Posted: November 8, 2014 at 12:40 am
Stem Cells Help Victim of Spinal Cord Injury to Walk
A young man that was paralyzed after a gunshot wound to the spine, and after 4 weeks of stem cell treatment he regained use of his legs. We look at video of his recovery and speak with his...
By: TheLipTV
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Stem Cells Help Victim of Spinal Cord Injury to Walk - Video
Posted: November 7, 2014 at 10:01 pm
All you sad sack Democrats looking for a glimmer of hope in that shellacking you took on Tuesday can take comfort in this:
At least you didn't lose a single race for dogcatcher.
Of course, that's because dogcatcher is one of the few government jobs in South Carolina that is not put up for popular election.
If it was, you would have lost that, too.
Sorry, but that's about as sunny as it gets.
At some point - and this would be a good time - Democrats need to get the message that people here just don't like you. Well, 60 percent of people anyway.
You can whine all you want about how talk radio and biased TV stations have turned people against you, that the GOP has folks voting against their economic self-interests, that you really aren't the party of the devil incarnate.
But none of that matters. Folks in South Carolina aren't interested in your politics.
It is so bad that voters in Georgetown County chose a Republican who is currently under federal indictment for some shady deal involving the sale of stem cells - stem cells! - over a durn Democrat for state representative.
That's just embarrassing.
Originally posted here:
Let's face it, Democrats - you are not going to win any popularity contests in South Carolina
Posted: November 7, 2014 at 9:58 pm
Harvard Stem Cell Institute (HSCI) researchers at Massachusetts General (MGH) and Boston Children's hospitals (BCH) for the first time have used a relatively new gene-editing technique to create what could prove to be an effective technique for blocking HIV from invading and destroying patients' immune systems.
This is the first published report of a group using CRISPR Cas technology to efficiently and precisely edit clinically relevant genes out of cells collected directly from people, in this case human blood forming stem cells and T-cells.
Though the researchers that believe this new approach to HIV therapy might be ready for human safety trials in less than five years, they themselves offered three strong points of caution:
The first and most obvious is that they could run into unexpected complications; the second is that the history of the HIV/AIDS epidemic is littered with "cures" that turned out not to be; and finally, even if this new approach works perfectly, it will require additional developments to be applicable in the areas of the world that have been the hardest hit by the epidemic.
The work, led by Chad Cowan, and Derrick Rossi, associate professors in Harvard's Department of Stem Cell and Regenerative Biology, is featured on the cover of today's issue of the journal Cell Stem Cell.
HIV specifically targets T cells, a principal portion of the blood-based immune system, and enters via a gene receptor called CCR5 that serves as a doorway into the cells. Once inside the T cells, HIV replicates and kills off the host cells, leaving patients at the mercy of a variety of opportunistic infections.
Using the CRISPR Cas gene-editing technology, the Cowan and Rossi teams knocked the CCR5 receptor out of blood stem cells that they showed could give rise to differentiated blood cells that did not have CCR5. In theory, such gene-edited stem cells could be introduced into HIV patients via bone marrow transplantation, the procedure used to transplant blood stem cells into leukemia patients, to give rise to HIV-resistant immune systems.
"We showed that you can knock out CCR5 very efficaciously, we showed that the cells are still functional, and we did very, very deep sequencing analysis to show that there were no unwanted mutations, so it appears to be safe," Cowan said, adding that "there is obviously much more work to do.
"The next step is animal trials in collaboration with the Ragon Institute at Mass General," Cowan said. "There are excellent mouse models you can give a human immune system and then infect with HIV. We can give our cells to the mice and see if they're protected from HIV." Once those studies are completed, and if they are successful and complications do not arise, the next step would be to apply to the U.S. Food and Drug Administration to launch phase I human trials, which are designed solely to test the safety of new treatments. Cowan said it is too early to predict how soon such trials might begin.
David Scadden, a hematologist/oncologist who is both co-director of HSCI and director of the Center for Regenerative Medicine at MGH, called the new work "a tremendous first step in editing out what makes human cells vulnerable to HIV. It makes possible the idea that a person's own immune cells can attack HIV without being susceptible to it. Since this was done in stem cells, the entire immune system may be durably brought to bear on the virus. That's a powerful concept.
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Human blood stem cells genetically 'edited'
Posted: November 7, 2014 at 9:55 pm
McLean Hospital and Harvard Stem Cell Institute scientists have new evidence that stem cell transplantation could be a worthwhile strategy to help epileptics who do not respond to anti-seizure drugs.
As reported in Cell Stem Cell, the laboratory of McLean Associate Neurobiologist Sangmi Chung, PhD, transplanted seizure-inhibiting, human embryonic stem cell-derived neurons into the brains of mice with a common form of epilepsy. Half of the mice who received the transplanted neurons no longer had seizures, while the other half experienced a significant drop in seizure frequency.
