Archive for February, 2015
Observing stem cells maturing into blood cells in living mouse
In the bone marrow, blood stem cells give rise to a large variety of mature blood cells via progenitor cells at various stages of maturation. Scientists from the German Cancer Research Center (DKFZ) have developed a way to equip mouse blood stem cells with a fluorescent marker that can be switched on from the outside. Using this tool, they were able to observe, for the first time, how stem cells mature into blood cells under normal conditions in a living organism. With these data, they developed a mathematical model of the dynamics of hematopoiesis. The researchers have now reported in the journal Nature that the normal process of blood formation differs from what scientists had previously assumed when using data from stem cell transplantations.
Since ancient times, humankind has been aware of how important blood is to life. Naturalists speculated for thousands of years on the source of the body's blood supply. For several centuries, the liver was believed to be the site where blood forms. In 1868, however, the German pathologist Ernst Neumann discovered immature precursor cells in bone marrow, which turned out to be the actual site of blood cell formation, also known as hematopoiesis. Blood formation was the first process for which scientists formulated and proved the theory that stem cells are the common origin that gives rise to various types of mature cells.
"However, a problem with almost all research on hematopoiesis in past decades is that it has been restricted to experiments in culture or using transplantation into mice," says Professor Hans-Reimer Rodewald from the German Cancer Research Center (Deutsches Krebsforschungszentrum, DKFZ). "We have now developed the first model where we can observe the development of a stem cell into a mature blood cell in a living organism."
Dr. Katrin Busch from Rodewald's team developed genetically modified mice by introducing a protein into their blood stem cells that sends out a yellow fluorescent signal. This fluorescent marker can be turned on at any time by administering a specific reagent to the animal. Correspondingly, all daughter cells that arise from a cell containing the marker also send out a light signal.
When Busch turned on the marker in adult animals, it became visible that at least one third (approximately 5000 cells) of a mouse's hematopoietic stem cells produce differentiated progenitor cells. "This was the first surprise," says Busch. "Until now, scientists had believed that in the normal state, very few stem cells -- only about ten -- are actively involved in blood formation."
However, it takes a very long time for the fluorescent marker to spread evenly into peripheral blood cells, an amount of time that even exceeds the lifespan of a mouse. Systems biologist Prof. Thomas Hfer and colleagues (also of the DKFZ) performed mathematical analysis of these experimental data to provide additional insight into blood stem cell dynamics. Their analysis showed that, surprisingly, under normal conditions, the replenishment of blood cells is not accomplished by the stem cells themselves. Instead, they are actually supplied by first progenitor cells that develop during the following differentiation step. These cells are able to regenerate themselves for a long time -- though not quite as long as stem cells do. To make sure that the population of this cell type never runs out, blood stem cells must occasionally produce a couple of new first progenitors.
During embryonic development of mice, however, the situation is different: To build up the system, all mature blood and immune cells develop much more rapidly and almost completely from stem cells.
The investigators were also able to accelerate this process in adult animals by artificially depleting their white blood cells. Under these conditions, blood stem cells increase the formation of first progenitor cells, which then immediately start supplying new, mature blood cells. In this process, several hundred times more cells of the so-called myeloid lineage (thrombocytes, erythrocytes, granulocytes, monocytes) form than long-lived lymphocytes (T cells, B cells, natural killer cells) do.
"When we transplanted our labeled blood stem cells from the bone marrow into other mice, only a few stem cells were active in the recipients, and many stem cells were lost," Rodewald explains. "Our new data therefore show that the findings obtained up until now using transplanted stem cells can surely not be reflective of normal hematopoiesis. On the contrary, transplantation is an exception [to the rule]. This shows how important it is that we actually follow hematopoiesis under normal conditions in a living organism."
The scientists in Rodewald's department, working together with Thomas Hfer, now also plan to use the new model to investigate the impact of pathogenic challenges to blood formation: for example, in cancer, cachexia or infection. This method would also enable them to follow potential aging processes that occur in blood stem cells in detail as they occur naturally in a living organism.
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Observing stem cells maturing into blood cells in living mouse
Stem cells offer promising key to new malaria drugs: US research
NEW YORK (Thomson Reuters Foundation) - Human stem cells engineered to produce renewable sources of mature, liver-like cells can be grown and infected with malaria to test potentially life-saving new drugs, according to researchers at the Massachusetts Institute of Technology.
