Space Station 13 : Genetics And Weird Sounds.
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Gene therapy could be a way to fix a genetic problem at its source. By adding a corrected copy of a defective gene, gene therapy promises to help diseased tissues and organs work properly. This approach is different from traditional drug-based approaches, which may treat symptoms but not the underlying genetic problems.

Most commonly, gene therapy uses a vector, typically a virus, to deliver a gene to the cells where it's needed. Once it's inside, the cell's gene-reading machinery uses the information in the gene to build RNA and protein molecules. The proteins (or RNA) can then carry out their job in the cells.

But gene therapy is not a molecular bandage that will automatically fix any genetic problem. While many disorders or medical conditions can potentially be treated using gene therapy, others are not suitable for this approach. So what makes a condition a good candidate for gene therapy?

Could the condition be corrected by adding one or a few functional genes? For you to even consider gene therapy, the answer must be "yes." For instance, genetic disorders caused by mutations in single genes tend to be good candidates for gene therapy, while diseases involving many genes and environmental factors tend to be poor candidates.

Do you know which genes are involved? If you plan to treat a genetic flaw, you need to know which gene(s) to pursue. You must also have a DNA copy of the gene available in your laboratory.

Do you understand the biology of the disorder? To design the best possible approach, you need to learn all you can about how the gene factors into the disorder. For example, which tissues the disorder affects, what role the protein encoded by the gene plays within the cells of that tissue, and exactly how mutations in the gene affect the protein's function.

Will adding a normal copy of the gene fix the problem in the affected tissue? Or could getting rid of the defective gene fix it? Sometimes when a gene is defective, no functional protein is being made from it. In cases like these, adding a functional copy of the gene could correct the problem. But sometimes a defective gene codes for a protein that starts doing something it shouldn't or prevents another protein from doing its job. In order to correct the problem, you would need to get rid of the misbehaving protein.

Can you deliver the gene to cells of the affected tissue? The answer will come from several pieces of information, including the tissue's accessibility and molecular signatures.

APA format: Genetic Science Learning Center (2014, June 22) What is Gene Therapy?. Learn.Genetics. Retrieved November 16, 2014, from http://learn.genetics.utah.edu/content/genetherapy/gtintro/ MLA format: Genetic Science Learning Center. "What is Gene Therapy?." Learn.Genetics 16 November 2014 <http://learn.genetics.utah.edu/content/genetherapy/gtintro/> Chicago format: Genetic Science Learning Center, "What is Gene Therapy?," Learn.Genetics, 22 June 2014, <http://learn.genetics.utah.edu/content/genetherapy/gtintro/> (16 November 2014)

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PUBLIC RELEASE DATE:

15-Nov-2014

Contact: Kurtis Pivert kpivert@asn-online.org 202-699-0238 American Society of Nephrology @ASNKidney

Philadelphia, PA (November 15, 2014) -- The results of numerous high-impact clinical trials that could affect kidney-related medical care will be presented at ASN Kidney Week 2014, November 11-16 at the Pennsylvania Convention Center in Philadelphia, PA.

ACT-AKI: A Phase 2 Multicenter, Randomized, Double-Blind, Placebo-Controlled Trial of AC607 for the Treatment of Acute Kidney Injury in Cardiac Surgery Subjects

ADVANCE-ON: long term benefits of intensive glucose control for end-stage kidney disease

HALT Progression of Polycystic Kidney Disease (HALT PKD) Trials: Primary Results of a 2x2 Factorial Trial in Early Stage CKD HALT Progression of Polycystic Kidney Disease Trials: Primary results of a randomized trial in moderately advanced stage CKD

Impact of Extended Weekly Hemodialysis Hours on Quality of Life and Clinical Outcomes: the ACTIVE Dialysis Multinational Trial

Randomized Clinical Trial of Ergocalciferol Supplementation in 25 Vitamin D Deficient Hemodialysis Patients

Renal Efficacy and Safety of Anti-TGF-1 Therapy in Patients with Diabetic Nephropathy

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High impact clinical trials yield results that could lead to improved kidney care

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What is a Stem Cell Support Serum? | RG Cell | Agerite Solutions
What is a Stem Cell Support Serum? Paloma: And I suppose my next question would be what is a stem cell support serum? Dean: Well, in skin care, serums are co...

