Archive for the ‘Gene Therapy Research’ Category

Provillus Review - Provillus Hair loss solution for Men and Women.
bit.ly Free Sample Bottles available Now! Rated NO.1 Hair Loss Treatment on the Market! Provillus Review Over the past couple of years a lot has been said about Provillus. Some people hate, some love it, and some sites simply give outrageous claims about Provillus and other natural hair loss treatments. So after buying and using it for the past year, this is my unbiased and honest Provillus review and experience with the product. What is Provillus? Provillus is claimed to be one the top natural hair loss treatments on the market. However, like most health products, there is a chance it may not work for you. Nothing works 100% of the time for everyone - our genetic make-up is just too diverse for any perfect, universal health product to exist! And that #39;s a fact! Any potential problems with Provillus? 1) Can take up to 6 months: Although it only took about 2 or 3 months for my hair loss to slow down and for new hair to appear on my bald spot, for some people it could take up to 6 months to see any noticeable results. I guess it all depends on your genetics, general well-being, and how soon you start the treatment. 2) Not 100% effective: With that said, Provillus sometimes may not work for you at all. Look, no treatment, no matter how advanced it is, can work for everyone 100% of the time. Our bodies are way too different for the perfect cure to ever exist! 3) Possible side-effects: Although Provillus claims to have no side-effects, sometimes people do not follow directions ...

By: jan robertson

Continue reading here:
Provillus Review - Provillus Hair loss solution for Men and Women. - Video

GZED pt 1
Leaked vid part 1 from classified program: Genetics and Zoological Engineering for Defense footage credits: militarychefs.com newscientist Boston University Twente University

By: anon ymouse

Read the original here:
GZED pt 1 - Video

Damon Elena || DNA
new vid! so i love this song i listen to it like every day and i think it #39;s written for Damon ..."It #39;s the blue in his eyes that help #39;s me see the future"...or"Perfect in every way i see it in his face nothing more to say it #39;s in his DDDD DNA" here are the lyrics Does he tell you he loves you When you least expect it Does he flutter your heart When he kisses your neck No scientist or biology It #39;s obvious, when he #39;s holding me It #39;s only natural That I #39;m so affected, ooh And my heart won #39;t beat again If I can #39;t feel him in my veins No need to question I already know It #39;s in his DNA, DD-DNA It #39;s in his DNA And he just takes my breath away Bb-breath away, I feel it every day And that #39;s what makes a man Not hard to understand, perfect in every way I see it in his face, nothing more to say It #39;s in his DD-DNA It #39;s the blue in his eyes That helps me see the future Fingerprints that leave me covered for days Yeah, hey, yeah Now I don #39;t have any first degree But I know what he does to me No need to work it out It #39;s so familiar, ohh And my heart won #39;t beat again If I can #39;t feel him in my veins No need to question I already know It #39;s in his DNA, DD-DNA It #39;s in his DNA And he just takes my breath away Bb-breath away, I feel it every day And that #39;s what makes a man Not hard to understand, perfect in every way I see it in his face, nothing more to say It #39;s in his DD-DNA It #39;s all about his kiss Contaminates my lips Our energy connects It #39;s simple genetics I #39;m the X to his Y It #39;s the ...

By: nikolkitty1

Excerpt from:
Damon

Public release date: 10-Jan-2013 [ | E-mail | Share ]

Contact: Octavi Lpez Coronado octavi.lopez@uab.cat 34-935-813-301 Universitat Autonoma de Barcelona

Scientists observed that blocking the expression of the gene TRIP-Br2 in mice protects them against obesity and insulin resistance. The study shows that the gene modulates fat storage by regulating energy expenditure and lipolysis, the process which transforms fat into lipids for the body's energy consumption. If the gene expression is blocked, the mice increase their lipolysis and their energy expenditure, thus reducing their obesity.

Obesity is the result of an alteration in the processes that regulate food absorption and energy production. This alteration tips the balance towards excessive storage of fat. According to the researchers, understanding the regulation of the factors that control the storage, mobilisation and use of excess energy in fat cells (the adipocytes) can lead to the development of therapies for obesity and its related illnesses, such as type 2 diabetes.

In the words of Cristina Mallol, a researcher at the Universitat Autnoma de Barcelona and co-author of the study: "The protection of mice with no expression of the gene TRIP-Br2, and its selective elevation in the visceral fat of humans point the way to a future gene therapy to counteract obesity, insulin resistance and excess lipids in the blood".

###

The research, whose findings were published this week in the online edition of the journal Nature Medicine, was led by researchers from the Joslin Diabetes Center, of the Harvard Medical School in Boston, Massachusetts (USA), with the participation of the University of Singapore (Singapore); the Centre for Animal Biotechnology and Gene Therapy (CBATEG) at the Universitat Autnoma de Barcelona (Spain); INSERM, Toulouse (France); the University of California, at Berkeley (USA); the University of Leipzig (Germany); and the University of Florida (USA); the University of Illinois, at Chicago (USA).

AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

Read more here:
Researchers identify a new gene with a key role in obesity and diabetes

Featured Article Academic Journal Main Category: Obesity / Weight Loss / Fitness Also Included In: Diabetes;Genetics Article Date: 11 Jan 2013 - 0:00 PST

Current ratings for: New Obesity, Type 2 Diabetes Gene Identified

5 (2 votes)

The researchers write about their work in a paper published online on 6 January in Nature Medicine.

