Archive for the ‘Gene Therapy Research’ Category

MarketResearchReports.biz Publishes Stem Cell Therapy Market in Asia-Pacific to 2018 Commercialization Supported by Favorable Government Policies, Strong Pipeline and Increased Licensing Activity. Buy the copy of this Report @ http://www.marketresearchreports.biz/analysis-details/stem-cell-therapy-market-in-asia-pacific-to-2018-commercialization-supported-by-favorable-government-policies-strong-pipeline-and-increased-licensing-activity

Albany, NY (PRWEB) March 29, 2013

To Read the Complete Report with TOC Visit: http://www.marketresearchreports.biz/analysis/155690

This report is built using data and information sourced from proprietary databases, primary and secondary research and in-house analysis by GBI Researchs team of industry experts.

GBI Research analysis finds the stem cell therapy market was valued at $545m in 2012, and is projected to grow at a Compound Annual Growth Rate (CAGR) of 10% from 2012 to 2018, to attain a value of $972m in 2018. The market is poised for significant growth in the forecast period due to the anticipated launch of JCR Pharmaceuticals JR-031 (2014) in Japan and FCB Pharmicells Cerecellgram (CCG) (2015) in South Korea.

Related Report: Mobile Health (mHealth) - Enhancing Healthcare and Improving Clinical Outcomes

The research is mainly in early stages, with the majority of the molecules being in early stages of development (Phase I/II and Phase II). Phase I/II and Phase II contribute 67% of the pipeline. Stem cell research is dominated by hospitals/universities/institutions, which contribute 63% of the molecules in the pipeline. The dominance of institutional research is attributable to uncertain therapeutic outcomes in stem cell research.The major companies conducting research in India include Reliance Life Sciences and Stempeutics Research Pvt Ltd, among others. The major institutions include PGIMER and AIIMS.

Latest Report: Global SMB Web Analytics Market 2012-2016

Scope

Country analysis of regulatory framework of India, China, South-Korea, Japan and Singapore

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Stem Cell Therapy Market in Asia-Pacific to 2018 Market Research Report Available at MarketResearchReports.biz

WASHINGTON, March 29, 2013 /PRNewswire-USNewswire/ --The injection of antisense molecules into the space around the spinal cord of people with ALS is safe according to research published today. The first-in-human trial of this new therapy was funded by The ALS Association. The study was published today in the scientific journal Lancet Neurology.

ALS, also known as Lou Gehrig 's Disease, is a progressive neurodegenerative disease that affects nerve cells in the brain and the spinal cord. The disease robs people of the ability to walk, to talk and even blink an eye. It traps them inside a body they no longer can control and ultimately prevents them from breathing as it takes their life. There is no known cause of the disease, although military veterans are approximately twice as likely to develop ALS as the general population.

"This trial is a landmark in ALS therapy," said Lucie Bruijn , Ph.D., Chief Scientist of The ALS Association. "By demonstrating the safety and practicality of this approach, it lays the groundwork for exciting new forms of treatment of ALS."

The study was led by Timothy Miller , M.D., Ph.D., of Washington University in Saint Louis, Mo. It compared the safety of delivering a single dose of antisense therapy versus placebo to the fluid surrounding the spinal cord in 21 patients with ALS. Several different doses were tested, and several patients re-enrolled and thus received more than one dose. The frequency of adverse events was similar between the two groups. The most common adverse event was post-lumbar puncture syndrome (characterized by a headache that is relieved by lying flat), as would be expected from the procedure. The study was not designed to test whether the antisense therapy had any effect on the disease, which would likely only emerge with longer-term treatment.

Antisense therapy targets a cellular messenger molecule, called messenger RNA, used to build proteins within cells. In this trial, the target was the messenger RNA for the protein Cu/Zn Superoxide Dismutase (SOD1). Mutations in the SOD1 gene account for about 20 percent of all familial, or inherited, ALS. The sequence of building blocks that make up the messenger RNA (the "sense" sequence) is used to design a complementary "antisense" molecule that will bind to it. That binding triggers the cell to destroy the messenger RNA, preventing the harmful SOD1 protein from being made. Results from SOD1-based animal models of ALS have indicated that reducing the level of SOD1 by antisense therapy increases lifespan.

The ALS Association's Translational Research Advancing Therapies for ALS (TREAT ALS) program provided funding at each stage of development for this therapy, beginning with establishing the proof of concept in pre-clinical work. That work was led by Don Cleveland , Ph.D., and Richard Smith , M.D., both of the University of California at San Diego, along with Dr. Miller, Dr. Cleveland's lab, and Frank Bennett , Ph.D., of Isis Pharmaceuticals, developer of the antisense molecules used in the research program. Merit Cudkowicz, M.D., of Massachusetts General Hospital, was co-investigator of the clinical trial.

This first-in-human trial of an antisense therapy for a neurodegenerative disease is the culmination of years of work by scores of people from academia and biotechnology, working in partnership to stop ALS," Dr. Bruijn said. "We still have much work to do before we know whether antisense therapy can offer benefit to patients with SOD1 mutations, but the evident safety of the procedure is very encouraging and should allow larger and longer trials in the near future that can tell us more about the potential of this form of treatment."

The ALS Association is grateful to have received funding to support this new groundbreaking research from the following:

The Kanter Family ALS Research Fund and The ALS Association Greater Philadelphia Chapter The Jeff Kaufman Fund and The ALS Association Wisconsin Chapter The Wallace Genetic Foundation and Mrs. Jean Wallace Douglas The George Yardley Company, the family of George Yardley , and The ALS Association Orange County Chapter Contributors to the Lou Gehrig Challenge campaign of The ALS Association

About The ALS AssociationThe ALS Association is the only national non-profit organization fighting Lou Gehrig 's Disease on every front. By leading the way in global research, providing assistance for people with ALS through a nationwide network of chapters, coordinating multidisciplinary care through certified clinical care centers, and fostering government partnerships, The Association builds hope and enhances quality of life while aggressively searching for new treatments and a cure. For more information about The ALS Association, visit our website at http://www.alsa.org.

