Public release date: 16-Jan-2013 [ | E-mail | Share ]

Contact: Sophie Mohin smophin@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, January 16, 2013Scientists invariably conduct debates in private about whether a body of scientific work or thought is worthy of presentation to the community. Behind closed doors scientists and editors tussle over when is the right time to publish their work. In a disruptive departure from this norm, Disruptive Science and Technology, a peer-reviewed journal from Mary Ann Liebert, Inc. publishers, has launched a Debate section in which ideas and counterpoints can be debated in public. The Journal seeks not to sway opinions but rather to inform them. It is fitting that the first series of debates is focused on the root cause of cancer.

Most cancer researchers would likely agree that not understanding how cancer develops is a major obstacle in the ongoing "war on cancer." However, in some scientists' minds the mechanism that underlies tumor development is not settled science. Under the Somatic Mutation Theory, cancers arise as a consequence of changes to DNA, while the Tissue Organization Field Theory states that they result from disruptions in normal cell communication needed to correctly form tissues. The initial debate explores these two major theories of cancer development in Disruptive Science and Technology, and the articles are available free on the Journal website at http://www.liebertpub.com/dst.

Stuart Baker, ScD, National Cancer Institute (Bethesda, MD), initiates the debate with the article, "Paradoxes in Carcinogenesis Should Spur New Avenues of Research: An Historical Perspective." Dr. Baker describes "paradigm instability" between the two main explanations of how cancer develops the more the dominant theory is investigated without a conclusive resolution, the more proponents think they are getting closer to understanding and the more others think the evidence is pointing to an alternative theory. Dr. Baker discusses paradoxes experimental and observational results that are not fully explained by one theory but which make sense under the other. He proposes focusing more research on explaining these paradoxes.

Vincent Wilson, PhD, Louisiana State University (Baton Rouge, LA), emphasizes that cancer develops as a result of both genetic and environmental factors in "Carcinogenesis as the Sum of Its Parts." Regardless of the specific causative event, multiple changes are required for an individual cancer cell and a tumor to develop. He suggests either combining the two main proposals for the mechanism of carcinogenesis, or subdividing cancer into subgroups developing specific hypotheses to explain the cause of each type.

Eric Lagasse, PharmD, PhD, University of Pittsburgh School of Medicine (PA), argues in "Battling Cancer: In the End What Matters the Most?" that while the initial event resulting in cancer is not yet clear, pointing out yet another cancer formation theory (Cancer Stem Cell Theory), cancer treatment can be improved by tailoring therapy to target the genetic characteristics of a patient's most aggressive tumor cells and to continue to monitor and modify treatment as needed to overcome drug resistance.

"The mechanisms underlying cancer formation are complex and not completely understood, even after some victories in the 'war on cancer,'" says Editor-in-Chief Alan J. Russell, PhD, Highmark Distinguished Career Professor, Carnegie Mellon University, Pittsburgh, PA. "Drs. Baker, Wilson, and Lagasse present different points of view as to the most likely explanations for carcinogenesis. A deeper understanding of cancer mechanisms is important for designing therapeutics and formulating new research questions."

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Contact: Alan J. Russell, PhD Highmark Distinguished Career Professor Carnegie Mellon University 914-740-2100 alanrussell@cmu.edu

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Embracing debate on how cancers develop: Without the answer, effective therapies remain elusive

Recommendation and review posted by Bethany Smith

Public release date: 15-Jan-2013 [ | E-mail | Share ]

Contact: Vicki Cohn vcohn@liebertpub.com 914-740-2100 x2156 Mary Ann Liebert, Inc./Genetic Engineering News

New Rochelle, NY, January 15, 2013A novel therapeutic approach called exon skipping involves bypassing a disease-causing mutation in a gene to restore normal gene expression and protein production. Two innovative examples of this strategy used to correct gene defects associated with muscular dystrophy are described in articles in Human Gene Therapy, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers. The articles are available free on the Human Gene Therapy website.

Willem Hoogaars and a team of researchers from France, the Netherlands, Finland, and Germany evaluated a combination of an exon-skipping treatment delivered via an adeno-associated virus (AAV) vector and a compound that inhibits myostatin signaling in a mouse model of Duchenne muscular dystrophy. The dual treatments led to improved muscle force and a decrease in ineffective muscle contractions, as well as increased body weight, muscle mass, and muscle fiber size. They did not, however, improve the effects of each treatment given individually. The results are reported in the article "Combined Effect of AAV-U7-Induced Dystrophin Exon Skipping and Soluble Activin Type IIB Receptor in mdx Mice."

Francesca Gualandi and colleagues, University of Ferrara and University of Padua, Italy, used exon skipping to inactivate mutated RNA messages responsible for defective collagen structure and function in muscle tissue affected by Ullrich muscular dystrophy or Bethlem myopathy. The authors describe their approach in "Antisense-Induced Messenger Depletion Corrects a COL6A2 Dominant Mutation in Ullrich Myopathy."