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Stem cells are the building blocks of your skin. They have a unique ability to replace damaged and diseased cells. As they divide, they can proliferate for long periods into millions of new skin cells.

As we age, our stem cells lose their potency. Your skin's ability to repair itself just isn't what it used to be. The result can be fine lines, wrinkles, age spots, and sagging skin. But non-embryonic stem cells -- the same stem cells active early in life -- are highly potent. Lifeline anti-aging stem cell serums tap into the potency of these stem cells to help renew your skin.

Scientists at Lifeline Skin Care discovered that human non-embryonic stem cell extracts can help renew skin -- by replacing old cells with healthy new ones. These stem cell extracts help stimulate your own skin's abilities to repair itself. And Lifeline anti-aging stem cell serums were born.

Where Stem Cells in Anti Aging Products Come From

The first types of human stem cells to be studied by researchers were embryonic stem cells, donated from in vitro fertilization labs. But because creating embryonic stem cells involves the destruction of a fertilized human embryo, many people have ethical concerns about the use of such cells.

Lifeline Skin Care (through its parent company, ISCO) is the first company in the world to discover how to create human non-embryonic stem cells -- and how to take extracts from them. As a result, you need never be concerned that a viable human embryo was damaged or destroyed to create these anti-aging products.

The non-embryonic stem cells in Lifeline stem cell serums are derived from unfertilized human oocytes (eggs) which are donated to ISCO from in vitro fertilization labs and clinics.

Lifeline Anti Aging Stem Cell Serums are Based in Science

Lifeline Skin Care's exclusive anti-aging products are a combination of several discoveries and unique high-technology, patent-pending formulations.

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Anti Aging Stem Cell Serums Renew Skin - Life Line Skin Care

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Gene Therapy: Choroideremia
It #39;s a form of blindness that some call especially cruel. People with choroideremia are born with perfect vision and then begin to lose their sight, sometimes as kids or teens.

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Eli Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA
In a specially designed facility that is compliant with FDA Good Manufacturing Practices (GMP) requirements, scientists with the Eli and Edythe Center of Regenerative Medicine and Stem Cell...

By: UCLA Eli Edythe Broad Center of Regenerative Medicine and Stem Cell Research

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SINGAPORE: It was anemotional meeting for bone marrow transplant recipient Ivan Wijaya. On Friday (Nov 14), he finally came face to face with his bone marrow donor Ms Enning Yeo, more than a year after his transplant operation last October.

Ivan, 29, was diagnosed with Acute Myelogenous Leukaemia in February last year and never imagined being alive today, because finding a match is 1 in 20,000.

"When I was diagnosed with leukaemia, I just felt that I will be dead soon. But I didn't cry and I toughened myself because I didn't want to let my wife down. But in my heart, I still felt scared and didn't know what to do, he said.

Enning, who is 28, signed up for the Bone Marrow Donor Programme in 2006. She likened being selected as a donor to striking a charity lottery.

"It is an altruistic act but on a personal level, I do feel a sense of satisfaction and achievement. People talk about a bucket list of things to do. I don't have my own bucket list but if I did have one, but if I could have check off - that I saved a life - even if it's simply by donating bone marrow is something I'm very proud of, she said.

This year, 19 local donors have taken part in successful bone marrow transplants in Singapore. There were seven such donors last year.

These numbers were revealed by the Bone Marrow Donor Programme, a non-profit organisation that manages Singapore's only register of volunteer bone marrow donors. But with about 50 bone marrow transplant requests received monthly, more donors are needed.

To date, the Bone Marrow Donor Programme has some 48,000 donors on its register. But with an increasing demand for bone marrow transplants, there is an urgent need to recruit more especially from the minority groups. The aim is to recruit 7,000 new donors each year to meet this increasing demand.

CLEARING MISCONCEPTION ABOUT HARVESTING PROCEDURE A CHALLENGE

But a main challenge to get more donors on board is clearing the misconception about the harvesting procedure.

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CANCER RESEARCH UK scientists have found more than 400 blind spots in DNA which could hide cancer-causing gene faults, according to research published in Cancer Research.

The researchers found hidden faults in areas that are tricky for gene-reading technology to decode. This technique, which unravels cancers genetic blueprint, is an important part of the research that scientists carry out to understand more about cancers biology.