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Therapy Funded by The ALS Association Involving Injection of Antisense Molecules Into Spinal Cord Area of People with ...

A huge international effort involving more than 100 institutions and genetic tests on 200,000 people has uncovered dozens of signposts in DNA that can help reveal further a person's risk for breast, ovarian or prostate cancer, scientists reported Wednesday.

It's the latest mega-collaboration to learn more about the intricate mechanisms that lead to cancer. And while the headway seems significant in many ways, the potential payoff for ordinary people is mostly this: Someday there may be genetic tests that help identify women with the most to gain from mammograms, and men who could benefit most from PSA tests and prostate biopsies.

And perhaps farther in the future these genetic clues might lead to new treatments.

"This adds another piece to the puzzle," said Harpal Kumar, chief executive of Cancer Research U.K., the charity which funded much of the research.

One analysis suggests that among men whose family history gives them roughly a 20 percent lifetime risk for prostate cancer, such genetic markers could identify those whose real risk is 60 percent.

The markers also could make a difference for women with BRCA gene mutations, which puts them at high risk for breast cancer. Researchers may be able to separate those whose lifetime risk exceeds 80 percent from women whose risk is about 20 to 50 percent. One doctor said that might mean some women would choose to monitor for cancer rather than taking the drastic step of having healthy breasts removed.

AP

Scientists have found risk markers for the three diseases before, but the new trove doubles the known list, said one author, Douglas Easton of Cambridge University. The discoveries also reveal clues about the biological underpinnings of these cancers, which may pay off someday in better therapies, he said.

Experts not connected with the work said it was encouraging but that more research is needed to see how useful it would be for guiding patient care. One suggested that using a gene test along with PSA testing and other factors might help determine which men have enough risk of a life-threatening prostate cancer that they should get a biopsy. Many prostate cancers found early are slow-growing and won't be fatal, but there is no way to differentiate and many men have surgery they may not need.

Easton said the prospects for a genetic test are greater for prostate and breast cancer than ovarian cancer.

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New Gene Markers Reveal Cancer Risk

Public release date: 28-Mar-2013 [ | E-mail | Share ]

Contact: Jim Fessenden james.fessenden@umassmed.edu 508-856-2000 University of Massachusetts Medical School

WORCESTER, MA Sometimes you just can't resist a tiny piece of chocolate cake. Even the most health-conscious eaters find themselves indulging in junk foods from time to time. New research by scientists at the University of Massachusetts Medical School (UMMS) raises the striking possibility that even small amounts of these occasional indulgences may produce significant changes in gene expression that could negatively impact physiology and health.

A pair of papers published in Cell by A.J. Marian Walhout, PhD, co-director of the Program in Systems Biology and professor of molecular medicine at UMMS, describe how metabolism and physiology are connected to diet. Using C. elegans, a transparent roundworm often used as a model organism in genetic studies, Dr. Walhout and colleagues observed how different diets produce differences in gene expression in the worm that can then be linked to crucial physiological changes.

"In short, we found that when C. elegans are fed diets of different types of bacteria, they respond by dramatically changing their gene expression program, leading to important changes in physiology," said Walhout. "Worms fed a natural diet of Comamonas bacteria have fewer offspring, live shorter and develop faster compared to worms fed the standard laboratory diet of E. coli bacteria."

Walhout and colleagues identified at least 87 changes in C. elegans gene expression between the two diets. Surprisingly, these changes were independent of the TOR and insulin signaling pathways, gene expression programs typically active in nutritional control. Instead, the changes occur, at least in part, in a regulator that controls molting, a gene program that determines development and growth in the worm. This connection provided one of the critical links between diet, gene expression and physiology detailed in "Diet-induced Development Acceleration Independent of TOR and Insulin in C. elegans." "Importantly, these same regulators that are influenced by diet in the worms control circadian rhythm in humans," said Lesley MacNeil, PhD, a postdoctoral student in the Walhout Lab and first author on the paper. "We already know that circadian rhythms are affected by diet. This points to the real possibility that we can now use C. elegans to study the complex connections between diet, gene expression and physiology and their relation to human disease."

Strikingly, Walhout and colleagues observed that even when fed a small amount of the Comamonas bacteria in a diet otherwise comprised of E. coli bacteria, C. elegans exhibited dramatic changes in gene expression and physiology. These results provide the tantalizing possibility that different diets are not "healthy" or "unhealthy" but that specific quantities of certain foods may be optimal under different conditions and for promoting different physiological outcomes.

"It's just as true that a small amount of a 'healthy' food in an otherwise unhealthy diet could elicit a beneficial change in gene expression that could have profound physiological effects," said Walhout.

Additional research by the Walhout Lab further explored the possibility of using C. elegans as a model system to answer complex questions about disease and dietary treatment in humans. Detailed in the "Integration of Metabolic and Gene Regulatory Networks Modulates the C. elegans Dietary Response," Walhout and colleagues found that disrupting gene expression involved with C. elegans metabolism lead to metabolic imbalances that interfered with the animal's dietary response; a result that may have a direct correlation to the treatment of a class of human genetic diseases.

