Myriad Genetics Slashes Outlook - Mar 6, 2015
Myriad Genetics cut its fiscal year forecast due to reimbursement delays and announced the retirement of longstanding CEO Peter Meldrum. The company said it ...

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Gene Therapy Oncology Insight: Trends and Challenges Analysed in Research Report
Gene Therapy Oncology Insight: Pipeline Assessment, Technology Trend, and Competitive Landscape provides the information across the gene therapy value chain covering gene therapy profiles core.

By: James Jacob

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Miracle stem cell therapy reverses multiple sclerosis
Latest research on stem cell therapy in curing MS.

By: Dulci Hill

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Medicine in the Digital Age | RiceX on edX | About Video
Enroll in Medicine in the Digital Age from RiceX at https://www.edx.org/course/medicine-digital-age-ricex-meddigx-0 The future of healthcare is connected, pa...

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Personalized Medicine Risk Assessment FInal Master

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Former Homeland Star David Harewood Has Written An Online Article Urging Black U.k. Residents To Sign Up To The Stem Cell Donor Register.

The actor has teamed up with stem cell charity Anthony Nolan and the African-Caribbean Leukaemia Trust (ACLT) to launch an appeal encouraging young, black Brits to donate bone marrow so leukaemia sufferers in ethnic minorities have a better chance of receiving pioneering stem cell treatment.

Harewood has written an online article for Independent.co.uk in which he details the stem cell donation process for the African-Caribbean community, and encourages them to take part.

He writes, "The black population is badly underrepresented on the bone marrow register compiled by the blood cancer charity Anthony Nolan. In fact, there are 30 times more white people than African-Caribbean people willing to donate their stem cells in this country.

"The result of this? If you're black and have leukaemia then you have less than a 20 per cent chance of finding the best possible match when your last hope of survival is a lifesaving transplant from a stranger. We are literally dying, not because a matching donor isn't out there somewhere - but because that person never joined the register.

"This isn't right, and it urgently needs to change. It's horrible to think that if my daughters needed a transplant they would be at a disadvantage because there aren't enough black and mixed race donors on the register."

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David Harewood Launches Appeal For Black Stem Cell Donors

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Fauza D: Amniotic fluid and placental stem cells.

Best Pract Res Clin Obstet Gynaecol 2004, 18:877-891. PubMedAbstract | PublisherFullText

Parolini O, Alviano F, Bagnara GP, Bilic G, Bhring HJ, Evangelista M, Hennerbichler S, Liu B, Magatti M, Mao N, Miki T, Marongiu F, Nakajima H, Nikaido T, Portmann-Lanz CB, Sankar V, Soncini M, Stadler G, Surbek D, Takahashi TA, Redl H, Sakuragawa N, Wolbank S, Zeisberger S, Zisch A, Strom SC: Concise review: isolation and characterization of cells from human term placenta: outcome of the first international workshop on placenta derived stem cells.

Stem Cells 2008, 26:300-311. PubMedAbstract | PublisherFullText

Pozzobon M, Ghionzoli M, De Coppi P: ES, iPS, MSC, and AFS cells. Stem cells exploitation for Pediatric Surgery: current research and perspective.

Pediatr Surg Int 2010, 26:3-10. PubMedAbstract | PublisherFullText

Miki T, Marongiu F, Dorko K, Ellis EC, Strom SC: Isolation of amniotic epithelial stem cells.

Curr Protoc Stem Cell Biol 2010, Chapter 1:Unit 1E 3. PubMedAbstract | PublisherFullText

Miki T, Strom SC: Amnion-derived pluripotent/multipotent stem cells.

Stem Cell Rev 2006, 2:133-142. PubMedAbstract | PublisherFullText

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Stem Cell Research & Therapy | Full text | Amnion-derived ...

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A call by scientists to halt to precision gene-editing of DNA in human embryos would allow time to work out safety and ethical issues

Sperm cell fertilizing an egg. Credit: Wikimedia Commons

Amid rumors that precision gene-editing techniques have been used to modify the DNA of human embryos, researchers have called for a moratorium on the use of the technology in reproductive cells.

In a Comment published on March 12 inNature, Edward Lanphier, chairman of the Alliance for Regenerative Medicine in Washington DC, and four co-authors call on scientists to agree not to modify human embryos even for research.