"This combines two very promising therapeutic approaches in a relevant animal model of muscular dystrophy," says James M. Wilson, MD, PhD, Editor-in-Chief, and Director of the Gene Therapy Program, Department of Pathology and Laboratory Medicine, University of Pennsylvania Perelman School of Medicine, Philadelphia.

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About the Journal

Human Gene Therapy, the Official Journal of the European Society of Gene and Cell Therapy, British Society for Gene and Cell Therapy, French Society of Cell and Gene Therapy, German Society of Gene Therapy, and five other gene therapy societies, is an authoritative peer-reviewed journal published monthly in print and online. Human Gene Therapy presents reports on the transfer and expression of genes in mammals, including humans. Related topics include improvements in vector development, delivery systems, and animal models, particularly in the areas of cancer, heart disease, viral disease, genetic disease, and neurological disease, as well as ethical, legal, and regulatory issues related to the gene transfer in humans. Its sister journal, Human Gene Therapy Methods, published bimonthly, focuses on the application of gene therapy to product testing and development, and Human Gene Therapy Clinical Development, launching in 2013, publishes data relevant to the regulatory review and commercial development of cell and gene therapy products. Tables of content for all three publications and a free sample issue may be viewed on the Human Gene Therapy website.

About the Publisher

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Exon skipping to restore gene expression is promising therapeutic strategy for muscular dystrophy

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Public release date: 15-Jan-2013 [ | E-mail | Share ]

Contact: Kathy Wallis kwallis3@uwo.ca 519-661-2111 x81136 University of Western Ontario

Researchers at Western University in London, Canada, have identified a new genetic mutation for amyotrophic lateral sclerosis (ALS), opening the door to future targeted therapies. Dr. Michael Strong, a scientist with Western's Robarts Research Institute and Distinguished University Professor in Clinical Neurological Sciences at the Schulich School of Medicine & Dentistry, and colleagues found that mutations within the ARHGEF28 gene are present in ALS. When they looked across both familial and sporadic forms of the disease, they found that virtually all cases of ALS demonstrated abnormal inclusions of the protein that arises from this gene. The research is published online in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneratio, the official journal of The World Federation of Neurology Research Group on Motor Neuron Diseases.

ALS, sometimes called Lou Gehrig's disease, is a progressive disease that affects the motor neurons that connect the brain to muscles throughout the body. It is a devastating disease with 90 per cent of patients dying within five years of diagnosis. As many as 30,000 Americans and 2,000 Canadians are living with ALS.

Strong's team is convinced ALS is a disorder of RNA metabolism. RNA is the intermediary or messenger between genes and the protein being made. This new protein appears to play a critical role. "Every time we look at a cell degenerating, this particular protein was deposited abnormally in the cell. It was a common denominator," explains Strong, who is also the Dean of Schulich Medicine & Dentistry. "Working with Dr. Rob Hegele at Robarts, we found there was a genetic mutation in the gene coding for this protein. So it's a huge discovery."

Unlike most proteins which have one key function, this one has two. "One side works with RNA. The other side has the capacity to regenerate or to deal with an injury. We think those are competitive activities so if it's doing one, it's not available to do the other," says Strong. In the case of ALS, Strong believes the protein is disturbed on the RNA side so it's no longer able to respond to cell injury. "We need to understand what causes the switch between the two functions, and then can we modulate it."

###

The research was funded by the Canadian Institutes of Health Research and the ALS Society of Canada.

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.

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Western University researchers identify new genetic mutation for ALS

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In 1968, Dr. Elliot Vesell, Penn State College of Medicines first chair of the Department of Pharmacology, discovered that a persons genetic makeup influences how a drug commonly used to thin blood is metabolized by the body. Four decades later, scientists have found the specific genetic sequences that determine this response. Physicians can now use a patients unique genetic signature to prescribe the right dose to be effective and not too much to cause excess bleeding.

Today, in the same halls where Vesell made his discovery, Penn State Hershey Institute for Personalized Medicine opened the doors to its new space, which will help scientists make the next important finds for improving health using genetic and biologic data and rapidly evolving computational techniques.

Launched in February 2012 under the leadership of James Broach, Ph.D., the institute works in close collaboration with departments and other institutes across the Hershey campus, including the Penn State Clinical and Translational Science Institute, to advance personalized medicine research and to translate that research into clinical applications.

During the dedication, Dr. Harold L. Paz, Penn State Milton S. Hershey Medical Center and Health System CEO, Penn States senior vice president for health affairs, and dean of the College of Medicine, said personalized medicine is the next frontier in medicine.