"Obesity develops as a result of altered energy homeostasis favoring fat storage."

In other words, obesity is what happens when the finely tuned processes that regulate food absorption and energy production go awry, and the balance (homeostasis) moves in the wrong direction: towards excessive storage of fat.

Insulin resistance is a risk factor for type 2 diabetes and other health problems. It develops when the body uses insulin, which is needed to control the amount of sugar in the body, less effectively than normal. The result is raised levels of blood sugar and fats.

Specific genes make people more likely to develop insulin resistance and diabetes. Excess weight and lack of exercise also contribute to insulin resistance.

When the team examined the fat storage cells (adipocytes) in the knockout mice, they discovered higher levels of "lipolysis" and energy expenditure. Liopolysis is a cellular process that converts fats into lipids to supply the body with energy.

Other studies have already shown that TRIP-Br2 is more highly expressed in the visceral fat of humans, so together with the results from the knockout mice, the researchers conclude that TRIP-Br2 could be a gene therapy target for treating obesity and related conditions.

Read the rest here:
New Obesity, Type 2 Diabetes Gene Identified

Jorge Paz MD: Adult Stem Cell Therapy for Arthritis, Sports Injury, and Autoimmune Disease || 3 of 3
Stem cell therapy for osteoarthritis using adipose (fat) stem cell. Case study of 76 year-old man with osteoarthritis in his knees. Stromal vasular fraction treatment statistics including side effects collected over 800 infusions. Stem cell treatments for sports injuries and why pro sports stars are seeking treatment. Case study of a professional dancer with knee and neck problems who returned to competition after stem cell treatment in Panama.

By: cellmedicine

Read more here:
Jorge Paz MD: Adult Stem Cell Therapy for Arthritis, Sports Injury, and Autoimmune Disease || 3 of 3 - Video

By JENNY F. MANONGDO

Manila, Philippines Doctors yesterday warned against fatal complications of the use of stem cell therapy.

According to the Philippine Society for Stem Cell Medicine (PSSCM), a stem cell transplant poses a host of complications, including fatal complications that depend on several factors such as the type of blood disorder, type of transplant and the age and health of the person receiving the transplant. If the stem cell that you received is not from your own body, it could lead to fatal complications, PSSCM said.

The Philippine Medical Association (PMA) also warned that a patients body may reject the transplant stem cells from a donor.

Although some people experience few problems with a transplant, others may develop complications that may require treatment or hospitalization. Some complications could even be life-threatening, said Dr. Leo Olarte, PMA vice-president.

According to Olarte, the complications that can arise with a stem cell transplant include graftversus-host disease, stem cell (graft) failure, organ injury, infections, cataracts, infertility, new cancers, and even death.

According to Olarte, a person who will undergo a stem cell transplant from a donor (allogeneic stem cell transplant) may be at risk of graft-versus-host disease.

This condition occurs when a donors transplanted stem cells attack your body. Graft-versushost disease can be mild or severe. It can occur soon after your transplant or months to years later. Aside from the graft-versushost disease, stem cell transplant from a donor can likewise affect any organ, commonly the skin (rash, often like sunburn), gut (mouth sores, abdominal pain, diarrhea, nausea or vomiting), liver (jaundice or yellowing of the skin), lungs (blocked airways) or eyes (irritation and light sensitivity).

Olarte said it could also lead to chronic disability arising from organ injury or infections that are potentially life-threatening.

Commercial establishments offering stem cell treatments have increased following its popularity in the treatment of various diseases.

Follow this link:
DOH: Stem cell therapy dangerous

Dr. Elliot Androphy on Finding SMA
Speaking from the 2012 FightSMA Annual Research Conference in Washington DC, Dr. Elliott Androphy talks about his role in discovering the gene that causes SMA and his relationship with the SMA community.

By: fightsmavideo

Original post:
Dr. Elliot Androphy on Finding SMA - Video

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/4gllbg/cell_therapy) has announced the addition of Jain PharmaBiotech's new report "Cell Therapy - Technologies, Markets and Companies" to their offering.

This report describes and evaluates cell therapy technologies and methods, which have already started to play an important role in the practice of medicine. Hematopoietic stem cell transplantation is replacing the old fashioned bone marrow transplants. Role of cells in drug discovery is also described. Cell therapy is bound to become a part of medical practice.

Stem cells are discussed in detail in one chapter. Some light is thrown on the current controversy of embryonic sources of stem cells and comparison with adult sources. Other sources of stem cells such as the placenta, cord blood and fat removed by liposuction are also discussed. Stem cells can also be genetically modified prior to transplantation.

Cell therapy technologies overlap with those of gene therapy, cancer vaccines, drug delivery, tissue engineering and regenerative medicine. Pharmaceutical applications of stem cells including those in drug discovery are also described. Various types of cells used, methods of preparation and culture, encapsulation and genetic engineering of cells are discussed. Sources of cells, both human and animal (xenotransplantation) are discussed. Methods of delivery of cell therapy range from injections to surgical implantation using special devices.

Cell therapy has applications in a large number of disorders. The most important are diseases of the nervous system and cancer which are the topics for separate chapters. Other applications include cardiac disorders (myocardial infarction and heart failure), diabetes mellitus, diseases of bones and joints, genetic disorders, and wounds of the skin and soft tissues.