"To better understand the molecular mechanisms by which diet effects gene expression in the worm, we performed complimentary genetic screens looking for genes that gave an abnormal response to diet," said Emma Watson, a doctoral student in the Walhout Lab and co-first author on the second Cell study together with Dr. MacNeil. "What we discovered was a large network of metabolic and regulator genes that can integrate internal cellular nutritional needs and imbalances with external availability," said Watson. "This information is then communicated to information processing genes in the worm to illicit the appropriate response in the animal."

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UMMS scientists tie dietary influences to changes in gene expression and physiology

Public release date: 28-Mar-2013 [ | E-mail | Share ]

Contact: Patricia Bailey pjbailey@ucdavis.edu 530-752-9843 University of California - Davis

A team of researchers, led by a University of California, Davis, plant scientist, has identified a lettuce gene and related enzyme that put the brakes on germination during hot weather a discovery that could lead to lettuces that can sprout year-round, even at high temperatures.

The study also included researchers from Arcadia Biosciences and Acharya N.G. Ranga Agricultural University, India.

The finding is particularly important to the nearly $2 billion lettuce industries of California and Arizona, which together produce more than 90 percent of the nation's lettuce. The study results appear online in the journal The Plant Cell.

"Discovery of the genes will enable plant breeders to develop lettuce varieties that can better germinate and grow to maturity under high temperatures," said the study's lead author Kent Bradford, a professor of plant sciences and director of the UC Davis Seed Biotechnology Center.

"And because this mechanism that inhibits hot-weather germination in lettuce seeds appears to be quite common in many plant species, we suspect that other crops also could be modified to improve their germination," he said. "This could be increasingly important as global temperatures are predicted to rise."

Most lettuce varieties flower in spring or early summer and then drop their seeds a trait that is likely linked to their origin in the Mediterranean region, which, like California, characteristically has dry summers. Scientists have observed for years that a built-in dormancy mechanism seems to prevent lettuce seeds from germinating under conditions that would be too hot and dry to sustain growth. While this naturally occurring inhibition works well in the wild, it is an obstacle to commercial lettuce production.

In the California and Arizona lettuce industries, lettuce seeds are planted somewhere every day of the year even in September in the Imperial Valley of California and near Yuma, Ariz., where fall temperatures frequently reach 110 degrees.

In order to jump-start seed germination for a winter crop in these hot climates, lettuce growers have turned to cooling the soil with sprinkler irrigation or priming the seeds to germinate by pre-soaking them at cool temperatures and re-drying them before planting methods that are expensive and not always successful.

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Gene discovery may yield lettuce that will sprout in hot weather

Is China Engineering Smarter Babies?

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Is China Engineering Smarter Babies? - Video

Genetic logic gates will enable biologists to program cells for chemical production and disease detection.

If biologists could put computational controls inside living cells, they could program them to sense and report on the presence of cancer, create drugs on site as theyre needed, or dynamically adjust their activities in fermentation tanks used to make drugs and other chemicals. Now researchers at Stanford University have developed a way to make genetic parts that can perform the logic calculations that might someday control such activities.

The Stanford researchers genetic logic gate can be used to perform the full complement of digital logic tasks, and it can store information, too. It works by making changes to the cells genome, creating a kind of transcript of the cells activities that can be read out later with a DNA sequencer. The researchers call their invention a transcriptor for its resemblance to the transistor in electronics. We want to make tools to put computers inside any living cella little bit of data storage, a way to communicate, and logic, says Drew Endy, the bioengineering professor at Stanford who led the work.

Timothy Lu, who leads the Synthetic Biology Group at MIT, is working on similar cellular logic tools. You cant deliver a silicon chip into cells inside the body, so you have to build circuits out of DNA and proteins, Lu says. The goal is not to replace computers, but to open up biological applications that conventional computing simply cannot address.

Biologists can give cells new functions through traditional genetic engineering, but Endy, Lu, and others working in the field of synthetic biology want to make modular parts that can be combined to build complex systems from the ground up. The cellular logic gates, Endy hopes, will be one key tool to enable this kind of engineering.

Cells genetically programmed with a biological AND gate might, for instance, be used to detect and treat cancer, says Endy. If protein A and protein B are presentwhere those proteins are characteristic of, say, breast cancerthen this could trigger the cell to produce protein C, a drug.

In the cancer example, says Endy, youd want the cell to respond to low levels of cancer markers (the signal) by producing a large amount of the drug. The case is the same for biological cells designed to detect pollutants in the water supplyideally, theyd generate a very large signal (for example, quantities of bright fluorescent proteins) when they detect a small amount of a pollutant.

The transcriptor triggers the production of enzymes that cause alterations in the cells genome. When the production of those enzymes is triggered by the signala protein of interest, for examplethese enzymes will delete or invert a particular stretch of DNA in the genome. Researchers can code the transcriptor to respond to one, or multiple, different such signals. The signal can be amplified because one change in the cells DNA can lead the cell to produce a large amount of the output protein over time.

Depending on how the transcriptor is designed, it can act as a different kind of logic gatean AND gate that turns on only in the presence of two proteins, an OR gate thats turned on by one signal or another, and so on. Endy says these gates could be combined into more complex circuits by making the output of one the input for the next. This work is described today in the journal Science.

MITs Lu says cellular circuits like his and Endys, which use enzymes to alter DNA, are admittedly slow. From input to output, it can take a few hours for a cell to respond and change its activity. Other researchers have made faster cellular logic systems that use other kinds of biomoleculesregulatory proteins or RNA, for example. But Lu says these faster systems lack signal amplification and memory. Future cellular circuits are likely to use some combination of different types of gates, Lu says.

