intensive care with flu revealed an unusually high number with a variant in a gene called IFITM3.

This gene produced a protein which hinders the spread of the flu virus in the lungs. The variant in this gene means less protein is produced and the flu virus can spread more easily.

Although the genetic variation is normally rare, it was 19-times more common than expected in people who needed hospital treatment.

Dr Kenneth Baillie, an expert in genetics and critical care at Edinburgh University's Roslin Institute, said: "During the pandemic it was very unusual for a healthy person to become desperately sick with flu but it did happen to some people.

"It was a mystery why it affected those people so severely when most people were hardly affected at all. This research explains a fraction of why those individuals were so susceptible."

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Gene clue found for flu mystery

* Gene appears to determine people's ability to fight flu

* People could be screened for gene

* It may help develop new medicines for other viruses too

LONDON, March 25 (Reuters) - A genetic discovery could help explain why flu makes some people seriously ill or kills them, while others seem able to bat it away with little more than a few aches, coughs and sneezes.

In a study published in the journal Nature on Sunday, British and American researchers said they had found for the first time a human gene that influences how people respond to flu infections, making some people more susceptible than others.

The finding helps explain why during the 2009/2010 pandemic of H1N1 or "swine flu", the vast majority of people infected had only mild symptoms, while others - many of them healthy young adults - got seriously ill and died.

In future, the genetic discovery could help doctors screen patients to identify those more likely to be brought down by flu, allowing them to be selected for priority vaccination or preventative treatment during outbreaks, the researchers said.

It could also help develop new vaccines or medicines against potentially more dangerous viruses such as bird flu.

Paul Kellam of Britain's Sanger Institute, who co-led the study and presented the findings in a telephone briefing, said the gene, called ITFITM3, appeared to be a "crucial first line of defence" against flu.

When IFITM3 was present in large quantities, the spread of the virus in lungs was hindered, he explained. But when IFITM3 levels were lower, the virus could replicate and spread more easily, causing more severe symptoms.

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Scientists find gene that can make flu a killer

25 March 2012 Last updated at 13:39 ET

Scientists have identified a genetic flaw that may explain why some people get more ill with flu than others.

Writing in Nature, the researchers said the variant of the IFITM3 gene was much more common in people hospitalised for flu than in the general population.

It controls a malformed protein, which makes cells more susceptible to viral infection.

Experts said those with the flaw could be given the flu jab, like other at-risk groups.

Researchers removed the gene from mice. They found that when they developed flu, their symptoms were much worse than those seen in mice with the gene.

Evidence from genetic databases covering thousands of people showed the flawed version of the gene is present in around one in 400 people.

The scientists, who came from the UK and US, then sequenced the IFITM3 genes of 53 patients who were in hospital with flu.

Three were found to have the variant - a rate of one in 20.

The researchers say these findings now need to be replicated in bigger studies. And they add it is probably only part of the genetic jigsaw that determines a person's response to flu.

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'Severe flu' gene flaw identified

Public release date: 25-Mar-2012 [ | E-mail | Share ]

Contact: Michael Bernstein m_bernstein@acs.org 619-525-6268 (March 23-28, San Diego Press Center) 202-872-6042

Michael Woods m_woods@acs.org 619-525-6268 (March 23-28, San Diego Press Center) 202-872-6293 American Chemical Society

SAN DIEGO, March 25, 2012 Just as aspiring authors often read hundreds of books before starting their own, scientists are using decades of knowledge garnered from sequencing or "reading" the genetic codes of thousands of living things to now start writing new volumes in the library of life. J. Craig Venter, Ph.D., one of the most renowned of those scientists, described the construction of the first synthetic cell and many new applications of this work today at the 243rd National Meeting & Exposition of the American Chemical Society (ACS), the world's largest scientific society, which is underway this week.

In a plenary talk titled, "From Reading to Writing the Genetic Code," Venter described a fundamental shift in his field of genomics, and its promise for producing synthetic life that could help provide 21st century society with new fuels, medicines, food and nutritional products, supplies of clean water and other resources. Venter, a pioneer in the field, led the team at Celera Genomics that went head-to-head with the government-and-foundation-funded Human Genome Project in the race to decode the human genome. This quest, in which the 23,000 human genes were deciphered, ended with the teams declaring a tie and publishing simultaneous publications in 2001.

"Genomics is a rapidly evolving field and my teams have been leading the way from reading the genetic code deciphering the sequences of genes in microbes, humans, plants and other organisms to writing code and constructing synthetic cells for a variety of uses. We can now construct fully synthetic bacterial cells that have the potential to more efficiently and economically produce vaccines, pharmaceuticals, biofuels, food and other products."

