Genetherapy

How genes link a mother's diet to the risk of obesity in her offspring

September 2nd, 2014

PUBLIC RELEASE DATE:

2-Sep-2014

Contact: Cody Mooneyhan cmooneyhan@faseb.org 301-634-7104 Federation of American Societies for Experimental Biology

Many research studies have made it clear that a mother's eating habits prior to pregnancy, during pregnancy and during lactation have a profound impact on her offspring and their propensity for developing weight problems, including obesity. However, until now, the mechanisms behind this phenomenon were unclear. According to new research published in the September 2014 issue of The FASEB JournalF, scientists using an animal model found an epigenetic link between a mother's diet and an offspring's risk of future obesity. This link hinges on the blocked expression of a gene called Pomc, which manages a discrete area of the brain that controls feeding behavior. Excess methylation on the DNA sequence blocks the ability to express this gene, leading to a late satiety response, increased food intake and eventually to obesity.

"Parental obesity and diet can affect the children's likelihood to overeat and develop obesity. Changes in epigenetic programming have been implicated as one of the mechanisms underlying this phenomenon," said Asaf Marco, Ph.D., a researcher involved in the work from the Faculty of Life Sciences at Bar Ilan University in Ramat-Gan, Israel. "We observed a clear correspondence between a specific epigenetic mechanism and weight gain, potentially allowing for early detection and prevention of obesity."

To make this discovery, Marco and colleagues fed female rats either a high-fat diet or a standard diet from post-weaning to adulthood and in separate groups, throughout pregnancy and lactation. All offspring, including those of the high-fat treated rats, received standard food after weaning until adulthood. Blood was analyzed for hormone levels and brain sections for epigenetic modification on the specific DNA sequence of interest. Results showed that unmated female rats, chronically fed a high-fat diet, presented obesity associated with disruptions in an epigenetic mechanism that controls the production of Pomc. However, due to the sharp weight loss during lactation, rats who consumed a high-fat diet presented normal weight and a normalized epigenetic mechanism. Because methylation on the genes is typically considered stable and relatively permanent, this opens the door for future drug development. Researchers found that epigenetic malprogramming induced by maternal high-fat diet had a long-term effect on the offspring's vulnerability to develop obesity. These effects were not reprogrammed by providing standard food to the pups after weaning and the offspring maintained their obesogenic phenotype until adulthood.

"Shining light on heritable, epigenetic factors that cause obesity should help us shed unwanted pounds in future generations," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. "This research shows that being overweight and obese has a direct impact on the genes we use to signal when it's time to stop eating."

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Receive monthly highlights from The FASEB Journal by e-mail. Sign up at http://www.faseb.org/fjupdate.aspx. The FASEB Journal is published by the Federation of the American Societies for Experimental Biology (FASEB). It is the world's most cited biology journal according to the Institute for Scientific Information and has been recognized by the Special Libraries Association as one of the top 100 most influential biomedical journals of the past century.

FASEB is composed of 27 societies with more than 120,000 members, making it the largest coalition of biomedical research associations in the United States. Our mission is to advance health and welfare by promoting progress and education in biological and biomedical sciences through service to our member societies and collaborative advocacy.

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How genes link a mother's diet to the risk of obesity in her offspring

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9.8% CAGR for Oligonucleotide Synthesis Market Globally to 2019 Says a New Research Report Available at …

September 2nd, 2014

(PRWEB) September 01, 2014

The global oligonucleotide synthesis market is expected to reach $1,712.1 million by 2019 from $1,070.7 million in 2014, growing at a CAGR of 9.8% from 2014 to 2019. The global oligonucleotide synthesis market is categorized on the basis of products and services, applications, end users, and geography. The synthesized oligonucleotides segment is expected to register the highest growth rate in the oligonucleotide synthesis market during the forecast period, owing to an increasing number of applications for synthesized oligonucleotides in research, diagnostics and therapeutics; and a growing demand for custom oligos. Complete report is available at http://www.rnrmarketresearch.com/oligonucleotide-synthesis-market-by-product-services-equipment-reagent-primer-probe-custom-oligos-end-user-research-pharmaceutical-biotechnology-application-diagnostics-pcr-qpcr-gen-market-report.html .