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How to Make a Computer from a Living Cell

When Charles Babbage prototyped the first computing machine in the 19th century, he imagined using mechanical gears and latches to control information. ENIAC, the first modern computer developed in the 1940s, used vacuum tubes and electricity. Today, computers use transistors made from highly engineered semiconducting materials to carry out their logical operations.

And now a team of Stanford University bioengineers has taken computing beyond mechanics and electronics into the living realm of biology. In a paper to be published March 28 in Science, the team details a biological transistor made from genetic materialDNA and RNAin place of gears or electrons. The team calls its biological transistor the "transcriptor."

"Transcriptors are the key component behind amplifying genetic logicakin to the transistor and electronics," said Jerome Bonnet, PhD, a postdoctoral scholar in bioengineering and the paper's lead author.

The creation of the transcriptor allows engineers to compute inside living cells to record, for instance, when cells have been exposed to certain external stimuli or environmental factors, or even to turn on and off cell reproduction as needed.

"Biological computers can be used to study and reprogram living systems, monitor environments and improve cellular therapeutics," said Drew Endy, PhD, assistant professor of bioengineering and the paper's senior author.

The biological computer

In electronics, a transistor controls the flow of electrons along a circuit. Similarly, in biologics, a transcriptor controls the flow of a specific protein, RNA polymerase, as it travels along a strand of DNA.

"We have repurposed a group of natural proteins, called integrases, to realize digital control over the flow of RNA polymerase along DNA, which in turn allowed us to engineer amplifying genetic logic," said Endy.

Using transcriptors, the team has created what are known in electrical engineering as logic gates that can derive true-false answers to virtually any biochemical question that might be posed within a cell.

They refer to their transcriptor-based logic gates as "Boolean Integrase Logic," or "BIL gates" for short.

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Cellular computers: ' Genetic circuit' biological transistor enables computing within living cells

What is being hailed as major news in the genetic science community this week -- the identification of more than 80 genomes that raise a person's risk of different cancers -- may receive a lukewarm reception from the general public until the ramifications of such discoveries is evident.

Collaborative Oncological Gene-Environment Study, COGS

Learning the causes of cancer can only mean positive things in the development of screening, treatment, and perhaps, one day, prevention of those cancers. A consortium of more than 160 EU-based research groups working together in the Collaborative Oncological Gene-Environment Study, COGS, brought science and medicine one step closer to these positive outcomes with the discovery of more than 80 genome regions that can increase an individual's risk for prostate, breast and ovarian cancers, reported MedicalNewsToday.com .

The COGS research was submitted as 13 different scientific papers and published in five journals this week, including PLOS Genetics . (PLOS is the Public Library of Science , a non-profit and open access

group of scientific journals.)

COGS Research Team Members Weigh in on Genome Discovery Value

Professor Ros Eeles of the Royal Marsden and the Institute of Cancer Research explained to the Telegraph that this discovery is hoped to leading to simple saliva testing for these risk factors that primary care physicians will be able to interpret within the next five years.

The researchers caution that although the discovery of these genomes is important, there is more work to be done, first in research, then in application of the findings.

Understanding the Genetic Science Hoopla Over New Genome Discoveries

To the layman, the science behind genetic discovery and its uses is mystifying until the scientific terms and methods are broken down into concepts that are readily understandable: The discovery of these genomes associated with increased cancer risks in individuals may lead to simplified genetic testing for those risks within the next five years and potentially new therapies to thwart those cancers.

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Researchers Identify 'Haul' of New Genetic Markers for Cancer Risks

Jose Luis Pelaez / Getty Images

Almost every toddler will sniffle through a cold by the time they are three, but if they wheeze while theyre sick, they may be at higher risk of developing asthma.

Previous research found that wheezing-related illnesses can increase a childs risk for developing asthma, and other studies connected certain genetic factors to this heightened tendency to wheeze. In a new study published in the New England Journal of Medicine, researchers connected the two and found that 90% of three-year-olds with a combination of specific genes and a particular wheezing illness were diagnosed with asthma by the age of 6.

The scientists focused on a region of chromosome 17, known as 17q21 that has been associated with an elevated risk of asthma early in life. Two genes in the region likely increase this risk ORMDL3 and GSDMB. Variants of these genes, which are relatively common, seemed to confer higher risk of wheezing when children were infected with the rhinovirus, which is responsible for the common cold. About half of the infants in the study had one copy of the variant, while a quarter had both copies, which significantly increased their likelihood of wheezing and developing asthma.

(MORE: Fast Food Linked to Asthma and Allergies in Kids)

The researchers included children from two separate study groups, all of whom came from families with a history of allergies or asthma. The first group included 200 children toddlers with at least one, and possibly two parents who had allergies or asthma while the second group consisted of Danish toddlers whose mothers were diagnosed with asthma. Among children without the high-risk genetic variants for asthma, 40% who wheezed when they caught a cold before age three developed asthma by age six, compared to 60% who had one copy of the variant and wheezed, and 90% of those who had two copies and also wheezed.

We found that the interaction between this specific wheezing illness and a gene or genes on a region of chromosome 17 determines childhood asthma risk. The combination of genetic predisposition and the childs response to this infection has a huge effect,said study author Carole Ober, a Blum-Riese Professor of Human Genetics at the University of Chicago in a statement.

Overall, the children with the genetic and wheezing illness combination were almost four times as likely to develop asthma compared to kids who did not have the genetic variation or did not wheeze, suggesting that wheezing might be a relatively easy marker for identifying toddlers who might be at highest risk of developing asthma later.

(MORE: BPA Exposure Linked To Asthma In Kids)

The biological mechanisms underlying the connection are not well understood, but to get a better idea of whats going on, the researchers collected blood from 100 healthy adults and exposed their immune cells to human rhinovirus. Infection with the cold virus seemed to make the asthma-related genes on chromosome 17 more active, possibly leading to more wheezing.

