Archive for the ‘Gene Therapy Research’ Category

Forearm Exercises | Behind The Back Wrist Curls
Forearm exercises are essential to making the forearms grow especially if you don #39;t have naturally well developed forearms like I do. Doing the behind the back wrist curl will help develop the forearms, especially toward the back of them (the flexor muscles). Forearm exercises can only help you reach the physique that you want. If you do have good genetics for the forearms, it would still help to do forearm exercises to make them look even bigger. http://www.rippedandjacked.com http

By: RippedAndJacked

Read the original:
Forearm Exercises | Behind The Back Wrist Curls - Video

New hereditary breast and ovarian cancer courses
Hereditary Breast and Ovarian Cancer syndrome (HBOC) is an inherited tendency to develop breast, ovarian, and other cancers, and at a younger age than usual. The majority of HBOC is due to a mutation in either the BRCA1 or BRCA2 genes. Dr. Banu Arun, co-medical director and clinical cancer genetics professor, describes new free continuing medical education courses that covers information on a woman #39;s risk of developing breast cancer, screening, chemoprevention, genetic testing for breast cancer, and management of disease.

By: mdandersonorg

Read more from the original source:
New hereditary breast and ovarian cancer courses - Video

Bodybuilding Routine - Routine Maintenance Ep. 2 Featuring Mischa Janiec
Routine maintenance is a series of videos that focuses on the analysis and breakdown of bodybuilding posing routines. This episode features Mischa Janiec from Polska Genetics. Mischa #39;s Pages: Polskagenetics.com http://www.youtube.com Please Read: The Better Aesthetics YouTube channel is dedicated to providing the viewer with relevant, informative videos that offer the opportunity to expand your knowledge base in an interactive way designed to promote good practices in regards to posing in bodybuilding. Although the process of making these videos (pre post production, including all other steps) is long and consuming, we do it without compensation from any persons or organizations. All that we ask of the viewer is this: if you enjoyed any of our videos and honestly appreciated any aspect of it, we ask that you LIKE, RATE and SHARE the video. These actions (specifically sharing) DIRECTLY influence a YouTube channels viewership, which is one of the most meaningful things we could ask for from our audience. Please take this passage seriously, and help us improve our viewership if you enjoy any of our work. Thank you -Nick Colvill

By: BetterAestheticsBB

Here is the original post:
Bodybuilding Routine - Routine Maintenance Ep. 2 Featuring Mischa Janiec - Video

Ambry Genetics RainDance Technologies "Fully Automated"
Ambry Genetics offers an inside look at RainDance #39;s new fully-automated, high-throughput targeted sequencing system.

By: RainDanceTechnologie

See the article here:
Ambry Genetics

Ep 2 - Peel Forest Estate Deer - PGG Wrightson Stud Tour 2012
Rural TV NZ in association with New Zealand #39;s leading agriculture company, PGG Wrightson, present the PGG Wrightson Stud Tour 2012. PEEL FOREST ESTATE DEER GENETICS, GERALDINE, SOUTH CANTERBURY, NEW ZEALAND - GRAHAM CARR Peel Forest is home to world class red deer and the exclusive purebred Furzeland herd. Graham and his team at Peel Forest breed outstanding deer for both the trophy and venison markets. Graham is passionate about his association with Prof. Frank Griffin of the Department of Microbology at the University of Otago in their research into the genetic corealation of Johnes disease in deer. Contact Graham Carr or Steve Blanchard at Peel Forest Estate for more information. W : http://www.peelforestdeergenetics.com E : deercarr@xtra.co.nz MAKE SURE YOU SUBSCRIBE TO OUR YOU-TUBE CHANNEL TO WATCH THE NEXT EPISODE OF THE PGG WRIGHTSON STUD TOUR! JOIN RURAL TV NZ on FACEBOOK : http://www.facebook.com FOLLOW Us on TWITTER : twitter.com

By: RURALTVNZ

Originally posted here:
Ep 2 - Peel Forest Estate Deer - PGG Wrightson Stud Tour 2012 - Video

BlueDawg StarHaze ~ Titan Genetics Test Grow Ep. 3
Hey guys! Back with the 3rd installment of the Titan Genetics test grow. We got KILLER germ rates on this gear! Star Haze cracked 100% and the Blue Dawgs cracked at 90%. I will keep that last bean in the wet paper towel for another 12-24 hrs... probly just 12... if nothing has happened or it hasnt cracked it gets tossed. Star Haze - 10/10 (60hrs from going into wet paper twoel) Blue Dawg - 8/9 (60hrs from going into wet paper towel)