Such research could be exploited for non-therapeutic modifications. We are concerned that a public outcry about such an ethical breach could hinder a promising area of therapeutic development, write Lanphier and his colleagues, who include Fyodor Urnov, a pioneer in gene-editing techniques and scientist at Sangamo BioSciences in Richmond, California. Many groups, including Urnov's company, are already using gene-editing tools to develop therapies that correct genetic defects in people (such as by editing white blood cells). They fear that attempts to produce designer babies by applying the methods to embryos will create a backlash against all use of the technology.

Known as germline modification, edits to embryos, eggs or sperm are of particular concern because a person created using such cells would have had their genetic make-up changed without consent, and would permanently pass down that change to future generations.

We need a halt on anything that approaches germline editing in human embryos, Lanphier, who is also chief executive of Sangamo, toldNatures news team.

But other scientists disagree with that stance. Although there needs to be a wide discussion of the safety and ethics of editing embryos and reproductive cells, they say, the potential to eliminate inherited diseases means that scientists should pursue research.

Related trials Geneticist Xingxu Huang of ShanghaiTech University in China, for example, is currently seeking permission from his institutions ethics committee to try genetically modifying discarded human embryos. In February 2014, he reportedusing a gene-editing technique to modify embryos that developed into live monkeys. Human embryos would not be allowed to develop to full term in his experiments, but the technique gives lots of potential for its application in humans, he says.

Besides Huangs work, gene-editing techniques are also being used by Juan Carlos Izpisua Belmonte, a developmental biologist at the Salk Institute for Biological Studies in La Jolla, California, to eliminate disease-causing mutations from mitochondria, the cell's energy-processing structures. Belmonte's work is on unfertilized eggs; human eggs with such modified mitochondria could one day be used inin vitrofertilization (IVF) procedures to prevent a woman's offspring from inheriting mitochondrial disease.

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DNA Editing of Human Embryos Alarms Scientists

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CALDWELL Eleni Christoforou, 32, hopes that a hematopoietic stem cell transplant (HSCT) will strike a decisive blow in her decade-long battle with multiple sclerosis (MS).

The Caldwell resident said the goal is to erase any memory of the disease from her body.

However, even with insurance coverage, the procedure will cost Christoforou roughly $20,000 between traveling to Chicago, where the transplant is done, and the other costs associated with removing and reinserting her stem cells, as well as fertility treatments.

Multiple sclerosis is an autoimmune disease that disrupts the brains ability to communicate with the body. The hematopoietic stem cell transplant will remove Christoforous stem cells from her bone marrow and then she will undergo chemotherapy before her own stem cells are injected back into her system with hopefully no memory of the MS, she explained.

Christoforous first symptoms left her unable to walk up the stairs, bumping into walls, losing her memory and confused. There were days where she would forget how to get home or how she arrived at work, she said.

She had a particularly bad episode in July of 2014 that left her unable to speak, walk, see and even feed herself. She spent a week in the hospital followed by two weeks at Kessler Institute for Rehabilitation, she said. She then spent another eight weeks in outpatient therapy in order to recover.

It was a long road, but with lots of hard work and praying, you would never know that had happened to me by looking at me, she said.

After this episode, she was perusing Facebook for MS groups when one of the suggestions was a group for patients of Dr. Richard K. Burts Stem Cell Study at Northwestern University in Chicago.

Christoforou was diagnosed with MS at age 22 in 2005. It was her senior year of college and for awhile, she thought the symptoms were stress accruing from a busy year, but it unfortunately ended up being much worse than that, she said.

At the time of her diagnosis, she joined AOL chat rooms, which she said were popular at that time, about the disease where she spoke to someone named Rob from Maryland who had the HSCT procedure during a more advanced stage of MS.

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Caldwell resident fighting battle with multiple sclerosis

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TALIA CARLISLE/Stuff.co.nz

HOLDING ON TO HOPE: Amy Clague needs to raise $100,000 to cover flights to Russia and a stem cell transplant which she hopes will give her a chance at a normal life.

A multiple sclerosis diagnosis was not the 20th birthday present Amy Clague was hoping for.

The Melrose nanny was celebrating with family last year when she noticed something wasn't right.

"My right side was kind of numb," Clague said.

"[The next day] I woke up and it hadn't gone away. Day three it was in my face. It had spread."

Clague had no feeling on her right side from her toes to her face when she visited Wellington Hospital's emergency department for tests.

Four possible outcomes weighed on Clague's mind as she awaited the doctor's results.

"It was going to be multiple sclerosis [MS], a brain tumour, a brain bleed or a stroke."

But Clague's mother, a neurological physiotherapist who treats MS patients, knew the answer.

