Genetics Intro - Who is Gregor Mendel?
This video is an introduction to Genetics and Gregor Mendel. The video concludes with a discussion on Genotypes and Phenotypes

By: Charles Filipek

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Genetics Intro - Who is Gregor Mendel? - Video

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#1 How to Train and Build Biceps. Hints and Tips. Bulking Up
How to Train and Build Biceps. Hints and Tips. Bulking Up Yurii Spasokukotskyi, a personal trainer and bodybuilding champion came into the sport in 1994. Initialy he used to have narrow shoulders, weak muscles and a big fat belly. But even after 7 years of regular gym training 3-4 times a week didn #39;t bring hime good results. The reason was that regular and hard workout vs bad genetics was not cool enough without a competent training system. Then Yurii has developed his own system which works 100% and may ba suitable for everybody. And he himself got much greater results in bodybuilding during that one year than during those 7 years of training before. Now all people, who want to get a significant progress in bodybuilding and fitness are getting success with Yurii. He gives personal trainings in Skype and has thousands of happy clients around the world. Build muscle really fast: biceps.com.ua In today #39;s episode, it #39;s time to build some MONSTER BICEPS! I #39;ve gotten a lot of questions lately in the comments about what I do for my arms, and how to develop a big biceps . In this video I #39;m going to show you two of the exact exercises I use to get big arms myself. Building a biceps "peak" will make a HUGE difference in how big your biceps appear. If they #39;re shaped right, your biceps will appear much bigger than someone whose are the same size, but whose biceps do not have a dramatic peak. Developing your bracs (muscles outside your biceps) with the other exercise I show in this ...

By: WorkoutTV24

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#1 How to Train and Build Biceps. Hints and Tips. Bulking Up - Video

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#2 Pretty girls don #39;t like strong men. Joke
Pretty girls don #39;t like strong men. Joke Yurii Spasokukotskyi, a personal trainer and bodybuilding champion came into the sport in 1994. Initialy he used to have narrow shoulders, weak muscles and a big fat belly. But even after 7 years of regular gym training 3-4 times a week didn #39;t bring hime good results. The reason was that regular and hard workout vs bad genetics was not cool enough without a competent training system. Then Yurii has developed his own system which works 100% and may ba suitable for everybody. And he himself got much greater results in bodybuilding during that one year than during those 7 years of training before. Now all people, who want to get a significant progress in bodybuilding and fitness are getting success with Yurii. He gives personal trainings in Skype and has thousands of happy clients around the world. Build muscle really fast: biceps.com.ua In today #39;s episode, it #39;s time to build some MONSTER BICEPS! I #39;ve gotten a lot of questions lately in the comments about what I do for my arms, and how to develop a big biceps . In this video I #39;m going to show you two of the exact exercises I use to get big arms myself. Building a biceps "peak" will make a HUGE difference in how big your biceps appear. If they #39;re shaped right, your biceps will appear much bigger than someone whose are the same size, but whose biceps do not have a dramatic peak. Developing your bracs (muscles outside your biceps) with the other exercise I show in this video will also ...

By: WorkoutTV24

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#2 Pretty girls don't like strong men. Joke - Video

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Thalassaemia - Introduction, Classification, Clinical Features, Diagnosis, Treatment Complications
A brief video to refresh the memories of my busy students with a dose of pathology ! Recording took only half an hour, editing 5 minutes - But uploading was taking for ever ... Hope some one finds this helpful ... peace Tags : Thalassemia, Definition, Classification, Role of Genetics in Thalassemia, Pathophysiology of Alpha and Beta Thalassemia, Clinical Features, Main Findings in Blood Picture, Target Cells, How and why Target Cells Formed in Thalassemia, Role of Parvo virus B19 in thalassemia, Treatment and complications.

