Archive for November, 2014

Katie Joyce, left, aged four, and Sophie Ryan Palmer, aged 12, were among the four children who died as a result of complications with transplants. Photograph: Steve Parsons/PA

Four children have died after failings in how stem cells used in life-saving operations were frozen at Great Ormond Street hospital, it emerged this week.

The four, who were between one and 12 years old, were among eight children with cancer whose bone marrow transplants did not work as a result of problems with the freezing process.

Britains best-known childrens hospital has admitted that one of them, four-year-old Katie Joyce, might have survived if it had acted more quickly when problems arose.

An inquest into the deaths this week heard that doctors were initially baffled as to why a decade of success using the procedures suddenly came to a halt in summer 2013. Despite extensive investigations, the hospital failed to pinpoint the source of the setbacks in its cryopreservation laboratory, used for freezing stem cells which were kept there for using in bone marrow transplants in children.

The transplanted stem cells were intended to help the childs bone marrow, damaged during chemotherapy, grow again to maximise the chance of recovery.

At the inquest, lawyers for two of the families whose children died accused Great Ormond Street of taking too long to halt the transplants once staff began having concerns.

The hospital has since overhauled its procedures to prevent further incidents and there are calls for the deaths to lead to tighter procedures around how stem cells are stored at hospitals and research centres across the UK.

Concerns were first raised in June 2013 when 12-year-old Sophie Ryan Palmer, who had acute lymphoblastic leukaemia, failed to make progress after her transplant at Great Ormond Street, which involved using a donors stem cells rather than her own.

By October 2013 the hospital had identified that a higher than usual proportion of eight patients who had undergone stem cell transplantation between March and August had suffered setbacks after encountering what doctors call delayed engraftment. It immediately stopped freezing stem cells on site at its base in Bloomsbury, central London, and launched an investigation.

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Great Ormond Street deaths caused by stem cell lab failures, inquest told

The Saint Mary's student club, SMC Stands up to Cancer, held a bone marrow registration drive Friday. Registrants' genetic information will be added to the Be the Match marrow database which searches for possible matches with blood cancer patients. Suitable donors can provide bone marrow or peripheral blood stem cells to patients, saving lives.

Allison Lukomski, a communicative sciences and disorders major, was a match for a female cancer patient from last years drive. She said it is very rewarding, knowing she was able to help someone else.

"You could save a life," Lukomski said, "and I just think it is so incredible and it is such an incredible experience I had, my family had, everyone in my family decided to join because they thought it was a really cool process." She said everyone asks about the pain, but once they realize how much information there is every step of the way, many people sign up.

This is the second year for the bone marrow drive. For more information on joining the bone marrow donation registry, visit Be The Match.

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Saint Mary's holds bone marrow drive

PUBLIC RELEASE DATE:

20-Nov-2014

Contact: Cristy Lytal lytal@med.usc.edu 323-442-2172 University of Southern California - Health Sciences

There are plenty of body parts that don't grow back when you lose them. Nails are an exception, and a new study published in the Proceedings of the National Academy of Sciences (PNAS) reveals some of the reasons why.

A team of USC Stem Cell researchers led by principal investigator Krzysztof Kobielak and co-first authors Yvonne Leung and Eve Kandyba has identified a new population of nail stem cells, which have the ability to either self-renew or undergo specialization or differentiation into multiple tissues.

To find these elusive stem cells, the team used a sophisticated system to attach fluorescent proteins and other visible "labels" to mouse nail cells. Many of these cells repeatedly divided, diluting the fluorescence and labels among their increasingly dim progeny. However, a few cells located in the soft tissue attached to the base of the nail retained strong fluorescence and labels because they either did not divide or divided slowly -- a known property of many stem cells.

The researchers then discovered that these slow-dividing stem cells have the flexibility to perform dual roles. Under normal circumstances, the stem cells contribute to the growth of both the nails and the adjacent skin. However, if the nail is injured or lost, a protein called "Bone Morphogenic Protein," or BMP, signals to the stem cells to shift their function exclusively to nail repair.

The researchers are now wondering whether or not the right signals or environmental cues could induce these nail stem cells to generate additional types of tissue -- potentially aiding in the repair of everything from nail and finger defects to severe skin injuries and amputations.

"That was very surprising discovery, since the dual characteristic of these nail stem cells to regenerate both the nail and skin under certain physiological conditions is quite unique and different from other skin stem cells, such as those of the hair follicle or sweat gland," said Kobielak.

