Wheelchair Camber and width determination
This e-learning course delivered online with a DVD supplement represents current approached to evaluating, treating a patient with spinal cord injury. Unique...

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European researchers have announced a breakthrough in the development of artificial bone marrow which expands the ability of scientists to reproduce stem cells in the lab and could lead to increased availability of treatment for leukemia sufferers.

One of the main treatments for the blood cancer is the injection of hematopoietic stem cells (HSCs). These HSCs can either be harvested from a compatible donor or cultivated from the patients own bone marrow in the lab.

The greatest challenges in producing HSCs in the lab has been their limited longevity outside of the bone marrow environment. This problem may soon be circumvented with the creation of an artificial bone marrow by the Young Investigators Group for Stem Cell Material Interactions.

Headed by Dr. Cornelia Lee-Thedieck the group consists of scientists from the KIT Institute of Functional Interfaces (IFG), the Max Planck Institute for Intelligent Systems, Stuttgart, and Tbingen University.

The cultivation of HSCs with current methods is limited as they quickly change into mature blood cells in culture in a process known as differentiation. HSCs are capable of developing into one of 10 different cell types. These mature cells are short lived and are not capable of self-renewal. HSCs, however, can continuously self-renew in healthy bone marrow. So the challenge facing researchers has been creating a surrogate for bone marrow in the lab which allows for the cultivation of HSCs.

Using macroporous hydrogel scaffolds the Young Investigators Group produced a substance that mimics the spongy structure of trabecular bone, the material within bone where bone marrow is held. To this hydrogel architecture a number of proteins found in bone marrow were added for the HSCs to bind to. Other conditions important for HSC self-renewal in trabecular bone were also created by adding mesenchymal stem cells (MSCs) from bone marrow and umbilical cord.

When tested by adding HSCs from umbilical cord blood to the artificial bone marrow it was found that the cells were both able to self-renew and retain their ability to differentiate. The next step for the research is to identify how the behavior of stem cells can be manipulated by synthetic materials.

The team hopes within the next ten to fifteen years this research could lead to the development of an artificial environment for the reproduction of stem cells and the treatment of leukemia.

The research was recently published in the journal Biomaterials.

Source: Karlsruhe Institute of Technology

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Leukemia treatment given shot in the arm by artificial bone marrow development

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Category: Science & Technology Posted: January 14, 2014 08:02AM Author: Guest_Jim_*

Our bones play a larger role in our bodies than simply creating a rigid structure as they also hold other cells and tissues, such as bone marrow. Within sponge-like bone marrow are special niches where hematopoietic stem cells reside and produce necessary immune cells. These stem cells can only exist in those niches as they change their properties when moved to a new environment. However, researchers at the Karlsruhe Institute of Technology, Max Planck Institute for Intelligent Systems, and Tbingen University have successfully created artificial bone marrow.

Diseases such as leukemia cause the body to incorrectly produce immune cells, which obviously puts the body at risk. A bone marrow transplant can treat the disease, but it is very hard to find matches for all of the patients out there, which is why artificial bone marrow could be invaluable. To create their artificial bone marrow, the researchers used synthetic polymers to form a properly porous structure and added protein building blocks to it. These blocks are important as they replicate those found in natural bone marrow, which the stem cells attach to. Additional cell types were also added to the niche, to mimic the natural environment as much as possible.

With artificial bone marrow, it may be possible for researchers to better study and understand how stem cells interact with different materials. Potentially ten to fifteen years from now that research could lead to treatments for leukemia, and other diseases.

Source: Karlsruhe Institute of Technology

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Artificial Bone Marrow Created

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PUBLIC RELEASE DATE:

14-Jan-2014

Contact: Michelle Quivey mquivey@isscr.org 224-592-5012 International Society for Stem Cell Research

CHICAGO The International Society for Stem Cell Research (ISSCR) has announced the following 2014 award recipients, who will be formally recognized at its 12th Annual Meeting in Vancouver, taking place June 18-21, 2014:

The McEwen Award for Innovation, supported by the McEwen Centre for Regenerative Medicine, recognizes original thinking and groundbreaking research pertaining to stem cells or regenerative medicine that opens new avenues of exploration toward the understanding or treatment of human disease or affliction. The winner receives $100,000 USD. Past winners include James Thomson, Rudolf Jaenisch, Kazutoshi Takahashi and Shinya Yamanaka.