Medicine has always been personal, but through the research conducted here, we will now be able to fulfill the promise envisioned by early pioneers like Dr. Vesell and create a future in which it is possible to help each person tailor the healthiest possible lifestyle, and when necessary, to treat each patient with an individually designed medication, Paz said.

Paz joined local dignitaries for the institute dedication, including Sen. Bob Casey and state Department of Health Acting Secretary Michael Wolf.

The institute is developing the necessary resources for personalized medicine research, including a biorepository to collect, process and storewith informed consentblood and tissue samples from patients who visit Penn State Hershey Medical Center and its outpatient practice sites, plus the technology and computing power needed to analyze these samples. Together with information stored in the electronic health record, this secure bank of de-identified biological samples will allow scientists and physicians to develop better ways to diagnose, treat or cure certain diseases and illnesses, particularly those more prevalent in people living in central Pennsylvania.

Our efforts to advance personalized medicine will not be confined to the laboratory and research space we are unveiling today, said Dr. Daniel Notterman, vice dean for research and graduate studies for the College of Medicine, Penn States associate vice president for health sciences research, and professor of pediatrics, biochemistry and molecular biology. We are also engaging the communities and patients we serve in our efforts. Patients who volunteer to give samples for use in this important research can take pride in knowing they are helping us to uncover better ways to diagnose, treat, and prevent diseases and conditions that affect not only them but others in their families and in our community.

The institutes new space and equipment were supported by $2.85 million in National Institutes of Health funds and by $1.5 million in state tobacco settlement CURE grant funds.

The public can learn more about personalized medicine and participating in the Penn State Hershey biorepository at two town hall sessions in March: March 5 at 7 p.m. at the University Conference Center on the Penn State Hershey campus, and March 19 at 7 p.m., at Penn State Hershey Medical GroupCamp Hill. More information on these sessions will be available soon on the institutes web site, med.psu.edu/ipm.

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Penn State Hershey dedicates new Institute for Personalized Medicine

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Investigators probe mechanisms of RNA synthesis

Newswise NEWARK, N.J. One of the most extraordinary properties of living cells is their ability to precisely reproduce themselves through processes that transfer genetic information from one cell to the next. However, there are times when one of the steps of information transfer, transcription, goes awry at the cellular level, potentially producing diseases such as cancer and other health disorders. Unraveling how those processes work and how substandard transcription can be prevented is a major goal of biomedical science. Progress in this area may also lead the way toward development of drugs that target the genetic transcription process in disease-causing microbes.

A research team led by Arkady Mustaev, PhD, of the Public Health Research Institute (PHRI) at the University of Medicine and Dentistry of New Jersey-New Jersey Medical School, has published a study posted online by the Journal of Biological Chemistry, that describes an effort by the investigators to understand the underlying mechanisms of high precision (fidelity) of RNA synthesis by RNA polymerase, the major enzyme that promotes the transcription process. They attempted to influence the role of active center tuning (ACT) -- a mechanism they first identified -- in the process of transcription fidelity, which is the accurate copying of genetic information.

ACT is a rearrangement of the RNA polymerase catalytic center from an inactive to a catalytically proficient state. The investigators found that both reactions of NTP polymerization and hydrolytic RNA proofreading are performed by the same active center that includes two magnesium (Mg) ions coordinated by aspartate triad. The active center is normally turned off since it is missing one of Mg ions. Correct NTP substrates as well as misincorporated RNA residues can promote ACT by inclusion of the missing Mg ion through establishing recognition contacts in the active center. Incorrect substrates cannot trigger ACT and are rejected. The investigators also demonstrate that transcript cleavage factors Gre build on ACT mechanism by providing the residues for stabilization of catalytic Mg ion and for activation of the attacking water causing 3000-4000-fold reaction enhancement thereby strongly reinforcing proofreading.

The suggested ACT mechanism is fundamentally different from that proposed for DNA replication enzyme, DNA polymerase (DNAP) in which the active centers for DNA synthesis and proofreading are separated and discrimination between deoxy- and ribo-substrate is achieved through strict fitting requirements for the sugar rather than through active center rearrangement. In DNAP active center carboxylates stem from rigid scaffolds, while in multisubunit RNAP they reside in an apparently flexible loop. ACT is accompanied by significant re-shaping of the loop, which would not be possible in DNAP.

This study was supported by NIH grant RO1 GM-30717-21.

Journalists who wish to speak with Dr. Arkady Mustaev should contact Rob Forman, UMDNJ Chief of News Services, at 973-972-7276 or formanra@umdnj.edu .

About PHRI: The Public Health Research Institute (PHRI) (www.phri.org) is a 71-year-old biomedical research organization that emphasizes translational approaches to overcome critical issues of infectious diseases. Founded in New York City, PHRI became an academic affiliate of the New Jersey Medical School-University of Medicine and Dentistry of New Jersey (UMDNJ) in 2006. PHRIs 23 laboratories work on a wide range of infectious diseases issues including HIV and other viruses, TB, hospital and community acquired bacterial infections, fungal infections, biodefense and drug resistance. Fundamental knowledge of the disease process and its components is used to develop a new generation of diagnostics, therapeutics and vaccines. For more than 7 decades, PHRIs culture of research innovation and excellence has led to important new discoveries in science and medicine.