By: PNWGardenOfFunk

See more here:
BlueDawg

Ep1 - Red Oak Angus - PGG Wrightson Stud Tour 2012
Rural TV NZ in association with New Zealand #39;s leading agriculture company, PGG Wrightson, present the PGG Wrightson Stud Tour 2012. RED OAK ANGUS STUD, WEKA PASS, NORTH CANTERBURY, NEW ZEALAND - RIC DEBS ORR With regard to genetics Red Oak advocate a balanced approached using Estimated Breeding Values as a guide depending on accuracies combined with actual figures and common sense stockmanship. Only sires which have been bred and performed under NZ hill country conditions are used at Red Oak in North Canterbury, New Zealand. Contact Ric Orr at Red Oak Angus Stud for more information. W : http://www.redoakstud.co.nz E : redoakstud@amuri.net MAKE SURE YOU SUBSCRIBE TO OUR YOU-TUBE CHANNEL TO WATCH THE NEXT EPISODE OF THE PGG WRIGHTSON STUD TOUR! JOIN RURAL TV NZ on FACEBOOK : http://www.facebook.com FOLLOW Us on TWITTER : twitter.com

By: RURALTVNZ

View original post here:
Ep1 - Red Oak Angus - PGG Wrightson Stud Tour 2012 - Video

A rogue gene that drives the spread of aggressive breast cancer could help scientists develop better forms of diagnosis and treatment.

The mutant gene, known as KLF6-SV1, may provide a test marker for more dangerous breast cancers.

Targeting it could also help to treat some women with a poor prognosis.

"Breast cancer is a genetically complex disease and it remains a challenge to predict disease outcomes and which patients may benefit from more aggressive treatment," said study leader Dr Goutham Narla, from Case Western Reserve University School of Medicine in the US.

"Our research has uncovered a promising gene marker that will not only help us better identify tumours that behave badly, but provide a basis for developing and personalising therapies to better treat our patients."

The gene is linked to disease recurrence and metastasis, the spread of cancer around the body.

Scientists looked at tissue samples from 671 breast cancer patients kept at a tumour bank in the Netherlands.

Women with high levels of the gene variant were 50% more likely to die from their disease.

The findings are published in the journal Science Translational Medicine.

Dr Narla said: "More studies need to be done, but this could provide an important prognostic marker to determine which patients need to be treated more aggressively or watched more closely."

Excerpt from:
Gene clue to breast cancer therapy

NEWARK, Calif., Jan. 23, 2013 (GLOBE NEWSWIRE) -- StemCells, Inc. (STEM) announced today that Ann Tsukamoto, Ph.D., Executive Vice President, Research and Development, will make a presentation on the Company's clinical development programs at the Phacilitate Cell & Gene Therapy Forum to be held January 28-30, in Washington, DC. Dr. Tsukamoto is scheduled to speak at 12:25 p.m. ET on Wednesday, January 30, as part of the session on "Clinical development updates from leading cell and gene therapy product candidates in the clinic for CNS indications."

The Phacilitate Cell & Gene Therapy Forum is a preeminent industry-led meeting designed to help advance regulatory, manufacturing, R&D and commercial strategies and drive cell and gene therapy products forward. The Forum enables executives from global cell therapy, gene therapy and tissue engineering companies, representatives of big pharma and big biotech, regulators and regulatory experts, and public and private investors to meet and share information on the leading edge of the regenerative medicine sector.

About StemCells, Inc.

StemCells, Inc. is engaged in the research, development, and commercialization of cell-based therapeutics and tools for use in stem cell-based research and drug discovery. The Company's lead therapeutic product candidate, HuCNS-SC(R) cells (purified human neural stem cells), is currently in development as a potential treatment for a broad range of central nervous system disorders. In a Phase I clinical trial in Pelizaeus-Merzbacher disease (PMD), a fatal myelination disorder in children, the Company has shown preliminary evidence of progressive and durable donor-derived myelination in all four patients transplanted with HuCNS-SC cells. The Company is conducting a Phase I/II clinical trial in chronic spinal cord injury in Switzerland and recently reported positive interim data for the first patient cohort. The Company is also conducting a Phase I/II clinical trial in dry age-related macular degeneration (AMD), and is pursuing preclinical studies in Alzheimer's disease. StemCells also markets stem cell research products, including media and reagents, under the SC Proven(R) brand. Further information about StemCells is available at http://www.stemcellsinc.com.

The StemCells, Inc. logo is available at http://www.globenewswire.com/newsroom/prs/?pkgid=7014

Apart from statements of historical fact, the text of this press release constitutes forward-looking statements within the meaning of the U.S. securities laws, and is subject to the safe harbors created therein. These statements include, but are not limited to, statements regarding the clinical development of its HuCNS-SC cells; the Company's ability to commercialize drug discovery and drug development tools; and the future business operations of the Company. These forward-looking statements speak only as of the date of this news release. The Company does not undertake to update any of these forward-looking statements to reflect events or circumstances that occur after the date hereof. Such statements reflect management's current views and are based on certain assumptions that may or may not ultimately prove valid. The Company's actual results may vary materially from those contemplated in such forward-looking statements due to risks and uncertainties to which the Company is subject, including those described under the heading "Risk Factors" in the Company's Annual Report on Form 10-K for the year ended December 31, 2011 and in its subsequent reports on Forms 10-Q and 8-K.