The work Venter described at the ACS session falls within an ambitious new field known as synthetic biology, which draws heavily on chemistry, metabolic engineering, genomics and other traditional scientific disciplines. Synthetic biology emerged from genetic engineering, the now-routine practice of inserting one or two new genes into a crop plant or bacterium. The genes can make tomatoes, for instance, ripen without softening or goad bacteria to produce human insulin for treating diabetes. Synthetic biology, however, involves rearranging genes on a much broader scale that of a genome, which is an organism's entire genetic code to reprogram entire organisms and even design new organisms.

Venter and his team at the not-for-profit J. Craig Venter Institute (JCVI), which has facilities in Rockville, Maryland, and San Diego, announced in 2010 that they had constructed the world's first completely synthetic bacterial cell. Using computer-designed genes made on synthesizer machines from four bottles of chemicals, the scientists arranged those genes into a package, a synthetic chromosome. When inserted into a bacterial cell, the chromosome booted up the cell and was capable of dividing and reproducing.

In the ACS talk, Venter described progress on major projects, including developing new synthetic cells and engineering genomes to produce biofuels, vaccines, clean water, food and other products. That work is ongoing at both JCVI and at his company, Synthetic Genomics Inc. (SGI). A project at SGI for instance, aims to engineer algae cells to capture carbon dioxide and use it as a raw material for producing new fuels. Another group uses synthetic genomic advances with the goal of making influenza vaccines in hours rather than months to better respond to sudden mutations in those viruses.

Venter also described his work in sequencing the first draft human genome in 2001 while he and his team were at Celera Genomics, as well as the work on his complete diploid genome published in 2007 by scientists at JCVI, along with collaborators at The Hospital for Sick Children in Toronto and the University of California, San Diego. In addition to continued analysis of Venter's genome, he and his team are also studying the human microbiome, the billions of bacteria that live in and on people, and how these microbes impact health and disease.

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J. Craig Venter, Ph.D., describes biofuels, vaccines and foods from made-to-order microbes

ScienceDaily (Mar. 25, 2012) A genetic finding could help explain why influenza becomes a life-threating disease to some people while it has only mild effects in others. New research led by the Wellcome Trust Sanger Institute has identified for the first time a human gene that influences how we respond to influenza infection.

People who carry a particular variant of a gene called IFITM3 are significantly more likely to be hospitalised when they fall ill with influenza than those who carry other variants, the team found. This gene plays a critical role in protecting the body against infection with influenza and a rare version of it appears to make people more susceptible to severe forms of the disease. The results are published in the journal Nature.

A central question about viruses is why some people suffer badly from an infection and others do not. IFITM3 is an important protein that protects cells against virus infection and is thought to play a critical role in the immune system's response against such viruses as H1N1 pandemic influenza, commonly known as 'swine flu'. When the protein is present in large quantities, the spread of the virus in lungs is hindered, but if the protein is defective or absent, the virus can spread more easily, causing severe disease.

"Although this protein is extremely important in limiting the spread of viruses in cells, little is known about how it works in lungs," explains Aaron Everitt, first author from the Wellcome Trust Sanger Institute. "Our research plays a fundamental part in explaining how both the gene and protein are linked to viral susceptibility."

The antiviral role of IFITM3 in humans was first suggested by studies using a genetic screen, which showed that the protein blocked the growth of influenza virus and dengue virus in cells. This led the team to ask whether IFITM3 protected mice from viral infections. They removed the IFITM3 gene in mice and found that once they contracted influenza, the symptoms became much more severe compared to mice with IFITM3. In effect, they found the loss of this single gene in mice can turn a mild case of influenza into a fatal infection.

The researchers then sequenced the IFITM3 genes of 53 patients hospitalised with influenza and found that some have a genetic mutant form of IFITM3, which is rare in normal people. This variant alters the IFITM3 gene and makes cells more susceptible to viral infection.

"Since IFITM3 appears to be a first line defender against infection, our efforts suggest that individuals and populations with less IFITM3 activity may be at increased risk during a pandemic and that IFITM3 could be vital for defending human populations against other viruses such as avian influenza virus and dengue virus" says Dr. Abraham Brass, co-senior author and Assistant Professor at the Ragon Institute of MGH, MIT and Harvard and the Gastrointestinal Unit of Massachusetts General Hospital.

This research was a collaboration between institutes in the United States and the United Kingdom. The samples for this study were obtained from the MOSAIC consortium in England and Scotland, co-ordinated from the Centre for Respiratory Infection (CRI) at Imperial College London, and the GenISIS consortium in Scotland at the Roslin Institute of University of Edinburgh. These were pivotal for the human genetics component of the work.