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21-year-old MS sufferer: 'I feel like my life is on hold'

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Newswise Researchers at the University of California, San Diego School of Medicine have identified a gene variant that may be used to predict people most likely to respond to an investigational therapy under development for Alzheimers disease (AD). The study, published March 12 in Cell Stem Cell, is based on experiments with cultured neurons derived from adult stem cells.

Our results suggest that certain gene variants allow us to reduce the amount of beta amyloid produced by neurons, said senior author Lawrence Goldstein, PhD, director of UC San Diego Sanford Stem Cell Clinical Center and UC San Diego Stem Cell Program. This is potentially significant for slowing the progression of Alzheimers disease. AD is the most common cause of dementia in the United States, afflicting one in nine people age 65 and older.

The genetic risk factor investigated are variants of the SORL1 gene. The gene codes for a protein that affects the processing and subsequent accumulation of beta amyloid peptides, small bits of sticky protein that build up in the spaces between neurons. These plaques are linked to neuronal death and related dementia.

Previous studies have shown that certain variants of the SORL1 gene confer some protection from AD, while other variants are associated with about a 30 percent higher likelihood of developing the disease. Approximately one-third of the U.S. adult population is believed to carry the non-protective gene variants.

The studys primary finding is that variants in the SORL1 gene may also be associated with how neurons respond to a natural compound in the brain that normally acts to protect nerve cell health. The protective compound, called BDNF, short for brain-derived neurotrophic factor, is currently being investigated as a potential therapy for a number of neurological diseases, including AD, because of its role in promoting neuronal survival.

For the study, UC San Diego researchers took skin cells from 13 people, seven of whom had AD and six of whom were healthy control subjects, and reprogrammed the skin cells into stem cells. These stem cells were coaxed to differentiate into neurons, and the neurons were cultured and then treated with BDNF.

The experiments revealed that neurons that carried disease-protective SORL1 variants responded to the therapy by reducing their baseline rate of beta amyloid peptide production by, on average, 20 percent. In contrast, the neurons carrying the risk variants of the gene, showed no change in baseline beta amyloid production.

BDNF is found in everyones brain, said first author Jessica Young, PhD, a postdoctoral fellow in the Goldstein laboratory. What we found is that if you add more BDNF to neurons that carry a genetic risk factor for the disease, the neurons dont respond. Those with the protective genetic profile do.

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Boosting A Natural Protection Against Alzheimer's Disease

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Hip and shoulder arthritis six months after bone marrow stem cell therapy by Harry Adelson ND
Mareen describes her outcome six months after her bone marrow stem cell treatment by Harry Adelson ND for arthritis of her hip and shoulder http://www.docereclinics.com.

By: Harry Adelson, N.D.

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Intervention Strategies for Spinal Cord Injury Patients Video: J.J. Mowder-Tinney | MedBridge
Watch the first chapter FREE: https://www.medbridgeeducation.com/courses/details/spinal-cord-injury-practical-rehabilitation-exercises Instructor: J.J. Mowde...

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Joining Forces: Wings for Life and the Christopher Dana Reeve Foundation
Wings for Life and the Christopher Dana Reeve Foundation unite to advance a groundbreaking therapy for spinal cord injury. The study, conducted by Universi...

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Orlando, Florida (PRWEB) March 12, 2015

The Miami Stem Cell Treatment Center announces a series of free public seminars on the use of adult stem cells for various degenerative and inflammatory conditions. They will be provided by Dr. Thomas A. Gionis, Surgeon-in-Chief and Dr. Nia Smyrniotis, Medical Director and Surgeon.

The seminars will be held on Tuesday, March 17, 2015, at 12:30 pm, 2:30 pm and 4:30 pm at Seasons 52, 7700 Sand Lake Road, Orlando, FL 32819. Please RSVP at (561) 331-2999.

The Miami Stem Cell Treatment Center (Miami; Boca Raton; Orlando; The Villages, FL), along with sister affiliates, the Irvine Stem Cell Treatment Center (Irvine; Westlake Villages, CA) and the Manhattan Regenerative Medicine Medical Group (Manhattan, NY), abide by approved investigational protocols using adult adipose derived stem cells (ADSCs) which can be deployed to improve patients quality of life for a number of chronic, degenerative and inflammatory conditions and diseases. ADSCs are taken from the patients own adipose (fat) tissue (found within a cellular mixture called stromal vascular fraction (SVF)). ADSCs are exceptionally abundant in adipose tissue. The adipose tissue is obtained from the patient during a 15 minute mini-liposuction performed under local anesthesia in the doctors office. SVF is a protein-rich solution containing mononuclear cell lines (predominantly adult autologous mesenchymal stem cells), macrophage cells, endothelial cells, red blood cells, and important Growth Factors that facilitate the stem cell process and promote their activity.