The rest is here:
StemCells, Inc. to Present at Phacilitate Cell & Gene Therapy Forum

DUBLIN--(BUSINESS WIRE)--

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

Gene therapy can be broadly defined as the transfer of defined genetic material to specific target cells of a patient for the ultimate purpose of preventing or altering a particular disease state. Genes and DNA are now being introduced without the use of vectors and various techniques are being used to modify the function of genes in vivo without gene transfer. If one adds to this the cell therapy particularly with use of genetically modified cells, the scope of gene therapy becomes much broader. Gene therapy can now combined with antisense techniques such as RNA interference (RNAi), further increasing the therapeutic applications. This report takes broad overview of gene therapy and is the most up-to-date presentation from the author on this topic built-up from a series of gene therapy report written by him during the past decade including a textbook of gene therapy and a book on gene therapy companies. This report describes the setbacks of gene therapy and renewed interest in the topic

Gene therapy technologies are described in detail including viral vectors, nonviral vectors and cell therapy with genetically modified vectors. Gene therapy is an excellent method of drug delivery and various routes of administration as well as targeted gene therapy are described. There is an introduction to technologies for gene suppression as well as molecular diagnostics to detect and monitor gene expression.

Clinical applications of gene therapy are extensive and cover most systems and their disorders. Full chapters are devoted to genetic syndromes, cancer, cardiovascular diseases, neurological disorders and viral infections with emphasis on AIDS. Applications of gene therapy in veterinary medicine, particularly for treating cats and dogs, are included.

The markets for gene therapy are difficult to estimate as there is only one approved gene therapy product and it is marketed in China since 2004. Gene therapy markets are estimated for the years 2012-2022. The estimates are based on epidemiology of diseases to be treated with gene therapy, the portion of those who will be eligible for these treatments, competing technologies and the technical developments anticipated in the next decades. In spite of some setbacks, the future for gene therapy is bright.The markets for DNA vaccines are calculated separately as only genetically modified vaccines and those using viral vectors are included in the gene therapy markets

The voluminous literature on gene therapy was reviewed and selected 710 references are appended in the bibliography.The references are constantly updated. The text is supplemented with 72 tables and 15 figures.

Profiles of 178 companies involved in developing gene therapy are presented along with 199 collaborations. There were only 44 companies involved in this area in 1995. In spite of some failures and mergers, the number of companies has increased more than 4-fold within a decade. These companies have been followed up since they were the topic of a book on gene therapy companies by the author of this report. John Wiley & Sons published the book in 2000 and from 2001 to 2003, updated versions of these companies (approximately 160 at mid-2003) were available on Wiley's web site. Since that free service was discontinued and the rights reverted to the author, this report remains the only authorized continuously updated version on gene therapy companies.

Benefits of this report

- Up-to-date on-stop information on gene therapy with 72 tables and 14 figures

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

Jan. 22, 2013 Muscular dystrophy is caused by the largest human gene, a complex chemical leviathan that has confounded scientists for decades. Research conducted at the University of Missouri and described this month in the Proceedings of the National Academy of Sciences has identified significant sections of the gene that could provide hope to young patients and families.

MU scientists Dongsheng Duan, PhD, and Yi Lai, PhD, identified a sequence in the dystrophin gene that is essential for helping muscle tissues function, a breakthrough discovery that could lead to treatments for the deadly hereditary disease. The MU researchers "found the proverbial needle in a haystack," according to Scott Harper, PhD, a muscular dystrophy expert at The Ohio State University who is not involved in the study.

Duchenne muscular dystrophy (DMD), predominantly affecting males, is the most common type of muscular dystrophy. Children with DMD face a future of rapidly weakening muscles, which usually leads to death by respiratory or cardiac failure before their 30th birthday.

Patients with DMD have a gene mutation that disrupts the production of dystrophin, a protein essential for muscle cell survival and function. Absence of dystrophin starts a chain reaction that eventually leads to muscle cell degeneration and death. While dystrophin is vital for muscle development, the protein also needs several "helpers" to maintain the muscle tissue. One of these "helper" molecular compounds is nNOS, which produces nitric oxide that can keep muscle cells healthy during exercise.

"Dystrophin not only helps build muscle cells, it's also a key factor to attracting nNOS to the muscle cell membrane, which is important during exercise," Lai said. "Prior to this discovery, we didn't know how dystrophin made nNOS bind to the cell membrane. What we found was that dystrophin has a special 'claw' that is used to grab nNOS and bring it to the muscle cell membrane. Now that we have that key, we hope to begin the process of developing a therapy for patients."

Duan and Lai, scientists with MU's Department of Molecular Microbiology and Immunology, found that two particular sections of the dystrophin gene must be present for nNOS to bind to the muscle cell membrane. The sections of the gene, known as "repeaters 16 & 17," contain a "claw" that can grab nNOS and bring it to the muscle cell membrane so that it will prevent ischemic damage from muscle activity. Without this "claw," nNOS doesn't bind to the cell membrane and the muscle cells are damaged, leading to further problems associated with muscular dystrophy.