By finding new ways to unlock these blind spots in the future, the researchers hope this will help us understand these mistakes and whether they lead to cancer. This could be a step towards developing tests to spot cancers earlier or provide new tactics for discovering future cancer treatments.

The team, from the Cancer Research UK Manchester Institute, compared two giant gene databases made from cancer cells grown in labs and cross-checked all the genes that are known or are likely to be involved in cancer to unearth the problem areas.

They found that the 400 blind spots in the genes were hidden in very repetitive DNA areas which cause the gene-reading technology to stutter. This problem reading the genes could conceal mistakes which might play a vital role in cancer.

Lead researcher Andrew Hudson, at the Cancer Research UK Manchester Institute at The University of Manchester, said: The genes behind cancer are like a story. While weve been able to read most of the book using gene-reading technology, the limits of these tools mean some pages are missing.

These pages could just be unimportant filler, but we wonder if they might hold important twists in the plot which could affect our understanding of cancer. The next step in our work will be to find a way to open up these areas to help piece together the full story.

Nell Barrie, Cancer Research UKs senior science information manager, said: Were at an unprecedented point in cancer research. As research accelerates were revealing more and more about cancers secrets and central to this is our better understanding of how genetic changes drive the disease.

By delving deeper into cancers genetic origins we can spot the ways the disease is triggered and develops. This could help us to tackle it from the root, giving more cancer patients a chance at surviving the disease.

The University of Manchester, including the Cancer Research UK Manchester Institute, joined forces with Cancer Research UK and The Christie NHS Foundation Trust to form the Manchester Cancer Research Centre, allowing doctors and scientists to work closely together to turn scientific advances into patient benefits sooner.

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Latest Infectious Disease News

THURSDAY, Nov. 13, 2014 (HealthDay News) -- It may be possible to identify different types of hemorrhagic fevers -- including one related to Ebola -- before people develop symptoms, according to new research.

Scientists studied two hemorrhagic fevers, including a cousin of Ebola called Marburg and another called Lassa. Marburg causes occasional outbreaks in Africa that have high death rates, and Lassa is common is Western Africa, the researchers reported.

Using genetic material from white blood cells, researchers from the Boston University School of Medicine and the U.S. Army Medical Research Institute were able to recognize changes in the way the genes behaved in the early stages of infection. These changes occur before someone would even have symptoms, according to the researchers. They also occur before the infection could be passed to others, according to the study published recently in the journal BMC Genomics.

The findings could help lead to better ways to diagnose hemorrhagic fevers during the early stages, when treatments and containment efforts are more likely to be effective, the researchers suggested.

They noted that early indications of hemorrhagic fevers (fever, flu symptoms) are similar, which makes proper diagnosis difficult. More disease-specific symptoms and the ability to spread the virus from person to person don't begin until after the virus has accumulated in the blood.

"The ability to distinguish between different types of infection before the appearance of overt clinical symptoms has important implications for guiding triage and containment during epidemics," study corresponding author Nacho Caballero, a Ph.D. candidate at Boston University School of Medicine, said in a university news release.

"We hope that our study will help in the development of better diagnostics, especially during the early stages of disease, when treatments have a greater chance of being effective," he added.

However, Caballero noted that "this is not a finding that can be translated into a test tomorrow. This study supports the idea that early markers of infection are there, but significant work will still need to be done to extend these findings."

-- Robert Preidt

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PUBLIC RELEASE DATE:

14-Nov-2014

Contact: Michael Kennedy m.kennedy@utoronto.ca 416-946-5025 University of Toronto @UofTNews

Researchers from the University of Toronto (U of T) report that personalized dietary advice based on a person's genetic makeup improves eating habits compared to current "one-size-fits-all" dietary recommendations. The findings were published online today in the journal PLoS One.

"We conducted the first randomized controlled trial to determine the impact of disclosing DNA-based dietary advice on eating habits," says Ahmed El-Sohemy, an Associate Professor in Nutritional Sciences at U of T and Canada Research Chair in Nutrigenomics. "We found that people who receive DNA-based advice improve their diet to a greater extent than those who receive the standard dietary advice. They're also the ones who need to change it the most."