Award recipient Surani is a world leader in the field of epigenetics and the development of the mammalian germ line. His work on early mammalian development led to his involvement in the discovery of genomic imprinting and ongoing contributions to understanding the mechanistic basis of imprinting. Most relevant to stem cell biology, is his work on the cellular and molecular specification of the mammalian germ cell lineage, which impacted the field's understanding of how the germ line is established and the molecular mechanisms responsible for reprogramming the epigenome in order to generate the totipotent state.

"The ISSCR is thrilled to announce the McEwen Award for Innovation, our most prestigious award, will be presented to Azim Surani," Janet Rossant, ISSCR president, said. "His pioneering research, which has changed the face of epigenetics and advanced the field of stem cell biology, is a rare and significant contribution from a single individual."

The ISSCR-BD Biosciences Outstanding Young Investigator Award recognizes exceptional achievements by an ISSCR member and investigator in the early part of their independent career in stem cell research. The winner receives a $7,500 USD personal award and an opportunity to present at the ISSCR Annual Meeting. Past winners include Marius Wernig, Cdric Blanpain, Robert Blelloch, Joanna Wysocka and Konrad Hochedlinger.

Award recipient Greco established a noninvasive method to directly visualize skin stem cell division in real time in living animals the first of its kind for imaging any stem cell. By combining this method with laser ablation and transgenic lineage tracing, she captured previously inaccessible key information on stem cell behavior during tissue maintenance and regeneration. She demonstrated that the niche location of stem cells dictates their fates, the niche is required for tissue maintenance, and that a -catenin-mediated extrinsic mechanism regulates stem cell activation.

"The ISSCR is looking forward to presenting our Outstanding Young Investigator Award to Valentina Greco," Rossant said. "Her enthusiastic nomination by over a dozen leaders in the field of stem cell research demonstrates the significance of her early-career contributions to stem cell biology and regenerative medicine."

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The International Society for Stem Cell Research announces its 2014 award recipients

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Published:Tuesday, January 14, 2014

Updated:Tuesday, January 14, 2014 18:01

A new tool that could help facilitate future stem cell therapy has recently been identified by a UVM professor and his colleagues, according to UVMs College of Medicine.

The development of this tool could potentially help more than 700,000 Americans who suffer a heart attack each year.

Because stem cells have the potential to develop into a variety of cell types in the body, they may offer a renewable source of replacement cells to treat diseases, conditions and disabilities, and even regenerate damaged tissue and organs.

However, the field of regenerative medicine has struggled to successfully graft cells from culture back into injured tissue.

UVM Associate Professor of Medicine Jeffrey Spees, Ph.D., collaborated with the Center for Gene Therapy at Tulane University. His research team recently set out to develop ways to enhance graft success.

Dr. Spees and his team focused on a type of bone marrow-derived progenitor cell or biological cell that forms stromal cells or connective tissue cells.

They found that the medium contained Connective Tissue Growth Factor (CTGF) and the hormone insulin, and together, they have a synergistic effect, Spees said to UVMs College of Medicine.

The group found that the protective ligands resulted in improved graft success, breaking the record for engraftment.

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Jan. 14, 2014 The presence of a gene variant in people with mild cognitive impairment (MCI) is associated with accelerated rates of brain atrophy, according to a new study published online in the journal Radiology.

The study focused on the gene apolipoprotein E (APOE), the most important genetic factor known in non-familial Alzheimer's disease (AD). APOE has different alleles, or gene variations, said the study's senior author, Jeffrey R. Petrella, M.D., associate professor of radiology at Duke University School of Medicine in Durham, N.C.

"We all carry two APOE alleles, and most people have at least one copy of the APOE epsilon 3 (3) variant, which is considered neutral with respect to Alzheimer's risk," Dr. Petrella said.

The less common epsilon 4 (4) allele, in contrast, is associated with a higher risk for development of AD, earlier age of onset, and faster progression in those affected, as compared with the other APOE alleles.