The other key to this puzzle is dystrophin. If the protein is not present in the body, no "claw" exists and nNOS would never make it to the muscle cell membrane. For years, scientists have been attempting to find ways to make the body manufacture dystrophin, and thus get nNOS to the muscle cell membrane. Duan and Lai said the answer might lie elsewhere.

"Everybody, including those individuals with muscular dystrophy, has another protein known as 'utrophin,' " said Duan, a Margaret Proctor Mulligan Distinguished Professor in Medical Research at MU. "Utrophin is nearly identical to dystrophin except that it is missing repeaters 16 & 17, so it cannot attract nNOS to the muscle cell membrane. In our study, we were able to modify utrophin so that it had the repeaters, and thus, the ability to grab nNOS and bring it to the muscle cell membrane to protect muscle. Our study was completed in mice, but if we can do the same thing in larger animals, we could eventually have a therapy for humans with this devastating disease."

Harper described the MU research as "as an exquisite example of a basic study with potentially important translational implications for therapy of Duchenne muscular dystrophy. The data from the Duan laboratory, reported in this paper and previous studies, demonstrates that the structural elements required for proper nNOS localization should be included in any DMD therapy for which dystrophin restoration is the goal."

For more than 10 years, Duan has been a leader in muscular dystrophy, gene therapy and biology research at MU. In addition to his recently published study in PNAS, Duan's lab continues to examine the basic scientific mechanisms behind muscular dystrophy as well as strategies for treating the disease. For example, his lab is studying the effectiveness of a gene therapy for treating heart failure associated with Duchenne muscular dystrophy. Using viruses as a means for delivering gene therapy, Duan is also testing how synthetic microgenes could improve muscle function in dystrophic dog and mouse models. In 2011, he and Lai were granted a patent for a synthetic microgene developed in his lab that has now proved to enhance muscle function in dogs. Those results were also published this month in the journal Molecular Therapy.

Go here to see the original:
Scientists discover 'needle in a haystack' for muscular dystrophy patients

DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/c4r24r/epigenetics) has announced the addition of the "Epigenetics Technology Market (Epigenomics, DNA Methylation, Histone Modifications, RNA Interference, Cancer Therapeutics, Personalized Medicine) (2012 - 2017)" report to their offering.

Over the last decade, genomics and proteomics have been used as key tools to discover potential drug targets and to better understand the complexities of biology. To balance research in these areas, epigenetics offers a potential opportunity in understanding the basis of various diseases in a different approach. Thus, epigenetics is study of heritable changes in genome function and gene expression had opened the new gate of biology to understand the basis of diseases and presents incredible opportunities for disease diagnosis and drug discovery.

Report covers the market by therapeutics sector in oncology conditions, non-oncology indications and personalized medicine. The report also covers the market by research and diagnostics sector in gene regulation studies, biomarker detection and drug discovery. In addition, it also includes the factors driving and restraining the market and covers the market scenario in the U.S., Europe, Asia and the Rest of the World (ROW). This report will provide the company profiles of key companies along with the competitive analysis.

The Global Epigenetics market is showing a double digit growth (CAGR 25%) due to supportive factors such as, (i) huge amount of funds and investments, (ii) increasing partnerships and collaborations, and (iii) rapid screening tools. Epigenetics is used in the identification of new epigenetic biomarkers, which will aid in better diagnosis and prognosis of diseases. While there are factors favoring the market growth, there are concerns such as change in re-imbursement systems and lack of predictive markers holding back the growth of this market. However, the positive aspects in this field may very well offset the market restraints to aid the market grow at an exceptional rate.

Key Topics Covered:

1. INTRODUCTION

2. EXECUTIVE SUMMARY

3. EPIGENETICS - TECHNOLOGY LANDSCAPE ANALYSIS

4. EPIGENETICS - MARKET LANDSCAPE ANALYSIS

Follow this link:
Research and Markets: Epigenetics Technology Market (Epigenomics, DNA Methylation, Histone Modifications, RNA ...

Public release date: 22-Jan-2013 [ | E-mail | Share ]

Contact: Leslie Capo lcapo@lsuhsc.edu 504-568-4806 Louisiana State University Health Sciences Center

New Orleans, LA Research led by Dr. Suresh Alahari, the Fred Brazda Professor of Biochemistry and Molecular Biology at LSU Health Sciences Center New Orleans and its Stanley S. Scott Cancer Center, details exactly how the Her2 cancer gene promotes the progression and spread of breast cancer cells. The inactivation of a tumor suppression gene called Nischarin is among the mechanisms identified. The findings provide a new therapeutic target to block the function of Her2. The research was published in Cancer Research, OnlineFirst on January 21, 2013.

About 30% of breast cancers are positive for the Her2 oncogene. Although this gene is implicated in breast cancer, the exact mechanism has been unknown. In this study, the researchers showed that the Her2 oncogene activates two short microRNAs, called miR-27b and miR-23b, which in turn regulate breast cancer progression and lung metastasis. The study also shows, for the first time, that these microRNAs inactivate the function of a tumor suppressor gene called Nischarin, that Dr. Alahari's lab discovered.