Nutrigenomics is a field of research that aims to understand why some people respond differently than others to the same foods. Personalized nutrition, a branch of personalized medicine, is an application of nutrigenomics that helps tailor dietary recommendations to a person's DNA.

The researchers collected data on the intake of caffeine, sodium, vitamin C and sugar from 138 healthy young adults. The subjects were then randomized into two different study groups--one was given DNA-based dietary advice for each of the four dietary components of interest, and the other group was given current standard dietary advice for the same dietary components with no genetic information.

Changes in their dietary habits were assessed after three and 12 months. The researchers found that subjects who received DNA-based dietary advice started to show improvements to their diets after three months and the changes became even more apparent after 12 months.

Specifically, those who were informed that they carried a version of a gene linked to salt intake and high blood pressure significantly reduced their sodium intake, in accordance with the recommendation, compared to the group that received the standard advice for sodium intake.

No effects were observed for the other components of the diet. However, most subjects were already meeting the dietary recommendations for the three other components at the start of the study, and the researchers believe this might explain why no significant changes were seen in these intakes.

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PUBLIC RELEASE DATE:

14-Nov-2014

Contact: Crystal Mackay crystal.mackay@schulich.uwo.ca 519-661-2111 x80387 University of Western Ontario @mediawesternu

Researchers at Western University are using cutting-edge genetic mutation-analysis software developed in their lab to interpret mutations in tumour genome that may provide insight into determining which breast cancer tumours are more likely spread to other parts of the body and which ones won't.

Their findings are published today in the journal, Nature Scientific Reports.

"We are using a unique software program in our lab that looks at a type of mutation called a splicing mutation that is typically overlooked using current methods," said lead author on the study, Stephanie Dorman, a PhD student in the department of biochemistry at Western University's Schulich School of Medicine & Dentistry. She said that where previous genetic studies of 445 tumours detected 429 of these splicing mutations, the Western-developed analysis software was able to find more than 5000.

Using this software and human tumour tissue sample genetic data from The Cancer Genome Atlas, the research team pinpointed that mutations in the Neural Cell Adhesion Molecule (NCAM) and other related genes in NCAM biology were present at a much higher rate in tumours which had metastasized to the lymph nodes than those that did not. NCAM, typically found in neural cells is also highly expressed in breast tissue, and is involved in communication between cells.

"We believe that mutations in these biological pathways in some patients might be causing some of the characteristics of the tumour that enable it to migrate to other parts of the body," said Dorman.

Dr. Peter Rogan, principal investigator on the study and a Professor in the Departments of Biochemistry and Computer Science, hopes that these findings will allow oncologists and clinical laboratories looking for these mutations in tumour biopsies to predict which women are at higher risk for more aggressive tumours that might metastasize.

"One of the big issues in breast oncology is that women are sometimes treated with chemotherapy even if their tumour isn't going to metastasize," said Rogan. "The ideal situation would be to be able to identify those patients where the side-effects and potential negative consequences of chemotherapy following surgery can be avoided or at least, minimized."

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November 14, 2014

Provided by Michael McCarthy, University of Washington Health Sciences/UW Medicine

New technology closes many gaps in mapping that have long resisted sequencing

Thousands of never-before-seen genetic variants in the human genome have been uncovered using a new sequencing technology. These discoveries close many human genome mapping gaps that have long resisted sequencing.

The technique, called single-molecule, real-time DNA sequencing (SMRT), may now make it possible for researchers to identify potential genetic mutations behind many conditions whose genetic causes have long eluded scientists, said Evan Eichler, professor of genome sciences at the University of Washington, who led the team that conducted the study.

We now have access to a whole new realm of genetic variation that was opaque to us before, Eichler said. He and his colleagues reported their findings Nov. 10 in the journal Nature.

To date, scientists have been able to identify the genetic causes of only about half of inherited conditions. This puzzle has been called the missing heritability problem. One reason for this problem may be that standard genome sequencing technologies cannot map many parts of the genome precisely.

These approaches map genomes by aligning hundreds of millions of small, overlapping snippets of DNA, typically about 100 bases long, and then analyzing their DNA sequences to construct a map of the genome.

This approach has successfully pinpointed millions of small variations in the human genome. These variations arise from substitution of a single nucleotide base, called a single-nucleotide polymorphisms or SNP.