ADSCs are the body's natural healing cells - they are recruited by chemical signals emitted by damaged tissues to repair and regenerate the bodys injured cells. The Miami Stem Cell Treatment Center only uses Adult Autologous Stem Cells from a persons own fat No embryonic stem cells are used; and No bone marrow stem cells are used. Current areas of study include: Emphysema, COPD, Asthma, Heart Failure, Heart Attack, Parkinsons Disease, Stroke, Traumatic Brain Injury, Lou Gehrigs Disease, Multiple Sclerosis, Lupus, Rheumatoid Arthritis, Crohns Disease, Muscular Dystrophy, Inflammatory Myopathies, and degenerative orthopedic joint conditions (Knee, Shoulder, Hip, Spine). For more information, or if someone thinks they may be a candidate for one of the adult stem cell protocols offered by the Miami Stem Cell Treatment Center, they may contact Dr. Gionis or Dr. Smyrniotis directly at (561) 331-2999, or see a complete list of the Centers study areas at: http://www.MiamiStemCellsUSA.com.

About the Miami Stem Cell Treatment Center: The Miami Stem Cell Treatment Center, along with sister affiliates, the Irvine Stem Cell Treatment Center and the Manhattan Regenerative Medicine Medical Group, is an affiliate of the California Stem Cell Treatment Center / Cell Surgical Network (CSN); we are located in Boca Raton, Orlando, Miami and The Villages, Florida. We provide care for people suffering from diseases that may be alleviated by access to adult stem cell based regenerative treatment. We utilize a fat transfer surgical technology to isolate and implant the patients own stem cells from a small quantity of fat harvested by a mini-liposuction on the same day. The investigational protocols utilized by the Miami Stem Cell Treatment Center have been reviewed and approved by an IRB (Institutional Review Board) which is registered with the U.S. Department of Health, Office of Human Research Protection (OHRP); and our studies are registered with Clinicaltrials.gov, a service of the U.S. National Institutes of Health (NIH). For more information, visit our websites: http://www.MiamiStemCellsUSA.com, http://www.IrvineStemCellsUSA.com , or http://www.NYStemCellsUSA.com.

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Newswise Researchers at the University of California, San Diego School of Medicine have identified a gene variant that may be used to predict people most likely to respond to an investigational therapy under development for Alzheimers disease (AD). The study, published March 12 in Cell Stem Cell, is based on experiments with cultured neurons derived from adult stem cells.

Our results suggest that certain gene variants allow us to reduce the amount of beta amyloid produced by neurons, said senior author Lawrence Goldstein, PhD, director of UC San Diego Sanford Stem Cell Clinical Center and UC San Diego Stem Cell Program. This is potentially significant for slowing the progression of Alzheimers disease. AD is the most common cause of dementia in the United States, afflicting one in nine people age 65 and older.

The genetic risk factor investigated are variants of the SORL1 gene. The gene codes for a protein that affects the processing and subsequent accumulation of beta amyloid peptides, small bits of sticky protein that build up in the spaces between neurons. These plaques are linked to neuronal death and related dementia.

Previous studies have shown that certain variants of the SORL1 gene confer some protection from AD, while other variants are associated with about a 30 percent higher likelihood of developing the disease. Approximately one-third of the U.S. adult population is believed to carry the non-protective gene variants.

The studys primary finding is that variants in the SORL1 gene may also be associated with how neurons respond to a natural compound in the brain that normally acts to protect nerve cell health. The protective compound, called BDNF, short for brain-derived neurotrophic factor, is currently being investigated as a potential therapy for a number of neurological diseases, including AD, because of its role in promoting neuronal survival.

For the study, UC San Diego researchers took skin cells from 13 people, seven of whom had AD and six of whom were healthy control subjects, and reprogrammed the skin cells into stem cells. These stem cells were coaxed to differentiate into neurons, and the neurons were cultured and then treated with BDNF.

The experiments revealed that neurons that carried disease-protective SORL1 variants responded to the therapy by reducing their baseline rate of beta amyloid peptide production by, on average, 20 percent. In contrast, the neurons carrying the risk variants of the gene, showed no change in baseline beta amyloid production.

BDNF is found in everyones brain, said first author Jessica Young, PhD, a postdoctoral fellow in the Goldstein laboratory. What we found is that if you add more BDNF to neurons that carry a genetic risk factor for the disease, the neurons dont respond. Those with the protective genetic profile do.