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Genetic Variants and Wheezing Put Kids At Risk For Asthma

Avis Gibons, a licensed and board-certified genetic counselor joins Northwest Community Healthcare's genetic counseling program.

Arlington Heights, IL (PRWEB) March 28, 2013

Avis Gibons, MS, CGC, a licensed and board-certified genetic counselor with experience in both clinical and research settings, is now serving patients whose personal or family medical histories indicate an increased risk of developing cancer. In her role, Gibons meets with patients to review personal and family medical histories, assesses patients risks of developing cancer, coordinates genetic testing and discusses results, and presents cancer screening and risk reduction options.

We are thrilled that Avis has joined NCHs genetic counseling team, Keith Ammons, director of cancer services at NCH, says. Her previous experience will be an asset to the genetic counseling team.

Before joining NCH, Gibons served as genetic counselor at John H. Stroger, Jr. Hospital in Chicago, where she assisted in establishing a formal high-risk cancer genetics clinic. Dedicated to raising awareness about genetic contributions to disease, she also has designed human genetics course curriculum for clinical research professionals, presented seminars in genetics to community members, and delivered continuing medical education in cancer risk assessment and hereditary cancer syndromes to healthcare providers. Gibons has completed a certificate in clinical cancer genetics from City of Hope, a National Cancer Institute-designated comprehensive cancer center and a founding member of the National Comprehensive Cancer Network.

Gibons is an adjunct faculty member in the Division of Science and Health Careers at Oakton Community College, where she prepares students for careers in medicine and health sciences. Her research on the impact of genetic medicine on the employer-based healthcare system and on coverage and reimbursement of genetic tests and services has been cited in a report to the U.S. Department of Health and Human Services. Gibons says that the multidisciplinary Commission on Cancer, established by the American College of Surgeons, considers genetic counseling a standard of service necessary to ensure quality and comprehensive cancer care delivery. By helping to identify patients at increased risk of developing cancer, genetic counseling can have dramatic effects on early detection and cancer outcome. In addition, genetic counseling empowers patients to make informed decisions about cancer screening, cancer prevention and genetic testing.

The NCH Genetic Counseling Team has more than 20 years of experience providing genetic counseling, including review of medical history, assessment of cancer risk, and consideration of early detection and risk reduction options.

About Northwest Community Healthcare (NCH)

Serving Chicagos northwest suburbs since 1959, NCH is a comprehensive, patient-centered system of care that serves more than 350,000 outpatients each year, as well as nearly 30,000 inpatients treated annually at the 496-bed acute care hospital in Arlington Heights. The award-winning hospital holds the prestigious Magnet designation for nursing excellence, is designated as a Primary Stroke Center, earned the Joint Commission's Gold Seal of Approval in 2011, and was awarded the Leapfrog Groups designation as one of the nations Top Hospitals based on quality and safety criteria. NCH has four Immediate Care locations in the northwest suburbs and operates a FastCare Clinic in Palatine. NCH has a medical staff of more than 1,000 physicians, which includes the board-certified primary care doctors and specialists of the NCH Medical Group. For more information or to find a doctor on the NCH Medical staff, visit http://www.nch.org.

Patrick Reilly Northwest Community Healthcare 847.618.5529 Email Information

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NCH Adds Genetic Counselor

By Barbara Bronson Gray HealthDay Reporter

WEDNESDAY, March 27 (HealthDay News) -- Critical clues to understanding who is at the greatest risk for particular types of cancer may be found in "spelling mistakes" contained in a person's DNA.

In a step toward personalized medicine and the ability to better understand individual risk factors for three common hormone-related cancers, a large team of international researchers have unveiled what might be the clearest picture to date of the genetic alterations associated with some forms of the disease.

Although more research is needed, the study authors predict that genetic testing to help determine a person's risk for some of the most potentially deadly cancers may be available within five to 10 years.

"We think the most immediately practical application will be in people already at risk for the disease and going through the genetic counseling process," said Douglas Easton, a professor of genetic epidemiology at the University of Cambridge, in England.

A combination of five studies that include work from 160 different research groups has identified more than 80 genetic errors that are linked to increased risk of breast, prostate and ovarian cancers. The research was published March 27 in the journal Nature Genetics.

More than 2.5 million people worldwide are diagnosed with these three types of cancers each year, according to the researchers.

Everyone has some of the so-called spelling mistakes, often called "snips" (single nucleotide polymorphisms, or SNPs), the researchers said. Problems are signaled by errors in the sequence of genetic elements (bases), where letters representing the elements -- A, G, C and T -- are incorrectly placed.

The sequence of bases in a portion of a DNA molecule, called a gene, carries the instructions that are needed to create a protein. Although some errors affect small things, others may be responsible for increasing vulnerability to certain forms of cancer. The impact on a person depends on where on the strand of DNA the genetic alteration is located.

The studies from the European-based consortium -- collectively known as the Collaborative Oncological Gene-Environment Study, or COGS -- compared 100,000 patients with breast, ovarian or prostate cancer to 100,000 healthy people.

Link:
More Genetic Insights Into 3 Types of Cancer

Every Woody Allen Stammer From Every Woody Allen Movie | HuffPost Mashup
Subscribe to the HuffPost Today: http://goo.gl/xW6HG Watch More HuffPost Originals Here: http://goo.gl/zZlXH The complete collection of Woody Allen stammers ...

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Haptography: Digitizing our sense of touch - Katherine Kuchenbecker
View full lesson: http://ed.ted.com/lessons/haptography-digitizing-our-sense-of-touch-katherine-kuchenbecker View on TED.com: Katherine Kuchenbecker: The tec...