Major factors contributing to growth of the oligonucleotide synthesis market include growing R&D expenditure in pharmaceutical and biotech companies; emerging applications of oligos in molecular diagnostics and synthetic biology; and evolving significance of RNA-interference oligos in therapeutics and diagnostics. Furthermore, government support and venture capital funding are other major factors that will boost the growth of this market. For instance, the U.S. National Institutes of Health (NIH) spend $1.5 billion per year to support their oligonucleotide-based applications. Further, in January 2013, Solstice Biologics, a South California start-up, raised $18 million in a series-A financing backed by venture capital funding for targeting and delivery of nucleic acid therapeutics. The relatively-untapped markets of the Asia-Pacific (APAC) region and the increasing R&D activities and funding there have opened up an array of opportunities for the oligonucleotide synthesis market. However, factors such as regulatory barriers, especially for therapeutic oligos, and downward pricing pressure may restrain the growth of this market.

The leading players of this industry include Bioautomation Corporation, Biosearch Technologies, Inc, Eurofins Genomics (A Subsidiary of Eurofins Scientific Group), Eurogentec (A Subsidiary of Kaneka Corporation), GE Healthcare (A Subsidiary of General Electric Company), Genedesign, Inc, Integrated Dna Technologies, Sigma-Aldrich Corporation, thermo Fisher Scientific Inc and Trilink Biotechnologies Inc Order a copy of this report at http://www.rnrmarketresearch.com/contacts/purchase?rname=208277 .

Apart from the comprehensive geographic and product analysis, and market sizing, the report also provides a competitive landscape that covers the growth strategies adopted by players in the industry over the last three years. In addition, the company profiles comprise the key players in the oligonucleotide synthesis market and their product portfolios, developments, and strategies. The above-mentioned market research data, current market size, and forecast of future trends will help key players and new entrants to make the necessary decisions regarding product offerings, geographic focus, change in strategic approach, R&D investments for innovations in products and technologies, and levels of output, in order to remain successful.

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Browse Related Report:

"Whole Exome Sequencing Market by Product (Systems, Kits (Library Preparation, Target Enrichment), by Services (Sequencing), by Technology (Sequencing by Synthesis), by Application (Cancer, Monogenic disorders) Global Forecast to 2018 research report is now available with RnRMarketResearch.com. Companies like Illumina Inc, Thermo Fisher Scientific Inc, Beijing Genomics Institute (Bgi), Macrogen Inc, Eurofins Genomics Inc, Agilent Technologies Inc, Ambry Genetics, Genewiz Inc, Knome Inc, Roche Nimblegen Inc and Sengenics are discussed in this research available at http://www.rnrmarketresearch.com/whole-exome-sequencing-market-by-product-systems-kits-library-preparation-target-enrichment-by-services-sequencing-by-technology-sequencing-by-synthesis-by-application-cancer-monogenic-d-market-report.html .

"Molecular Biology Enzymes, Kits, & Reagents Market by Application (Cloning, Epigenetics, PCR, Restriction Digestion, Sequencing), Product (Ligase, Phosphatase, Polymerase, Protease, Restriction Endonuclease, Reverse Transcriptase) Global Forecast to 2018" research report is now available with RnRMarketResearch.com. Companies like Affymetrix, Agilent Technologies, Enzymatics, Illumina, New England Biolabs, Qiagen, Roche, Sigma-Aldrich Co, Takara Bio Ltd and Changshu Thermo Fisher Scientific are discussed in this research available at http://www.rnrmarketresearch.com/molecular-biology-enzymes-kits-reagents-market-by-application-cloning-epigenetics-pcr-restriction-digestion-sequencing-product-ligase-phosphatase-polymerase-protease-restriction-endonu-market-report.html .

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9.8% CAGR for Oligonucleotide Synthesis Market Globally to 2019 Says a New Research Report Available at ...

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Sebastian helps to find a gene

September 2nd, 2014

The West Australian

Happy to be home after a visit to the emergency department at Princess Margaret Hospital, Sebastian Rodriguez-Rios is ready for his favourite game of hide-and-seek.

What the three-year-old is too young to understand is that his stint in hospital could help save millions of children's lives.

Sebastian is taking part in a Telethon Kids Institute world-first research project led by Anthony Bosco that will attempt to block the activity of genes that cause asthma using "repurposed" drugs.

"Recently it's been shown that drugs used to treat one condition may be re-used to treat an unrelated condition," Dr Bosco said.

"This research will find the genes that cause asthma and then we'll search through thousands of drugs to find which drugs hit these (asthma) genes."