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Nail stem cells prove more versatile than press ons

Elite Emage Stem Cell Therapy
Elite Emage Stem Cell Therapy.

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Elite Emage Stem Cell Therapy - Video

PUBLIC RELEASE DATE:

21-Nov-2014

Contact: Quinn Eastman qeastma@emory.edu 404-727-7829 Emory Health Sciences @emoryhealthsci

Patients who receive more cells get significant benefits. That's a key lesson emerging from a clinical trial that was reported this week at the American Heart Association meeting in Chicago.

In this study, doctors treated heart attack patients with their own bone marrow cells, selected for their healing potential and then reinjected into the heart, in an effort to improve the heart's recovery.

In the PreSERVE-AMI phase II trial, physicians from 60 sites treated 161 patients, making the study one of the largest to assess cell therapy for heart attacks in the United States. The study was sponsored by NeoStem, Inc.

"This was an enormous undertaking, one that broke new ground in terms of assessing cell therapy rigorously," says the study's principal investigator, Arshed Quyyumi, MD, professor of medicine at Emory University School of Medicine and co-director of the Emory Clinical Cardiovascular Research Institute.

"We made some real progress in determining the cell type and doses that can benefit patients, in a group for whom the risks of progression to heart failure are high."

All participating patients received the standard of care -- stent placement -- and were only enrolled if, four days after heart attack and stenting, their ejection fraction (a measure of the heart's pumping capacity) was less than 48 percent. The average starting ejection fraction was 34 percent, a sign of severe injury to the heart.

After enrollment, patients had cells extracted from their bone marrow and received an intracoronary injection of sorted bone marrow cells or a placebo. Not all patients received the same dose of cells. Patients were supposed to receive a minimum of 10 million cells but some received more, up to 40 million.

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In landmark study of cell therapy for heart attack, more cells make a difference

Scientists from Universit Laval, the University of British Columbia and the University of Oxford have discovered a natural resistance gene against spruce budworm in the white spruce. The breakthrough, reported in The Plant Journal, paves the way to identifying and selecting naturally resistant trees to replant forests devastated by the destructive pest.

A research team composed of professors ric Bauce, Joerg Bohlmann and John Mackay as well as their students and postdocs discovered the gene in spruces that had remained relatively undamaged by a local budworm outbreak. The scientists compared the genomes of the more resilient trees and those that suffered substantial damage. "We measured expression levels of nearly 24,000 genes in the two groups of trees, explains Professor Mackay. We discovered a gene, betaglucosidase-1, whose expression in the needles of resistant spruce trees is up to 1,000 times higher than in non-resistant trees."

Postdoctoral scientist Melissa Mageroy then produced the protein encoded by the gene. Tests showed that the protein plays an essential part in chemical reactions resulting in the production of two compounds that are toxic to the budworm, piceol and pungenol, identified in 2011 by a research team supervised by Dr. ric Bauce. "We could say the gene we discovered produces natural insecticides in the tree foliage," sums up Dr. Mackay.

The resistance gene is present in all white spruces, but is expressed to varying degrees. "Theoretically, we could create white spruce stands that are less vulnerable to the budworm by reforesting areas with plantings from trees with a high expression of the resistance gene," says postdoctoral fellow and study coauthor Genevive Parent. Universit Laval and University of British Columbia researchers have partnered with Quebec's Ministre des Forts, de la Faune et des Parcs and the British Columbia Ministry of Forests, Lands and Natural Resource Operations to evaluate applications of their discoveries.

The spruce budworm is a moth whose caterpillar feeds primarily on balsam fir and white spruce needles. It is the most devastating insect to coniferous stands in Eastern North America. The last major outbreak that took place between 1970 and 1990 caused an estimated loss of half a billion cubic meters of wood in the province of Quebec alone, roughly the equivalent of 15 years of harvesting. Since 2003, the total affected forest area has been increasing steadily. Related caterpillars are affecting other types of conifer trees across Canada.

Story Source:

The above story is based on materials provided by Universit Laval. Note: Materials may be edited for content and length.

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Natural resistance gene against spruce budworm found

PUBLIC RELEASE DATE:

21-Nov-2014

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

Quebec City, November 21, 2014--Scientists from Universit Laval, the University of British Columbia and the University of Oxford have discovered a natural resistance gene against spruce budworm in the white spruce. The breakthrough, reported in The Plant Journal, paves the way to identifying and selecting naturally resistant trees to replant forests devastated by the destructive pest.