By: Rabiul Haque

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Thalassaemia - Introduction, Classification, Clinical Features, Diagnosis, Treatment

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#4 Shoulder Dumbell Fly, one arm style. My own Shoulder Workout
Shoulder Dumbell Fly, one arm style. My own Shoulder Workout Yurii Spasokukotskyi, a personal trainer and bodybuilding champion came into the sport in 1994. Initialy he used to have narrow shoulders, weak muscles and a big fat belly. But even after 7 years of regular gym training 3-4 times a week didn #39;t bring hime good results. The reason was that regular and hard workout vs bad genetics was not cool enough without a competent training system. Then Yurii has developed his own system which works 100% and may ba suitable for everybody. And he himself got much greater results in bodybuilding during that one year than during those 7 years of training before. Now all people, who want to get a significant progress in bodybuilding and fitness are getting success with Yurii. He gives personal trainings in Skype and has thousands of happy clients around the world. Build muscle really fast: biceps.com.ua In today #39;s episode, it #39;s time to build some MONSTER BICEPS! I #39;ve gotten a lot of questions lately in the comments about what I do for my arms, and how to develop a big biceps . In this video I #39;m going to show you two of the exact exercises I use to get big arms myself. Building a biceps "peak" will make a HUGE difference in how big your biceps appear. If they #39;re shaped right, your biceps will appear much bigger than someone whose are the same size, but whose biceps do not have a dramatic peak. Developing your bracs (muscles outside your biceps) with the other exercise I show in ...

By: WorkoutTV24

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#4 Shoulder Dumbell Fly, one arm style. My own Shoulder Workout - Video

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Synastry - Cryolife
A song from an awesome band from new album Our Memetic Imprints, download or buy it from here synastry.bandcamp.com Song will be removed at the request of the author as I do not own it and this video is for promotional purposes of an awesome band. Jimmy Anastasopoulos - Vocals Pavel Ikonomov - Guitars Garen Vartivarian - Bass Kegham Kesserian - Drums All Music by Synastry All Lyrics by Jimmy Anastasopoulos Drums, Guitars and Bass Recorded by JF Dagenais Vocals Recorded by Chris Donaldson Mixed by JF Dagenais Samples production by Kevin Jardine Mastering by Jef Fortin GUITAR SOLO on Negative Genetics by Chris Donaldson. LEAD GUITAR OUTRO on Negative Genetics by JF Dagenais. Artwork by Mikio Murakami @ SILENT Q Design.

By: Necromael21

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Synastry - Cryolife - Video

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J-Don - Bad Odour
J-Don with his reply to Emre Lyrics: [Chorus] Oh Oh sometimes I smell a bad odour, yeah I smell an odour that i #39;ve never never never never smelt before no no i smell a bad odour, yeah Oh Oh sometimes I smell a bad odour, yeah I smell an odour that i #39;ve never never never never smelt before no no i smell a bad odour, yeah Why you sending back and foreskin me to do this I #39;m going to crucify your ass so you can call me Judas I #39;m gonna sharpen up my act cause before my bars were useless standing harmless with an axe pretending to be ruthless stealing my chromosome bar was kind of pathetic lets forget the racism and skip to genetics your mom gives head for bus fare and gets the camel home at least I know no why you #39;ve got down syndrome you follow me around school constantly lurking your skin complexion reminds me of a greasy gherkin your dads a sikh he wears a turban you write crap bars and you think your urban [Chorus] Oh Oh sometimes I smell a bad odour, yeah I smell an odour that i #39;ve never never never never smelt before no no i smell a bad odour, yeah Oh Oh sometimes I smell a bad odour, yeah I smell an odour that i #39;ve never never never never smelt before no no i smell a bad odour, I don #39;t know why I knocked on your door anymore considering I have a key I bet if I opened the door you mom would be waiting for me flicking her bean so vigorously in perfect syncronicity to the theme tune of sesame street flicking it so hard an vigorous, told her not to be so brave and shiverous ...