About UMDNJ: The University of Medicine and Dentistry of New Jersey (UMDNJ) is New Jerseys only health sciences university with more than 6,000 students on five campuses attending three medical schools, the States only dental school, a graduate school of biomedical sciences, a school of health related professions, a school of nursing and New Jerseys only school of public health. UMDNJ operates University Hospital, a Level I Trauma Center in Newark, and University Behavioral HealthCare, which provides a continuum of healthcare services with multiple locations throughout the State.

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New Paths Explored for Curbing Genetic Malfunctions

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Jan. 15, 2013 Western researchers have identified a new genetic mutation for amyotrophic lateral sclerosis (ALS), opening the door to future targeted therapies.

Dr. Michael Strong, Schulich School of Medicine & Dentistry dean, and colleagues discovered mutations within the ARHGEF28 gene are present in ALS. When they looked across both familial and sporadic forms of the disease, they found virtually all cases of ALS demonstrated abnormal inclusions of the protein that arises from this gene.

Strong is a scientist with Western's Robarts Research Institute and Distinguished University Professor in Clinical Neurological Sciences at Schulich.

The study is published online in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, the official journal of The World Federation of Neurology Research Group on Motor Neuron Diseases.

ALS, sometimes called Lou Gehrig's disease, is a progressive disease that affects the motor neurons connecting the brain to muscles throughout the body. It is a devastating disease with 90 per cent of patients dying within five years of diagnosis. As many as 2,000 Canadians and 30,000 Americans are living with ALS.

Strong's team is convinced ALS is a disorder of RNA metabolism. RNA is the intermediary or messenger between genes and the protein being made. This new protein appears to play a critical role.

"Every time we look at a cell degenerating, this particular protein was deposited abnormally in the cell. It was a common denominator," Strong said. "Working with Dr. Rob Hegele at Robarts, we found there was a genetic mutation in the gene coding for this protein. So it's a huge discovery."

Unlike most proteins which have one key function, this one has two.

"One side works with RNA. The other side has the capacity to regenerate or to deal with an injury. We think those are competitive activities so if it's doing one, it's not available to do the other," Strong said.

In the case of ALS, Strong believes the protein is disturbed on the RNA side so it's no longer able to respond to cell injury.

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New genetic mutation for amyotrophic lateral sclerosis identified

Recommendation and review posted by Bethany Smith

London researchers have identified a genetic mutation that may open doors to better understand, and potentially treat, Lou Gehrigs disease.

Led by Michael Strong, the dean of Schulich Medicine and Dentistry at Western University, the researchers believe theyve fingered a genetic culprit behind a disease called amyotrophic lateral sclerosis (ALS) that disrupts motor neurons that connect the brain to muscles and kills its victims, 90% of them within five years of diagnosis.

Ive been working in ALS research for 25 years. Its a tough disease ... But this is a big opening. This is a London discovery, Strong said Tuesday,

Researchers found mutations in a gene that were present in nearly all ALS patients but not in healthy individuals, a gene called ARHGEF28.

The gene is linked to the production of proteins that help to stabilize and repair cells in health people researchers suspect the repair function is compromised by the defects.

Strongs work is published online in Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration, the official journal of The World Federation of Neurology Research Group on Motor Neuron Diseases.

While there are other genetic defects linked to ALS, including one Strong pinpointed six years ago, he believes those in ARHGEF28 appear to be the common denominator.

His research has already sparked inquiries from labs in Germany, Israel and Italy.

There will be a lot of interest worldwide, Strong said.

No wonder as many as 30,000 Americans and 2,000 Canadians are living with ALS.

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Western University researchers discover genetic mutation linked to Lou Gehrig's disease

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A technique which allows genetic editing has been successfully tested on human cells meaning that genetic medicine -- previously an expensive and complex endeavour -- could become simple and affordable.

The process was discovered in 2012 by Jennifer Doudna and Martin Jinek of the Howard Hughes Medical Institute at the University of California, Berkeley working with Emmanuelle Charpentier of the Laboratory for Molecular Infection Medicine Sweden. Initially it described genomic editing in bacterial cells but has now been tested on human DNA .

"The ability to modify specific elements of an organism's genes has been essential to advance our understanding of biology, including human health," said Doudna. "This is going to remove a major bottleneck in the field, because it means that essentially anybody can use this kind of genome editing or reprogramming to introduce genetic changes into mammalian or, quite likely, other eukaryotic systems."