The advance comes at a time when the parasitic mosquito-borne disease, which kills nearly 600,000 people every year, is showing increased resistance to current treatment, especially in Southeast Asia, according to the World Health Organization.
The liver-like cells, or hepatocytes, in the MIT study were manufactured from stem cells derived from donated skin and blood samples.
The resulting cells provide a potentially replenishable platform for testing drugs that target the early stage of malaria, when parasites may linger and multiply in the liver for weeks before spreading into the bloodstream.
Sangeeta Bhatia, a biomedical engineer and senior author of the MIT report, told the Thomson Reuters Foundation that the breakthrough study not only showed that these liver-like cells could host a malaria infection but also described a way to mature the young cells so that an adult-like metabolism, necessary for drug development, could be established.
The study is published in the Feb. 5 online issue of Stem Cell Reports.
Stem cells retain the genetic makeup of their donors, affording researchers the potential to test drugs against a large variety of genetic types and a variety of diseases.
"This allows us to explore in depth how different diseases affect different people, in this case malaria," Bob Palay, chairman and CEO of Cellular Dynamics International (CDI), told the Thomson Reuters Foundation.
"This allows you to study it in a dish and find new drugs," he added, noting that CDI uses blood samples for its stem cells.
Before this development, researchers tested new drugs using human liver cells from cadavers and cancerous liver cells.
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Stem cells offer promising key to new malaria drugs: US research
Theres a lot to love at The Body Shop
DROPS of Youth Bouncy Sleeping Mask is designed to be left on overnight without washing off. The lightweight, pliable mask molds itself like a second skin, making skin look younger and fresher.
The Body Shop introduces its Drops of Youth, Red Musk Fragrance, and Limited-Edition Forbidden Flower collections.
Drops of Youth, made from edelweiss flower stem cells sourced from the Alps, replenishes your skin in the most natural way. Left on overnight, the lightweight mask is like a second skin. In the morning, skin feels smooth and hydrated, and looks younger and fresher.
Red Musk, The Body Shops most unconventional scent to date, turns up the heat.
The Limited-Edition Forbidden Flower Collection is a body care and fragrance line inspired by the poppy flower.
DROPS of YouthWonderblur is a skin smoother that reduce fine lines and pores for an even, flawless finish.
Known for its thrust in protecting the planet, The Body Shop never tests its products on animals. The line has a Community Fair Trade program, where high-quality natural ingredients are sourced in different parts of the world where small stakeholders and artisans can benefit.
The Drops of Youth and Red Musk collections are available at The Body Shop stores nationwide, while Forbidden Flower Collection is available at selected The Body Shop branches. SM Advantage Card members can now earn and redeem points in all The Body Shop stores.
THE RED Musk Fragrance Collection. I wanted to create a fragrance that wasnt the typical girly girl scent. I wanted to change the rules of fragrance. Instead, I used the sensuality and the warmth of spices blended withmusk to approach femininity differently, says Corinne Cachen, master perfumer.
FORBIDDEN Flower Body Butter gives your skin the pleasure of pure potent moisture.
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Theres a lot to love at The Body Shop
FAQ Part 1: MEsenchymal Stem cell therapy for CAnadian MS patients (MESCAMS) – Video
FAQ Part 1: MEsenchymal Stem cell therapy for CAnadian MS patients (MESCAMS)
The Multiple Sclerosis Society of Canada and the Multiple Sclerosis Scientific Research Foundation have announced a $4.2 million grant in support of the MEse...
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FAQ Part 1: MEsenchymal Stem cell therapy for CAnadian MS patients (MESCAMS) - Video
Creation Of Rejuvenated Cell By Stem Cell Therapy – The Line Clinic – Video
Creation Of Rejuvenated Cell By Stem Cell Therapy - The Line Clinic
Stem cell therapy has become reality which was just possibilities and thoughts of science few days before. This amazing innovation makes life more secured an...
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Creation Of Rejuvenated Cell By Stem Cell Therapy - The Line Clinic - Video
Comment: T cell therapy for children with aggressive leukaemia – Video
Comment: T cell therapy for children with aggressive leukaemia
Visit http://www.ecancer.org for more. Dr Bollard (George Washington University, Washington, USA) discusses key abstracts showcased at ASH 2014 with ecancert...