Regulatory and ethical issues involving cell therapy are important and are discussed. Current political debate on the use of stem cells from embryonic sources (hESCs) is also presented. Safety is an essential consideration of any new therapy and regulations for cell therapy are those for biological preparations.

The cell-based markets was analyzed for 2012, and projected to 2022.The markets are analyzed according to therapeutic categories, technologies and geographical areas. The largest expansion will be in diseases of the central nervous system, cancer and cardiovascular disorders. Skin and soft tissue repair as well as diabetes mellitus will be other major markets.

The number of companies involved in cell therapy has increased remarkably during the past few years. More than 500 companies have been identified to be involved in cell therapy and 285 of these are profiled in part II of the report along with tabulation of 272 alliances. Of these companies, 156 are involved in stem cells. Profiles of 70 academic institutions in the US involved in cell therapy are also included in part II along with their commercial collaborations. The text is supplemented with 55 Tables and 11 Figures. The bibliography contains 1,050 selected references, which are cited in the text.

Key Topics Covered:

Read the original post:
Research and Markets: Cell Therapy - Technologies, Markets and Companies - 2013 Report

Newswise Scientists have discovered a gene that interferes with the clearance of hepatitis C virus infection. They also identified an inherited variant within this gene, Interferon Lambda 4 (IFNL4), that predicts how people respond to treatment for hepatitis C infection. The results of this study, by investigators at the National Cancer Institute (NCI), part of the NIH, and their collaborators at NIH and other institutions, were published online in Nature Genetics on Jan. 6, 2013.

Chronic infection with hepatitis C virus is a cause of liver cirrhosis and liver cancer. Up to 80 percent of people who are acutely infected with hepatitis C fail to clear the virus and develop chronic hepatitis C infection, and of these, approximately 5 percent develop liver cancer. Individuals of African ancestry do not respond as well to current treatments of hepatitis C infection compared to patients of European or Asian ancestry.

Previously, results from genome-wide association studies (GWAS) identified common inherited genetic markers that were associated with response to hepatitis C virus treatment and spontaneous clearance of the infection. Those markers are located on chromosome 19 near a known interferon gene, IFNL3 (IL28B). However, molecular investigations into IFNL3 did not explain the GWAS association with spontaneous virus clearance or treatment response. To find the new gene, the investigators used a technology involving RNA sequencing on human liver cells treated to mimic hepatitis C virus infection.

By using RNA sequencing we looked outside the box to search for something beyond what was already known in this region. We hit the jackpot with the discovery of a new gene. It is possible that other important genes may be discovered using this approach, said co-lead investigator Ludmila Prokunina-Olsson, Ph.D., of the Laboratory of Translational Genomics in NCIs Division of Cancer Epidemiology and Genetics (DCEG).

The researchers found that the IFNL4 region harbors a variant that is found in two alternative forms. One form, called deltaG, results in a deletion in one of the four bases that comprise DNA. The change creates an alteration known as a frameshift, which produces the IFNL4 protein, while the form without the deletion does not produce IFNL4. By analyzing data from hepatitis C-infected African-Americans and European-Americans participating in clinical studies, the authors found that the presence of the IFNL4 protein is associated with poorer clearance and response to treatment than the form that does not produce IFNL4. The deletion variant is more common in people of African ancestry, which helps partially explain why African-Americans have a lower response to current hepatitis C treatments than patients of Asian and European ancestry.

Our work fulfills several promises of the genomic era, said NCIs Thomas R. OBrien, M.D., Infections and Immunoepidemiology Branch, DCEG. One, a better understanding of biology; two, personalized medicine; and three, new potential treatments. We deliver immediately on the first two. Weve identified a new gene that may help us better understand response to viral infection and the new genetic marker may transition to clinical practice because it predicts treatment outcome for African-American patients better than the current genetic test. For the third, the INFL4 protein may be used as a novel therapeutic target for hepatitis C virus infection, and possibly other diseases.

The new gene belongs to what is now a family of four interferon-lambda protein-encoding genes, three of which were discovered more than ten years ago (IFNL1, IFNL2 and IFNL3) The mechanism by which the IFNL 4 protein impairs hepatitis C virus clearance remains unknown. Further studies will explore molecular function of this novel protein in normal and disease conditions.

This study was conducted collaboratively with the National Institute of Diabetes and Digestive and Kidney Diseases at NIH, as well as the U.S. Food and Drug Administration, and a number of universities and research institutions. Funding was provided by NCI grant Z01 CP005782.

Originally posted here:
Investigators Discover New Gene That Affects Clearance of Hepatitis C Virus

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/rfv8l2/biochips_and) has announced the addition of Jain PharmaBiotech's new report "Biochips and Microarrays - Technologies, Markets and Companies" to their offering.

This report is an analysis of biochip/microarray markets based on technologies and applications. The report starts with a description of technologies as a basis for estimation of markets. Technologies include array comparative genomic hybridization (CGH), copy number variation (CNV), DNA methylation, ChIP-Chip, RNA splice variants, and microRNA. Separate chapters are devoted to protein biochips/microarrays, microfluidics and nanobiotechnology-based nano-arrays.

Various applications of biochips and microarrays are described throughout the report. Areas of application such as point-of-care, genetic screening, cancer, and diagnosis of infections are included. Separate chapters are devoted to applications in drug discovery and development as well as personalized medicine

The report provides current share of each segment: market size in 2012 and projected value for the years 2017 and 2022. Gene expression has the largest share and is an established market. Share of microarray technologies in other areas will grow with the maximum growth in RNA splice variants followed by epigenetics. The growth in protein microarrays is somewhat less, partly because it is more mature than the other submarkets and has already shown considerable growth in the past. Impact of next generation sequencing on segments of microarray markets is identified. Customer requirements and unmet needs are described. Markets are also analyzed according to geographical areas.