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Boosting A Natural Protection Against Alzheimer's Disease

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Posted: Thursday, March 12, 2015 7:08 PM

UCLA stem-cell researchers have shown that a novel stem-cell gene therapy method could one day provide a one-time, lasting treatment for the most common inherited blood disorder in the U.S. sickle cell disease. Publishedin the journal Blood, the study outlines a method that corrects the mutated gene that causes sickle cell disease and shows, for the first time, the gene correction method leads to the production of normal red blood cells. The study was directed by renowned stem cell researcher and UCLA Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research member, Dr. Donald Kohn.

People with sickle cell disease are born with a mutation in their beta-globin gene, which is responsible for delivering oxygen to the body through blood circulation. The mutation causes blood stem cellswhich are made in the bone marrowto produce distorted and rigid red blood cells that resemble a crescent or sickle shape. Consequently, the abnormally shaped red blood cells do not move smoothly through blood vessels, resulting in insufficient oxygen supply to vital organs. Anyone can be born with sickle cell disease, but it occurs more frequently in African Americans and Hispanic Americans.

The stem-cell gene therapy method described in the study seeks to directly correct the mutation in the beta-globin gene so bone marrow stem cells then produce normal, circular-shaped blood cells that do not sickle. The fascinating gene correction technique used specially engineered enzymes, called zinc-finger nucleases, tocut out the mutated genetic code and replace it with a corrected version that repairs the beta-globin mutation.

For the study, bone marrow stem cells donated by people with the sickle cell gene mutation were treated in the laboratory with the zinc-finger nucleases enzyme cutting method.Kohn and his team then demonstrated in mouse models that thecorrected bone-marrow stem cells have the capability to replicate successfully. The research showed that the method holds the potential to permanently treat the disease if a higher level of correction is achieved.

This is a very exciting result,said Dr. Kohn, professor of pediatrics atUCLAs David Geffen School of Medicine, professor of microbiology, immunology and molecular genetics in Life Sciences at UCLA, member of the UCLA Childrens Discovery and Innovation Institute at Mattel Childrens Hospital and senior author on the study. It suggests the future direction for treating genetic diseases will be by correcting the specific mutation in a patients genetic code. Since sickle cell disease was the first human genetic disease where we understood the fundamental gene defect,and since everyone with sickle cell has the exact same mutation in the beta-globin gene, it is a great target for this gene correction method.

To make the cut in the genetic code, Dr. Kohn and his team used zinc-finger nucleases engineered by Sangamo BioSciences, Inc., in Richmond. The enzymes can be designed to recognize a specific and targeted point in the genetic code. For the study, scientists at Sangamo BioSciences engineered the enzymes to create a cut at the site of the mutated genetic code that causes sickle cell disease. This break triggered a natural process of repair in the cell and at the same time, a molecule containing the correct genetic code was inserted to replace the mutated code.

The next steps in this research will involve improving the efficiency of the mutation correction process and performing pre-clinical studies to demonstrate that the method is effective and safe enough to move to clinical trials.

Symptoms of sickle cell disease usually begin in early childhood and include a low number of red blood cells (anemia), repeated infections and periodic episodes of pain. People with sickle cell disease typically have a shortened lifespan of just 36-40 years of age. The disease impacts more than 250,000 new patients worldwide each year. The only cure currently available for sickle cell disease is a transplant of bone marrow stem cells from a matched sibling, but matches are rare or can result in rejection of the transplanted cells.

This is a promising first step in showing that gene correction has the potential to help patients with sickle cell disease, said Megan Hoban, a senior graduate student in microbiology, immunology and molecular genetics and first author on the study. The study data provide the foundational evidence that the method is viable.

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UCLA Research Shows Promising Method For Correcting Genetic Code To Treat Sickle Cell Disease

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The Genetic Engineering of Humans
by Taylor Davidson.

By: STS1 2015 Student Media Productions

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The Genetic Engineering of Humans - Video

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IMAGE:This photo is of the sighted, surface-dwelling fish related to the ancient, eyeless Astyanax mexicanus. view more

Credit: Jay Yocis

A $1.92 million, five-year R01 Award from the National Institutes of Health will support University of Cincinnati research into the genetic aspects of craniofacial asymmetries that could address a wide spectrum of human conditions, from non-syndromic cleft palate to hemifacial microsomia - conditions that can impair breathing or lead to emotional suffering from distorted appearance. In addition, UC biology researcher Joshua Gross, an assistant professor of biological sciences, was awarded $519,343 from the National Science Foundation to explore the genetic explanation for pigmentation loss in cave animals, which could also hold links to pigmentation changes in humans. Both awards get underway in March.