Analysis to determine which of a number of cancer-related genes could be potential targets for miR-23b/27b found that only one other gene and Nischarin were directly targeted, and these microRNAs repressed its function. Nischarin is a novel protein that regulates breast cancer cell migration and movement. In a previous study, Dr. Alahari found that breast tumor growth and metastasis were reduced in the samples where they manipulated the overproduction of Nischarin.

"Our data for the first time show that these two microRNAs are highly expressed in breast cancer patients, and we were able suppress the expression of microRNAs using a novel antisense compound that led to inhibition of breast tumor growth in a mouse model," notes Dr. Alahari. "This study will be helpful in developing novel breast cancer therapeutic drugs that target mciroRNAs in breast cancer patients."

Excluding skin cancer, breast cancer is the most common type of cancer among women in the United States. The American Cancer Society estimates 232,340 new cases of invasive breast cancer among American women this year, and 2,240 among men in the US, with 39,620 deaths in women and 410 deaths in men.

Risk factors include aging, weight gain, combined hormone therapy, physical inactivity, and alcohol consumption. A family history increases risk, as does never having had children or having a first child after age 30. Mammography can often detect breast cancer at an early stage when treatment options are greatest and a cure is possible.

###

Researchers from the Cleveland Clinic, Regulus Therapeutics, and the University of Texas MD Anderson Cancer Center also contributed.

See the article here:
LSUHSC research provides new drug target for Her-2 related breast cancer

Public release date: 22-Jan-2013 [ | E-mail | Share ]

Contact: Wolfgang Sadee Wolfgang.Sadee@osumc.edu 614-292-1597 Ohio State University

COLUMBUS, Ohio Scientists have identified genetic circumstances under which common mutations on two genes interact in the presence of cocaine to produce a nearly eight-fold increased risk of death as a result of abusing the drug.

An estimated one in three whites who died of cocaine exposure is a carrier of variants that make cocaine abuse particularly deadly.

The variants are found in two genes that affect how dopamine modulates brain activity. Dopamine is a chemical messenger vital to the regular function of the central nervous system, and cocaine is known to block transporters in the brain from absorbing dopamine after its release.

The same dopamine genes are also targeted by medications for a number of psychiatric disorders. The researchers say that these findings could help determine how patients will respond to certain drugs based on whether they, too, have mutations that interact in ways that affect dopamine flow and signaling.

The scientists had previously identified a total of seven mutations on two dopamine-related genes, some of which were linked to the risk for cocaine abuse death. Years of molecular genetics studies showed that the mutations had specific functions a single variant alone was associated with an almost three-fold increase in risk of dying of cocaine abuse and led researchers to hypothesize that the variants probably interacted because the genes themselves relied on each other for proper function.

A statistical analysis that dissected the complex interactions among the variants combined with cocaine exposure revealed gene-gene-environment interactions that would dramatically increase the risk of death from cocaine abuse.

"Finding an impact factor of 8 just blew us away," said Wolfgang Sadee, professor of pharmacology and director of the Program in Pharmacogenomics at Ohio State University and senior author of the study. "Beyond that, this represents a new paradigm. Going forward, we can ask whether such interactions do exist between variants that may be a normal variation in the population. These kinds of interactions may underlie the genetics of behavior."

These specific findings apply primarily to whites. The researchers found that a different combination of variants affect the risk of cocaine abuse death in African Americans, and that in this population, some of the variants had protective properties.

Continue reading here:
Scientists find gene interactions that make cocaine abuse death 8 times more likely

Jan. 22, 2013 A novel software tool, developed at The Children's Hospital of Philadelphia, streamlines the detection of disease-causing genetic changes through more sensitive detection methods and by automatically correcting for variations that reduce the accuracy of results in conventional software. The software, called ParseCNV, is freely available to the scientific-academic community, and significantly advances the identification of gene variants associated with genetic diseases.

"The algorithm we developed detects copy number variation associations with a higher level of accuracy than that available in existing software," said the lead inventor of ParseCNV, Joseph T. Glessner, of the Center for Applied Genomics at The Children's Hospital of Philadelphia. "By automatically correcting for variations in the length of deleted or duplicated DNA sequences from one individual to another, ParseCNV produces high-quality, highly replicable results for researchers studying genetic contributions to disease."

Glessner is the lead author of a study describing ParseCNV, published Jan. 4 in Nucleic Acids Research.

Copy number variations (CNVs) are particular sequences of DNA, ranging in length from 1000 to millions of nucleotide bases, which may be deleted or duplicated. While in any given region of a person's DNA, CNVs are very rare, everyone's genome has CNVs, many of which play important roles in causing or influencing disease.

In searching for associations between CNVs and diseases, researchers typically perform case-control studies, comparing DNA samples from patients to DNA from healthy individuals, looking for telltale differences in how CNVs are overrepresented or underrepresented.