Brief profiles of companies involved in biochip/microarray technologies are provided. Currently selected 85 companies are included along with listing of 113 collaborations between companies. The text is supplemented by 19 tables, 8 figures and 100 references to literature.

Key Topics Covered:

Executive Summary

1. Introduction

2. Biochip and Microarray Technologies

See the original post here:
Research and Markets: Biochips and Microarrays - Technologies, Markets and Companies - Updated 2013 Report

Jan. 9, 2013 Scientists have discovered a gene that interferes with the clearance of hepatitis C virus infection. They also identified an inherited variant within this gene, Interferon Lambda 4 (IFNL4), that predicts how people respond to treatment for hepatitis C infection.

The results of this study, by investigators at the National Cancer Institute (NCI), part of the NIH, and their collaborators at NIH and other institutions, were published online in Nature Genetics on Jan. 6, 2013.

Chronic infection with hepatitis C virus is a cause of liver cirrhosis and liver cancer. Up to 80 percent of people who are acutely infected with hepatitis C fail to clear the virus and develop chronic hepatitis C infection, and of these, approximately 5 percent develop liver cancer. Individuals of African ancestry do not respond as well to current treatments of hepatitis C infection compared to patients of European or Asian ancestry.

Previously, results from genome-wide association studies (GWAS) identified common inherited genetic markers that were associated with response to hepatitis C virus treatment and spontaneous clearance of the infection. Those markers are located on chromosome 19 near a known interferon gene, IFNL3 (IL28B). However, molecular investigations into IFNL3 did not explain the GWAS association with spontaneous virus clearance or treatment response. To find the new gene, the investigators used a technology involving RNA sequencing on human liver cells treated to mimic hepatitis C virus infection.

"By using RNA sequencing we looked outside the box to search for something beyond what was already known in this region. We hit the jackpot with the discovery of a new gene. It is possible that other important genes may be discovered using this approach," said co-lead investigator Ludmila Prokunina-Olsson, Ph.D., of the Laboratory of Translational Genomics in NCI's Division of Cancer Epidemiology and Genetics (DCEG).

The researchers found that the IFNL4 region harbors a variant that is found in two alternative forms. One form, called deltaG, results in a deletion in one of the four bases that comprise DNA. The change creates an alteration known as a frameshift, which produces the IFNL4 protein, while the form without the deletion does not produce IFNL4. By analyzing data from hepatitis C-infected African-Americans and European-Americans participating in clinical studies, the authors found that the presence of the IFNL4 protein is associated with poorer clearance and response to treatment than the form that does not produce IFNL4. The deletion variant is more common in people of African ancestry, which helps partially explain why African-Americans have a lower response to current hepatitis C treatments than patients of Asian and European ancestry.

"Our work fulfills several promises of the genomic era," said NCI's Thomas R. O'Brien, M.D., Infections and Immunoepidemiology Branch, DCEG. "One, a better understanding of biology; two, personalized medicine; and three, new potential treatments. We deliver immediately on the first two. We've identified a new gene that may help us better understand response to viral infection and the new genetic marker may transition to clinical practice because it predicts treatment outcome for African-American patients better than the current genetic test. For the third, the INFL4 protein may be used as a novel therapeutic target for hepatitis C virus infection, and possibly other diseases."

The new gene belongs to what is now a family of four interferon-lambda protein-encoding genes, three of which were discovered more than ten years ago (IFNL1, IFNL2 and IFNL3) The mechanism by which the IFNL 4 protein impairs hepatitis C virus clearance remains unknown. Further studies will explore molecular function of this novel protein in normal and disease conditions.

This study was conducted collaboratively with the National Institute of Diabetes and Digestive and Kidney Diseases at NIH, as well as the U.S. Food and Drug Administration, and a number of universities and research institutions. Funding was provided by NCI grant Z01 CP005782.

Share this story on Facebook, Twitter, and Google:

See the original post:
Scientists discover new gene that affects clearance of hepatitis C virus

In a long life of scholarship and dissent, Gene Sharp has been imprisoned and persecuted, but never silenced. His ideas continue to inspire resistance movements across the world.

Gene Sharp is not a typical pacifist. When I used to lecture, I would always get complaints from the pacifists, says the academic, who turns 85 this month. They would say I wasnt pure. They said that what I was proposing was still conflict. Military people often understood him better. A retired US army colonel, Robert Helvey, heard Sharp lecture 20 years ago and persuaded him to visit Burma, where rebels asked Sharp to give them advice.

He wrote a pamphlet. I didnt know Burma well, he recalls. So I had to write generically: if a movement wanted to bring a dictatorship to an end, how would they do it? That pamphlet, From Dictatorship to Democracy (1993), contained the idea for which Sharp is now known all over the world that power is held only by the consent of the people over whom it is exercised, and that consent can be withdrawn. All regimes depend on certain pillars of support and, with a proper strategy, resisters can remove those pillars non-violently.

The book was originally published in English and Burmese. And I thought that was it, Sharp says. But it went on display in a bookshop in Bangkok. From there, nobody knows exactly how it spread. But it did everywhere. Im still amazed. It didnt spread because of propaganda or some sales pitch but because people found it usable, and important.