The researchers are searching for genetic hints by examining a species of eyeless, cave-dwelling fish, Astyanax mexicanus - which has lived in the pitch-black caves of the Sierra de El Abra region of Mexico for millions of years. These fish can be compared with the closely related sighted surface-dwelling fish that are found in Mexico, Texas and New Mexico. Previous research suggests that genetic mutations leading to craniofacial distortions in the cavefish may be similar to human facial abnormalities that often result in painful, corrective surgeries as early as infancy. The closely-related surface-dwelling fish do not have these facial abnormalities.

The funding will support genome-wide mapping which will allow researchers to zero in on the precise region of the genome - specific genes as well as mutations within genes - that will explain these facial asymmetries.

The research project will examine these three levels:

Hello, Gorgeous - The 'Beautiful Reflection,' or Brangelina Factor

Gross says the project began with an appreciation for the fact that symmetry is an important component of human perceptions of facial attractiveness. "This trait evolves under intense sexual selection as a signal of robust physical health and genetic quality in potential mates," states the research proposal. "Think of couples like Brad Pitt and Angelina Jolie, who are admired worldwide for their physical features," says Gross. "The logical flow of this is that facial attractiveness is believed to be an indication of strong genetic composition - a strong mate who will provide for your offspring - and so indirectly there may have been evolutionary pressures acting on our ancestors to maintain facial symmetry in humans.

"Cavefish have naturally lost their eyes over the course of evolution," continues Gross. "The fish can't see one another anymore, so the left and right sides of their faces become uncoupled and begin to exhibit random asymmetries. One of our most surprising discoveries is that there's actually a genetic basis for that asymmetry. Some changes in the genome have resulted in one side of the face developing differently from the other side of the face. Because this process occurs so often, cavefish are a powerful natural model system for learning about this fundamental biological phenomenon of craniofacial symmetry."

The UC researchers have previously found two genes in the cavefish that are closely tied to non-syndromic cleft palate in humans.

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NIH awards UC biologist $1.9 million for genetic research

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Case Western Reserve scientists have discovered that speed matters when it comes to how messenger RNA (mRNA) deciphers critical information within the genetic code -- the complex chain of instructions critical to sustaining life. The investigators' findings, which appear in the March 12 journal Cell, give scientists critical new information in determining how best to engage cells to treat illness -- and, ultimately, keep them from emerging in the first place.

"Our discovery is that the genetic code is more complex than we knew," said senior researcher Jeff Coller, PhD, associate professor, Division of General Medical Sciences, and associate director, The Center for RNA Molecular Biology, Case Western Reserve University School of Medicine. "With this information, researchers can manipulate the genetic code to achieve more predictable outcomes in an exquisite fashion."

The genetic code is a system of instructions embedded within DNA. The code tells a cell how to generate proteins that control cellular functions. mRNA transmits the instructions from DNA to ribosomes. Ribosomes translate the information contained within the mRNA and produce the instructed protein. The genetic code comprises 61 words, called "codons," and a single codon, a sequence of three nucleotides, instructs the ribosome how to build proteins.

The code not only dictates what amino acids are incorporated into proteins, it also tells the cell how fast they should be incorporated. With this information, researchers can manipulate the genetic code to achieve predictable protein levels in an exquisite fashion."

The most significant breakthrough in the Case Western Reserve work is that all of the words, or codons, in the genetic code are deciphered at different rates; some are deciphered rapidly while others are deciphered slowly. The speed of how mRNA decodes its information is the sum of all the codons it contains. This imposed speed limit then ultimately affects the amount of protein produced. Sometimes faster is better to express a high level of protein. Sometimes slower is better to limit the amount protein. Importantly, codons are redundant -- many of these words mean the same thing.

Coller and colleagues found that each of the codons is recognized differently by a ribosome. Some codons are recognized faster than others, but these differences in speed are tiny. Over the entire span of an mRNA, however, each tiny difference in speed is powerfully additive.

"Many codons mean the same thing, but they influence decoding rate differently. Because of this, we can change an mRNA without changing its protein sequence and cause it to be highly expressed or poorly expressed and anywhere in between," he said. "We can literally dial up or down protein levels any way we want now that we know this information."

During their research, investigators measured the mRNA decay rate for every transcript within the cell. They were seeking answers for why different RNAs had different stabilities. With statistical analysis, investigators compared the half-lives of mRNAs to the codons used within these messages. A strong correlation emerged between codon identity and mRNA message stability. They ultimately linked these observations back to the process of mRNA translation.