Repurposed drugs were already approved for use in patients, making them "much faster and cheaper to get these drugs to patients for different diseases".

Asthma affects 300 million people worldwide, including two million Australians, and is among the most frequent reasons for children's hospital admission.

Dr Bosco said his project, which involves collecting samples from about 50 children taken to PMH's emergency department with a life-threatening asthma attack, would not be possible without funding.

His study is one of 16 Perth-based research projects to benefit from nearly $3 million in grants announced by Health Minister Kim Hames in the second round of the Telethon-Perth Children's Hospital Research Fund, a collaboration between the Channel 7 Telethon Trust and the Department of Health.

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Sebastian helps to find a gene

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Throwing a loop to silence gene expression

September 2nd, 2014

PUBLIC RELEASE DATE:

2-Sep-2014

Contact: Dr. Sibylle Kohlstdt s.kohlstaedt@dkfz.de German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ)

All human cells contain essentially the same DNA sequence their genetic information. How is it possible that shapes and functions of cells in the different parts of the body are so different? While every cell's DNA contains the same construction master plan, an additional regulatory layer exists that determines which of the many possible DNA programs are active. This mechanism involves modifications of genome-bound histone proteins or the DNA itself with small chemical groups (e.g. methylation). It acts on top of the genetic information and is thus called 'epi'-genetic from the corresponding Greek word that means 'above' or 'attached to'.

"Epigenetics has fundamentally changed our view on how the genetic information is used", says Dr. Karsten Rippe from the German Cancer Research Center, who is studying this process with his team. "Epigenetic modifications can be rapidly set or removed to reversibly change cell function. At the same time, epigenetic patterns can be stably inherited through cell division and possibly also to the next generation."

It turns out that deciphering the cell's 'epigenetic code' is a challenging task: Hundreds of proteins in the cell are linked in large networks to 'write', 'erase' or 'read' about 140 different chemical modifications of histone proteins and DNA that have been identified so far. Understanding how epigenetic regulation operates for a specific part of the genome thus requires an integrative approach that considers the connections between different factors. Accordingly, the researchers, together with their colleagues from the DKFZ and the LMU Munich, conducted a comprehensive analysis of a prototypic epigenetic network. They studied how certain DNA sequences were silenced by histone and DNA methylation that would make the genome instable if active and would thus favor cancer development.

Based on maps of epigenetic signals and interactions of proteins with the genome, they developed a mathematical model for epigenetic silencing. "The silencing mechanism we found works much like throwing a loop with a lasso to catch something", says Katharina Mller-Ott, the first author of the study: "Several factors bind the silencing enzyme stably to certain sites in the genome. Because the DNA randomly moves around and forms transient loops, the enzyme hits other regions in the genome nearby, which then become modified and are switched off."

By virtue of their quantitative description of this process, the researchers were able to predict how the silencing network would react in response to perturbations like changes of the abundance of proteins or the activity of the enzymes involved. The scientists in the groups of Karsten Rippe and Thomas Hfer at the DKFZ are now continuing to further develop and apply their model to deregulated epigenetic signaling in leukemia. By evaluating genome-wide maps of epigenetic signals with mathematical models they are identifying tumor-specific changes in cell samples from patients with blood cancer. Furthermore, they are dissecting how epigenetic signals can be used to predict therapy response and how drugs affect the epigenetic program.

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The project was supported by the German Federal Ministry of Education and Research (BMBF).

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Throwing a loop to silence gene expression

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GENETOS – Genetic Engineering – Video

September 2nd, 2014

GENETOS - Genetic Engineering
In which I show off the game #39;s highest difficulty the only way I possibly could: cheating and making myself invincible. This was made for the Shooting Galler...

By: Oblivion4568238SA

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GENETOS - Genetic Engineering - Video

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MPs' protests fail to derail "three parent family" plans

September 2nd, 2014

First published in News Last updated by Robert Merrick, Parliamentary Correspondent

PROTESTS by a group of MPs have failed to derail plans for a controversial gene therapy, to stop incurable diseases passing to the next generations.

Ministers vowed to plough ahead with preparations for the DNA-altering procedure, which is being pioneered by a team at Newcastle University.

However, the department of health declined to say when the issue would be put to a vote in Parliament, despite suggestions that it could be before the end of the year.

The treatment involves replacing faulty mitochondria responsible for inherited diseases, including muscle wasting, heart problems, vision loss, organ failure and epilepsy.