The standard approach also made it possible to identify very large variations, typically involving segments of DNA that are 5,000 bases long or longer. But for technical reasons, scientists had previously not been able to reliably detect variations whose lengths range from about 50 bases to 5,000 bases in length.

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Cartilage Regeneration
Christopher H. Evans, Ph.D., Director of Rehabilitation Medicine Research Center, Mayo Clinic PM R, discusses his lecture at AAPM R 2014 on the damage done to cartilage from trauma and arthritis.

By: Mayo Clinic

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BA2762: The Balancing Act on Lifetime Talks Organic Produce, Personalized Medicine
Today #39;s show focuses on organic produce from farm to plate -- and healthy recipes that help kids eat more vegetables; plus personalized medicine and advancem...

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Segway seat - AddSeat - Brake by sliding
This man has a Th 9 - Th 10 Spinal cord injury. As you can see he will need some leg support. We provide such an adjustment for this type of injury.

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Segway seat - AddSeat - Brake by sliding - Video

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Life Can Change in a Second:Doris Dennison #39;s Personal Injury Story
In 1986, Doris Dennison sustained a severe spinal cord injury when the car she was a passenger in, hit a patch of black ice on a remote road in Utah, rolled over 3 times and ejected her, her...

By: Eve #39;s Fund for Native American Health Initiatives

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PUBLIC RELEASE DATE:

13-Nov-2014

Contact: Kurtis Pivert kpivert@asn-online.org 202-699-0238 American Society of Nephrology @ASNKidney

Philadelphia, PA (November 13, 2014) -- Transplanted kidneys may not function long-term if they come from donors with variants in a particular gene, according to a study that will be presented at ASN Kidney Week 2014 November 11-16 at the Pennsylvania Convention Center in Philadelphia, PA.

Previous research from a single center in North Carolina found that risk variants in the apolipoprotein L1 gene (APOL1) in African American deceased kidney donors were linked with shorter survival of transplanted kidneys. The APOL1 gene creates a protein that is a component of HDL, or good cholesterol. Variation in the APOL1 gene is associated with up to 40% of all kidney disease in African Americans who undergo dialysis or kidney transplantation, and APOL1 kidney risk variants are present only on the chromosomes of individuals who possess recent African ancestry.

Researchers led by Barry Freedman (Wake Forest School of Medicine) looked for the potential link between APOL1 risk variants and shorter survival of transplanted kidneys in a larger group of patients. The new multi-center study included 675 deceased donor kidney transplants from African American donors.

Results from the study confirmed that 2 APOL1 gene variants in donor kidneys were associated with more than a 2-fold increased risk of organ failure after transplantation.

"These results warrant consideration of rapidly genotyping deceased African American kidney donors for APOL1 risk variants at the time of organ recovery," said Dr. Freedman. "APOL1 genotype data should be incorporated in the organ allocation and informed-consent processes."

###

Study: "Apolipoprotein L1 Gene Variants in Deceased Organ Donors Are Associated with Renal Allograft Failure" (Abstract TH-OR165)

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Gene variants in organ donors linked to shorter survival of transplanted kidneys

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By Randy Dotinga HealthDay Reporter

WEDNESDAY, Nov. 12, 2014 (HealthDay News) -- Many American doctors may not support genetic testing in patients without a major family history of certain illnesses, suggests a new survey of physicians.

When presented with the hypothetical case of a middle-aged man with a family history of cancer in an aunt and uncle, more than a third of 180 U.S. doctors surveyed said they wouldn't recommend any genetic testing. Almost half would only recommend testing for cancer genes, and fewer than one in five would recommend whole-genome testing, according to the survey.

The genome is the complete genetic "blueprint" for an individual.

So what's going on? "Most doctors still feel uncomfortable with genetic testing," said Dr. Robert Klitzman, who studies genetic testing and is a professor of psychiatry at Columbia University's Joseph Mailman School of Public Health in New York City.

"Most doctors feel uncomfortable with knowing how to order genetic information, interpret it and counsel patients," explained Klitzman, who was not part of the study.

And even when genetic testing is done, the results may provide plenty of frustrating uncertainty about a patient's future health, he said.