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Basics Fun with Mazzel
Mazzel and I have fun with the basics. These are very basic exercises, but are a lot of fun as we quickly switch between them. Music: Owl City - Deer in the ...

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Top 5 WORST Homophobic Quotes from Justice Scalia
"Justice Antonin Scalia has written that "it is our moral heritage that one should not hate any human being or class of human beings." Judging by the things ...

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Top 5 WORST Homophobic Quotes from Justice Scalia - Video

Magnify Your Strengths to Become Your Best
Sign up Grow Stronger Newsletter: http://hulsestrength.com/go/youtube Elliott #39;s Other Channel: http://www.youtube.com/user/elliottsaidwhat Elliott #39;s Facebook...

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Elliott in Yoga class (iphone video)
YOGA FOR STRENGTH http://www.hulsestrength.com/recommends/yoke Sign up Grow Stronger Newsletter: http://hulsestrength.com/go/youtube Elliott #39;s Other Channel:...

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Want to be happier? Stay in the moment - Matt Killingsworth
View full lesson: http://ed.ted.com/lessons/want-to-be-happier-stay-in-the-moment-matt-killingsworth When are humans most happy? To gather data on this quest...

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Public release date: 28-Mar-2013 [ | E-mail | Share ]

Contact: Kathy Ridgely Beal kbeal@acmg.net 301-238-4582 American College of Medical Genetics

Caleb P. Bupp MD was honored as the 2013 recipient of the ACMG Foundation/Signature Genomics from PerkinElmer, Inc. Travel Award at the American College of Medical Genetics and Genomics (ACMG) 2013 Annual Clinical Genetics Meeting in Phoenix, AZ.

Dr. Bupp was selected to receive the award for his platform presentation, "Twenty years of neural tube defect surveillance and prevention in South Carolina."

Dr. Bupp completed his MD degree at the University of Toledo College of Medicine. He completed his residency in Pediatrics at the University of Louisville and is currently completing his Medical Genetics Residency at the Greenwood Genetics Center.. Dr. Bupp received his Bachelor of Science in Molecular Biology and graduated Magna Cum Laude from Grove City College. He is currently a Medical Consultant for the U.S. Department of Justice.

The ACMG Foundation/Signature Genomics Travel Award is given to a trainee ACMG member whose abstract submission was chosen as a platform presentation during the ACMG Annual Clinical Genetics Meeting. The ACMG program committee selects the Travel Award recipient based on scientific merit. In recognition of the selected presentation, Signature Genomics covers the travel costs for the recipient to the ACMG meeting.

"The Foundation for Genetic and Genomic Medicine is grateful to Signature Genomics' for its continued generous support of the development of medical genetic researchers through this Travel Award," said Bruce R. Korf, MD, PhD FACMG, president of the ACMG Foundation for Genetic and Genomic Medicine.

"Signature Genomics is pleased to support the recognition of young researchers like Dr. Bupp who are working in the field of medical genetics and genomics. This presentation is just one of the many outstanding presentations at this year's ACMG meeting," said Beth Torchia, PhD, FACMG, Technical Laboratory Director at Signature Genomics.

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About the ACMG and ACMG Foundation

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2013 ACMG Foundation/Signature Genomic, PerkinElmer Inc., Travel Award Winner announced

Individuals who pick up smoking as teenagers have a much higher risk of becoming heavy smokers as adults. And for some, the risk is even greater depending on their genetics.

A team of researchers from the United States, the U.K. and New Zealand utilized previous research on genetics and smoking to develop a genetic risk profile for individuals who eventually become heavy smokers.

The research revealed individuals with a high-genetic risk for smoking were much more likely to become heavy smokers as adults, but only if they had tried cigarettes as teenagers. Those who were determined to have low-genetic risk were much less likely to progress into heavy smoking, even if they had tried cigarettes when they were younger.

Smoking behavior is a major public health problem, which develops relatively early in life, lead author Dan Belsky, a post-doctoral research fellow at Duke Universitys Center for the Study of Aging and Human Development, told FoxNews.com. We know from studies in families that genetics makes a difference in who becomes hooked on cigarettes and who doesnt. Relatives who share more genes are more similar in their smoking behavior.

- Dan Belsky, lead author for the study

Belsky noted their research was based on large genome-wide association studies (GWAS) from 2010 on smoking behavior, in which scientists looked across entire genomes to identify variants linked with heavy smoking. Those studies identified variants in single nucleotide polymorphisms located in and around two groups of genes the nicotine receptor genes, which control how the brain responds to nicotine, and the CYP2A6 region, which is responsible for nicotine metabolism in the liver.

What the studies did not show was when these genetic risks first manifest. Belsky and his team also wanted to know if early manifestation of these genetic risk factors were critical to the genetic influence on adult smoking problems.

To better understand how these genetic variations influence behavior, the scientists followed 1,000 New Zealanders from birth to the age of 38, analyzing their smoking habits in relation to their known genetic risk. Utilizing the genetic risk score developed to predict heavy smoking among individuals, the researchers cross analyzed an individuals risk score with their smoking habits throughout the course of the lives.

Pack-a-day by 18

Ultimately, the results showed that genetic risk was best at predicting whether or not a teenager who tried cigarettes grew to become a heavy smoker.

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Genetics may determine who becomes a heavy smoker

Public release date: 28-Mar-2013 [ | E-mail | Share ]

Contact: Kathy Beal kbeal@acmg.net 301-238-4582 American College of Medical Genetics

Lindsay C. Burrage, MD, PhD of Baylor College of Medicine/Texas Children's Hospital and Shane C. Quinonez, MD of The University of Michigan were honored as the 2013-2014 recipients of the Genzyme/ACMG Foundation Medical Genetics Training Award in Clinical Biochemical Genetics at the ACMG 2013 Annual Clinical Genetics Meeting in Phoenix, AZ.