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Comment: T cell therapy for children with aggressive leukaemia - Video
terapia celular para cinomose – distemper stem cell therapy – Video
terapia celular para cinomose - distemper stem cell therapy
Caso de cinomose tratado com terapia celular - unesp - botucatu Stem cell therapy for distemper in a dog.
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terapia celular para cinomose - distemper stem cell therapy - Video
MPN Research Foundation initiates exploratory gene editing project
Chicago, IL (PRWEB) February 12, 2015
One of the primary goals of the MPN Research Foundation is to catalyze new avenues of research into the cause(s) and potential treatments for the blood cancer group polycythemia vera, essential thrombocythemia and myelofibrosis. As an increasing number of new approaches to cancer research are emerging, the Foundation has a new project which hopefully will ensure any applicable technology is tested in MPNs.
One such approach to cancer treatment is CRISPR-cas9, an acronym for Clustered Regularly Interspaced Short Palindromic Repeats. CRISPR-cas9 allows for the targeting of specific mutations. This approach is currently being tested in cystic fibrosis, sickle cell anemia, and some cancers. It is believed to be particularly effective for diseases associated with single point genetic mutations, which suggests that it may be applicable to MPNs, for which there are several known genetic mutations suck as JAK2V617F and CALR.
Currently MPNs are under-represented among the conditions being studied by CRISPR researchers. In addition, not enough is known about the potential impact of this treatment on the people living with MPNs. To ensure that MPNs are sufficiently explored by the CRISPR research world the MPN Research Foundation will be taking action on two fronts:
As a cautionary note, this technology, although exciting and currently the subject of much scientific and commercial activity, is in its preliminary stages. The long-term costs and benefits are not yet clear. But given its potential to fundamentally alter the course of MPNs and other diseases, the Foundation believes that further study is critical. The RFP is scheduled to go out in the end of February. Check http://www.mpnresearchfoundation.org for further details.
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MPN Research Foundation initiates exploratory gene editing project
Mutated gene causes 70% cancer risk
Health officials hit back at e-cig claims
Health professionals say more research is needed to prove using e-cigarettes is a good way to quit smoking.
According to new health figures, Australian women are far less likely to survive a heart attack than men.
Research says high factor sunscreen can't be relied on to protect against the deadliest skin cancer form.
A British study using skin electrodes has found men experience greater levels of emotion than women.
High protein diets may protect against stroke, especially if they contain a lot of fish, scientists say.
Driving too much is bad for your health, according to a study of 40-thousand middle-aged Australians.
Researchers say the financial crisis may have led to thousands of suicides in Europe and North America.
Biologists have devised a new weapon against malaria by genetically engineering mosquitoes.
Stomach-shrinking bariatric surgery beats other forms of treatment in bringing about remission of diabetes.
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Mutated gene causes 70% cancer risk
Studies Find More Genetic Links to Obesity
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WEDNESDAY, Feb. 11, 2015 (HealthDay News) -- New research offers more evidence that genes play a significant role in obesity.
The findings may help explain why some people are more likely to put on extra pounds and develop obesity-linked conditions, the investigators said.
The researchers analyzed genetic samples from more than 300,000 people and identified more than 140 locations across their sets of DNA that play a role in obesity. They also pinpointed new biological pathways that play important roles in body weight and fat distribution.
The findings appear in two companion papers published Feb. 11 in the journal Nature.
This is the first step toward identifying individual genes involved in body shape and size, the researchers said. The proteins produced by the genes could offer targets for the development of new drugs to fight obesity.
One of the papers focused on genes that affect where fat is stored in the body, which affects health risk. For example, people with more belly fat are more likely to have metabolic conditions such as type 2 diabetes and cardiovascular disease than those with more fat in the hips or distributed throughout the body.
"We need to know these genetic locations because different fat deposits pose different health risks," senior author Karen Mohlke, a professor of genetics at the University of North Carolina School of Medicine, said in a University of Michigan Health System news release.
"If we can figure out which genes influence where fat is deposited, it could help us understand the biology that leads to various health conditions, such as insulin resistance/diabetes, metabolic syndrome and heart disease," she explained.
The other paper looked at the link between genes and body mass index (BMI), an estimate of body fat based on height and weight. The researchers said they found 97 genetic associations linked to BMI. They also found that genetic locations associated with BMI are linked to areas that control factors such as appetite and energy use.