Dr. Petrella and colleagues recently analyzed data from the Alzheimer's Disease Neuroimaging Initiative (ADNI) involving 237 patients, mean age 79.9, with MCI, a slight but noticeable decline in cognitive ability that is tied to a higher risk of AD. The researchers used MRI to measure brain atrophy rates in these patients over a 12- to 48-month period.

The 4 carriers in the study group exhibited markedly greater atrophy rates than 3 carriers in 13 of 15 brain regions hypothesized to be key components of the cognitive networks disrupted in AD.

"The results showed atrophy in brain regions we know are affected by AD, in a population of patients who do not have AD, but are at risk for it," Dr. Petrella said. "This suggests the possibility of a genotype-specific network of related brain regions that undergo faster atrophy in MCI and potentially underlies the observed cognitive decline."

The researchers did not explore why APOE 4 might accelerate atrophy, but the affect is likely due to a combination of factors, noted Dr. Petrella.

"The protein has a broad role in the transport and normal metabolism of lipids and a protective function on behalf of brain cells, including its role in the breakdown of beta-amyloid, one of the proteins implicated in the pathophysiology of AD," he said.

With MRI playing an increasingly prominent role in MCI research, Dr. Petrella predicted that increased knowledge about the effects of APOE will improve the design and execution of future clinical trials. For instance, researchers could enrich their samples with 4 patients in MCI prevention trials to better determine potential treatment effects on brain regions vulnerable to degeneration.

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Gene variation associated with brain atrophy in mild cognitive impairment

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PUBLIC RELEASE DATE:

14-Jan-2014

Contact: Beverly Clark beverly.clark@emory.edu 404-712-8780 Emory Health Sciences

A unique study of the white-throated sparrow has identified a biological pathway connecting variation in the birds' aggression and parenting behaviors in the wild to variation in their genome.

The Proceedings of the National Academy of Sciences (PNAS) is publishing the results of the experiments, conducted by the lab of neuroscientist Donna Maney in Emory University's Department of Psychology.

The research, which comprised behavioral observations of the study subjects in the field and laboratory analyses of their gene expression in the brain, showed that variation in the expression of the estrogen receptor alpha (ER-alpha) gene strongly predicts the birds' behavior.

"We believe this is the most comprehensive study yet of how the rearrangement of a chromosome affects social behavior in a vertebrate," says Brent Horton, a post-doctoral fellow in the Maney lab and lead author of the study. "So much of the process of genetic discovery is restricted behind closed doors in a laboratory. But our study began in the woods, where we first observed the social behaviors of the actual subjects of our experiments in their natural setting. The results provide valuable insight into the mechanistic basis of aggression and parenting in all vertebrates, including humans."

Such integrated studies "are exceedingly rare," Horton adds, "because they require such a variety of resources, expertise and well-balanced collaboration."

In addition to Horton and Maney, the principal investigators included Eric Ortlund, a biochemist and an expert in the ER-alpha gene at the Emory School of Medicine; and James Thomas, a human geneticist who was formerly with Emory and now works at the National Institutes of Health. Co-authors include William Hudson, a graduate fellow in Ortland's lab; Wendy Zinzow-Kramer, a post-doc in the Maney lab; Sandra Shirk, a research associate; and Emily Young, an undergraduate student of biology at Georgia Tech.

The white-throated sparrow is considered a good model organism for the genetic basis of behavior due to a genetic event that has divided the species into two distinct forms that differ in their behavior. These two forms, the white-striped morph and the tan-striped morph, are easily distinguished by their plumage markings.

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Wild sparrow study traces social behaviors in the field to specific gene

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AAP A new system bought by Sydney's Garvan Institute can map the genetic makeup of 350 people a week.

Australian medicine has taken a leap into the future with the purchase of a system that can quickly and cheaply map a person's genetic makeup.

The new system bought by Sydney's Garvan Institute can map 350 people a week at a cost of $1000 each.

This means doctors will receive quick feedback on the best way to treat cancer patients and scientists will have massive power to build an Australian genetic database.

The system differs from current genetic testing in that it maps the entire genome rather than specific gene mutations such as BRCA1 and BRCA2 that cause breast and ovarian cancer.

The first whole human genome was mapped more than a decade ago by an international team of scientists at a cost $1 billion.