A research team composed of professors ric Bauce, Joerg Bohlmann and John Mackay as well as their students and postdocs discovered the gene in spruces that had remained relatively undamaged by a local budworm outbreak. The scientists compared the genomes of the more resilient trees and those that suffered substantial damage. "We measured expression levels of nearly 24,000 genes in the two groups of trees, explains Professor Mackay. We discovered a gene, betaglucosidase-1, whose expression in the needles of resistant spruce trees is up to 1,000 times higher than in non-resistant trees."

Postdoctoral scientist Melissa Mageroy then produced the protein encoded by the gene. Tests showed that the protein plays an essential part in chemical reactions resulting in the production of two compounds that are toxic to the budworm, piceol and pungenol, identified in 2011 by a research team supervised by Dr. ric Bauce. "We could say the gene we discovered produces natural insecticides in the tree foliage," sums up Dr. Mackay.

The resistance gene is present in all white spruces, but is expressed to varying degrees. "Theoretically, we could create white spruce stands that are less vulnerable to the budworm by reforesting areas with plantings from trees with a high expression of the resistance gene," says postdoctoral fellow and study coauthor Genevive Parent. Universit Laval and University of British Columbia researchers have partnered with Quebec's Ministre des Forts, de la Faune et des Parcs and the British Columbia Ministry of Forests, Lands and Natural Resource Operations to evaluate applications of their discoveries.

The spruce budworm is a moth whose caterpillar feeds primarily on balsam fir and white spruce needles. It is the most devastating insect to coniferous stands in Eastern North America. The last major outbreak that took place between 1970 and 1990 caused an estimated loss of half a billion cubic meters of wood in the province of Quebec alone, roughly the equivalent of 15 years of harvesting. Since 2003, the total affected forest area has been increasing steadily. Related caterpillars are affecting other types of conifer trees across Canada.

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The study's coauthors are: Genevive Parent, Gaby Germanos, Isabelle Gigure, Nathalie Delvas, Halim Maaroufi, and ric Bauce (Universit Laval); John Mackay (Universit Laval and University of Oxford); Melissa Mageroy and Joerg Bohlmann (University of British Columbia). The research was supported by Genome Canada, Genome Qubec, Genome British Columbia, the iFor Research Consortium and the Natural Sciences and Engineering Research Council of Canada.

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Researchers discover natural resistance gene against spruce budworm

Scientists in China say they've identified a gene that may play a role in some people being uncomfortable in relationships.

Perhaps your incompatibility is simply genetic. What a relief. Wahbanana/YouTube screenshot by Chris Matyszczyk/CNET

You often get the call late at night.

There's a sniffling at the other end. Then the words: "We just broke up."

You try and be sympathetic, even though this is the fifth time this year that your friend has broken up with the love of his life. Yes, there have been five loves of his life this year. And now, it may well be that it isn't entirely his fault.

Researcher from Peking University in China believe they have identified a gene variant that might be partly responsible for people not being very good at relationships.

Published this week in Scientific Reports, the research examined "a polymorphism (C-1019G)...of 5-HT1A gene," and found it was "significantly associated with the odds of being single both before and after controlling for socioeconomic status, external appearance, religious beliefs, parenting style, and depressive symptoms."

You can't blame God. You can't blame looks. You can't even blame your parents. Well, actually you can. They gave you the gene.

Still, the ultimate conclusion is quite dramatic. The researchers wrote: "These findings provide, for the first time, direct evidence for the genetic contribution to romantic relationship formation."

Surely we always feel that there are strange genetic things going on in terms of both attraction and relationship maintenance. There are people who, according to objective criteria, aren't attractive at all. Yet, to us, there's something viscerally alluring about them. There are also people with whom, for no obvious reason, we simply get on.

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Is there a gene that keeps you single?

UNIV 100 Genetic Engineering

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6.5.1 Genetic Engineering

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BIOLOGY: Genetic Engineering - Robin Hesketh
Good News for cancer therapy. Trials show genetic engineering of T-cells in the treatment of B-Cell Acute Lymphocitic Leukemia works.

By: Hay Levels

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Future Gene Therapy for Cancer
Future Gene Therapy for Cancer. Video streamed by http://www.AllthingsScience.com.

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Scientists at The Scripps Research Institute (TSRI) have discovered how one gene is essential to hearing, uncovering a cause of deafness and suggesting new avenues for therapies.