In some cases where potential treatment options are clearer, such as women with histories of breast and ovarian cancer on one side of the family, doctors may be likely to order genetic tests, Klitzman said. Genetic tests can indicate that certain women have much higher risks of breast and ovarian cancers, according to the National Cancer Institute.

The survey asked readers of The New England Journal of Medicine to consider genetic testing in a made-up 45-year-old patient who requested it. The hypothetical man didn't appear to have any significant risks based on his health or family history.

Doctors responded from 77 countries. The responses from the United States were similar overall to those in the rest of the world. Of the 929 respondents, 74 wrote comments and expressed concern about what to tell the patient if testing showed a risk of cancer. Would the patient be stressed out or even be able to do anything? What about cost and the potential for discrimination against the patient based on his medical future?

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Many U.S. Doctors Wary of Genetic Testing: Survey

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Newswise Mice bred to carry a gene variant found in a third of ALS patients have a faster disease progression and die sooner than mice with the standard genetic model of the disease, according to Penn State College of Medicine researchers. Understanding the molecular pathway of this accelerated model could lead to more successful drug trials for all ALS patients.

Amyotrophic lateral sclerosis, commonly known as Lou Gehrig's disease, is a degeneration of lower and upper motor neurons in the brainstem, spinal cord and the motor cortex. The disease, which affects 12,000 Americans, leads to loss of muscle control. People with ALS typically die of respiratory failure when the muscles that control breathing fail.

Penn State researchers were the first to discover increased iron levels in the brains of some patients with the late-onset neurodegenerative disorders Parkinson's disease and Alzheimer's disease. A decade ago, they also identified a relationship between ALS and excess iron accumulation when they found that 30 percent of ALS patients in their clinic carried a variant of a gene known as HFE that is associated with iron overload disease.

For this study, the researchers crossbred mice with the HFE gene variant with the standard mice used in ALS research.

"When we followed the disease progression and the behavior of our crossbred mice compared to the standard mice, we saw significant differences," said James Connor, vice chair of neurosurgery research and director of the Center for Aging and Neurodegenerative Diseases. The crossbred mice performed significantly worse on tests of forelimb and hindlimb grip strength and had a 4 percent shorter life-span. The researchers published their findings in BBA Molecular Basis of Disease.

"The disease progression was much faster in the crossbred mice than in the standard mice," Connor said. "What we found is that when ALS happens in the presence of the HFE gene variant, things go downhill more quickly."

The lead investigator on this project, graduate student Wint Nandar, noticed that the HFE gene variant sped up disease progression and death in females but not males. Males with ALS die faster, on average, than females.

Connor said the variant may not have had time to accelerate the pace of the disease in male mice. An accelerated progression may show up in clinical trials in human males, who live longer with the disease than mice.

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Genotype Found in 30 Percent of ALS Patients Speeds Up Disease Progression

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Nutrition and Genetics 4
Produced with CyberLink PowerDirector 13.

By: Tom Ballard, ND

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Rafael Nadal to Receive Stem Cell Treatment for Back Pain - TOI
Rafael Nadal to Receive Stem Cell Treatment for Back Pain Rafael Nadal #39;s doctor says the 14-time Grand Slam winner will receive stem cell treatment on his ailing back. Angel Ruiz-Cotorro...

By: The Times of India

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PUBLIC RELEASE DATE:

13-Nov-2014

Contact: Krista Conger kristac@stanford.edu 650-725-5371 Stanford University Medical Center @sumedicine

A protein that plays a critical role in preventing the development of many types of human cancers has been shown also to inhibit a vital stem cell property called pluripotency, according to a study by researchers at the Stanford University School of Medicine.

Blocking expression of the protein, called retinoblastoma, in mouse cells allowed the researchers to more easily transform them into what are known as induced pluripotent stem cells, or iPS cells. Pluripotent is a term used to describe a cell that is similar to an embryonic stem cell and can become any tissue in the body.

The study provides a direct and unexpected molecular link between cancer and stem cell science through retinoblastoma, or Rb, one of the best known of a class of proteins called tumor suppressors. Although Rb has long been known to control the rate of cell division, the researchers found that it also directly binds and inhibits the expression of genes involved in pluripotency.