The editing system uses an enzyme-RNA complex, Cas9, present in some bacteria which conduct genetic editing for self preservation. The bacteria can cut up viral DNA strands and integrate it with their own DNA. They are then able to synthesise working copies of the genetic material in the form of RNA which binds to and inactivates the attacking virus.

"The beauty of this compared to any of the other systems that have come along over the past few decades for doing genome engineering is that it uses a single enzyme," explained Doudna. "The enzyme doesn't have to change for every site that you want to target -- you simply have to reprogram it with a different RNA transcript, which is easy to design and implement."

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Editing tool successfully created for human genome

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How To Gain Weight If You Have Skinny Genetics?
SUBSCRIBE TO MY VERTICAL JUMP CHANNEL! http://www.youtube.com LIKE ON FACEBOOK! http://www.facebook.com MY VERTICAL JUMP PROGRAM theverticaljumptruth.blogspot.com Everyone has the potential to gain weight, even with skinny genes. If you are genetically skinny than it is important for you to stay CONSISTENT. CONSISTENCY IS KEY TO SUCCESS. To gain weight you must eat more calories than you are burning. You also need to focus on compound movements such as squats, deadlifts, bench press and military press,

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Mendelian Genetics Experiment
HSA Euless STEM Project 2012-2013

By: Mendel Genetics

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Mendelian Genetics Experiment - Video

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Advanced Genetics Athlete Melanie Gardner
Contest Prep for the Arnolds I do not own the rights to the music heard in this video. It belongs to the respective copyright owners. I upload these videos to promote the artists to an audience that may not otherwise take notice of the artist and for nothing more. Do NOT duplicate and/or sell this video at any time or to anyone. No copyright infringement intended. If you would like me to remove this video because of any legal issues, please message me and I will promptly and gladly do so

By: Jason Green

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Advanced Genetics Athlete Melanie Gardner - Video

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Daily Weight Loss Weight Loss Quick Weight loss
#9658; #9658;goo.gl #9658; #9658;goo.gl #9658; #9658;goo.gl Watch My Full Video http://www.youtube.com Daily Weight Loss Weight Loss Quick Weight loss Software BLAST Basic Local Alignment Search Tool . Splign Vector Alignment Search Tool VAST . Conserved Domain Search Service CD Search . Database of Genotypes and Phenotypes dbGaP . Map Viewer Online Mendelian Inheritance in Man OMIM . Bookshelf Database of Genotypes and Phenotypes dbGaP . RefSeqGene All Genetics Medicine Resources. Genomes Maps Database of Genomic Structural Variation dbVar . Homology BLAST Basic Local Alignment Search Tool . BLAST Link BLink Conserved Domain Database CDD . Conserved Domain Search Service CD Search . Protein Clusters All Homology Resources. Sequence Analysis BLAST Basic Local Alignment Search Tool . BLAST Link BLink Conserved Domain Search Service CD Search . Variation Database of Genomic Structural Variation dbVar . Database of Single Nucleotide Polymorphisms dbSNP . But y,ou s_hould tr,y the alternative ,m+edication! Large a mount of fa,t food -lack #39; of activity i #39;n your lif e can caus #39;e ob_esity. Total Price: Depends on the product properties you select. Place of Origin: Guangdong China Mainland is_customized:. Shipment : You can have your goods shipped by. Please note that buyers are responsible for all other potential fees or taxes, for instance, customs fees, duties, commissions/brokerage, or taxes for the importation. We can not guarantee the delivery time on all international shipments due to the ...

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Daily Weight Loss Weight Loss Quick Weight loss - Video

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How to get a flat stomach in a day
#9658; #9658;goo.gl #9658; #9658;goo.gl #9658; #9658;goo.gl Watch My Full Video http://www.youtube.com how to get a flat stomach in a day people with Hashi #39;s www ahsta com is a website that supports people who are using LDN for autoimmune thyroid disease. Hashi #39;s, AI, Celiac, Low Aldo, menopause, MVP, pyroluria. Another possibility is that the doc subscribes to the "the gut is the source" school of thought and will want you on a very strict diet, plus antifungals and probiotics. Thanks everyone! I wish I could post to his website directly, but I don #39;t know if that is allowed since we aren #39;t supposed to drop the names of doctors on here and it is the site for his clinic. He has almost all his alternative therapies listed on there, but none of them seem to target thyroid specifically. I will go back on and look for the ones mentioned here though. Citations may include links to full-text content from PubMed Central and publisher web sites. PubChem Substance All Chemicals Bioassays Resources. DNA RNA BLAST Basic Local Alignment Search Tool . Data Software BLAST Basic Local Alignment Search Tool . Splign Vector Alignment Search Tool VAST . Conserved Domain Search Service CD Search . Database of Genotypes and Phenotypes dbGaP . Map Viewer Online Mendelian Inheritance in Man OMIM . Bookshelf Database of Genotypes and Phenotypes dbGaP . RefSeqGene All Genetics Medicine Resources. Genomes Maps Database of Genomic Structural Variation dbVar . Homology BLAST Basic Local Alignment Search Tool . BLAST Link ...