I had no idea how useful it would be, confirms Srdja Popovic, a leader of Otpor, the movement that toppled Slobodan Milosevic in Serbia in 2000. Others have described the effect of reading Sharps work as mind-blowing, because it showed that what had seemed impossible might not be impossible after all.

For nearly 20 years, From Dictatorship to Democracy circulated clandestinely in as many as 40 countries. It was being printed in Moscow when the FSB (the successor to the KGB) raided the printer. It later went on sale at two independent Russian bookshops both of which, remarkably, soon caught fire.

The British film-maker Ruaridh Arrow first heard about Sharp while covering Ukraines Orange Revolution. He decided to find out more, and the result of his research was a film, How to Start a Revolution, which has been shown in more than 22 countries and became an underground hit with the Occupy movement.

Now Sharps teachings are winning interest from the mainstream, too. From Dictatorship to Democracy finally had its official publication in the UK. The Archbishop of Canterbury invited Sharp to meet bishops from around the world. And the All-Party Parliamentary Group on Conflict Issues asked him to address MPs, peers and senior civil servants at the House of Commons. The room was packed thanks to a crowd of Occupy activists and he received a standing ovation. He has been nominated for the Nobel Peace Prize, and early last month in the Swedish Parliament he was presented with the so-called Alternative Nobel, the Right Livelihood Award.

After a lifetime of lonely academic toil, Sharp is suddenly finding that people all over the world are ready to hear his theory of power and how to seize it. This is a very strange experience, he says. But is the acclaim overblown? The Occupy movement has largely fizzled out and the Arab spring has not been quite the success that people hoped it would be. Is he worried that his reputation will fall again? I dont give a damn about my reputation. The point is that bringing down one regime does not produce political nirvana. You still have tough times ahead. I have always been very clear about that.

But people used to say non-violence cant work. After Tunisia and Egypt, people can no longer deny that non-violent regime change is possible. The old theory of a just war is that there must be no viable alternative. I think thats false now. Its no longer a theological question its an empirical question. He quotes Kenneth Boulding: That which is, is possible. The breakthrough has happened.

Follow this link:
Gene Sharp: The Machiavelli of non-violence

A research team consisting of scientists from two countries has completed a study showing a relationship between a gene and the makeup of gastrointestinal bacteria, a suspected culprit in the development of Crohn's disease.

The scientists represented the Karolinska Institutet in Sweden and Scotland's University of Glasgow. Their findings suggest that the human genome -- billions of particles organized into DNA molecules -- might be at least partially responsible for which microbes reside in the digestive tract, according to Medical News Today. The collection of these microbes, also numbering in the billions, is known as the gut microbiota. Its composition varies among humans.

The hypothesis suggested by the small study is that an individual's genetic makeup customizes his or her microbiota. While much more research will be necessary to determine how specific microbiota profiles are created, the hypothesis has significant implications for treating diseases associated with bacterial composition of the gut. Among them are Crohn's disease and obesity.

Crohn's disease is one of the two main types of inflammatory bowel disease (IBD). The Mayo Clinic says that the inflammation it leaves behind spreads deep into the layers of the intestine, though the illness can strike anywhere in the digestive tract. This incurable disease causes abdominal pain, severe diarrhea, and a host of other symptoms, some of which are also common to its cousin, ulcerative colitis, the other primary type of IBD.

Around 700,000 Americans suffer from Crohn's disease, according to the Crohn's & Colitis Foundation of America. Despite decades of research, scientists have not identified a specific cause of the illness. However, most blame a combination of issues. The most likely are a faulty immune system that causes the body to attack normally benign substances like "good" bacteria, genetics, and environmental factors.

The European study included a statistical analysis on DNA involving 30 specific genes for 51 healthy subjects with no history of intestinal disorders. These genes had already been linked to elevated risk of developing Crohn's.

A variation in one, known as the IRGM gene, was connected to higher-than-normal amounts of a microbe called Prevotella. Genetics Home Reference indicates that this gene furnishes instructions to make a protein with a role in surrounding and destroying invaders like bacteria and viruses.

Several variations in or near this gene are associated with an elevated risk for Crohn's. The study suggested that the IRGM gene could influence the makeup of a person's microbiota so that it favors a bacteria like Prevotella over a close relative, Bacteroides.

For Crohn's patients like me, the study offers the possibility of treating the disease by restoring normal intestinal flora rather than turning to surgery or anti-inflammatory or immunosuppressant medications with significant side effects. Linking a specific gene to gut flora and Crohn's disease could be the beginning of highly individualized treatment for the disorder.

Vonda J. Sines has published thousands of print and online health and medical articles. She specialized in diseases and other conditions that affect the quality of life.

See the article here:
Study Links Gene to Gut Flora and Crohn's Disease

Genetic analysis added to procedure offers way to reveal malignancies

By Nathan Seppa

Web edition: January 9, 2013

A multipurpose version of a Pap smear can detect genetic signs of ovarian or uterine cancer in women, researchers report. When applied to the cervical swabs, the experimental analysis spotted genetic mutations in every sample from uterine cancer patients and in many from those with ovarian cancer.

The test is far from clinic-ready. But if confirmed in larger studies and developed into a usable Papgene test, as the study authors propose, the new approach could change cancer testing in women. The study appears in the Jan. 9 Science Translational Medicine.