Embryos are given healthy DNA from donor eggs, meaning a baby has the DNA of three people from two parents, plus less than one per cent from the donor.

Professor Doug Turnbull, who leads the Newcastle team, has urged the Government to draw up legislation as soon as possible, because of the number of patients waiting for treatment.

But, in the Commons, MPs brought forward a motion demanding further research and for new regulations to be delayed in light of public safety concerns.

Fiona Bruce, a Conservative backbencher, claimed the Human Fertilisation and Embryology Authority (HFEA) wanted further research, saying: This is a case of genetic engineering.

It is the alteration of a potential human being - the removal of certain genes and their replacement with others, to create children.

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MPs' protests fail to derail "three parent family" plans

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Scientists devise a bar code for the bacteria that causes tuberculosis

September 2nd, 2014

PUBLIC RELEASE DATE:

1-Sep-2014

Contact: Jenny Orton press@lshtm.ac.uk 44-207-927-2802 London School of Hygiene & Tropical Medicine

Doctors and researchers will be able to easily identify different types of tuberculosis (TB) thanks to a new genetic barcode devised by scientists from the London School of Hygiene & Tropical Medicine.

The bacteria that cause the deadly respiratory disease have evolved into families of strains, or lineages, which may affect people differently.

To help identify the different origins and map how tuberculosis moves around the world, spreading from person to person through the air, the research team studied over 90,000 genetic mutations.

According to the study published in Nature Communications the researchers found that just 62 mutations are needed to code the global family of strains.

Dr Taane Clark, Reader in Genetic Epidemiology and Statistical Genomics at the London School of Hygiene & Tropical Medicine, who led the study, said: "There is increasing interest in new technologies that can assist those treating tuberculosis patients.

"This new barcode can be easily implemented and used to determine the strain-type that is a surrogate for virulence.

"We are making this information available to the doctors and scientists working with tuberculosis so that they can more easily know what strains they are dealing with."

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Scientists devise a bar code for the bacteria that causes tuberculosis

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Pharmacogenetics advances personalized medicine

September 2nd, 2014

John Hwa is a professor of medicine and the director of cardiovascular pharmacogenetics at Yale School of Medicine. Along with Dartmouth genetics professor Jason H. Moore, Hwa recently coauthored an editorial in the journal Current Molecular Medicine. The article, titled Pharmacogenetics and Molecular Medicine: So Close and Yet So Far introduces a new review series of eight articles contributed by different researchers in the field of pharmacogenomics. The News sat down with Hwa and his colleague, Yale postdoctoral fellow Jeremiah Stitham, to understand the latest advances in the field.

Q. How would you define the fields of pharmacogenomics and personalized medicine to the general public? What are the basic underlying principles and ideas?

H. About 100,000 people die each year from adverse side effects to medications, and millions of others have some sort of harmful drug reaction. The idea of pharmacogenetics is to try and figure out, based on genetics, who is going to suffer problems and who will benefit the most from taking a particular drug. Though there are actually many definitions out there, the simplest definition is that it is a combination of pharmacology and genetics: pharmacogenetics. It is the use of genetic data to understand how a disease process is influenced by genetics, progresses as a result of genetics, and responds to drugs. In terms of the pharmacology, there are two main components, pharmacodynamics and pharmacokinetics: the former dealing with how genetics influences the drugs effect on the disease and the latter dealing with how genetics influences the metabolism of the drug.

Q. As your lab specializes in cardiovascular medicine, what has been the core focus of your research in particular?

H. Commonly used drugs that are taken for pain, arthritis and fever can have a profound effect on the cardiovascular system and one of the main reasons for this is because of problems with [the molecules] prostacyclin and thromboxane. This has become a very major concern in cardiovascular medicine and the clinical sciences. I am part of a large consortium based at the University of Pennsylvania that has come together to address this problem. We are trying to figure out who would benefit from these common drugs without adverse side effects and who should be careful about taking these medications: essentially the concept of personalized medicine. Currently, my lab is focusing our efforts on the diabetic population, because they are particularly at risk for cardiovascular diseases. We have all the tools now and are beginning to make sense of the data. There is not doubt that in the near future, we will be able to predict who is going to have adverse side effects as a result of a drug and who is going be fine and benefit from the treatment.