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Races and Human Genetic Variation
Many people are under the mistaken impression that people from different racial backgrounds have big differences in their DNA instructions. But this is not the case. The entire human race has an incredibly low level of genetic variety. Some biologists have remarked that if you sequenced the DNA instruction of two humans on opposite sides of the globe they #39;d have less change in their DNA than two chimps on the same mountain in Africa. These discoveries have profound implications. Since the human race has relatively low genetic variety that means it must have originated recently. The racial groups have not therefore evolved independently over long periods of time. These discoveries are consistent with the bible #39;s timeframe, whereby the human race originated from a single set of parents, only thousands of years ago and the people groups have originated since then. Related Articles: Noah and Genetics (creation.com Could Adam and Eve have given rise to all races? (creation.com The non-mythological Adam and Eve (creation.com Related Products: Mitochondrial Eve and the Daughters of Noah DVD (creation.com Genetic Entropy and the Mystery of the Human Genome (creation.com

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Farmer Testimonials on GM Alfalfa
Farmers from across Canada describe how genetically engineered (genetically modified or GM) alfalfa would affect them. Do farmers need GM alfalfa? This year there is a new industry push to pave the way to introduce GM alfalfa into Canada. The company Forage Genetics wants to sell GM alfalfa seeds in Canada (seeds with Monsanto #39;s Roundup Ready herbicide tolerant trait). Its not legal to sell GM alfalfa seeds in Canada until Forage Genetics gets variety registration. In October 2012, the industry group called the Canadian Seed Trade Association began to push a plan for "co-existence" of GM and non-GM alfalfa, to pave the way to introduce GM alfalfa in Canada via Ontario. However, "co-existence" is not possible - GM alfalfa cannot be controlled but will contaminate farmers #39; fields across the country. Take action today or find out more info at http://www.cban.ca Thank you to the National Farmers Union and the NFU Youth for these testimonials.

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learn how to lose weight fast.mp4
find out new stategies for weight loss 2013 a75005stqin2q89--0icj8orv6.hop.clickbank.net get a FREE copy of our "Food Factor" book sent immediately to your email. Dr. Charles DC Licensed Chiropractor, Wellness Professional, and Author of The Fat Loss Factor Being fat is not genetic. True, your entire family may be overweight but it doesn #39;t mean that you have to be. There are success stories all the time of people overcoming their "genetics" and possibly increasing your chances of rapid fat loss. Just watch the TV show "The Biggest Loser" (google it if you #39;ve never seen it) It is full of people who have overcome their "genetics". Want to know a sort of secret? Your genes do not control your weight... your lifestyle does. Your genes are like a light switch, you can turn them on and off depending what you do with your life. Don #39;t be a victim of yourself and everything that you hear! Most over eating is due to STRESS. People will eat when they are nervous, worried, sad, depressed, anxious, scared, etc. This is a very common problem facing our society and there is a simple solution. Manage your stress. We dedicate a giant section of the book to this problem alone. One easy way to lose weight quickly without actually doing ANYTHING physical or to your diet, decrease your stress levels. When your stress levels are high, your stress hormones sky rocket which make you hungry. For many, it can be harder to control your portions, to stop emotional eating, and stop binge eating ...

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color genetics for rabbits

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LDSF Conference 2012 Dr. Bart Loeys
Dr. Bart Loeys, Professor of Medical Genetics, Antwerp University Hospital, and member of the Loeys-Dietz Syndrome Foundation Medical Advisory Council (MAC), present, "Introduction to Loeys-Dietz Syndrome: A Broad overview of genetics and medical features of individuals with Loeys-Dietz syndrome," at the 2012 LDSF Conference in Baltimore, Maryland, USA.

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The simple entrance of this oldfield mouse burrow should not mislead you about its architectural complexity.

Vera Domingues/Hopi Hoekstra, Harvard University

Humans engage in a lot of complex behaviors, but many of them are learned. Genetics gives us a nervous system that's flexible enough to incorporate new behaviors, and we pick them up socially. But many animals display highly complex behavior that appears to be instinctual. Which raises the question of how these sorts of behaviors can be programmed into the nervous system genetically.

Pretty simply, if a new study of mice is to be believed. The work compared the architecture of burrows built by two closely related species. The researchers find the design of the animals' burrows is modular, and the two modules are largely controlled by a handful of genesperhaps as few as four in total.

The work relied on two closely related species. One is the deer mouse, which is widespread in North America. This species makes very simple burrows, with a short entry passage leading to a nest. In the southeastern US, however, there's a closely related species, the oldfield mouse, that builds a far more complex home. This includes a much longer entrance passage and a secondary "escape tunnel" from the back of the nest that allows it a safe route out should a predator come in the front door.