The objective of the two Genzyme/ACMG Foundation Awards is to support a national training program to encourage the recruitment and training of clinicians in the field of clinical biochemical genetics and especially in the diagnosis, management and treatment of individuals with metabolic diseases. Two awardees will be given the opportunity to participate in an in-depth clinical experience at a premier medical center with expertise and significant clinical volume in the area of biochemical genetics.

The Award grants $75,000 per year to each of two recipients selected by the ACMG Foundation through a competitive process and will provide for the sponsorship of one year of the trainees' clinical genetics subspecialty in biochemical genetics following residency.

Dr. Burrage is currently in the second year of residency in Medical Genetics at Baylor College of Medicine. She said, "The Medical Biochemical Genetics Fellowship at Baylor will provide an environment where I can obtain both clinical and research training in inborn errors of metabolism. This training will prepare me for an academic career in biochemical genetics, where I can continue to pursue my research interests focusing on metabolic disorders." Dr. Burrage completed her M.D. and Ph.D. at Case Western Reserve University School of Medicine in Cleveland, OH and a Pediatrics Residency at Rainbow Babies and Children's Hospital, Cleveland, OH. Her research during the Award period will involve a randomized clinical trial to evaluate the utility of sodium phenylbutyrate as a therapeutic agent in Maple Syrup Urine Disease.

The second award recipient, Dr. Quinonez, received his M.D from the University of Michigan, completed his residency in Pediatrics at the University of Michigan, and began his residency in Medical Genetics in 2011. His research focuses on Cystinosis and the potential correction of cystine storage via microvesicles. He will continue his training as part of the Clinical Biochemical Genetics Program.

"I am extremely honored to be one of the recipients of the Genzyme/ACMG Foundation award. It is my hope that the opportunities, both research and clinical, afforded to me as a result of this award will allow me to provide the best possible clinical care to the patients I manage in the future."

"The Genzyme/ACMG Foundation Clinical Genetics Award in Clinical Biochemical Genetics is critical to the development of the genetics workforce. Biochemical genetics is undergoing particular rapid change, as new insights into disease mechanisms are leading to new methods of treatment," said Bruce R. Korf, MD, PhD, FACMG, president of the ACMG Foundation.

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2013-14 Genzyme/ACMG Foundation Training Award in Clinical Biochemical Genetics announced

SEATTLE, WA--(Marketwire - Mar 28, 2013) - Atossa Genetics, Inc. (NASDAQ: ATOS), a healthcare company focused on the prevention of breast cancer, has entered into a $30 million stock purchase agreement with Aspire Capital, LLC. Under terms of the agreement, Aspire has made an initial purchase of $1 million of Atossa common stock at a price of $12.00 per share. In addition, after the SEC declares the registration statement related to the transaction effective, Aspire has committed to purchase up to an additional $29 million of Atossa's common stock over the next three years at prices based on prevailing market prices over a period preceding each sale.

"We look forward to working with Aspire Capital as a financial partner and to Aspire Capital being a long-term investor in Atossa," stated Dr. Steven Quay, chairman, CEO and president. "Our agreement with Aspire provides added financial strength and flexibility, allowing us to raise equity opportunistically based on market conditions and our working capital needs. We believe that Aspire's initial investment and ongoing commitment, along with their reputation as a long-term, institutional investor, demonstrates confidence in our ForeCYTE and ArgusCYTE tests, other breast health tests in development, and our business model. We presently do not expect to need to raise additional equity capital in the near term other than under this agreement. However, we may decide to opportunistically raise equity or debt capital or enter into a strategic transaction in which equity capital is issued."

"Over the past few months we have spent a lot of time with the management team and done significant due diligence on Atossa as well as talked with physicians and users of its products. During this process, we have come to see the tremendous opportunity that Atossa presents as the 'Pap Smear' for the breast and for early non-invasive treatment of breast cancer," commented Steven G. Martin, Managing Member of Aspire Capital. "Atossa's products can help save the lives of our mothers, our daughters and our wives. The Company's success is personal to all of us. We are extremely proud to be a long-term shareholder in Atossa and a financial partner to this experienced management team."

Key aspects of the agreement with Aspire Capital include:

Atossa will use the net proceeds from the sales of common stock for general corporate purposes and working capital requirements. Dawson James Securities, Inc. was the placement agent for the sale of 83,333 shares of common shares at $12 per share as well as the $30 million stock purchase agreement.

Atossa also entered into a registration rights agreement with Aspire in connection with its entry into the purchase agreement that requires the Company to file a registration statement regarding the shares sold to Aspire Capital. A more complete and detailed description of the transaction is set forth in the Company's Annual Report on Form 10-K, filed today with the U.S. Securities and Exchange Commission.

About Atossa Genetics, Inc.

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

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

About Aspire Capital Fund, LLC

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Atossa Genetics Announces $30 Million At-the-Market Common Stock Purchase Agreement With Aspire Capital, LLC

SEATTLE, WA--(Marketwire - Mar 28, 2013) - Atossa Genetics, Inc. (NASDAQ: ATOS), a healthcare company focused on the prevention of breast cancer through the commercialization of diagnostic medical devices and laboratory developed tests that can detect precursors to breast cancer, and through the research, development, and ultimate commercialization of treatments for pre-cancerous lesions and ductal carcinoma in situ, today announced its 2012 financial results and corporate developments.