CNVs, however, occur in multiple types among individuals, said senior author Hakon Hakonarson, M.D., Ph.D., director of the Center for Applied Genomics at The Children's Hospital of Philadelphia. "One person may have a 60-kilobase deletion, while another may have a 100-kilobase deletion; that may determine the difference between a healthy state versus disease. Many CNV detection softwares may misread the boundary of a CNV region, which could lead to a misclassification and result in false-positive or false-negative associations."

ParseCNV is designed with built-in corrections to adjust for these size variations and other red flags that confound results. Using polymerase chain reaction testing to validate the initial findings, the study team determined that the software had called 90 percent of the CNVs accurately -- a better rate than conventional CNV association softwares, which typically produce validation rates that are notably lower.

The authors say the program's comprehensive design, statistical capabilities, and quality-control features lend it versatility, applicable not just to case-control studies, but also to family studies, and quantitative analyses of continuous traits, such as obesity or height.

Glessner says the Center for Applied Genomics team will continue to refine ParseCNV's features as CNV research progresses. Hakonarson adds that the ParseCNV algorithm will advance genomic diagnostics: "It is likely to play a future key role as a research tool in improving detection of CNV association in individual patients enrolled in disease studies -- perhaps through an initial diagnostic screen, to be followed up with a CLIA-certified laboratory test."

An Institutional Development Award from The Children's Hospital of Philadelphia supported this research, along with the Cotswold Foundation and a donation from Adele and Daniel Kubert. The third co-author, also from the Children's Hospital genome center, was Jin Li.

See more here:
Novel gene-searching software improves accuracy in disease studies

Jan. 22, 2013 Scientists have identified genetic circumstances under which common mutations on two genes interact in the presence of cocaine to produce a nearly eight-fold increased risk of death as a result of abusing the drug.

An estimated one in three whites who died of cocaine exposure is a carrier of variants that make cocaine abuse particularly deadly.

The variants are found in two genes that affect how dopamine modulates brain activity. Dopamine is a chemical messenger vital to the regular function of the central nervous system, and cocaine is known to block transporters in the brain from absorbing dopamine after its release.

The same dopamine genes are also targeted by medications for a number of psychiatric disorders. The researchers say that these findings could help determine how patients will respond to certain drugs based on whether they, too, have mutations that interact in ways that affect dopamine flow and signaling.

The scientists had previously identified a total of seven mutations on two dopamine-related genes, some of which were linked to the risk for cocaine abuse death. Years of molecular genetics studies showed that the mutations had specific functions -- a single variant alone was associated with an almost three-fold increase in risk of dying of cocaine abuse -- and led researchers to hypothesize that the variants probably interacted because the genes themselves relied on each other for proper function.

A statistical analysis that dissected the complex interactions among the variants combined with cocaine exposure revealed gene-gene-environment interactions that would dramatically increase the risk of death from cocaine abuse.

"Finding an impact factor of 8 just blew us away," said Wolfgang Sadee, professor of pharmacology and director of the Program in Pharmacogenomics at Ohio State University and senior author of the study. "Beyond that, this represents a new paradigm. Going forward, we can ask whether such interactions do exist between variants that may be a normal variation in the population. These kinds of interactions may underlie the genetics of behavior."

These specific findings apply primarily to whites. The researchers found that a different combination of variants affect the risk of cocaine abuse death in African Americans, and that in this population, some of the variants had protective properties.

The research is published in the online journal Translational Psychiatry.

The mutations are mostly single-nucleotide polymorphisms, or SNPs (pronounced "snips"). Each gene contains two alternative forms -- called alleles -- that are functionally identical in most people. However, in some cases, the activity level, or expression, of an allele can differ from its partner allele in a single gene.

Read the original here:
Gene interactions make cocaine abuse death eight times more likely

IB Genetic Engineering Biotechnology Part 2
Discussion of Cloning, Genetically Modified Organisms, Nuclear Transplantation, Gene Transfer between organisms.

By: Dan Rott

Go here to see the original:
IB Genetic Engineering

Space Hacker Alpha
An early version of a mobile game I #39;m creating. You #39;re a hacker that #39;s had your mind swapped into a purple octopus(or sextopus, damn Genetic Engineering), sent into orbit to hack computer systems around the globe from the comfort of your own satellite. Over the course of the game you get increasingly difficult jobs, to complete the jobs, first you must successfully connect to a computer, then you are presented with a hacking screen, which you have to get a number of file symbols in a row to complete the job, all without getting traced, if you get traced you fail the job and don #39;t receive the reward, when you succeed you will earn valuable cash to upgrade in the way you see fit to complete new hacking jobs. Through various upgrades you can increase your Hacking (which dictates how fast you hack Level of server you can connect to), your Programming (decreases chance of alarm) Luck (increases chance of bonus) Alpha 0.01

By: Daniel Whyte

Read more here:
Space Hacker Alpha - Video

Genetic Engineering Video
Filming

By: DarkRCT

Excerpt from:
Genetic Engineering Video - Video

2012 Biometric Lexicon of Cognitive States - Iasi Romania
Joe Ferguson presents his ideas about machines reading human minds at the Humascend 2012 conference in Iasi, Romaina, where his buddy Adrian Stoica held a conference on Robotics, Cyborgs, Genetic Engineering and Orthopedic surgery in his home town in Romania for Joe #39;s entertainment during his visit to Romania with Adrian. Briefly, the history of biometric signal analysis has peaked at the lie detector, which nobody really trusts but which has clear psychological advantages under interrogation. But the indisputable reality of body language, prosody and other nonverbal and involuntary communication channels reveal the possibility of reading some higher level cognitive states from involuntary biometric information.