"mRNA translation and mRNA decay are intimately connected. This can be very beneficial to scientists. If you would like a gene to be expressed really well, you simply change the protein sequence to be derived by all optimal codons. This will both stabilize the mRNA and cause it to be translated more efficiently," Coller said. "If you need an mRNA to express at a low level, you fill it with non-optimal codons. The mRNA will be poorly translated and thus unstable. Evolution has used codon optimization to shape the expression of the proteome. Genes of similar function use similar codons; therefore, they are expressed at similar levels."

His discovery has a variety of practical implications for medicine. From a bioengineering perspective, molecular biology techniques can be applied to manipulate the gene to contain ideal codons and obtain the gene expression pattern that is most beneficial to the application. From a human physiological standpoint, it's possible to learn the speed limit for each and every mRNA and then determine if this changes in specific pathologies such as cancer. Currently, it is unknown whether codons convey different speeds in disease states. A future direction for research will be to link codon speeds to specific illnesses. The potential is also there to develop drugs that can manipulate higher or lower gene expression by changing the decoding rate.

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Hidden meaning and 'speed limits' found within genetic code

Recommendation and review posted by Bethany Smith

Case Western Reserve scientists have discovered that speed matters when it comes to how messenger RNA (mRNA) deciphers critical information within the genetic code -- the complex chain of instructions critical to sustaining life. The investigators' findings, which appear in the March 12 journal Cell, give scientists critical new information in determining how best to engage cells to treat illness -- and, ultimately, keep them from emerging in the first place.

"Our discovery is that the genetic code is more complex than we knew," said senior researcher Jeff Coller, PhD, associate professor, Division of General Medical Sciences, and associate director, The Center for RNA Molecular Biology, Case Western Reserve University School of Medicine. "With this information, researchers can manipulate the genetic code to achieve more predictable outcomes in an exquisite fashion."

The genetic code is a system of instructions embedded within DNA. The code tells a cell how to generate proteins that control cellular functions. mRNA transmits the instructions from DNA to ribosomes. Ribosomes translate the information contained within the mRNA and produce the instructed protein. The genetic code comprises 61 words, called "codons," and a single codon, a sequence of three nucleotides, instructs the ribosome how to build proteins.

The code not only dictates what amino acids are incorporated into proteins, it also tells the cell how fast they should be incorporated. With this information, researchers can manipulate the genetic code to achieve predictable protein levels in an exquisite fashion."

The most significant breakthrough in the Case Western Reserve work is that all of the words, or codons, in the genetic code are deciphered at different rates; some are deciphered rapidly while others are deciphered slowly. The speed of how mRNA decodes its information is the sum of all the codons it contains. This imposed speed limit then ultimately affects the amount of protein produced. Sometimes faster is better to express a high level of protein. Sometimes slower is better to limit the amount protein. Importantly, codons are redundant -- many of these words mean the same thing.

Coller and colleagues found that each of the codons is recognized differently by a ribosome. Some codons are recognized faster than others, but these differences in speed are tiny. Over the entire span of an mRNA, however, each tiny difference in speed is powerfully additive.

"Many codons mean the same thing, but they influence decoding rate differently. Because of this, we can change an mRNA without changing its protein sequence and cause it to be highly expressed or poorly expressed and anywhere in between," he said. "We can literally dial up or down protein levels any way we want now that we know this information."

During their research, investigators measured the mRNA decay rate for every transcript within the cell. They were seeking answers for why different RNAs had different stabilities. With statistical analysis, investigators compared the half-lives of mRNAs to the codons used within these messages. A strong correlation emerged between codon identity and mRNA message stability. They ultimately linked these observations back to the process of mRNA translation.

"mRNA translation and mRNA decay are intimately connected. This can be very beneficial to scientists. If you would like a gene to be expressed really well, you simply change the protein sequence to be derived by all optimal codons. This will both stabilize the mRNA and cause it to be translated more efficiently," Coller said. "If you need an mRNA to express at a low level, you fill it with non-optimal codons. The mRNA will be poorly translated and thus unstable. Evolution has used codon optimization to shape the expression of the proteome. Genes of similar function use similar codons; therefore, they are expressed at similar levels."