"Collectively, these data reveal that the action of a single antiviral protein, IFITM3, can profoundly alter the course of the flu and potentially other viruses in both human and mouse," explains Professor Paul Kellam, co-senior author from the Wellcome Trust Sanger Institute. "To fully understand how both the protein and gene control our susceptibility to viral infections, we need to study the mechanisms of the gene variant more closely.

"Our research is important for people who have this variant as we predict their immune defences could be weakened to some virus infections. Ultimately as we learn more about the genetics of susceptibility to viruses, then people can take informed precautions, such as vaccination to prevent infection."

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Genetics of flu susceptibility: Why the flu is life-threatening for some, and quite mild for others

Public release date: 25-Mar-2012 [ | E-mail | Share ]

Contact: Aileen Sheehy as22@sanger.ac.uk 44-122-349-2368 Wellcome Trust Sanger Institute

A genetic finding could help explain why influenza becomes a life-threating disease to some people while it has only mild effects in others. New research led by the Wellcome Trust Sanger Institute has identified for the first time a human gene that influences how we respond to influenza infection.

People who carry a particular variant of a gene called IFITM3 are significantly more likely to be hospitalised when they fall ill with influenza than those who carry other variants, the team found. This gene plays a critical role in protecting the body against infection with influenza and a rare version of it appears to make people more susceptible to severe forms of the disease. The results are published in the journal Nature.

A central question about viruses is why some people suffer badly from an infection and others do not. IFITM3 is an important protein that protects cells against virus infection and is thought to play a critical role in the immune system's response against such viruses as H1N1 pandemic influenza, commonly known as 'swine flu'. When the protein is present in large quantities, the spread of the virus in lungs is hindered, but if the protein is defective or absent, the virus can spread more easily, causing severe disease.

"Although this protein is extremely important in limiting the spread of viruses in cells, little is known about how it works in lungs," explains Aaron Everitt, first author from the Wellcome Trust Sanger Institute. "Our research plays a fundamental part in explaining how both the gene and protein are linked to viral susceptibility."

The antiviral role of IFITM3 in humans was first suggested by studies using a genetic screen, which showed that the protein blocked the growth of influenza virus and dengue virus in cells. This led the team to ask whether IFITM3 protected mice from viral infections. They removed the IFITM3 gene in mice and found that once they contracted influenza, the symptoms became much more severe compared to mice with IFITM3. In effect, they found the loss of this single gene in mice can turn a mild case of influenza into a fatal infection.

The researchers then sequenced the IFITM3 genes of 53 patients hospitalised with influenza and found that some have a genetic mutant form of IFITM3, which is rare in normal people. This variant gene encodes a shortened version of the protein which makes cells more susceptible to viral infection.

"Since IFITM3 appears to be a first line defender against infection, our efforts suggest that individuals and populations with less IFITM3 activity may be at increased risk during a pandemic and that IFITM3 could be vital for defending human populations against other viruses such as avian influenza virus and dengue virus" says Dr. Abraham Brass, co-senior author and Assistant Professor at the Ragon Institute and Gastrointestinal Unit of Massachusetts General Hospital.

This research was a collaboration between institutes in the United States and the United Kingdom. The samples for this study were obtained from the MOSAIC consortium in England and Scotland, co-ordinated from the Centre for Respiratory Infection (CRI) at Imperial College London, and the GenISIS consortium in Scotland at the Roslin Institute of the University of Edinburgh. These were pivotal for the human genetics component of the work.

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Genetics of flu susceptibility

Published on Mar 25, 2012

CHICAGO (AFP) - Patients with advanced heart disease who received an experimental stem cell therapy showed slight improvements in blood pumping but no change in most of their symptoms, United States researchers said on Saturday.

Study authors described the trial as the largest to date to examine stem cell therapy as a route to repairing the heart in patients with chronic ischemic heart disease and left ventricular dysfunction.

Previous studies have established that the approach is safe in human patients, but none had examined how well it worked on a variety of heart ailments.

The clinical trial involved 92 patients, with an average age of 63, who were picked at random to get either a placebo or a series of injections of their own stem cells, taken from their bone marrow, into damaged areas of their hearts.

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Stem cell therapy could repair some heart damage: Study

SATURDAY, March 24 (HealthDay News) -- An innovative approach using patients' own bone marrow cells to treat chronic heart failure came up short in terms of effectiveness, researchers report.

Use of stem cell therapy to repair the slow, steady damage done to heart muscle and improve heart function is safe, but has not been shown to improve most measures of heart function, the study authors said.