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Studies Find More Genetic Links to Obesity
More genetic links to obesity discovered
New research offers more evidence that genes play a significant role in obesity.
The findings may help explain why some people are more likely to put on extra pounds and develop obesity-linked conditions, the investigators said.
The researchers analyzed genetic samples from more than 300,000 people and identified more than 140 locations across their sets of DNA that play a role in obesity. They also pinpointed new biological pathways that play important roles in body weight and fat distribution.
The findings appear in two companion papers published Feb. 11 in the journal Nature.
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This is the first step toward identifying individual genes involved in body shape and size, the researchers said. The proteins produced by the genes could offer targets for the development of new drugs to fight obesity.
One of the papers focused on genes that affect where fat is stored in the body, which affects health risk. For example, people with more belly fat are more likely to have metabolic conditions such as type 2 diabetes and cardiovascular disease than those with more fat in the hips or distributed throughout the body.
"We need to know these genetic locations because different fat deposits pose different health risks," senior author Karen Mohlke, a professor of genetics at the University of North Carolina School of Medicine, said in a University of Michigan Health System news release.
"If we can figure out which genes influence where fat is deposited, it could help us understand the biology that leads to various health conditions, such as insulin resistance/diabetes, metabolic syndrome and heart disease," she explained.
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More genetic links to obesity discovered
New option for Jewish genetic testing
Image via shutterstock.com
When a Jewish couple is planning their wedding or anticipating starting a family, they probably arent thinking much about rare genetic conditions. But JScreen, an educational and screening program, urges couples to add genetic testing to their to-do list. And by offering home-based testing, JScreen hopes to eliminate any obstacles to this process.
Based at Emory Universitys Department of Human Genetics, JScreen (jscreen.org) provides a Web-based portal for individuals to request a genetic-screening kit. Participants provide a saliva sample most genetic tests involve a blood draw and mail it back for analysis. Before receiving the kit, participants must view an educational video and enter health information that is reviewed by an Emory genetic counselor.
We all carry [recessive genes for] various genetic diseases. We just dont know what they are, said Karen Grinzaid, a genetic counselor and instructor at Emory University School of Medicine and the senior director of outreach initiatives for JScreen.
The problem occurs when both parents are carriers of the same disease. In that case, each of their offspring has a 25 percent chance of manifesting the condition.
According to Emorys Department of Human Genetics, about one in five Ashkenazi Jews in the U.S. carries a genetic disease. However, most dont have a family history of the disease and are unaware of their status of carriers. In fact, 80 percent of babies with genetic diseases are born to parents with no known family history of that disease.
The only way to know if you are a carrier for a Jewish genetic disease is to have an affected child or be screened, Grinzaid said. For the vast majority of couples, genetic screening gives couples reassurance that theyre not at risk.
Saliva samples returned to Emorys lab are tested for 40 diseases prevalent in the Jewish community. Nineteen of them are more common in Ashkenazi populations, and 21 of them are common in Jews of Sephardic or Mizrahi (Middle Eastern) origins. Testing for an additional 47 diseases found in the general population is available at no extra cost. Many of the diseases included in the tests are fatal, and all impact the individuals quality of life.
Results take less than four weeks. If they are negative, individuals are notified via email. Those who are identified as carriers speak via phone or videoconference to an Emory University genetic counselor about their results and options. They might also be referred to a local genetic counselor for more extensive counseling. Grinzaid said that about 2 percent of couples will be found to be carriers of the same disease.
If both members of a couple carry the same genetic disease, they have several options. One is to undergo in-vitro fertilization using pre-implantation genetic diagnosis. This technology allows embryos to be tested for the affected gene before being implanted. Other options include using a donor egg or sperm, or pursuing adoption.
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New option for Jewish genetic testing
Lecture 2 Developmental Genetics – Video
Lecture 2 Developmental Genetics
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Lecture 2 Developmental Genetics - Video
The Origin of Nations Pt 2 – ‘GENETICS’ Nat Stock – Video
The Origin of Nations Pt 2 - #39;GENETICS #39; Nat Stock
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The Origin of Nations Pt 2 - 'GENETICS' Nat Stock - Video
Quick Medical Genetics – Pseudohypoparathyroidism, Albright hereditary osteodystrophy – Video
Quick Medical Genetics - Pseudohypoparathyroidism, Albright hereditary osteodystrophy
This is a lecture about the genetic diseases pseudohypoparathyroidism (PHP), pseudopseudohypoparathyroidism (PPHP), and Albright hereditary osteodystrophy (A...