Although the genetic screen caught uterine cancers more consistently, it is more apt to have a major impact on diagnosing ovarian cancer, says Shannon Westin, a gynecologic oncologist at the University of Texas M.D. Anderson Cancer Center in Houston who wasnt part of the study team. While uterine cancers are often found due to vaginal bleeding and diagnosed with ultrasound tests, ovarian cancers remain hidden because they lack obvious symptoms and reliable screening tests. That makes the cancer deadly, she says.

Researchers identified 12 genetic mutations that show up in uterine or ovarian tumors. They reasoned that a Pap test could detect these mutations since some cancerous cells get shed from the ovaries and uterus and travel to the cervix, the conical structure where the uterus meets the vagina. A doctor swabs the cervix with a brush to get a sample of cells for a Pap smear, an exam that normally checks for aberrant cell growth related to cervical cancer and can also look for the genetic signature of the virus that causes it.

The researchers tested 46 Pap smears from cancer patients. The new test found at least one genetic mutation in all 24 samples taken from uterine cancer patients and in nine of 22 samples from ovarian cancer patients. Many of the cancers were still in an early stage at the time the Pap smears were performed, says study coauthor Luis Diaz Jr., an oncologist at Johns Hopkins University.

Tests on Pap smears from 14 women without cancer showed no signs of the 12 mutations.

This study is really encouraging, says Michael Melner, a molecular biologist and scientific program director for the American Cancer Society, based in Atlanta. The strength of this is that Pap tests are already being done. You could just expand on that.

Continue reading here:
Updated Pap smear detects ovarian, uterine cancers

Connie K. Ho for redOrbit.com Your Universe Online

If youre thinking of eating a burger and have the right DNA, you might just get away with eating this fatty culinary delight without doing too much damage to your waistline. Researchers from the Health Sciences Department at the University of California, Los Angeles (UCLA) recently found that genetics can affect the way a persons body-fat levels react to a fast-food diet. The researchers found a number of genes that they believe manage those reactions, adding further fuel to the debate over whether genes or environment are the main culprit in obesity, and providing at least a partial answer to the question: Is obesity genetic?

The findings of the study were recently featured in the online edition of the journal Cell Metabolism. The scientists believe that the study is unique in its observation of metabolic responses in regards to a diet high in sugar and fat content.

The team studied a diverse mouse population in specific environmental conditions, allowing them to create a model that resembled the diversity of natural human populations. What they found is that the risk of obesity was only partially affected by the amount and type of food consumed.

Our research demonstrates that body-fat responses to high-fat, high-sugar diets have a very strong genetic component, and we have identified several genetic factors potentially regulating these responses, explained the studys first author Brian Parks, a postdoctoral researcher at UCLA, in a prepared statement.

We found that obesity has similar genetic signatures in mice and humans, indicating the mice are a highly relevant model system to study obesity. Overall, our work has broad implications concerning the genetic nature of obesity and weight gain.

The project shows that while fatty diets and a sedentary lifestyle can definitely impact an individuals chances of becoming obese, peoples body-fat reactions may also be a large part attributed to their inherited DNA. The study was conducted over a period of two years, during which scientists tracked adipose (fat) tissue, global gene expression, intestinal flora (normal intestinal bacteria), and obesity traits in regards to a diet high in sugar and fat.

The team experimented with a group of over 100 inbred strains of mice that were first placed on a normal diet for eight weeks and then given a diet high in fat and sugar the following eight weeks. The researchers determined 11 genome-wide regions that were linked to fat gain and obesity that were affected by diets high in fat and sugar.

We measured the change in fat dynamically, at five different points following a high-fat, high-sugar feeding, providing strong evidence for a genetically controlled body-fat set-point, continued Parks in the statement. Our use of inbred mice strains also enabled detailed analysis of the relationship between obesity traits, gene expression, intestinal flora and diet.

There was a range of dietary responses from the different strains of mice, with increase of body-fat percentage between zero to over 600 percent. During the first four weeks of the high-fat, high-sugar diet, many of the strains of the mice responded to the diet. However, following this initial period, there was no more accumulation of extra fat. Researchers believe that this shows that there is a certain set-point at which the body stops gaining fat due to genetic factors.

Continued here:
Is Obesity Genetic? Study Highlights New Link Between DNA And Body Fat

CHAPEL HILL, N.C. Even if the patients hadnt been as young as 4 months old, the surgery would have been harrowing: six holes bored into the skull, six tiny tubes inserted directly into targeted parts of the brain, then a solution containing hundreds of millions of viruses pumped in.

But the rare degenerative illness it fights is even scarier. Canavan disease strikes infants, essentially making the brain attack itself with a toxic chemical, stopping and reversing development. It then kills, usually before age 10.

The procedure used in the study though, slows Canavans progress and improves and may even help extend their lives, according to a study that appeared last month in the online journal Science Translational Medicine. It does that by using viruses as microscopic trucks to deliver missing genetic material precisely where its needed in the kids brains.

This form of gene therapy was created at UNC-Chapel Hill, and the viral vehicle and genetic cargo used in the study were developed there at the medical schools Gene Therapy Center. Center director R. Jude Samulski was a senior author of the study, which began in 2001 and tracked 13 children who received the treatment.

The youngest was 4 months old, the oldest 83 months when they got the operation. After the procedure, the researchers, led by Paola Leone, an associate professor of cell biology at the University of Medicine and Dentistry of New Jersey, followed them to see how the therapy affected their illness.