The new study, published November 20 in the journal Neuron, shows how mutations in a gene called Tmie can cause deafness from birth. Underlining the critical nature of their findings, researchers were able to reintroduce the gene in mice and restore the process underpinning hearing.

"This raises hopes that we could, in principle, use gene-therapy approaches to restore function in hair cells and thus develop new treatment options for hearing loss," said Professor Ulrich Mller, senior author of the new study, chair of the Department of Molecular and Cellular Neuroscience and director of the Dorris Neuroscience Center at TSRI.

The Gene Responsible

The ear is a complex machine that converts mechanical sound waves into electric signals for the brain to process. When a sound wave enters the ear, the uneven ends (stereocilia) of the inner ear's hair cells are pushed back, like blades of grass bent by a heavy wind. The movement causes tension in the strings of proteins (tip links) connecting the stereocilia, which sends a signal to the brain through ion channels that run through the tips of the hair cell bundles.

This process of converting mechanical force into electrical activity, called mechanotransduction, still poses many mysteries. In this case, researchers were in the dark about how signals were passed along the tip links to the ion channels, which shape electrical signals.

To track down this unknown component, researchers in the new study built a library of thousands of genes with the potential to affect mechanotransduction.

The team spent six months screening the genes to see if the proteins the genes produced interacted with tip link proteins. Eventually, the team found a gene, Tmie, whose protein, TMIE, interacts with tip link proteins and connects the tip links to a piece of machinery near the ion channel.

A Path to New Treatments

This discovery answers a long-standing question in neuroscience. Scientists have long known that mutations in the Tmie gene could cause deafness -- but they weren't sure how.

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How mutant gene can cause deafness

SOUTH BEND, Ind.--- Little Hunter Miller's motor is always running.

Like most toddlers he's sometimes one step away from trouble, but for Hunter being rough and tumble can have serious side effects. Hunter has severe hemophilia.

Twenty-thousand Americans live with hemophilia; it's a condition preventing the blood from clotting easily after a cut or injury.

Patients are also more susceptible to internal bleeding, which can damage joints, organs and tissue.

Three days after Hunter was born a routine circumcision caused a major scare.

"You know a baby gets up in the morning and their diapers are just full, said Tina Miller, Hunters grandmother. Well his was full, but it was full of blood."

Doctors diagnosed Hunter with hemophilia a, which means his blood is missing a protein known as clotting factor eight.

When he gets hurt doctors need to inject the clotting factor to stop the bleeding.

He's had eight emergency room visits in 19 months.

"Him falling, bumping his head too hard; just little cuts, said Heather Frederick, Hunters mother. He cut the roof of his mouth with a tortilla chip and that was a hospital trip."

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Doctors working on gene therapy to help patients with hemophilia

PUBLIC RELEASE DATE:

20-Nov-2014

Contact: Scott LaFee slafee@ucsd.edu 619-543-5232 University of California - San Diego @UCSanDiego

While investigating a rare genetic disorder, researchers at the University of California, San Diego School of Medicine have discovered that a ubiquitous signaling molecule is crucial to cellular reprogramming, a finding with significant implications for stem cell-based regenerative medicine, wound repair therapies and potential cancer treatments.

The findings are published in the Nov. 20 online issue of Cell Reports.

Karl Willert, PhD, assistant professor in the Department of Cellular and Molecular Medicine, and colleagues were attempting to use induced pluripotent stem cells (iPSC) to create a "disease-in-a-dish" model for focal dermal hypoplasia (FDH), a rare inherited disorder caused by mutations in a gene called PORCN. Study co-authors V. Reid Sutton and Ignatia Van den Veyver at Baylor College of Medicine had published the observation that PORCN mutations underlie FDH in humans in 2007.

FDH is characterized by skin abnormalities such as streaks of very thin skin or different shades, clusters of visible veins and wartlike growths. Many individuals with FDH also suffer from hand and foot abnormalities and distinct facial features. The condition is also known as Goltz syndrome after Robert Goltz, who first described it in the 1960s. Goltz spent the last portion of his career as a professor at UC San Diego School of Medicine. He retired in 2004 and passed away earlier this year.

To their surprise, Willert and colleagues discovered that attempts to reprogram FDH fibroblasts or skin cells with the requisite PORCN mutation into iPSCs failed using standard methods, but succeeded when they added WNT proteins - a family of highly conserved signaling molecules that regulate cell-to-cell interactions during embryogenesis.