Garvan is one of a few organisations in the world to buy the HiSeq X Ten Sequencing System, according to an announcement in San Diego on Tuesday (Wednesday AEDT).

"Over the next few years, we have an opportunity to learn as much about the genetics of human disease as we have learned in the history of medicine," said Garvan executive director Professor John Mattick.

"We have reached a tipping point where genome sequencing has become achievable on a broad scale."

He expected genomic sequencing to become widely available to the general public in the next few years.

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Australia takes genetic medicine leap

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AAP A new system bought by Sydney's Garvan Institute can map the genetic makeup of 350 people a week.

Australian medicine has taken a leap into the future with the purchase of a system that can quickly and cheaply map a person's genetic makeup.

The new system bought by Sydney's Garvan Institute can map 350 people a week at a cost of $1000 each.

This means doctors will receive quick feedback on the best way to treat cancer patients and scientists will have massive power to build an Australian genetic database.

The system differs from current genetic testing in that it maps the entire genome rather than specific gene mutations such as BRCA1 and BRCA2 that cause breast and ovarian cancer.

The first whole human genome was mapped more than a decade ago by an international team of scientists at a cost $1 billion.

Garvan is one of a few organisations in the world to buy the HiSeq X Ten Sequencing System, according to an announcement in San Diego on Tuesday (Wednesday AEDT).

"Over the next few years, we have an opportunity to learn as much about the genetics of human disease as we have learned in the history of medicine," said Garvan executive director Professor John Mattick.

"We have reached a tipping point where genome sequencing has become achievable on a broad scale."

He expected genomic sequencing to become widely available to the general public in the next few years.

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Major leap for Aust genetic medicine

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Durham, NC (PRWEB) January 14, 2014

A new study released in STEM CELLS Translational Medicine indicates that stem cells can be effective in treating a debilitating and sometimes lethal genetic disorder called brittle bone disease.

Brittle bone disease, or osteogenesis imperfecta (OI), is characterized by fragile bones causing some patients to suffer hundreds of fractures over the course of a lifetime. In addition, according to the OI Foundation, other symptoms include muscle weakness, hearing loss, fatigue, joint laxity, curved bones, scoliosis, brittle teeth and short stature. Restrictive pulmonary disease occurs in the more severe cases. Currently there is no cure.

OI can be detected prenatally by ultrasound. In the study reported on in STEM CELLS Translational Medicine, an international team of researchers treated two patients for the disease using mesenchymal stem cells (MSCs) while the infants were still in the womb, followed by stem cell boosts after they were born.

We had previously reported on the prenatal transplantation for the patient with OI type III, which is the most severe form in children who survive the neonatal period, said Cecilia Gtherstrm, Ph.D., of the Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden. She and Jerry Chan, M.D., Ph.D., of the Yong Loo Lin School of Medicine and National University of Singapore, and KK Womens and Childrens Hospital, led the study that also included colleagues from the United States, Canada, Taiwan and Australia.

The first eight years after the prenatal transplant, our patient did well and grew at an acceptable rate. However, she then began to experience multiple complications, including fractures, scoliosis and reduction in growth, so the decision was made to give her another MSC infusion. In the two years since, she has not suffered any more fractures and improved her growth.

She was even able to start dance classes, increase her participation in gymnastics at school and play modified indoor hockey, Dr. Gtherstrm added.

The second child, which was experiencing a milder form of OI, received a stem cell transfusion 31 weeks into gestation and did not suffer any new fractures for the remainder of the pregnancy or during infancy. She followed her normal growth pattern just under the third percentile in height until 13 months of age, when she stopped growing. Six months later, the doctors gave her another infusion of stem cells and she resumed growing at her previous rate.

Our findings suggest that prenatal transplantation of autologous stem cells in OI appears safe and is of likely clinical benefit and that re-transplantation with same-donor cells is feasible. However, the limited experience to date means that it is not possible to be conclusive, for which further studies are required, Dr. Chan said.

Although the findings are preliminary, this report is encouraging in suggesting that prenatal transplantation may be a safe and effective treatment for this condition, said Anthony Atala, M.D., editor of STEM CELLS Translational Medicine and director of the Wake Forest Institute for Regenerative Medicine.