By: Rap Battles

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J-Don - Bad Odour - Video

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#10 Results before and after. A 50 years old man loses 31 kilo! Diet plus fitness
Results before and after. A 50 years old man loses 31 kilo! Diet plus fitness Yurii Spasokukotskyi, a personal trainer and bodybuilding champion came into the sport in 1994. Initialy he used to have narrow shoulders, weak muscles and a big fat belly. But even after 7 years of regular gym training 3-4 times a week didn #39;t bring hime good results. The reason was that regular and hard workout vs bad genetics was not cool enough without a competent training system. Then Yurii has developed his own system which works 100% and may ba suitable for everybody. And he himself got much greater results in bodybuilding during that one year than during those 7 years of training before. Now all people, who want to get a significant progress in bodybuilding and fitness are getting success with Yurii. He gives personal trainings in Skype and has thousands of happy clients around the world. Build muscle really fast: biceps.com.ua In today #39;s episode, it #39;s time to build some MONSTER BICEPS! I #39;ve gotten a lot of questions lately in the comments about what I do for my arms, and how to develop a big biceps . In this video I #39;m going to show you two of the exact exercises I use to get big arms myself. Building a biceps "peak" will make a HUGE difference in how big your biceps appear. If they #39;re shaped right, your biceps will appear much bigger than someone whose are the same size, but whose biceps do not have a dramatic peak. Developing your bracs (muscles outside your biceps) with the other ...

By: WorkoutTV24

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#10 Results before and after. A 50 years old man loses 31 kilo! Diet plus fitness - Video

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SEATTLE, WA--(Marketwire - Jan 17, 2013) - Atossa Genetics, Inc. ( NASDAQ : ATOS ) announced today that Steven C. Quay, M.D., Ph.D., FCAP, Chairman, CEO and President of Atossa, will make two presentations at the Personalized Medicine World Conference (PWMC) being held at the Computer History Museum in Mountain View, California, on January 28th and 29th, 2013. Dr. Quay will discuss a strategy for providing care to patients at every stage of a disease or condition, and how it may be possible to actually prevent breast cancer.

Here are summaries of his two presentations:

The "CarePath" Business Model in Personalized Medicine - 9:45 am Pacific Time, Jan. 28, 2013

Abstract: Medical practice is moving toward treatments that are based on simple protocols. For example, if a woman has a lump in her breast, she typically gets a standard biopsy. These so-called protocol-driven treatment paradigms thus make it hard for genomics-based diagnostic companies to launch innovative tests that may offer better care but which don't fit the established protocol. There is another possible approach, however -- designing a suite of tests and procedures that work together to help patients at every stage of a disease or condition. Atossa Genetics calls this the 'CarePath' business model, and believes it offers an insightful way to distinguish a truly innovative company from the crowd, to better treat a medical condition by establishing synergies across all parts of the business, and to build stakeholder value for the organization. Atossa Genetics has created such a CarePath for breast health with eleven FDA-cleared medical devices, four CLIA-validated Laboratory Developed Tests, and a planned pharmaceutical/biotech treatment program.

Breast Cancer Prevention through Diagnosis and Treatment - 4:15 pm Pacific Time, Jan. 28, 2013

Abstract: Dr. Quay will discuss how to obtain routine, repeated, painless breast biopsy samples non-invasively for cytopathology, next-generation sequencing, proteome, and transcriptome analysis of precursors to breast cancer. This approach makes it possible to identify the earliest "-omic" changes in reversible precursor lesions of the breast, such as atypical ductal hyperplasia. The test not only provides more accurate assessments of patients' risks of future breast cancer, it also offers a source of breast specimens for potential use in biomarker discovery, clinical trial support and patient selection. And most importantly, it opens the door to ultimately preventing breast cancer through the treatment of reversible hyperplastic lesions within the breast ducts.

"Our personalized medicine approach to breast health represents a new paradigm in the way we think about and approach breast cancer and breast cancer prevention," stated Dr. Quay. "I appreciate the opportunity to make two presentations at this important conference, which brings together thought leaders from many prestigious institutions, including Stanford University, Harvard University and other world-renowned institutions."