"We were very surprised to see that retinoblastoma directly connects control of the cell cycle with pluripotency," said Julien Sage, PhD, associate professor of pediatrics and of genetics. "This is a completely new idea as to how retinoblastoma functions. It physically prevents the reacquisition of stem cellness and pluripotency by inhibiting gene expression."

Marius Wernig, MD, associate professor of pathology, said, "The loss of Rb appears to directly change a cell's identity. Without the protein, the cell is much more developmentally fluid and is easier to reprogram into an iPS cell."

Wernig and Sage, both members of the Stanford Cancer Institute, share senior authorship of the study, which will be published online Nov. 13 in Cell Stem Cell. Postdoctoral scholar Michael Kareta, PhD, is the lead author.

Tumor Suppressor

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Newswise Led by Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research member Dr. Hanna Mikkola, UCLA scientists have discovered a unique protein that is integral to the self-renewal of hematopoietic stem cells (HSCs) during human development.

This discovery lays the groundwork for researchers to generate HSCs in the lab (in vitro) that better mirror those that develop in their natural environment (in vivo). This could lead to improved therapies for blood-related diseases and cancers by enabling the creation of patient-specific blood stem cells for transplantation.

The findings are reported online November 13, 2014, ahead of print in the journal Cell Stem Cell.

The research community has long sought to harness the promise of pluripotent stem cells (PSCs) to overcome a significant roadblock in making cell-based therapies blood and immune diseases more broadly available, which has been hampered by the inability to generate and expand human HSCs in culture. HSCs are the blood forming cells that serve as the critical link between PSCs and fully differentiated cells of the blood system. The ability of HSCs to self-renew (replicate themselves) and differentiate to all blood cell types, is determined in part by the environment that the stem cell came from, called the niche.

In the five-year study, Mikkola and Drs. Sacha Prashad and Vincenzo Calvanese, members of Mikkolas lab and lead authors of the study, investigated a unique HSC surface protein called GPI-80. They found that it was produced by a specific subpopulation of human fetal hematopoietic cells that were the only group that could self-renew and differentiate into various blood cell types. They also found that this subpopulation of hematopoietic cells was the sole population able to permanently integrate into and thrive within the blood system of a recipient mouse.

Mikkola and colleagues further discovered that GPI-80 identifies HSCs during multiple phases of human HSC development and migration. These include the early first trimester of fetal development when newly generated HSCs can be found in the placenta, and the second trimester when HSCs are actively replicating in the fetal liver and the fetal bone marrow.

We found that whatever HSC niche we investigated, we could use GPI-80 as the best determinant to find the stem cell as it was being generated or colonized different hematopoietic tissues, said Mikkola, associate professor of molecular, cell and development biology at UCLA and also a member of the Jonsson Comprehensive Cancer Center. Moreover, loss of GPI-80 caused the stem cells to differentiate. This essentially tells us that GPI-80 must be present to make HSCs. We now have a very unique marker for investigating how human hematopoietic cells develop, migrate and function.

Mikkolas team is actively exploring different stages of human HSC development and PSC differentiation based on the GPI-80 marker, and comparing how blood stem cells are being generated in vitro and in vivo. This paves the way for scientists to redirect PSCs into patient-specific HSCs for transplantation into the patient without the need to find a suitable donor.

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November 13, 2014

Marc-Andr Skelling of East Angus needs help. The 23-year-old man has Hodgkins Lymphoma, a cancer affecting the bodys white blood cells and lymph nodes. He has been told that without a viable donation of bone marrow stem cells he has less than a month to live.

We need to find a donor, its urgent, said Muguette Skelling, Marc-Andrs mother. Were inviting everyone, no matter who they are, to register with Hma-Quebec.

Bone marrow is responsible for the production of red and white blood cells in the body and therefore a bone marrow transplant can be an effective treatment for a range of blood related diseases. Depending on the context, individuals can receive a transplant either from another part of their own body, or from an outside donor.

Individuals in good health who are between 18 and 35 years of age can register to donate in Quebec. Registration is done online through the Hma-Quebec website. Once registration is complete, a test kit containing a cheek swab is mailed to the registrant that must then be returned. According to Mnard, the whole process from registration to getting onto the list takes twelve weeks.

Read the full story in Thursday's Record.

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East Angus man looking for stem cells

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