"WNT signaling is ubiquitous," said Willert. "Every cell expresses one or more WNT genes and every cell is able to receive WNT signals. Individual cells in a dish can grow and divide without WNT, but in an organism, WNT is critical for cell-cell communication so that cells distinguish themselves from neighbors and thus generate distinct tissues, organs and body parts."

WNT signaling is also critical in limb regeneration (in some organisms) and tissue repair.

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Signaling molecule crucial to stem cell reprogramming

PUBLIC RELEASE DATE:

20-Nov-2014

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

Mouse cells and tissues created through nuclear transfer can be rejected by the body because of a previously unknown immune response to the cell's mitochondria, according to a study in mice by researchers at the Stanford University School of Medicine and colleagues in Germany, England and at MIT.

The findings reveal a likely, but surmountable, hurdle if such therapies are ever used in humans, the researchers said.

Stem cell therapies hold vast potential for repairing organs and treating disease. The greatest hope rests on the potential of pluripotent stem cells, which can become nearly any kind of cell in the body. One method of creating pluripotent stem cells is called somatic cell nuclear transfer, and involves taking the nucleus of an adult cell and injecting it into an egg cell from which the nucleus has been removed.

The promise of the SCNT method is that the nucleus of a patient's skin cell, for example, could be used to create pluripotent cells that might be able to repair a part of that patient's body. "One attraction of SCNT has always been that the genetic identity of the new pluripotent cell would be the same as the patient's, since the transplanted nucleus carries the patient's DNA," said cardiothoracic surgeon Sonja Schrepfer, MD, PhD, a co-senior author of the study, which will be published online Nov. 20 in Cell Stem Cell.

"The hope has been that this would eliminate the problem of the patient's immune system attacking the pluripotent cells as foreign tissue, which is a problem with most organs and tissues when they are transplanted from one patient to another," added Schrepfer, who is a visiting scholar at Stanford's Cardiovascular Institute. She is also a Heisenberg Professor of the German Research Foundation at the University Heart Center in Hamburg, and at the German Center for Cardiovascular Research.

Possibility of rejection

A dozen years ago, when Irving Weissman, MD, professor of pathology and of developmental biology at Stanford, headed a National Academy of Sciences panel on stem cells, he raised the possibility that the immune system of a patient who received SCNT-derived cells might still react against the cells' mitochondria, which act as the energy factories for the cell and have their own DNA. This reaction could occur because cells created through SCNT contain mitochondria from the egg donor and not from the patient, and therefore could still look like foreign tissue to the recipient's immune system, said Weissman, the other co-senior author of the paper. Weissman is the Virginia and D.K. Ludwig Professor for Clinical Investigation in Cancer Research and the director of the Stanford Institute for Stem Cell Biology and Regenerative Medicine.

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Pluripotent cells created by nuclear transfer can prompt immune reaction, researchers find

DNA Sequencing s Promise for Personalized Medicine ca

By: Wenjia Fan

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SINAInnovations 2014: Keynote Address - Genomics and Personalized Medicine
Jun Wang, Director, Dept of Bioinformatics, BGI Shenzhen, speaks on the history of genome sequencing and what BGI is doing to drive the pricing of sequencing technology to meet the need of...

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SCI BC TV - Exoskeleton
"It #39;s like riding a bike." After 23 years of not walking, our host takes the Ekso Bionics Exoskeleton out for a test drive at Vancouver #39;s Blusson Spinal Cord...

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LAGUNA BEACH, Calif. (KABC) --

"I could not bend my arms, could not bend my legs, couldn't even open my mouth and it was just getting worse and worse," said Joselyn.

Her son, Rex Miller, knew his mother might die.

"The doctor said there was a 30 percent chance that she wasn't going to make it. I was just so distraught," he said.

Finally, a neurologist diagnosed her with Shulman's syndrome, an extremely rare disease with no cure. It can lead to leukemia so she began chemotherapy and taking hundreds of pills.

But nothing worked.

"My bone marrow stopped producing white blood cells, red blood cells, and platelets," Joselyn recalled.

She endured more than 100 blood transfusions just to survive.

Doctors told her only a bone marrow transplant would save her. Her brother, a perfect match, agreed to be her donor.

After the procedure, she grew stronger and committed herself to finding donors for others.