About Atossa Genetics, Inc.

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

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

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Atossa Genetics, Inc. to Present at the Personalized Medicine World Conference in Mountain View, California

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An Australian researcher has developed a gene therapy for HIV - which has the potential to stop the virus from turning deadly.

David Harrich, an associate professor at the Queensland Institute of Medical Research (QIMR), will begin animal trials this year, but experiments in humans are still five years away.

Harrich has manipulated an HIV protein involved in gene expression, known as Tat, and turned it into a weapon against the virus.Using human immune system cells, known as T-cells, in the laboratory, he's shown the mutant protein prevents HIV replication.

At the same time, Harrich said the modified protein, dubbed Nullbasic, did not appear to adversely affect the human cells.

"So far we haven't found that Nullbasic causes toxicity in the cells we've tested," he said.

"I'm excited. Every test I've done with this agent has succeeded. It makes me optimistic it will work in humans. At the same time, I'm a skeptical scientist, and I'm going to require proof it can jump every hurdle."

QIMR researchers will soon begin testing the protein in mice.

"Before you can trial it on humans, it's going to have to go through rigorous testing in animals for safety," Harrich said.

In order for human cells to make the HIV-inhibitory protein in the laboratory, Harrich had to insert a new gene - a process known as gene therapy.

He said the idea of gene therapy being used as a treatment for HIV had gained momentum since the case of a man known as the Berlin Patient, considered by doctors to have been cured of the virus.

The rest is here:
Australian researcher may have developed the cure for AIDS

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Pressure Ulcers Can Wreck Your Life! Preventing and Managing Skin Problems After Spinal Cord Injury
Pressure ulcers are a serious and scary matter. This presentation illustrates why you should care about pressure ulcers and the potential consequences of developing one. Learn about the risk factors and common causes of skin breakdown after spinal cord injury, how to recognize the early signs of skin trouble, what to do if you think you are developing a pressure ulcer, appropriate treatments for ulcers of different stages, and the specific things that you and your support system can do to help prevent a pressure ulcer from happening to you.

By: UWSpinalCordInjury

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Pressure Ulcers Can Wreck Your Life! Preventing and Managing Skin Problems After Spinal Cord Injury - Video

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MFIII Swiss Cell Therapy for Regeneration, Rejuvenation and Revitalisation
MFIII Swiss Cell Therapy for Regeneration, Rejuvenation and Revitalisation

By: Vina Higgs

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MFIII Swiss Cell Therapy for Regeneration, Rejuvenation and Revitalisation - Video

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ALLENDALE, N.J. and OXFORD, United Kingdom, Jan. 16, 2013 (GLOBE NEWSWIRE) -- NeoStem, Inc. (NYSE MKT:NBS) and its subsidiary, Progenitor Cell Therapy LLC ("PCT"), together with Adaptimmune Limited and Adaptimmune LLC (collectively, "Adaptimmune"), announced today a Services Agreement under which PCT will provide services to support Adaptimmune's NYESO-1c259-T cell therapy product being developed for multiple oncology indications (for more information with respect to Adaptimmune's clinical trials, see clinicaltrials.gov, identifiers NCT01350401, NCT01343043 and NCT01352286).

PCT's services will include the transfer and qualification of Adaptimmune's manufacturing process for its NYESO-1c259-T cell therapy product candidate at PCT's facility in Allendale, New Jersey and subsequent manufacturing of the product for Adaptimmune's clinical trials.

Adaptimmune develops products containing unique engineered T cell receptors for the treatment of cancer and infectious diseases. The company has a research base in Oxford, UK and a clinical base in Philadelphia, Pennsylvania.

In December, at the American Society of Hematology conference, Adaptimmune announced encouraging preliminary results from its expanded multiple myeloma trial. Related trials in melanoma and sarcoma are also recruiting patients.