By: Joe Ferguson

Read the original here:
2012 Biometric Lexicon of Cognitive States - Iasi Romania - Video

Online narrated tutorial suite teaches you how to effectively and efficiently use OMIM

Seattle, WA (PRWEB) January 22, 2013

OMIM is a catalog of human genes and genetic conditions that helps researchers and clinicians understand the relationship between genes and genetic disease. OMIM is a foundational resource in genomics, and OMIM links and data are found at sites all around the bioinformatics sphere. Knowledge of the full scope of OMIMs data and resources provides access to the most comprehensive understanding of human phenotypes and disease. OMIM contains full text summaries of information from the scientific literature, and provides extensive links to the literature resources and other genomic resource tools as well.

The new tutorial reflects the many changes and enhancements to OMIM, including the new face it received during the move from NCBI to omim.org. New search functions enable more precise and relevant searches for different user communities, including clinical geneticists, genetic counselors, and basic researchers. In addition, OMIM now has more links to other relevant genetics and biomedical research resources around the world.

The online narrated tutorial runs in just about any browser and can be navigated in a number of ways. In just under 30 minutes, the tutorial highlights and explains the features and functionality needed to start using OMIM effectively. The tutorial can be used as an introduction to the catalog of human genes and genetic disorders, as a quick way to view new features and functionality, or simply as a reference tool to understand specific features.

In addition to the tutorial, users can also access training and teaching materials, including the animated PowerPoint slides that serve as a basis for the tutorial, suggested script for the slides, slide handouts, and exercises. This can save a tremendous amount of time and effort for teachers and professors when creating classroom content.

Users can view the tutorials and download the free materials at http://www.openhelix.com/omim.

About OMIM

OMIM is a comprehensive, authoritative compendium of human genes and genetic phenotypes that is freely available and updated daily. The free-text, referenced overviews in OMIM contain information on all known mendelian disorders and over 12,000 genes. OMIM focuses on the relationship between phenotype and genotype. OMIM entries contain copious links to other genetics resources. OMIM is funded by a grant from the National Human Genome Research Institute (NHGRI).

About OpenHelix

Here is the original post:
OpenHelix Announces an Updated Sponsored Tutorial and Training Materials for Online Mendelian Inheritance in Man (OMIM)

Public release date: 22-Jan-2013 [ | E-mail | Share ]

Contact: Bruce Goldman goldmanb@stanford.edu 650-725-2106 Stanford University Medical Center

STANFORD, Calif. Stanford University School of Medicine investigators have found that for people harboring a genetic predisposition that is prevalent among Americans, beta carotene, which the body converts to a close cousin of vitamin A, may lower the risk for the most common form of diabetes, while gamma tocopherol, the major form of vitamin E in the American diet, may increase risk for the disease.

The scientists used a "big data" approach to hunt down interactions between gene variants previously associated with increased risk for type-2 diabetes and blood levels of substances previously implicated in type-2 diabetes risk. In people carrying a double dose of one such predisposing gene variant, the researchers pinpointed a highly statistically significant inverse association of beta carotene blood levels with type-2 diabetes risk, along with a suspiciously high positive association of gamma tocopherol with risk for the disease.

"Type-2 diabetes affects about 15 percent of the world's population, and the numbers are increasing," said Atul Butte, MD, PhD, associate professor of systems medicine in pediatrics. "Government health authorities estimate that one-third of all children born in the United States since the year 2000 will get this disease at some point in their lives, possibly knocking decades off their life expectancies."

Butte is the senior author of the new study, which will be published online Jan. 22 in Human Genetics. The first author, Chirag Patel, PhD, is a former graduate student in Butte's lab and now a postdoctoral scholar at the Stanford Prevention Research Center.

The findings point the way to further experiments that could establish whether beta carotene and gamma tocopherol are, respectively, protective and harmful themselves, or merely "markers" whose blood levels dovetail with the presence or absence of some other substance, process or defect that is a true causal factor.

Moreover, the fact that both beta carotene and gamma tocopherol interact with the same gene variant to influence diabetes risk, albeit in opposite directions, suggests that the protein the gene called, SLC30A4, codes for may play a crucial role in the disease. Indeed, that protein is relatively abundant in insulin-producing islet cells of the pancreas, where it aids the transport of zinc into those cells. This, in turn, triggers the release of insulin, whose adequate secretion by the pancreas and efficient uptake in muscle, liver and fat tissue counters the dangerous buildup of glucose in the blood and, in the long run, the onset of type-2 diabetes.