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Stem Cells Could Prove Effective in Treating Brittle Bone Disease

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Genetics of Sickle Cell Disease
Sickle cell disease is an inherited genetic disorder and is a recessive trait. This video describes how the genetic mutation causing sickle cell disease is p...

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Mutants Genetics Gladiators: Omega Boss Neo Paris | Medusas lvl 33 and Dracus nobilis.
en este video muestro como matar al dracus nobilis de omega aunk me sobro un poco de suerte XD ya k este si fue algo dificil MI FB: https://www.facebook.com/...

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Mutants Genetics Gladiators: Omega Boss Neo Paris | Medusas lvl 33 and Dracus nobilis. - Video

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How to analyze and solve genetics problems
Solving Genetic Problems What is a Genetic Problem? A genetic problem is a type examination question that involves both a knowledge of Mendel #39;s experiments, ...

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How to analyze and solve genetics problems - Video

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MineCraft Modded Survival Grouer Adventure #5 Advanced genetics

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MineCraft Modded Survival Grouer Adventure #5 Advanced genetics - Video

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Minecraft Mod Spotlight - Advanced Genetics
Now that Tom (A.K.A.) has defeated the Ender Dragon he has now begun searching for cool mods made by the community! Get Advanced Genetics: http://www.minecra...

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Lets play the sims3 perfect genetics challenge pt9

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2014 Pediatrics Genetics Video Excerpt
This excerpt is a lecture from our 2014 Pediatrics Board Review. Find out more by going to: http://www.medstudy.com.

By: MedStudycom

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2014 Pediatrics Genetics Video Excerpt - Video

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Jan. 14, 2014 Ryan Zurakowski, assistant professor of electrical and computer engineering at the University of Delaware, is co-author of a paper appearing in Nature Medicine on Jan. 12 highlighting the role of T-cells in HIV.

The paper, titled "HIV-1 Persistence in CD4+ T-Cells with Stem Cell-Like Properties," provides evidence that a particular T-cell type may help researchers better understand why HIV can persist despite treatment.

Zurakowski's co-authors include Mathias Lichterfeld, the paper's lead author, and researchers from Massachusetts General Hospital (MGH); Ragon Institute of MGH, the Massachusetts Institute of Technology and Harvard University; the First Affiliated Hospital of China Medical University; Brigham and Women's Hospital; and Howard Hughes Medical Institute.

Zurakowski explained that HIV treatments do not kill infected cells. Instead, they stop the infection of new cells, and rely on the virus itself to kill the infected cells. Unfortunately, some cells infected by the virus -- memory T-cells -- are not killed by the virus.

T-cells are a type of lymphocyte, or white blood cell, produced by the thymus gland, that actively participates in the body's immune response. "Memory" T-cells can live for years, or even decades, providing life-long immunity to previously encountered diseases. They can form "quiescent" infections, which last for years, and cause HIV to rebound whenever a patient stops treatment.

During a decade-long study, the researchers discovered that not all memory T-cells are alike. A subgroup of memory T-cells, called "Stem-Cell Memory T-cells" (Tscm), are different, particularly in their ability to produce daughter cells.

The researchers were able to show that the HIV-infected Tscm cells in patients on HIV therapy decayed more slowly than any other type of T-cell. As a result, after 10 years of therapy, the Tscm cells represented 24 percent of the total HIV infected cell population, despite being only 1 percent of the total T-cell population.

This finding is significant, Zurakowski said, because it demonstrates that Tscm cells are the slowest-decaying portion of the HIV reservoir.

"Over time this particular cell type plays an increasingly significant role in sustaining HIV infection in patients that have remained on therapy," he said.

Zurakowski credits the finding to the diligence of Lichterfeld and the researchers at the Ragon Institute in carefully following the same HIV patients for a decade.

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T-cell research sheds light on why HIV can persist despite treatment

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Introduction

Over the last year, there have been over 1,500 articles published in medical journals on multiple sclerosis or animal models of the disease. The majority of these articles represent new research into MS, its causes, its mode of action or potential treatments for it. In addition, there has been an even greater amount of new research into cell biology, genetics, the immune system, other autoimmune, inflammatory and neurological diseases, virology and stem cell research - all of which give us a better understanding of the biological environment in which the disease operates.