PCT is an internationally recognized contract development and manufacturing organization with facilities in Allendale, New Jersey and Mountain View, California. The company has expertise in GMP manufacture for cell therapies, including dendritic cells, stem cells and T cells. Notably, PCT provided manufacturing for the pivotal studies for Dendreon's Provenge(R), the first cell therapy approved for cancer treatment.

"With our sights set on future pivotal trials for our T cell therapy products, we have invested significant effort towards establishing capabilities within Adaptimmune that support expansion of our clinical platform in terms of both scale and compliance with FDA requirements beyond phase I/II. Our relationship with PCT is an important component," said James Noble, Chief Executive Officer of Adaptimmune. "PCT's impressive level of experience in the burgeoning field of cell therapy, combined with their flexible capacity and professionalism, are among the reasons we selected them for this critical role for our T cell product."

"We are excited to enter into this agreement with Adaptimmune, an innovator for T cell therapy to treat cancers," said Robert A. Preti, PhD, President and Chief Scientific Officer of PCT. "Given our extensive experience with technology transfer, process qualification and GMP manufacturing, we feel PCT will be an asset to Adaptimmune as it develops its product for the U.S. commercial market."

Dr. Robin L. Smith, NeoStem's Chairman and Chief Executive Officer, stated that, "PCT's expertise is recognized globally as demonstrated by the services agreement executed with Adaptimmune. As PCT continues to expand its GMP manufacturing capabilities and focus to support the development of an increasingly wide range of cell therapies under development, it remains focused on providing outstanding client services."

About Adaptimmune

Adaptimmune focuses on the use of T cell therapy to treat cancer and infectious disease. It aims to use the body's own machinery -- the T cell -- to target and destroy cancerous or infected cells.

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NeoStem's Subsidiary, Progenitor Cell Therapy, Enters Into a Cell Therapy Manufacturing Services Agreement With ...

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A GENE has been uncovered that may help to create born leaders.

The leadership gene, known as rs4950, is an inherited DNA sequence associated with people taking charge.

Scientists accept that leadership skills are also learned. But the gene may provide the vital push needed to make someone into a manager rather than a minion.

Researchers found the gene after analysing DNA samples from around 4000 individuals and matching them to information about jobs and relationships. Workplace supervisory roles were used as a measurement of leadership behaviour.

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The study showed that a quarter of the observed variation in leadership traits between individuals could be explained by genetics.

Lead scientist Jan-Emmanuel De Neve, from University College London, said: We have identified a genotype, called rs4950, which appears to be associated with the passing of leadership ability down through generations.

The conventional wisdom - that leadership is a skill - remains largely true, but we show it is also, in part, a genetic trait.

The findings appear online today in the journal Leadership Quarterly.

Some of the greatest leaders in recent history include Martin Luther King, Mohandas Gandhi, Nelson Mandela and Sir Winston Churchill.

More here:
Leadership is in the gene, say scientists

Recommendation and review posted by Bethany Smith

STUD Merino breeders wanting to cash in on the swing to polled sheep can now fast-track the process.

DNA technology can allow breeders to lessen the chances of getting a horned ram by 80 per cent in just one year.

And it is possible to remove the horned gene from the flock within seven years, according to work done by the Co-operative Research Centre for Sheep.

Sales of Poll Merino rams have skyrocketed in the past few years as the quality of polled animals increases and demand spikes.

Studs such as Woodpark Merinos at Jerilderie sell out of their polled sires, in a dramatic change of heart by their clients.

The process of switching from horned to Poll Merinos can be achieved in the shortest time frame by testing all sheep.

But even if only rams are tested, it will take just 20 years to remove the horn gene.

The speed with which horns can be removed from the flock is thanks to its genetic control. "The development of horns in sheep appears to be controlled by a single gene for which there is a good DNA marker," Sheep CRC chief executive James Rowe said.

"The new genomic test for the horn gene means that, in poll flocks, we can avoid breeding from rams that are carriers of the horn gene."