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Quick Medical Genetics - Pseudohypoparathyroidism, Albright hereditary osteodystrophy - Video
Mendelian Genetics 2 – Video
Mendelian Genetics 2
Table of Contents: 00:16 - Independent assortment 01:08 - Incomplete dominance 01:09 - Independent assortment 01:27 - Incomplete dominance 03:05 - Codominanc...
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Choice Genetics Drives Pork Producer Productivity. – Video
Choice Genetics Drives Pork Producer Productivity.
Dr Derek Petry of Choice Genetics provides an overview of the focus of the company on how they help pork producers achieve better results. For more information visit Choice Genetics at http://www....
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LYSOGENE, UMM and AU Collaborate To Develop IND-supporting Preclinical Studies In GM1-gangliosidosis
Collaboration entails development of gene therapy treatment for severe neurodegenerative disease GM1-gangliosidosis
LYSOGENE, a leading, clinical stage gene therapy biotechnology company committed to the development and commercialization of breakthrough treatments for severe orphan pathologies affecting the central nervous system (CNS), recently announced that it has entered into a strategic collaboration with the University of Massachusetts Medical School (UMMS) in Worcester, Massachusetts, and Auburn University (AU) in Auburn, Alabama. Through the collaboration, LYSOGENE, UMMS and AU will develop IND-supporting preclinical studies in GM1-gangliosidosis, a rare, inherited disorder characterized by severe neurological impairment, using adeno-associated virus (AAV) gene therapy technology.
The collaboration will combine LYSOGENEs outstanding translational and clinical expertise in gene therapy for CNS disorders with the unique preclinical expertise and infrastructure of UMMS and AU to design and test innovative AAV-based gene therapy approaches to treat GM1-gangliosidosis.
The development of a potential treatment for GM1-gangliosidosis using AAV gene therapy was initiated in 2005 by Miguel Sena-Esteves, PhD, associate professor in the Neurology Department and the Gene Therapy Center at UMMS, and Douglas R. Martin, PhD, associate professor in the Scott-Ritchey Research Center and Department of Anatomy, Physiology & Pharmacology at AU. The approach developed by the investigators uses AAV vectors to treat the entire brain and spinal cord after injection of only a few intracranial sites. Preclinical studies demonstrated a remarkable extension in lifespan from 8 months in untreated GM1 cats to greater than 4.5 years in AAV-treated cats, with dramatic improvements in quality of life. Results were published in Science Translational Medicine in 2014 (McCurdy, V.J., et al., Sustained normalization of neurological disease after intracranial gene therapy in a feline model. Science Translational Medicine, 2014. 6(231): p. 231ra48).
We are thrilled by our collaboration with University of Massachusetts Medical School and Auburn University, which constitutes a significant step towards the development of a treatment for patients affected with GM1-gangliosidosis, a severely debilitating disease. For each of these patients and their families, there is currently no option and an urgent need for a safe and effective therapy, said Karen Aiach, founding president and CEO of LYSOGENE. AAV-based therapies are particularly suitable for inherited disorders of the CNS. In this new program, LYSOGENE will leverage its unique capacity to develop these therapies and bring them to patients with unmet needs. We will also reinforce our scientific and technology base through our collaboration with leaders in the field.
Collaborating with LYSOGENE will allow us to leverage their clinical and translational expertise and advance the development of a gene transfer therapy for treating patients affected with GM1-gangliosidosis, said Sena-Esteves. In our minds, what ultimately matters is the ability to deliver a potential treatment to the children suffering from this horrible disease. Ultimately, thats what drives us all.
About Gangliosidosis with GM1 GM1-gangliosidosis is a rare inherited neurodegenerative disorder characterized by severe cognitive and motor developmental delays resulting in death of most patients at a very young age.
It is caused by mutations in the GLB1 gene, which encodes an enzyme called beta-galactosidase necessary for recycling of a molecule (GM1-ganglioside) in neurons. This brain lipid is indispensable for normal function, but its overabundance causes neurodegeneration, resulting in the severe neurological symptoms of GM1-gangliosidosis.