Various information, such as the species' geographic ranges and their close similarity, suggest the oldfield mice are offshoots of the more widely ranging deer mouse. If accurate, this would suggest the oldfield's burrowing behavior evolved since its separation from the parent species.

To confirm the burrowing behavior was under genetic control, the authors brought some of each species into the lab and raised offspring in cages that lacked any material for them to dig burrows. Then, when the mice were mature, they were set loose into a larger area filled with a sandy soil. Despite never having seen a parent's burrow, the mice quickly dug one that was similar to those that their fellow species members dig in the wild. You can see an example of how the authors managed to study the burrow's properties in the video below.

The researchers obtained casts of the mice's burrows in order to measure them. (video courtesy of Jesse Weber, Harvard University)

With the importance of genetics established, the authors set about studying it. Because the two species are so closely related, they were able to get the mice to mate, creating an offspring that was a 50/50 mix of the DNA of the two species. They tested these hybrids for behavior, and in all cases, they acted like the oldfield mice, making longer burrows with an escape tunnel. That, in a classic Mendelian way, suggests the genes that control these behaviors are dominant.

At first glance, it also suggested the suite of behaviors might all be inherited together. But the authors did further crosses to test that by mating the hybrids with regular deer mice (which build simple burrows). The burrows made by the animals that resulted tended to be a bit shorter, on average, than those of the oldfield mice, and only some of these offspring made escape tunnels. The presence of an escape tunnel did not correlate with the length of the burrow, suggesting these two traits are unlinked.

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Complex behaviors driven by remarkably simple genetics

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Public release date: 16-Jan-2013 [ | E-mail | Share ]

Contact: Jean-Franois Hupp jean-francois.huppe@dc.ulaval.ca 418-656-7785 Universit Laval

This press release is available in French.

Quebec City, January 16, 2013Genetics plays a major role in peer rejection and victimization in early elementary school, according to a study recently published on the website of the journal Child Development by a team directed by Dr. Michel Boivin, a research professor at Universit Laval's School of Psychology.

To come to this conclusion, Boivin and his team tested over 800 twins at three time points: when they were in kindergarten, Grade 1, and Grade 4. This sample consisted of 41% monozygotic twins"true" twins who share 100% of their genesand 59% "false," or fraternal twins who share an average of 50% of their genes. Each subject, their classmates, and their teacher were asked questions relating to peer rejection and victimization.

The research revealed that pairs of twins presented significant similarities with respect to relationship problems. Their analyses determined that these similarities were over 73% attributable to genetic factors. "Certain genetically transmissible traits that underlie physical appearance or behaviorparticularly aggressive, impulsive, and hyperactive behaviorsincrease the risk of rejection or victimization," asserts Michel Boivin, holder of the Canada Research Chair in Child Development.

Researchers also noted that relationship problems persisted between kindergarten and Grade 4, largely due to genetic factors.

"The good news is that it is possible, in kindergarten if not earlier, to identify children who might have trouble relating to their peers and quickly intervene," stresses Boivin. "We have to keep the personal characteristics that make them less popular with other kids from creating a vicious circle of rejection and victimization."

Between 5 and 10% of children experience chronic rejection or victimization in elementary school. These relationship difficulties can lead to academic problems, health issues, and a series of mental health complications like depression, anxiety, and suicidal ideation. "That's why it's so important to know when and how these problems appear and develop," concludes Dr. Boivin.

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Genetics plays major role in victimization in elementary school

Recommendation and review posted by Bethany Smith

SALT LAKE CITY, Jan. 15, 2013 (GLOBE NEWSWIRE) -- Myriad Genetics, Inc. (MYGN) today announced that it will issue financial results for the second fiscal quarter 2013 following the close of market on Tuesday, February 5, 2013.

The Company will also host a conference call on Tuesday, February 5, 2013 at 4:30 P.M. Eastern to review the financial results. Participating on the call will be: Peter Meldrum, President and Chief Executive Officer, Mark Capone, President of Myriad Genetic Laboratories, Inc. and Jim Evans, Chief Financial Officer.

To listen to the call, interested parties within the U.S. may dial 800-732-6870, or +1 212-231-2900 for international callers. All callers will be asked to reference reservation number 21645936.

The conference call will also be available through a live webcast at http://www.myriad.com.

A replay of the call will be available two hours after the end of the call for seven days and may be accessed by dialing 800-633-8284 within the U.S. or +1 402-977-9140 for international callers, and entering reservation number 21645936.