The test for the poll/horn gene is $17 per animal, which Professor Rowe said represented "a clear return on investment for breeders and ram buyers wanting polled Merinos".

Read more from the original source:
CRC in poll gene find

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irishtimes.com - Last Updated: Tuesday, January 15, 2013, 13:48

A gene has been uncovered that may help to create born leaders.

The leadership gene, known as rs4950, is an inherited DNA sequence associated with people taking charge.

Scientists accept that leadership skills are also learned. But the gene may provide the vital push needed to make someone into a manager rather than a minion. Researchers found the gene after analysing DNA samples from around 4,000 individuals and matching them to information about jobs and relationships.

Workplace supervisory roles were used as a measurement of leadership behaviour.

The study showed that a quarter of the observed variation in leadership traits between individuals could be explained by genetics.

Lead scientist Dr Jan-Emmanuel De Neve, from University College London, said: We have identified a genotype, called rs4950, which appears to be associated with the passing of leadership ability down through generations.

The conventional wisdom that leadership is a skill remains largely true, but we show it is also, in part, a genetic trait.

The findings appear online today in the journal Leadership Quarterly. Some of the greatest leaders in recent history include Martin Luther King, Gandhi, Nelson Mandela and Sir Winston Churchill.

But leaders do not necessarily have to be heroic or good. Adolf Hitler, Joseph Stalin and Genghis Khan were also great leaders in their own way. The new research suggests at least the possibility that some of these historic figures were blessed with the leadership gene.

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Scientists discover 'leadership' gene

Recommendation and review posted by Bethany Smith

Charly Franklin / Getty Images

In one of the largest-ever studies of genetics and autism, researchers have identified 24 new gene variants associated with autism spectrum disorders (ASD). The work also confirms that 31 variants previously linked to the developmental disorder may serve as useful genetic markers for identifying those with the condition.

Understanding autisms genetic roots is a priority, researchers say, since it may lead to earlier diagnosis and behavioral intervention, which can improve patient outcomes.

(MORE: Behavior Therapy Normalizes Brains of Autistic Children)

Oftentimes findings like this get published in academic journals, but they dont get translated into clinical use, says Chuck Hensel, an author on the new research study, published in PLoS ONE, who is the senior manager of research at the genetic diagnostics company Lineagen. Our goal, Hensel says, is to try to get these markers into the clinic.

Hensel teamed with researchers at the University of Utah and the Childrens Hospital of Philadelphia and devised a two-pronged approach for hunting down genetic markers of autism.

First, the researchers chose 55 people living with autism, all from families with many members diagnosed with ASDs. The scientists then sequenced the genomes of these subjects, and compared the genetic profiles to those from a reference population, using the Utah Genetics Reference Project. That allowed them to find regions where the autistic individuals differed from people without the disorder, and led to 153 gene variants, or genetic red flags for the condition.

(MORE: Researchers Discover Genetic Patterns of Autism)

But because ASDs occur in a spectrum of mild to severe symptoms, and the genetic contribution of each of these variants likely varied, they needed to find out which of the 153 aberrations were most strongly linked to autism; some were likely indirectly connected to the disorder, and the scientists wanted to weed out those potential red herrings. So Hensel and his collaborators built a new molecular test, or probe, that would identify the 153 variants from a patient sample of blood, as well as for 185 other gene variants that previous studies had linked to autism. Running this probe on genetic samples collected from 2,175 children with clinically diagnosed autism spectrum disorders and also from 5,801 children with normal development, they could compare how well each of the variants matched up with an ASD.

Of the 153 initial candidate gene variants, 15 were confirmed as autism-related. The test also picked up another nine autism-related variants that had never been linked to autism spectrum disorders before. Participants with any of the 24 variants had a two-fold greater risk of developing an ASD than those without the genetic changes.

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Gene Variants Linked to Autism

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DUBLIN--(BUSINESS WIRE)--

Research and Markets (http://www.researchandmarkets.com/research/ssc94x/chinese_markets) has announced the addition of the "Chinese Markets for Biotechnology" report to their offering.