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Woman saved by bone marrow transplant sets out to pay it forward

CLEVELAND -

Our bodies contain 23 pairs of them, 46 total, but if chromosomes are damaged, they can cause birth defects, disabilities, growth problems, even death.

Case Western Reserve University scientist Anthony Wynshaw-Boris is studying how to repair damaged chromosomes with the help of a recent discovery. He's taking skin cells and reprogramming them to work like embryonic stem cells, which can grow into different cell types.

"You're taking adult or a child's skin cells. You're not causing any loss of an embryo, and you're taking those skin cells to make a stem cell," said Wynshaw-Boris.

Scientists studied patients with a specific defective chromosome that was shaped like a ring. They took the patients' skin cells and reprogrammed them into embryonic-like cells in the lab. They found this process caused the damaged "ring" chromosomes to be replaced by normal chromosomes.

"It at least raises the possibility that ring chromosomes will be lost in stem cells," said Wynshaw-Boris.

While this research was only conducted in lab cultures on the rare ring-shaped chromosomes, scientists hope it will work in patients with common abnormalities like Down syndrome.

"What we're hoping happens is we might be able to use, modify, what we did, to rescue cell lines from any patient that has any severe chromosome defect," Wynshaw-Boris explained.

It's research that could one day repair faulty chromosomes and stop genetic diseases in their tracks.

The reprogramming technique that transforms skin cells to stem cells was so groundbreaking that a Japanese physician won the Nobel Prize in medicine in 2012 for developing it.

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Health Beat: Stem cells to repair broken chromosomes

Durham, NC (PRWEB) November 20, 2014

With more soldiers returning from combat suffering devastating injuries, doctors are turning to a reconstructive surgery that uses tissue transplantation along with immuno-suppression therapy. This approach has had encouraging results; however, rejection of transplanted tissue from an unmatched donor remains a critical complication. A new study found in the latest issue of STEM CELLS Translational Medicine reports that researchers may have found a way around that.

We demonstrated in mice that a single infusion of adipose-derived stromal cells (ASC) which are stem cells taken from fat in a minimally invasive procedure from an unmatched donor combined with an extremely low dose of bone marrow cells resulted in stable long-term tolerance of the skin graft without undo consequences such as graft versus host disease, said Thomas Davis, Ph.D., a contractor from the Henry M. Jackson Foundation who is working at the Naval Medical Research Centers Regenerative Medicine Department. Dr. Davis is lead author of the study.

He added, As we move forward, we are cautiously optimistic, appreciating that the transition from these laboratory models to proof-of-principle preclinical studies is challenging and not straightforward. If successful, the technology has diverse therapeutic applications in clinical transplantation in both military and civilian settings.

The research team wanted to try using ASCs because these cells have proven to be more potent than bone marrow and cord-blood derived stem cells when it comes to inhibiting the bodys rejection of transplantations from an unmatched donor. They conducted the study by doing skin grafts in mice. One group of grafted mice received no stem cell transfusions; one group received human-derived ASCs after the graft occurred; and another group received a combination of human ASCs and stem cells harvested from the mouses own bone marrow, also after placement of the graft.

More than 200 days later, the combination of human ASC and limited numbers of blood marrow stem cells effectively prevented rejection, with no evidence of graft versus host disease, Dr. Davis reported.

Navy Capt. Eric A. Elster, M.D., professor and chair of the surgery department at Uniformed Services University of the Health Sciences, helped lead the study. ASC constitutively produced high levels of anti-inflammatory/immunoregulatory factors, he said. While further work is needed to validate this approach in other laboratory models before clinical trials can begin, the ability to use ASC, which are non-donor specific and clinically feasible, to induce tolerance opens a new horizon in transplantation.

The implications of this research are broad, said Anthony Atala, MD, editor of STEM CELLS Translational Medicine and director of the Wake Forest Institute for Regenerative Medicine. If these findings are duplicated in additional models and in human trials, there is potential to apply this strategy to many areas of transplantation.

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This article, Adipose-derived Stromal Cells Promote Allograft Tolerance Induction, and more can be accessed at http://www.stemcellsTM.com.

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Fat and Bone Marrow-Derived Stem Cells Combo Shows Promise in Preventing Transplant Rejection

PUBLIC RELEASE DATE:

20-Nov-2014

Contact: Jessica Mikulski jmikulski@nyee.edu 212-979-4274 The Mount Sinai Hospital / Mount Sinai School of Medicine @mountsinainyc

The National Eye Institute (NEI), a division of the National Institutes of Health, has awarded researchers at the Icahn School of Medicine at Mount Sinai a five-year grant totaling $1 million that will support an effort to re-create a patients' ocular stem cells and restore vision in those blinded by corneal disease.