It is impossible to sum up all of this research in a single essay and, for this reason, I intend to concentrate on those areas which seem to me to be particularly hopeful. This is, therefore, a personal view. This section will take a while to complete but I'm publishing it in installments.

There is no global authority coordinating the MS research effort. This is probably a good thing because it allows researchers to attack the problem from oblique angles and provide novel and unexpected insights into the disease. However, I intend to structure this article as if it were a progress report for just such a global research project. This project would group the research into four areas:

2. Arresting the progress of the disease

Of course, those of us who are already carrying significant deficits as a result of MS might wish to reorder these priorities. In any event, researchers are making significant progress in all these areas.

Finding the Cause of Multiple Sclerosis

Looking for the genes that convey a susceptibility to Multiple Sclerosis

Introduction

Recently, there has been a lot of interest in the genetics of complex diseases such as multiple sclerosis. The human genome has recently been mapped in its entirety and the hope is that this will allow researchers to isolate the genes for such diseases by statistical analysis of affected populations.

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Research in Multiple Sclerosis

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Conquering Diabetes by Anne Peters M.D. 01-12-2014
Diabetes and obesity are in an epidemic proportion in the US and around the globe including Michigan and Manipur. Ann Peters, a Los Angeles diabetologist and...

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Get Moving! Exercise after Spinal Cord Injury
http://sci.washington.edu There are so many barriers to getting exercise after you #39;ve had a spinal cord injury that it is easy to be discouraged or feel that...

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ST. LOUIS -

Sickle cell is a serious disease that causes pain, anemia, infection, organ damage and even stroke. Its the most common inherited blood disorder in the United States.

The good news is bone marrow transplants can be a cure. The bad news is not every patient has a matching donor. Now, researchers are looking at a new way to offer more patients transplants.

Madisyn Travis is like any other 9-year-old, but theres something that sets Madisyn apart. She has sickle cell, an inherited red blood cell disease.

"It makes me feel bad, and sometimes I have to go to the hospital," Madisyn said.

"It's really hard to see her life interrupted," said Denise Travis, Madisyn's mom.

Soon, however, Madisyn will get a bone marrow transplant to cure her disease. Her little brother or sister are both matches, and one will be the donor.

Madisyn is one of the lucky ones. Only 14 percent of patients have a matching sibling.

"Ten years ago, we'd just tell them, 'Sorry, you have no family member. We cant transplant you,'" said Dr. Shalini Shenoy, professor of pediatrics and medical director, pediatric stem cell transplant program, Washington University School of Medicine, St. Louis Children's Hospital.

Shenoy is studying a new option for patients without related donors. Stem cells from a baby's umbilical cord can be infused in the arm. They travel to the bone marrow, settle there and make new cells.

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Health Beat: Stem cells to cure sickle cell

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Contact Information

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Newswise Ryan Zurakowski, assistant professor of electrical and computer engineering at the University of Delaware, is co-author of a paper appearing in Nature Medicine on Jan. 12 highlighting the role of T-cells in HIV.

The paper, titled HIV-1 Persistence in CD4+ T-Cells with Stem Cell-Like Properties, provides evidence that a particular T-cell type may help researchers better understand why HIV can persist despite treatment.

Zurakowskis co-authors include Mathias Lichterfeld, the papers lead author, and researchers from Massachusetts General Hospital (MGH); Ragon Institute of MGH, the Massachusetts Institute of Technology and Harvard University; the First Affiliated Hospital of China Medical University; Brigham and Womens Hospital; and Howard Hughes Medical Institute.

Zurakowski explained that HIV treatments do not kill infected cells. Instead, they stop the infection of new cells, and rely on the virus itself to kill the infected cells. Unfortunately, some cells infected by the virus memory T-cells are not killed by the virus.

T-cells are a type of lymphocyte, or white blood cell, produced by the thymus gland, that actively participates in the bodys immune response. Memory T-cells can live for years, or even decades, providing life-long immunity to previously encountered diseases. They can form "quiescent" infections, which last for years, and cause HIV to rebound whenever a patient stops treatment.

During a decade-long study, the researchers discovered that not all memory T-cells are alike. A subgroup of memory T-cells, called "Stem-Cell Memory T-cells" (Tscm), are different, particularly in their ability to produce daughter cells.