GM1 affects 1 in 100,000 - 200,000 newborns and is inherited in an autosomal recessive pattern. GM1-gangliosidosis can be classified into three major clinical phenotypes according to the age of onset and severity of symptoms: Type I (infantile), Type II (late infantile/juvenile) and Type III (adult). There is currently no treatment for this disease.
About LYSOGENE LYSOGENE is a clinical stage biotechnology company committed to the development and commercialization of innovative therapies for patients affected with rare disorders and high unmet medical needs. LYSOGENEs team translated its rAAVrh10 lead product for Sanfilippo from bench to bedside in an unprecedented fashion over the last years. Its lead product is for Sanfilippo syndrome, a neurodegenerative lysosomal storage disorder considered to be a perfect model for gene therapy. LYSOGENE is currently expanding its pipeline to additional diseases with high unmet medical needs. Lysogene was launched in 2009. It completed a Series A financing in May 2014 with leading life sciences investors Sofinnova Partners, BPI Innobio and Novo AIS.
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LYSOGENE, UMM and AU Collaborate To Develop IND-supporting Preclinical Studies In GM1-gangliosidosis
Spinal Cord Injury Program at Children’s Specialized Hospital – Video
Spinal Cord Injury Program at Children #39;s Specialized Hospital
Details description of the Spinal Cord Injury program at Children #39;s Specialized Hospital.
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Morphine Undermines Recovery of Function Following a Spinal Cord Injury – Video
Morphine Undermines Recovery of Function Following a Spinal Cord Injury
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Morphine Undermines Recovery of Function Following a Spinal Cord Injury - Video
Stem Cell Transplants May Work Better than Existing Drug for Severe Multiple Sclerosis
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Newswise MINNEAPOLIS Stem cell transplants may be more effective than the drug mitoxantrone for people with severe cases of multiple sclerosis (MS), according to a new study published in the February 11, 2015, online issue of Neurology, the medical journal of the American Academy of Neurology.
The study involved 21 people whose disability due to MS had increased during the previous year even though they were taking conventional medications (also known as first-line treatments). The participants, who were an average age of 36, were at an average disability level where a cane or crutch was needed to walk.
In MS, the bodys immune system attacks its own central nervous system. In this phase II study, all of the participants received medications to suppress immune system activity. Then 12 of the participants received the MS drug mitoxantrone, which reduces immune system activity. For the other nine participants, stem cells were harvested from their bone marrow. After the immune system was suppressed, the stem cells were reintroduced through a vein. Over time, the cells migrate to the bone marrow and produce new cells that become immune cells. The participants were followed for up to four years.
This process appears to reset the immune system, said study author Giovanni Mancardi, MD, of the University of Genova in Italy. With these results, we can speculate that stem cell treatment may profoundly affect the course of the disease.
Intense immunosupression followed by stem cell treatment reduced disease activity significantly more than the mitoxantrone treatment. Those who received the stem cell transplants had 80 percent fewer new areas of brain damage called T2 lesions than those who received mitoxantrone, with an average of 2.5 new T2 lesions for those receiving stem cells compared to eight new T2 lesions for those receiving mitoxantrone.
For another type of lesion associated with MS, called gadolinium-enhancing lesions, none of the people who received the stem cell treatment had a new lesion during the study, while 56 percent of those taking mitoxantrone had at least one new lesion.
Mancardi noted that the serious side effects that occurred with the stem cell treatment were expected and resolved without permanent consequences.
More research is needed with larger numbers of patients who are randomized to receive either the stem cell transplant or an approved therapy, but its very exciting to see that this treatment may be so superior to a current treatment for people with severe MS that is not responding well to standard treatments, Mancardi said.
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Stem Cell Transplants May Work Better than Existing Drug for Severe Multiple Sclerosis
Stem cells reduce MS brain damage
Structure of a typical neuron, showing the protective myelin sheath that is attacked in multiple sclerosis
In what could herald a major advance in treating multiple sclerosis, brain damage was significantly reduced in patients getting stem cell transplants, compared to a control group. Results of the small Phase 2 trial -- the first of its kind -- are preliminary but promising, according to experts not involved with the trial.
The four-year study compared the results of intense immune suppression followed by transplants of the patient's own blood-forming, or hematopoietic stem cells to those of a control group given immune suppression alone. Dr. Giovanni L. Mancardi of the University of Genova in Italy led the 21-patient study, released Wednesday in the journal Neurology.