About six million people worldwide have been blinded by burns, trauma, infection, genetic diseases, and chronic inflammation that result in corneal stem cell death and corneal scarring.

There are currently no treatments for related vision loss that are effective over the long term. Corneal stem cell transplantation is an option in the short term, but availability of donor corneas is limited, and patients must take medications that suppress their immune systems for the rest of their lives to prevent rejection of the transplanted tissue.

A newer proposed treatment option is the replacement of corneal stem cells to restore vision. The grant from the NEI will fund Mount Sinai research to re-create a patient's own stem cells and restore vision in those blinded by corneal disease. Technological advances in recent years have enabled researchers to take mature cells, in this case eyelid or oral skin cells, and coax them backward along the development pathways to become stem cells again. These eye-specific stem cells would then be redirected down pathways that become needed replacements for damaged cells in the cornea, in theory restoring vision.

"Our findings will allow the creation of transplantable eye tissue that can restore the ocular surface," said Albert Y. Wu, MD, PhD, Assistant Professor, Department of Ophthalmology at the Icahn School of Medicine at Mount Sinai and principle investigator for the grant-funded effort. "In the future, we will be able to re-create a patient's own corneal stem cells to restore vision after being blind," added Dr. Wu, also Director of the Ophthalmic Plastic and Reconstructive Surgery, Stem Cell and Regenerative Medicine Laboratory in the Department of Ophthalmology and a member of the Black Family Stem Cell Institute at Icahn School of Medicine. "Since the stem cells are their own, patient's will not require immunosuppressive drugs, which would greatly improve their quality of life."

Specifically, the grant will support efforts to discover new stem cell therapies for ocular surface disease and make regenerative medicine a reality for people who have lost their vision. The research team will investigate the most viable stem cell sources, seek to create ocular stem cells from eyelid or oral skin cells, explore the molecular pathways involved in ocular and orbital development, and develop cutting-edge biomaterials to engraft a patient's own stem cells and restore vision.

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Mount Sinai researchers awarded grant to find new stem cell therapies for vision recovery

By Estel Grace Masangkay

A team of researchers at the Washington University School of Medicine in St. Louis reported that they have discovered a way to directly convert human skin cells into a type of brain cell that has been damaged by Huntingtons disease.

The team chose to produce a certain type of brain cell known as medium spiny neurons, which play a key part in controlling movement. Medium spiny neurons are the cells most affected by Huntingtons disease, a neurodegenerative disorder characterized by involuntary muscle movements and cognitive decline. The disease symptoms typically begin showing in mid-adulthood, and they steadily worsen over time.

For their experiment, the scientists used adult human skin cells instead of the typical mouse cells or embryonic human cells. The team placed the skin cells in an environment similar to the environment of brain cells and then exposed them to two small molecules of RNA named miR-9 and miR-124. In their past research, the scientists have discovered that these microRNAs turn skin cells into a mix of various neuron types. Dr. Yoo and his colleagues fine-tuned the chemical signals by further exposing the cells to transcription factors they knew are found in the part of the brain where medium spiny neurons thrive. Results show that the converted cells survived for at least six months after they were injected into mices brains. The cells also behaved in a similar fashion to native brain cells.

Not only did these transplanted cells survive in the mouse brain, they showed functional properties similar to those of native cells. These cells are known to extend projections into certain brain regions. And we found the human transplanted cells also connected to these distant targets in the mouse brain. That's a landmark point about this paper, said Dr. Andrew S. Yoo, assistant professor of developmental biology in Washington University School of Medicine and senior author of the study.

The new process differs from other techniques in that it does not need to undergo a stem cell phase, thereby avoiding production of multiple cell types. The scientists added that using adult human cells offers the opportunity to use the patients own cells in future procedures, which would radically minimize the risk of rejection by the patients immune system. Dr. Yoos team is now preparing to test skin cells taken from patients with Huntingtons disease using the approach. They also intend to inject healthy reprogrammed human cells into mice models of Huntingtons disease to check whether these have any effect on the diseases symptoms.

The researchers work was published in the previous months issue of the journal Neuron.

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Researchers Convert Skin Cells To Replace HD-Damaged Brain Cells