The researchers were able to show that the HIV-infected Tscm cells in patients on HIV therapy decayed more slowly than any other type of T-cell. As a result, after 10 years of therapy, the Tscm cells represented 24 percent of the total HIV infected cell population, despite being only 1 percent of the total T-cell population.

This finding is significant, Zurakowski said, because it demonstrates that Tscm cells are the slowest-decaying portion of the HIV reservoir.

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T-Cell Finding Sheds Light on Why HIV Can Persist Despite Treatment

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PUBLIC RELEASE DATE:

12-Jan-2014

Contact: Jessica Studeny jessica.studeny@case.edu 216-368-4692 Case Western Reserve University

Geneticists from Ohio, California and Japan joined forces in a quest to correct a faulty chromosome through cellular reprogramming. Their study, published online today in Nature, used stem cells to correct a defective "ring chromosome" with a normal chromosome. Such therapy has the promise to correct chromosome abnormalities that give rise to birth defects, mental disabilities and growth limitations.

"In the future, it may be possible to use this approach to take cells from a patient that has a defective chromosome with multiple missing or duplicated genes and rescue those cells by removing the defective chromosome and replacing it with a normal chromosome," said senior author Anthony Wynshaw-Boris, MD, PhD, James H. Jewell MD '34 Professor of Genetics and chair of Case Western Reserve School of Medicine Department of Genetics and Genome Sciences and University Hospitals Case Medical Center.

Wynshaw-Boris led this research while a professor in pediatrics, the Institute for Human Genetics and the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UC, San Francisco (UCSF) before joining the faculty at Case Western Reserve in June 2013.

Individuals with ring chromosomes may display a variety of birth defects, but nearly all persons with ring chromosomes at least display short stature due to problems with cell division. A normal chromosome is linear, with its ends protected, but with ring chromosomes, the two ends of the chromosome fuse together, forming a circle. This fusion can be associated with large terminal deletions, a process where portions of the chromosome or DNA sequences are missing. These deletions can result in disabling genetic disorders if the genes in the deletion are necessary for normal cellular functions.

The prospect for effective counter measures has evaded scientistsuntil now. The international research team discovered the potential for substituting the malfunctioning ring chromosome with an appropriately functioning one during reprogramming of patient cells into induced pluripotent stem cells (iPSCs). iPSC reprogramming is a technique that was developed by Shinya Yamanaka, MD, PhD, a co-corresponding author on the Nature paper. Yamanaka is a senior investigator at the UCSF-affiliated Gladstone Institutes, a professor of anatomy at UCSF, and the director of the Center for iPS Cell Research and Application (CiRA) at the Institute for Integrated Cell-Material Sciences (iCeMS) in Kyoto University. He won the Nobel Prize in Medicine in 2012 for developing the reprogramming technique.

Marina Bershteyn, PhD, a postdoctoral fellow in the Wynshaw-Boris lab at UCSF, along with Yohei Hayashi, PhD, a postdoctoral fellow in the Yamanaka lab at the Gladstone Institutes, reprogrammed skin cells from three patients with abnormal brain development due to a rare disorder called Miller Dieker Syndrome, which results from large terminal deletions in one arm of chromosome 17. One patient had a ring chromosome 17 with the deletion and the other two patients had large terminal deletions in one of their chromosome 17, but not a ring. Additionally, each of these patients had one normal chromosome 17.

The researchers observed that, after reprogramming, the ring chromosome 17 that had the deletion vanished entirely and was replaced by a duplicated copy of the normal chromosome 17. However, the terminal deletions in the other two patients remained after reprogramming. To make sure this phenomenon was not unique to ring chromosome 17, they reprogrammed cells from two different patients that each had ring chromosomes 13. These reprogrammed cells also lost the ring chromosome, and contained a duplicated copy of the normal chromosome 13.

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Nature study discovers chromosome therapy to correct a severe chromosome defect

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14 months after Stem Cell Therapy by Dr Harry Adelson for arthritis of the knee
Nona discusses her outcome 14 months after Stem Cell Therapy by Dr Harry Adelson for arthritis of the knee http://www.docereclinics.com.

By: Harry Adelson

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14 months after Stem Cell Therapy by Dr Harry Adelson for arthritis of the knee - Video

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