Patients in the treatment group had 80 percent fewer new damaged brain areas called T2 lesions, compared to those who got the immune-suppressing chemotherapy drug mitoxantrone but no stem cells. The Phase 3 trial will look for signs of effectiveness in reducing disability. The goal is to "reboot" the immune system, which is maladjusted in MS and attacks the nervous system, impairing movement and balance.
Patients were randomly assigned to either the treatment or control group, something that hasn't been done in previous trials of stem cell therapy for MS, according to an accompanying editorial in Neurology.
Randomizing patient assignment gives the results more value, said UC San Diego stem cell researcher Larry Goldstein and neurologist Dr. Jody Corey-Bloom.
"It's a very exciting advance," said Goldstein, who heads UCSD's stem cell program. "It's a small study, but it sure looks like it was well controlled and carefully done."
Goldstein and Corey-Bloom, and the study authors themselves, cautioned that because the trial was so small, results must be regarded as preliminary. No improvement in disability was found in the trial, although there were so few patients that even a strong benefit might not have been noticed.
The Phase 3 trial now underway, which will include more patients, has been designed to find that benefit, if it exists. It can be found at clinicaltrials.gov under the identifier NCT00273364.
In the Phase 2 trial, nine patients received immune suppression followed by stem cell transplants. Immune suppression alone was administered to a control group of 12 patients, for a total of 21 patients. The patients receiving stem cells were given their own, or autologous, hematopoietic stem cells, reducing the risk of rejection.
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Stem cells reduce MS brain damage
Stem Cells from Placenta Show Promise for Treating Heart Failure
Durham, NC (PRWEB) February 11, 2015
Stem cells collected from placenta, which is generally discarded after childbirth, show promise as a treatment for heart failure. Found in the latest issue of STEM CELLS Translational Medicine, a new study using mice determined that human-derived adherent cells (PDAC cells) significantly improved cardiac function when injected into the heart muscle.
Currently, about 6 million people in the United States alone suffer from heart failure, which is when the hearts pumping power is weaker than normal. Despite intensive medical care, almost 80 percent of people die within eight years of diagnosis, making it the worlds leading cause of death. Heart failure can be the result of coronary artery disease, heart attack and other conditions such as high blood pressure and valve disease.
Cell therapies for cardiac repair have generated considerable interest in recent years. While earlier studies using autologous bone marrow transplantation (that is, stem cells collected from the patients own bone marrow) helped improve cardiac function after myocardial infarction (MI), more recent studies showed no benefit in the early stages after MI. This has led researchers to question whether mesenchymal stem cells from sources other than bone marrow, such as cord blood and placenta tissue, might yield better results.
Among those interested in this is an international team co-led by Patrick C.H. Hsieh of Taiwans Institute of Biomedical Sciences, Academia Sinica, Taipei, and Uri Herzberg of Celgene Cellular Therapeutics, Warren, New Jersey, U.S. They recently undertook a study to test the therapeutic effects of PDA-001, an intravenous formulation of PDAC cells, in mice. The researchers were also testing the best way to deliver the therapy.
Three weeks after chronic heart failure was induced in the animals they were treated with the stem cells by either direct intramyocardial (IM) or intravenous (IV) injection, Dr. Hsieh said. The results showed that the IM injections significantly improved the left ventricle systolic and diastolic functions compared with injection of vehicle or IV injection of PDA-001.
The IM injections also decreased cardiac fibrosis in the vicinity of the injection sites. We repeatedly observed improvement of cardiac function in the injected sites following IM PDA-001 treatment, Dr. Herzberg added. Based on these results, we want to continue our investigations to optimize the effect through controlling the dose, timing and delivery.
In this animal model of progressive heart injury, stem cells isolated from placenta showed promise as an off-the-shelf therapy for cardiac repair, warranting the need for testing in additional models," said Anthony Atala, M.D., Editor-in-Chief of STEM CELLS Translational Medicine and director of the Wake Forest Institute for Regenerative Medicine.
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The full article, Human Placenta-derived Adherent Cells Improve Cardiac Performance in Mice with Chronic Heart Failure, can be accessed at http://stemcellstm.alphamedpress.org/content/early/2015/02/09/sctm.2014-0135.full.pdf+html.