His discovery has a variety of practical implications for medicine. From a bioengineering perspective, molecular biology techniques can be applied to manipulate the gene to contain ideal codons and obtain the gene expression pattern that is most beneficial to the application. From a human physiological standpoint, it's possible to learn the speed limit for each and every mRNA and then determine if this changes in specific pathologies such as cancer. Currently, it is unknown whether codons convey different speeds in disease states. A future direction for research will be to link codon speeds to specific illnesses. The potential is also there to develop drugs that can manipulate higher or lower gene expression by changing the decoding rate.

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Case Western Reserve scientists find hidden meaning and 'speed limits' within genetic code

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Newswise Case Western Reserve scientists have discovered that speed matters when it comes to how messenger RNA (mRNA) deciphers critical information within the genetic code the complex chain of instructions critical to sustaining life. The investigators findings, which appear in the March 12 journal Cell, give scientists critical new information in determining how best to engage cells to treat illness and, ultimately, keep them from emerging in the first place.

Our discovery is that the genetic code is more complex than we knew, said senior researcher Jeff Coller, PhD, associate professor, Division of General Medical Sciences, and associate director, The Center for RNA Molecular Biology, Case Western Reserve University School of Medicine. With this information, researchers can manipulate the genetic code to achieve more predictable outcomes in an exquisite fashion.

The genetic code is a system of instructions embedded within DNA. The code tells a cell how to generate proteins that control cellular functions. mRNA transmits the instructions from DNA to ribosomes. Ribosomes translate the information contained within the mRNA and produce the instructed protein. The genetic code comprises 61 words, called codons, and a single codon, a sequence of three nucleotides, instructs the ribosome how to build proteins.

The code not only dictates what amino acids are incorporated into proteins, it also tells the cell how fast they should be incorporated. With this information, researchers can manipulate the genetic code to achieve predictable protein levels in an exquisite fashion.

The most significant breakthrough in the Case Western Reserve work is that all of the words, or codons, in the genetic code are deciphered at different rates; some are deciphered rapidly while others are deciphered slowly. The speed of how mRNA decodes its information is the sum of all the codons it contains. This imposed speed limit then ultimately affects the amount of protein produced. Sometimes faster is better to express a high level of protein. Sometimes slower is better to limit the amount protein. Importantly, codons are redundant many of these words mean the same thing.

Coller and colleagues found that each of the codons is recognized differently by a ribosome. Some codons are recognized faster than others, but these differences in speed are tiny. Over the entire span of an mRNA, however, each tiny difference in speed is powerfully additive.

Many codons mean the same thing, but they influence decoding rate differently. Because of this, we can change an mRNA without changing its protein sequence and cause it to be highly expressed or poorly expressed and anywhere in between, he said. We can literally dial up or down protein levels any way we want now that we know this information.

During their research, investigators measured the mRNA decay rate for every transcript within the cell. They were seeking answers for why different RNAs had different stabilities. With statistical analysis, investigators compared the half-lives of mRNAs to the codons used within these messages. A strong correlation emerged between codon identity and mRNA message stability. They ultimately linked these observations back to the process of mRNA translation.

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Case Western Reserve Scientists Discover Hidden Meaning and 'Speed Limits' within the Genetic Code

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LONDON: Pakistani and Bangladeshi people in London's least healthy boroughs are being asked to provide spit samples and health records to researchers hoping to find genetic clues to why they are disproportionately affected by certain diseases.

The East London Genes and Health project will focus partly on so-called knock-out genes, rare in the general population but more frequent in communities where cousins and other close relatives marry and have children, as is more common in Pakistani and Bangladeshi communities.

Read: Have Bangladeshis overtaken Pakistanis in Britain?

The largest community genetics study in the world will recruit 100,000 volunteers from East London, which have substantial South Asian populations.

Researchers leading the study say health signals buried in the data could have a big impact on peoples' health worldwide.

This is the first time a large-scale genetics study has focused on two distinct ethnic minority groups, with high levels of health concerns in the community and the potential for significant genetic variation, Richard Trembath, a professor at Queen Mary University of London, told reporters at a briefing.

These findings will play a key role in tackling health inequality locally and in the UK, (and) we hope to reveal crucial information about the link between genetics and common diseases which will have significant international impact.

Studying genetic variation is crucial to improving understanding of the normal variation in genes in certain populations, which can then help the diagnosis of inherited rare diseases.

So-called knock-out genes occur when a healthy person has two copies, inherited from both parents, of a gene that functions differently to the norm.

The team hopes to use these findings to understand how knock-out genes impact health and eventually to help develop new drugs or treatments which block bad genes and enhance good ones.

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Genetics study seeks South Asian health clues in East London - Pakistan - DAWN.COM

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