China's demand for biotechnology has grown at a fast pace in the past decade. In the next five years, both production and demand will continue to grow. This new study examines China's economic trends, investment environment, industry development, supply and demand, industry capacity, industry structure, marketing channels and major industry participants. Historical data (2001, 2006 and 2011) and long-term forecasts through 2016 and 2021 are presented. Major producers in China are profiled.

Companies Mentioned

Changchun Institute of Biological Products (CCIBP)

Chengdu Institute of Biological Products (CDIBP)

Guangxi Yuefeng Bioengineering Corporation Ltd.

GeneScience Pharmaceuticals Co., Ltd. (GenSci)

Hainan Xindazhou Pharmaceuticals Co., Ltd.

Hangzhou Jiuyuan Gene Engineering Co., Ltd.

Follow this link:
Research and Markets: Chinese Markets for Biotechnology - 2012 Report Features Players such as Hangzhou Jiuyuan Gene ...

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Paul jackman/Nature

Even as home experiments go, Hopi Hoekstras one was peculiar: she built a giant plywood box in her garage in San Diego, California, filled it with more than a tonne of soil and then let a pet mouse dig away.

This thing was bursting at its seams and held together with duct tape, says the evolutionary biologist, now at Harvard University in Cambridge, Massachusetts. But it worked. It allowed her to study the genetics of burrowing behaviour in a controlled setting. Armed with plastic casts of the burrows and state-of-the-art sequencing, Hoekstras team discovered clusters of genes that partly explain why the oldfield mouse (Peromyscus polionotus) builds elaborate two-tunnel burrows, whereas its close relative, the deer mouse (Peromyscus maniculatus), goes for a simple hole in the ground1.

The findings highlight an underappreciated benefit of a genomics revolution that is moving at breakneck speed. Thanks to cheap and quick DNA sequencing, scientists interested in the genetics of behaviour need not limit themselves to a handful of favourite lab organisms. Instead, they can probe the genetic underpinnings of behaviours observed in the wild, and glean insights into how they evolved. In my mind, the link between genes and behaviour in natural populations and organisms is the next great frontier in biology, says Hoekstra.

Hopi Hoekstra talks about what mouse burrows can reveal about the genetics of complex behaviours.

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Oldfield mice are native to the southeastern United States, where they burrow in soils ranging from sandy beaches to silt-rich clays. Wherever they dig, their holes look much the same, with a long entrance tunnel and a second tunnel that stops short of the surface and allows them to escape predators. Such invariability hints that the trait is encoded in DNA, says Hoekstra.

To find out where, she and her Harvard colleagues Jesse Weber and Brant Peterson cross-bred oldfield mice with deer mice, whose burrows are shallow and lack escape routes. The offspring continued to build complex tunnels, suggesting that the oldfield burrowing genes were dominant (see The genetics of burrowing).

A second round of breeding between the first-generation crosses and deer mice revealed that genes linked to burrow length were distinct from those influencing the escape tunnel. Some offspring produced short tunnels with escape routes, whereas others produced long tunnels without them. DNA analysis revealed that three genetic regions are responsible for much of the variation in tunnel length, and a fourth affects escape-tunnel digging.

This paper is awesome, says Cornelia Bargmann, a neurogeneticist at Rockefeller University in New York, noting that it combines cutting-edge molecular-genetics tools with established cross-breeding techniques to study behaviours that have been observed for more than a century in the wild. In the past, geneticists interested in unravelling behaviour had to focus on lab animals for which mutant and transgenic strains and genetic data were available, she says. But there were always questions we knew would be more interesting in wild animals. Bargmann and her team studied various wild strains of Caenorhabditis elegans flatworms to identify genes and brain circuits involved in seeking out new sources of food2.

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Behaviour genes unearthed

Recommendation and review posted by Bethany Smith

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

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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

Recommendation and review posted by Bethany Smith

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."

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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