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Stem Cells from Placenta Show Promise for Treating Heart Failure
Taking after Darwin, scientists discover beak gene for famous finches
Nearly two centuries after Charles Darwin jotted down his notes about the Galapagos finches, scientists are still gaining insights into just how the iconic birds evolved.
By sequencing the genomes of more than 100 finches, an international research team has pinpointed the gene that determines how the birds beaks develop. The findings, published on Wednesday in the journal Nature, help to fill in the details of Darwins early research on evolutionary adaptation.
Darwin didn't realize it at the time, but in observing these finches, he was witnessing signs of what would become a central concept in evolutionary biology: adaptive radiation. In response to changes in the environment or the availability of new resources, species can tend to rapidly develop new and different traits, eventually diversifying into distinct species. With Darwin's finches, the fragmented environments of the Galapagos islands promptedthis diversification, most prominently withthe birds' beaks.
Its assumed that the ancestor of the bird came to the islands about 1.5 to 2 million years agoand if you compare the sequences they are very similar to each other, Leif Andersson, Uppsala University genetics professor and study co-author, told the Monitor. But perhaps the most striking difference between them is this variation in beak shape.
Because of this variety, finches with differently shaped beaks could exploit different food resources. For example, a pointed beak may be more successful at catching insects while a blunt beak may be suited for picking up seeds from the ground. But the genetics behind these adaptations has been, until now, unclear.
So the research team re-sequenced the genomes of all 15 finch species studied by Darwin in the Galapagos and on Cocos Island, as well as two close relatives of the species. And in the process of mapping out the radiation of these species, Anderssons team determined the location of a gene that appears to play a critical role in determining beak shape.
After characterizing the gene, the team was able to classify two variants: one for blunt beaks and one for pointed beaks.
We looked at that region across all birds and we saw that there was a very strong correlation between the characterization of the beak in the birds and the presence and absence of these two variants, says Andersson.
Andersson and his colleagues also found evidence for what is known as interspecific gene flow, where species that are closely related can continue to breed successfully despite the existence of slightly different characteristics. His team says that this process of hybridization may have also contributed to the diversification of finches on the islands.
While the researchers found evidence suggesting that several genes have played a role in producing this variation among finches, the gene located in this study, entitled ALX1, is likely the most prominent determinant of beak shape, according to Andersson. And now the team can investigate other genes more closely.
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Taking after Darwin, scientists discover beak gene for famous finches
Research at Frozen Zoo gene bank aims to resurrect extinct species
By Julie Watson The Associated Press
Nola, a 40-year-old northern white rhino who is only one of five remaining of the species, wanders around her enclosure at the San Diego Zoo Safari Park on a cold winter day in Escondido, Calf. The survival of the northern white rhinoceros and dozens of other species could hinge on the Frozen Zoo, whose collection amassed over nearly 40 years has become the largest gene bank of its kind.
ESCONDIDO, Calif. Whenever an endangered animal dies at the San Diego Zoo, researchers race out, regardless of the hour, to remove its sperm or eggs, maybe a bit of ear or eyeball, and carefully freeze the cells in liquid nitrogen.
Today, the survival of the northern white rhinoceros and dozens of other species could hinge on the collection amassed over nearly 40 years that has become the largest gene bank of its kind: The Frozen Zoo.
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The icy vials may one day be used in experiments to resurrect recently extinct animals, like the Hawaiian Poouli bird. The stainless steel tanks hold the genetic material of more than 10,000 individual animals from more than 1,000 species and subspecies.
The Frozen Zoos work has taken on renewed urgency since the San Diego Safari Park lost 42-year-old Angalifu to cancer in December, leaving only five northern white rhinos left in the world and all unable to reproduce.
Barbara Durant, director of reproductive physiology at the San Diego Zoo Institute for Conservation Research, a.k.a. the Frozen Zoo, stands on the rail of a nitrogen-cooled stainless steel vat holding hundreds of vials of animal cells at the Beckman Center at the San Diego Zoos Safari Park in Escondido, Calif.
Scientists are racing to find the best way to utilize the banks frozen sperm to produce another one before the northern white goes extinct, which could happen within a decade.
Critics question whether its worth spending millions of dollars on species that are down to so few.
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Research at Frozen Zoo gene bank aims to resurrect extinct species