To an outsider, the results might not even be noticeable. To the families, though, the changes began quickly and were nothing short of dramatic.

Right away, we saw a significant change in his eyes, said Jordana Holovach of Rye, N.Y., whose son Jacob participated in the study. He then was able to regain some of the strength he had lost in grasping, improved his head control, his immune system clearly got better, and he was even with some assistance able to take steps, something we never thought wed be able to see.

Jacob, who had the operation in 2001, will be 17 years old in February. He has grown so much that he doesnt have the strength to take steps now, but attends a mainstream high school, albeit with substantial help.

Ilyce Randell of Buffalo Grove, Ill., whose son Max was diagnosed when he was little more than 4 months old, said that he hadnt seemed to use his eyes at all before the operation, which he had when he was 3 years old. Not long after it, though, he clearly was focusing on things, and began using his arms.

To this day, his sight is improving, and he barely needs glasses. Thats a huge thing, when youre trapped in your body, she said.

Excerpt from:
UNC scientists use virus to deliver genetic material to slow kids' illness

For those who are overweight, it is not entirely your fault. Researchers at UCLA say it's not just what you eat that makes those pants tighter it's also genetics. In a new study, scientists discovered that body-fat responses to a typical fast-food diet are determined in large part by genetic factors, and they have identified several genes they say may control those responses. The study is the first of its kind to detail metabolic responses to a high-fat, high-sugar diet in a large and diverse mouse population under defined environmental conditions, modeling closely what is likely to occur in human populations. The researchers found that the amount of food consumed contributed only modestly to the degree of obesity.

The findings are published Jan. 8 in the online edition of the journal Cell Metabolism and will appear Jan. 9 in the print version.

Like many other medical conditions, obesity is the result of an interplay between genetic and environmental factors. Polymorphisms in various genes controlling appetite and metabolism predispose to obesity under certain dietary conditions. The percentage of obesity that can be attributed to genetics varies widely, depending on the population examined, from 6% to 85% as reported in various studies. As of 2006, more than 41 sites on the human genome have been linked to the development of obesity when a favorable environment is present. "Our research demonstrates that body-fat responses to high-fat, high-sugar diets have a very strong genetic component, and we have identified several genetic factors potentially regulating these responses," said first author Dr. Brian Parks, a postdoctoral researcher at the David Geffen School of Medicine at UCLA. "We found that obesity has similar genetic signatures in mice and humans, indicating the mice are a highly relevant model system to study obesity. Overall, our work has broad implications concerning the genetic nature of obesity and weight gain." The dramatic increase in obesity in the world over the past few decades has been tightly associated with an increase in obesity-related conditions such as type 2 diabetes, heart disease and cancer. While high-calorie diets containing high levels of fat and sugar, along with sedentary lifestyles, have been considered the most significant environmental factors contributing to this epidemic, the new UCLA research demonstrates that body-fat responses to food are strongly inherited and linked to the DNA in genes. During the two-year study, researchers measured obesity traits, adipose (fat) tissue, global gene expression and intestinal flora (normal intestinal bacteria) in response to a high-fat, high-sugar diet in more than 100 inbred strains of mice. They identified 11 genome-wide regions associated with obesity and fat gain due to high-fat, high-sugar intake. Several identified regions overlap with genes identified in human studies. For the study, the mice were placed on a normal diet for the first eight weeks of life and were subsequently switched to a high-fat, high-sugar diet for eight weeks. "We measured the change in fat dynamically, at five different points following a high-fat, high-sugar feeding, providing strong evidence for a genetically controlled body-fat set-point," Parks said. "Our use of inbred mice strains also enabled detailed analysis of the relationship between obesity traits, gene expression, intestinal flora and diet." Dietary responses, as assessed by the body-fat percentage increase during high-fat, high-sugar feeding, varied widely among the strains, with increases in body-fat percentage ranging from 0 to more than 600 percent in the various strains of mice. Most strains responded during the first four weeks of the high-fat, high-sugar feeding and did not accumulate additional fat during the remainder of the study. This suggests an upper body-fat set-point whereby continued gain in body fat is resisted by genetic mechanisms, the researchers said. Additionally, "We observed high heritability of about 80 percent for body-fat percentage across the study timeline," said principal investigator Dr. Jake Lusis, a professor of medicine and human genetics and of microbiology, immunology and molecular genetics at the Geffen School of Medicine. "Changes in body-fat percentage after high-fat, high-sugar feeding were also highly heritable, suggesting that dietary responses are strongly controlled by genetics." The results are consistent with the inheritance of body mass index (BMI) and obesity in humans and emphasize the importance of genetics in controlling obesity, the study authors said. The researchers note that over consumption of high-calorie, high-sugar food is an important factor contributing to the obesity epidemic but stress that food consumption is only one of many environmental factors that affect obesity. "Our results emphasize the importance of gene-by-environment interactions, with important implications for an understanding of the overall genetic architecture of obesity," Lusis said. "In particular, it will be of interest to examine behavioral and neurological differences among the strains as they relate to obesity traits." The researchers conclude that, based on their data, there appears to be a strong link between DNA and the amount of fat gained when a high-calorie, high-sugar diet is consumed.

For further information see Genetics.

Gene Diet image via UCLA.