The genomes of some 50 to 60 percent of the U.S. population carry two copies of that very gene variant, which previous studies have shown to confer a slightly increased risk of contracting type-2 diabetes. This variant was one of 18, each found by other researchers to have a mild association with type-2 diabetes risk, that the Butte team incorporated into its analysis.

These gene/disease connections had been identified via so-called "genome-wide association studies," or GWAS. In such analyses, the genomes of large numbers of people with a disease are compared with those of people without it to see if certain versions of any gene variants occur with substantially greater frequency in one group than in the other.

See the original post here:
Beta carotene may protect people with common genetic risk factor for type-2 diabetes

Cancer Risk Factors - The Risk Factors of Cancer
Cancer Risk Factors. http://www.CancerUncensored.com Welcome to today #39;s issue of cancer uncensored. Hi, I #39;m Chris, and I am the author of cancer uncensored, a step-by-step guide to cancer prevention, early detection and cancer survival. In today #39;s video,I would like to present you with an overview of cancer. I am going to briefly go over exactly what cancer is, what triggers it, what the symptoms are, how you can actively avoid it. We will also go over current treatment methods and alternative medicine. I #39;ll also tell you where you should go to get the most up-to-date news and advancements. Before we get stuck in, I should address two points Firstly, most people are afraid of cancer. I can understand that, as my wife has recently been diagnosed with cancer, but as a society, we must not allow the dread of the disease stop us from taking steps to understand it, because that way we can actively prevent it. One in three of us will be diagnosed with cancer during our lifetimes, and yet 85% of cancer is preventable! This video, and my book, cancer uncensored, can tell you how. So take in as much of this information as you can, because it could save your life. Secondly, you need to realise that cancer is not entirely understood. We have a number of very solid theories, and a lot of study data, but if cancer was fully understood, we might be even closer to a cure. To quote Thomas Edison, "The doctor of the future will no longer treat the human frame with drugs, but rather will cure and ...

By: CancerUncensored

Go here to read the rest:
Cancer Risk Factors - The Risk Factors of Cancer - Video

Cancer Symptoms - Symptoms of Cancer
Cancer Symptoms. http://www.CancerUncensored.com. Welcome to today #39;s issue of cancer uncensored. Hi, I #39;m Chris, and I am the author of cancer uncensored, a step-by-step guide to cancer prevention, early detection and cancer survival. In today #39;s video,I want to give you an overview of cancer. I am going to briefly talk about what cancer is, what triggers it, what the symptoms are, how you can actively avoid it. We #39;ll also go over current treatment options and alternative treatment. I #39;m going to also tell you where you can go to get the most up-to-date news and breakthroughs. Before we get stuck in, I ought to address two points Firstly, people are afraid of cancer. I can fully understand that, as my wife has cancer, but as a society, we must not let the dread of the disease stop us from taking steps to understand it, because that way we can actively prevent it. One in three of us will be diagnosed with cancer during our lifetimes, yet 85% of cancer is avoidable! This video, and my book, cancer uncensored, will tell you how. So take in as much of this data as you can, because it could save your life. Secondly, you need to realise that cancer isn #39;t entirely understood. We have a number of very solid theories, and lots of study data, but if cancer was fully understood, we might be closer to a cure. As Thomas Edison once said, "The doctor of the future will no longer treat the human frame with drugs, but rather will cure and prevent disease with nutrition." But as things currently ...

By: CancerUncensored

Read the original here:
Cancer Symptoms - Symptoms of Cancer - Video

Cancer Therapy - Therapy for Cancer
Cancer Therapy. http://www.CancerUncensored.com. Welcome to today #39;s issue of cancer uncensored. Hi, I #39;m Chris, and I am the author of cancer uncensored, a step-by-step guide to cancer prevention, early detection and cancer survival. In today #39;s video,I would like to present you with an overview of cancer. I #39;m going to briefly talk about exactly what cancer is, what triggers it, what the symptoms are, how you can avoid it. We #39;ll also go over current treatment procedures and alternative treatment. I #39;m going to also let you know where you can go to get the most up-to-date news and breakthroughs. Before we get stuck in, I ought to address two points Firstly, people are afraid of cancer. I can fully understand that, as my wife has cancer, but as a society, we must not allow the fear of the condition stop us from taking steps to understand it, because that way we can actively prevent it. One in three of us will be diagnosed with cancer within our lifetimes, yet 85% of cancer is preventable! This video, and my book, cancer uncensored, can tell you how. So take in as much of this information as you can, because it could save your life. Secondly, you must understand that cancer is not entirely understood. We have quite a few very solid theories, and lots of study data, but if cancer was fully understood, we would be even closer to a cure. As Thomas Edison once said, "The doctor of the future will no longer treat the human frame with drugs, but rather will cure and prevent disease with ...

By: CancerUncensored

Go here to read the rest:
Cancer Therapy - Therapy for Cancer - Video