"For the measures we paid most attention to, we saw no effect, there is no question about that," said researcher Dr. Lemuel Moye, a professor of biostatistics at the University of Texas School of Public Health in Houston.

"Ultimately, this is going to pay off handsomely for individuals and for public health in general, but it's going to take years of work," Moye said. "We are the vanguard looking for new promising lines of research."

While the hoped-for results didn't materialize, there appeared to be a small improvement in some patients, he said. "When we looked at another commonly used measure of heart function called ejection fraction, or the strength of the heart's pumping, that's where all the action was," Moye noted.

It's hard to know which measures of heart function to look at, Moye explained. "We have had some difficulty with that," he said.

Future research will look at other measures of heart function, pay more attention to the characteristics of the cells that are injected and determine which cells are best, he added.

Cardiac cells and other types of specially prepared cells are available now that were not accessible when this study started in 2009, Moye pointed out.

The results of the trial, which was sponsored by the U.S. National Heart, Lung, and Blood Institute, were to be presented Saturday at the American College of Cardiology's annual meeting in Chicago. The report was also published online March 24 in the Journal of the American Medical Association.

For the study, Moye and colleagues worked with 92 patients, average age 63 and mostly male, who had heart failure with and without chest pain. They were randomly assigned to receive either an injection of 100 million bone marrow cells from their own bone marrow, or an inactive placebo. Patients in both groups also received aggressive medical therapy.

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Stem-Cell Trial Failed to Treat Heart Failure

Public release date: 24-Mar-2012 [ | E-mail | Share ]

Contact: Kristin Wincek kwincek@mhif.org 612-863-0249 Minneapolis Heart Institute Foundation

CHICAGO Cell therapy may present an option for patients with ischemic heart disease to use their own bone marrow cells to repair the damaged areas of their hearts, and may pave the way for future treatment options, according to the FOCUS trial, which will be presented as a late-breaking clinical trial March 24 at the 61st annual American College of Cardiology (ACC) scientific session.

This is the largest study to date to look at stem cell therapy, using a patient's own stem cells, to repair damaged areas of the heart in patients with chronic ischemic heart disease and left ventricular dysfunction. Researchers found that left ventricular ejection fraction (the percentage of blood leaving the heart's main pumping chamber) increased by a small but significant amount (2.7 percent) in patients who received stem cell therapy. The study also revealed that the improvement in ejection fraction correlated with the number of progenitor cells (CD34+ and CD133+) in the bone marrow; and this information will help in evaluating and designing future therapies and trials.

"FOCUS is an incredibly important trial, as it has informed the cell therapy community how to better treat this high-risk patient population, and allows us to enter into an exciting, next generation of stem cell therapy armed with more data," said study investigator Timothy D. Henry, MD, an interventional cardiologist at the Minneapolis Heart Institute (MHI) at Abbott Northwestern Hospital in Minneapolis and director of research with the Minneapolis Heart Institute Foundation.

This multicenter study was conducted by the Cardiovascular Cell Therapy Research Network (CCTRN), which is supported through a research grant from the National Institutes of Health's National, Heart, Lung and Blood Institute (NHLBI), with the goal to evaluate novel stem cell-based treatment strategies for individuals with cardiovascular disease.

FOCUS will be presented at ACC.12 by its lead investigator Emerson C. Perin, MD, PhD, director of clinical research for cardiovascular medicine at the Texas Heart Institute, one of the five sites in the CCTRN. The Minneapolis Heart Institute is another site of the five in the network, and a large number of CCTRN patients were enrolled in Minnesota.

For this study, which took place between April 2009 and April 2011, the five sites randomly selected 92 patients to receive stem cell treatment or placebo. The symptomatic patients, with an average age 63, all had chronic ischemic heart disease and an ejection fraction of less than 45 percent (baseline 34 percent) along with heart failure and/or angina and were no longer candidates for revascularization. "These patients had no other options, as medical management failed to improve their symptoms," explained the study's co-investigator Jay Traverse, MD, an interventionalist cardiologist at the Minneapolis Heart Institute at Abbott Northwestern Hospital and physician researcher with the Minneapolis Heart Institute Foundation.

Bone marrow was aspirated from the patients and processed to obtain just the mononuclear fraction of the marrow. In patients randomly selected to receive stem cell therapy, physicians inserted a catheter into the heart's left ventricle to inject 100 million stem cells in more than 15 sites that showed damage on the electromechanical mapping image of the heart.

"Studies such as these are able to be completed much faster because of the team approach of the network" said Sonia I. Skarlatos, PhD, NHBLI's deputy director of the division of cardiovascular sciences and program director of CCTRN.

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Cell therapy using patient's own bone marrow may present option for heart disease