About Myriad Genetics

Myriad Genetics is a leading molecular diagnostic company dedicated to making a difference in patients' lives through the discovery and commercialization of transformative tests to assess a person's risk of developing disease, guide treatment decisions and assess risk of disease progression and recurrence. Myriad's portfolio of molecular diagnostic tests are based on an understanding of the role genes play in human disease and were developed with a commitment to improving an individual's decision making process for monitoring and treating disease. Myriad is focused on strategic directives to introduce new products, including companion diagnostics, as well as expanding internationally. For more information on how Myriad is making a difference, please visit the Company's website: http://www.myriad.com

Myriad, the Myriad logo, BRACAnalysis, Colaris, Colaris AP, Melaris, TheraGuide, Prezeon, OnDose, Panexia and Prolaris are trademarks or registered trademarks of Myriad Genetics, Inc. in the United States and foreign countries. MYGN-F, MYGN-G

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Myriad Genetics to Announce Second Fiscal Quarter 2013 Results on Tuesday, February 5, 2013

Recommendation and review posted by Bethany Smith

The Sea Slug That Eats The Sun: Sidney Pierce at TEDx TampaBay (The Future of Stories)
Dr. Sidney Pierce is currently a professor at the University of South Florida #39;s Department of Integrative Biology. His current research involves photosynthetic animals, especially the molecular biology behind the intracellular symbiosis between the digestive cells of a sea slug (Elysia chlorotica) and algal (Vaucheria litorea) chloroplasts, with applications in medicine mdash;gene therapy. Dr. Pierce #39;s work has been featured on radio, TV, newspapers, magazines, and even Weekly Reader, internationally as well as domestically. In fact, his research was recently featured in a French documentary, "The Power of Plants" on the France 5 network in France.

By: TEDxTalks

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The Sea Slug That Eats The Sun: Sidney Pierce at TEDx TampaBay (The Future of Stories) - Video

Recommendation and review posted by Bethany Smith

Washington, January 16 (ANI): In a preliminary study in a canine model of Duchenne muscular dystrophy (DMD), researchers have shown a giant leap using gene therapy to treat muscular dystrophy.

Muscular dystrophy occurs when damaged muscle tissue is replaced with fibrous, bony or fatty tissue and loses function. Duchenne muscular dystrophy is the most common type of muscular dystrophy predominantly affecting boys.

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.

For years, scientists have been working to find the key to restoring dystrophin, but they have faced many challenges.

One of the largest hurdles in DMD gene therapy is the large size of the gene. Dystrophin is the largest gene in the human genome, containing approximately 4,000 amino acids.

To fit the dystrophin gene into a vehicle that could deliver the gene to the appropriate site in the body, one has to delete 70 percent of the gene. The highly abbreviated gene is known as the "micro-dystrophin" gene.

Previous studies suggest that micro-dystrophin can effectively stop muscle disease in mice that are missing dystrophin. However, mice that are missing dystrophin show minimal DMD symptoms, and results from mice often do not predict what will happen in humans.

In contrast to mice, loss of dystrophin results in severe muscular dystrophy in dogs. If micro-dystrophin can work in dystrophic dogs, it will likely work in human patients. Unfortunately, when micro-dystrophin was tested in dogs in previous studies, it was not successful.

To overcome these hurdles, a team led by Dongsheng Duan, the Margaret Proctor Mulligan Professor in Medical Research at the University of Missouri School of Medicine, engineered a new micro-dystrophin gene that carries an important functional region missing in previously tested micro-dystrophins.

"We placed the new microgene into a virus and then injected the virus into dystrophic dogs' muscles," Duan said.

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Experts take quantum leap in gene therapy to treat muscular dystrophy

Recommendation and review posted by Bethany Smith

Sleep problems and sleep apnea in persons with spinal cord injury
In this video you will learn about the causes and consequences of sleep problems, including a detailed discussion of sleep apnea, and treatments that can improve your health and well-being. Presented by Don Fogelberg, PhD, assistant professor, Department of Rehabilitation Medicine, University of Washington, and Stephen Burns, MD, associate professor, Department of Rehabilitation Medicine, University of Washington and director, SCI Service, VA Puget Sound Health Care System, Seattle, Washington. Sleep problems are common in persons with SCI.

By: UWSpinalCordInjury

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Sleep problems and sleep apnea in persons with spinal cord injury - Video

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#33 - Tissue regeneration, stem cells, regenerative medicine
The ability of tissues to repair themselves is influenced by their capacity to regenerate the missing tissue and their ability that is inherent for them to divide and undergo mitosis. In most continuously dividing tissues the mature cells are terminally differentiated and short-lived. As mature cells die the tissue is replenished by the differentiation of cells generated from stem cells. Thus, in these tissues there is a homeostatic equilibrium between the replication and differentiation of stem cells and the death of the mature, fully differentiated cells. Regenerative medicine is the "process of replacing or regenerating human cells, tissues or organs to restore or establish normal function".

By: Kevin Mangum

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#33 - Tissue regeneration, stem cells, regenerative medicine - Video

Recommendation and review posted by sam