Read the rest here:
Genetic Obesity

Do genetics play a role in eosinophilic esophagitis?
APFED #39;s Educational Webinar Series Presents... Answers from Experts Do genetics play a role in eosinophilic esophagitis? Ikuo Hirano, MD Professor of Medicine Fellowship Program Director Northwestern University School of Medicine Created through a collaboration between the American Partnership for Eosinophilic Disorders http://www.APFED.org and the Center for Managing Chronic Disease at the University of Michigan http

By: APFED

Read more:
Do genetics play a role in eosinophilic esophagitis? - Video

Joey Swoll training shoulders at Jersey Shore Fitness
Team Shredz athlete Joey Swoll trains shoulders at Jersey Shore Fitness. Joey starts off the video with his #trainharderthanme movement quote and takes us through an intense shoulder workout. Check out Joey Swoll and the complete Product Line of Beyond Genetics Supplements the makers of Shredz at: ** wwww.breakingpastgenetics.com ** ** http://www.facebook.com/getshredz **

By: GetShredz

See the original post:
Joey Swoll training shoulders at Jersey Shore Fitness - Video

Sex linked Genetics
Mrs. K explains sex-linked traits and how to complete punnett squares for sex-linked traits.

By: Meredith Kersting

Read this article:
Sex linked Genetics - Video

Escutcheon - Kill Mode
Taken from the album "Battle Order" (2009) Melodic Death metal inspired by the old Swedisch Gothenburg style LYRICS: Awakening, it #39;s hard to breathe The darkness is surrounding Cannot move, fear returns to pain I close my eyes Drift away, again The fluid is pumped away My lungs are expanding with air As we #39;re brought back to life once again I #39;ll never get used to this, panic will overtake Gasping, shaking, screaming, fighting, free Expanding cells, regaining life, reborn again Bio-genetics will complete this war machine The memories of the fight, so vividly Can #39;t tell the dream from reality Relive the past once more Regiment is going down Big red blur, then it fades away ... fades away Thirty years and the second battle we have just won It #39;s time to go, back to hell and fight for our good cause Not all is lost, Renewed with strength, armor and more men We were meant to fight this war and Victory was ours to take No matter what the cost was going to be Conquer all the worlds, our destiny All worn out, defending armor The reason that I get this chance Another tour, another mission Maybe it #39;s my last and go down in a bang Let #39;s go now and ride out to fight Don #39;t stop, hesitate, give it all Send them back to where they came from Finally... avenge our grief, for so long Approaching the field, pitch black night Switch into kill mode, attack

By: Alwin Bassphyx

See more here:
Escutcheon - Kill Mode - Video

James Gilliland and Giles Campbell, January 8th 2013
*I do not own this work, it belongs to James Gilliland, the world puja network and the great artists who took part in all aspects of it. Copyright Disclaimer Under Section 107 of the Copyright Act 1976, allowance is made for "fair use" for purposes such as criticism, comment, news reporting, teaching, scholarship, and research. Fair use is a use permitted by copyright statute that might otherwise be infringing. Non-profit, educational or personal use tips the balance in favor of fair use.* bull; Contact with multiple Beings bull; Out of body experiences manifested by meditation bull; Understanding self, realization and forgiveness bull; The struggle with this reality continues...... Giles Campbell has a degree in Zoology and a Masters in Biodiversity and conservation genetics. He worked within the Australian government scientific research organization (CSIRO) for 9-10 years. Over the past five years he has experienced different types of contact with different beings, been followed by lights and this finally led to a great awakening. This transformation accelerated in recent years and months as his life has radically changed and set in a new direction after having had a number of paradigm shattering experiences, including contact with extra dimensional entities and spontaneous out of body experiences. Giles has visited the ECETI Ranch numerous times in 2012 and has traveled to other power points on the planet in his travels. For more information have a look here: - ECETI.org Insulting ...

By: EroSeninka

Read more:
James Gilliland and Giles Campbell, January 8th 2013 - Video

Teresa Edmondson, Natural Health Practitioner
Invitation to our Nutrition Genetics presentation at the Link Centre in Tupelo.

By: Genes Don #39;t Lie

See original here:
Teresa Edmondson, Natural Health Practitioner - Video

Congressional Briefing 2012
A Congressional briefing "The Multi-Generational Impact of Autoimmune Disease: America #39;s Silent Health Crisis" was held March 28th, 2012, at the Rayburn House Office Building on Capitol Hill, in Washington, DC. The briefing to bring national attention to the serious issue of autoimmune disease was co-sponsored by the National Coalition of Autoimmune Patient Groups (NCAPG) and the American Autoimmune Related Diseases Association (AARDA). The briefing opened with Dr. Lindsey Criswell of the University of California who presented "Introduction to the Autoimmune Problem: Genetics and Autoimmune Disease". Next, Dr. Nicole McDonald and her family shared their family #39;s range of members affected with some type of autoimmune disease. Dr. McDonald #39;s teen daughter has Graves #39; disease (thyroid), her mother has ulcerative colitis (an autoimmune disease of the colon), her father has Hashimoto #39;s (thyroid disease), her sister has vitiligo and psoriasis (skin conditions), and her first cousin has Ankylosing Spondylitis (autoimmune degeneration in the backbone). Dr. Robert Phillips, Director of the Center for Coping, in Long Island, NY (familiar to those who have attended past ITP conferences), discussed the emotional and family cost implications of autoimmune diseases. Info via http://www.pdsa.org

By: AARDATube

See the original post here:
Congressional Briefing 2012 - Video