Recent Accomplishments and Highlights

"We continue to make steady progress in the national rollout of our patented ForeCYTE Breast Health Test, advancing our ambition to arm women and their physicians with information that will enable improved breast health management and prevent breast cancer," stated Dr. Steven Quay, chairman, CEO and president. "We are very encouraged by the enthusiastic response we are seeing from doctors and their patients for the ForeCYTE test during the early phases of our national rollout. We believe that widespread adoption of the ForeCYTE test could lead to a dramatic lowering of the incidence of breast cancer, much as the Pap smear has led to a 75 percent reduction in cervical cancer."

Developments in 2012 and early 2013 include:

Full-Year 2012 Financial Results

Net loss for the year ended December 31, 2012 was $5.1 million, or $(0.41) per share, compared with net loss of $3.4 million, or $(0.38) per share, for the year ended December 31, 2011. The increase in net loss was primarily attributable to an increasein general and administrative expense of $1.8 million.

Revenues for the twelve months ended December 31, 2012 were $481,842, which included $6,440 of product revenue from the sale of MASCT Systems and $475,402 of diagnostic testing service revenue from the ForeCYTE and ArgusCYTE breast health tests. This compares with total revenues of $1,500 for the year ended December 31, 2011. The year-over-year increase in total revenues was driven by the launch of the ForeCYTE test near the end of 2011 in a field experience trial and sales of the ArgusCYTE test.

Gross profit for the twelve months ended December 31, 2012 was $416,213. This compares to gross loss of $95,690 for the year ended December 31, 2011. Loss on reduction of inventory to lower of cost or market was $29,884 for the twelve months ended December 31, 2012, and $92,026 for the twelve months ended December 31, 2011, primarily due to write-off of parts purchased during the year for the assembly of MASCT System which was determined at zero net realizable value as a result of lower of cost or market analysis at year end. The MASCT System is currently sold at a price substantially lower than its cost to encourage sales and because the MASCT System is currently manufactured by Atossa's suppliers only in small quantities. For these reasons, the manufacturing cost allocated to each inventory unit is high.

Total operating expenses were $5.5 million for the twelve months ended December 31, 2012, consisting of G&A expenses of $5.0 million and selling expenses of $0.5 million.This compares to total operating expenses of $3.3 million for the twelve months ended December 31, 2011, consisting of G&A expenses of $3.2 million and selling expenses of $0.1 million.The increase in G&A expenses of $1.8 million, or approximately 56%, from 2011 to 2012 is attributed to the launch of the Company's MASCT System, ForeCYTE test and ArgusCYTE test and the related growth in expenses to hire additional staff, expand our operations, invest additional funds in research and development and increased legal fees and other costs associated with our initial public offering.Atossa expects that its G&A expenses will continue to increase as it adds additional full time employees and incurs additional costs as a publicly traded company. Additionally, G&A costs are expected to rise as the Company increases headcount to coordinate the production and manufacture of the MASCT System, and the expected increase in service revenues.

At December 31, 2012, Atossa had cash and cash equivalents of $1.7 million.

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Atossa Genetics Reports 2012 Results and Operating Highlights

WALTHAM, Mass.--(BUSINESS WIRE)--

Interleukin Genetics,Inc. (ILIU) today issued financial and operational results for its fiscal fourth quarter and full fiscal year ended December 31, 2012.

In 2012, with the successful completion of the University of Michigan study showing the value of our periodontal disease test, PST, in guiding preventive dental care, Interleukin Genetics achieved a key milestone on the path to what we believe will be growth in commercialization of our proprietary molecular diagnostic technology, reported Dr. Ken Kornman, Chief Executive Officer of Interleukin Genetics. We are now focused on preparing to make PST widely available to guide more effective and efficient preventive care in dentistry. In addition, we continue to work with our weight management test partner, Amway, to integrate more directly with their new weight loss programs that launch in 2013. We are optimistic that our advances in 2012 will help to make Interleukin one of the leading commercial providers of molecular diagnostics as personalized healthcare becomes a reality.

2012 Financial Highlights

The Company reported revenues of $2.2 million and a loss from continuing operations of $5.1 million, or $(0.14) per basic and diluted common share, for the year ended December31, 2012, compared to revenues in 2011 of $2.9 million and a loss from continuing operations of $5.2 million, or $(0.14) per basic and diluted common share. The revenue decrease is primarily attributable to decreased sales of the Companys Inherent Health brand of genetic tests through the Amway Global sales channel.

Research and development expenses were $1.3 million for the year ended December 31, 2012, compared to $1.4 million for the year ended December 31, 2011. The decrease is primarily attributable to decreased consulting costs partially offset by increased compensation expenses as compared to the year ended December 31, 2011.

Selling, general and administrative expenses were $4.2 million for the year ended December 31, 2012, compared to $4.7 million for the year ended December 31, 2011. The decrease is primarily attributable to decreases in sales commissions paid to Amway Global as part of our Merchant Channel and Partner Store Agreement, compensation expenses and depreciation, partially offset by increased professional fees and employee separation costs attributable to the resignation of the Companys former Chief Executive Officer on August 23, 2012.

Fourth Quarter Results

Revenue for the quarter ended December31, 2012 was $0.3 million, compared to $0.6 million for the same period in 2011. The decrease is primarily attributable to decreased genetic testing revenue as a result of sales through the Amway Global sales channel.

Research and development expenses were $0.3 million for the quarter ended December 31, 2012, compared to $0.4 million for the quarter ended December 31, 2011. The decrease is primarily attributable to decreased consulting costs partially offset by increased compensation expenses as compared to the year ended December 31, 2011.

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Interleukin Genetics Reports Fourth Quarter and Year End 2012 Financial Results