S. That is basically the third component of pharmacogenomics: the first two being how genetics affects drug response and drug metabolism and the final component being how it is going to affect people with adverse reactions.

Q. Which recent advances and discoveries have been game-changers? Have any new experimental techniques and technologies really impacted the way the scientific community studies this field?

H. One major advance has been the advent of genetic sequencing. Back in 2001, sequencing used to cost a fortune, but now prices have gotten significantly lower. Whole-genome sequencing now costs a few thousand dollars, and the price is going to drop even further. I have no doubt that one day everyone will sequence his or her genome.

In many ways, we are overwhelmed with data from all of these sources. The real question now is the hypothesis-generation procedure: how are you going to make sense of all of this information? Certainly with an area like pharmacogenetics, there is a vast amount of data that is being collected, at multiple levels, and ultimately it is going to be a cross-disciplinary collaboration between the basic scientists, the translational scientists, the clinicians, the bioinformaticists, and the outcomes specialists. It is going to be a collaboration that makes sense of the massive data sets that are being generated and applies this knowledge to clinical practice.

Q. In the title of your editorial, you state that the scientific community in this field is so close and yet so far. What are the major challenges currently faced by the fields of pharmacogenomics and personalized medicine?

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Pharmacogenetics advances personalized medicine

Recommendation and review posted by Bethany Smith

The Sims 3 | Perfect Genetics Challenge Part 23: So Close – Video

September 2nd, 2014

The Sims 3 | Perfect Genetics Challenge Part 23: So Close
In this part, we give birth to our 9th baby! The Sims 3 Perfect Genetics Playlist: https://www.youtube.com/playlist?list=PL0BV_YFL-2I77acu9TBO5aor9CgMW97mo...

By: simplyapril

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The Sims 3 | Perfect Genetics Challenge Part 23: So Close - Video

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Let’s play FTB Monster #49 [FR HD] : Advanced genetics partie 2 – Video

September 2nd, 2014

Let #39;s play FTB Monster #49 [FR HD] : Advanced genetics partie 2
On continue avec advanced genetics, et on commence se modifier gntiquement. Au programme, on installe un DNA Splitter, un DNA breeder, une centrifuge, un...

By: Raunok Toutencube

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Let's play FTB Monster #49 [FR HD] : Advanced genetics partie 2 - Video

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Exploring the Labyrinth of Human Genetics – Video

September 2nd, 2014

Exploring the Labyrinth of Human Genetics
Hannah Isaacson, State Fair oral presentation 2014.

By: Dan Isaacson

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Exploring the Labyrinth of Human Genetics - Video

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A One-Two Punch for Brain Tumors? New Clinical Trial Opens at U-M

September 2nd, 2014

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Newswise ANN ARBOR, Mich. University of Michigan Health System doctors have started testing a unique new approach to fighting brain tumors -- one that delivers a one-two punch designed to knock out the most dangerous brain cancer.

The experimental approach, based on U-M research, delivers two different genes directly into the brains of patients following the operation to remove the bulk of their tumors.

The idea: trigger immune activity within the brain itself to kill remaining tumor cells -- the ones neurosurgeons cant take out, which make this type of tumor so dangerous.

Its the first time this gene therapy approach is being tried in humans, after more than a decade of research in experimental models.

One of the genes is designed to kill tumor cells directly, and is turned on when the patient takes a certain drug. The other gene spurs the bodys own immune system to attack remaining cancer cells. Both are delivered into brain cells via a harmless virus.

The Phase I clinical trial has already enrolled two patients who have tolerated the gene delivery without complications. All patients in the study must have a presumptive diagnosis of WHO grade 3 or 4 malignant primary glioma, such as glioblastoma multiforme; patients must not have been treated yet by any therapy. They must also meet other criteria for inclusion in the trial.

More patients will be able to enroll at a pace of about one every three weeks, through a careful selection process. In addition to surgery and gene therapy at U-M, each will receive standard chemotherapy and radiation therapy as well as follow-up assessments for up to two years.

Were very pleased to see our years of research lead to a clinical trial, because based on our prior work we believe this combination of cell-killing and immune-stimulating approaches holds important promise, says principal investigator Pedro Lowenstein, M.D., Ph.D., the U-M Medical School Department of Neurosurgery professor who has co-led the basic research effort to develop and test the strategy.

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A One-Two Punch for Brain Tumors? New Clinical Trial Opens at U-M

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MPs' protests fail to derail gene therapy plans