"After the transplantation we observed that the human neurons integrate into the epileptic brain," said Chung, who is also a Harvard Stem Cell Institute affiliated faculty member and an assistant professor at Harvard Medical School. "The transplanted neurons begin to receive excitatory input from host neurons and in turn generate inhibitory responses that reverse the electrical hyperactivity that cause seizures."
The recovery seen after the human stem cell-derived neuron transplants, which were done while the cells were still maturing into their full-grown form, is similar to that published in a 2013 study by University of California, San Francisco, scientists who transplanted fetal mouse brain cells into epileptic mice.
While encouraging, Chung noted that further primate studies and a process to purify the neurons, so only those known to inhibit seizures are transplanted (called interneurons), would need to be completed before a treatment in humans could be considered.
"Because embryonic stem cells can differentiate into many different cell types, even when we drive them into neurons, there are always other cell types," she said. "For clinical purposes, we need to make sure the cells are safe, without any contaminant. Currently we are working on a different method to specifically isolate interneurons."
Over 65 million people worldwide are affected by epileptic seizures, which can cause convulsions, loss of consciousness and other neurological symptoms. The exact cause of the condition is unknown, but it is hypothesized that diminished populations of interneurons is a contributor.
Most epileptic patients can be treated with anti-seizure drugs, which contain molecules that can inhibit electrical symptoms, similar to the normal function of interneurons. But about one-third do not benefit from existing medication. Patients may opt to have a portion of their brain cut out to control symptoms.
"This seems to be an area that needs a novel therapy," Chung said. "Before starting this project, I was a stem cell biologist mostly interested in the development of neural stem cells, but as I've come to know about epilepsy, I've become motivated to continue this research."
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Human stem cell-derived neuron transplants reduce seizures in mice
Posted: November 6, 2014 at 11:56 pm
PUBLIC RELEASE DATE:
6-Nov-2014
Contact: B. D. Colen bd_colen@harvard.edu 617-413-1224 Harvard University @HarvardResearch
Harvard Stem Cell Institute (HSCI) researchers at Massachusetts General (MGH) and Boston Children's hospitals (BCH) for the first time have used a relatively new gene-editing technique to create what could prove to be an effective technique for blocking HIV from invading and destroying patients' immune systems.
This is the first published report of a group using CRISPR Cas technology to efficiently and precisely edit clinically relevant genes out of cells collected directly from people, in this case human blood forming stem cells and T-cells.
Though the researchers that believe this new approach to HIV therapy might be ready for human safety trials in less than five years, they themselves offered three strong points of caution:
The first and most obvious is that they could run into unexpected complications; the second is that the history of the HIV/AIDS epidemic is littered with "cures" that turned out not to be; and finally, even if this new approach works perfectly, it will require additional developments to be applicable in the areas of the world that have been the hardest hit by the epidemic.
The work, led by Chad Cowan, and Derrick Rossi, associate professors in Harvard's Department of Stem Cell and Regenerative Biology, is featured on the cover of today's issue of the journal "Cell Stem Cell."
HIV specifically targets T cells, a principal portion of the blood-based immune system, and enters via a gene receptor called CCR5 that serves as a doorway into the cells. Once inside the T cells, HIV replicates and kills off the host cells, leaving patients at the mercy of a variety of opportunistic infections.
Using the CRISPR Cas gene-editing technology, the Cowan and Rossi teams knocked the CCR5 receptor out of blood stem cells that they showed could give rise to differentiated blood cells that did not have CCR5. In theory, such gene-edited stem cells could be introduced into HIV patients via bone marrow transplantation, the procedure used to transplant blood stem cells into leukemia patients, to give rise to HIV-resistant immune systems.
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Harvard researchers genetically 'edit' human blood stem cells
Posted: November 6, 2014 at 11:54 pm
The University of Floridas John Pastor reports that researchers at the university have programmed bone marrow stem cells to repair damaged retinas in mice. This suggests that there is potential to treat common causes of vision loss in humans, such as macular degeneration, which affects nearly 2 million people in the United States, and some forms of blindness related to diabetes. Researchers removed blood stem cells from the bone marrow of mice, modified the cells in cultures, and injected them back into the animals circulatory systems. From there, the stem cells were able to hone in on the eye injury and become retinal cells. At 28 days after receiving the modified stem cells, mice that had previously demonstrated no retinal function were no different than normal mice in electrical measures of their response to light. The University of Floridas College of Medicine reports that the success in repairing a damaged layer of retinal cells in mice implies that blood stem cells take
GAINESVILLE, Fla. University of Florida researchers were able to program bone marrow stem cells to repair damaged retinas in mice, suggesting a potential treatment for one of the most common causes of vision loss in older people.
The success in repairing a damaged layer of retinal cells in mice implies that blood stem cells taken from bone marrow can be programmed to restore a variety of cells and tissues, including ones involved in cardiovascular disorders such as atherosclerosis and coronary artery disease.
To our knowledge, this is the first report using targeted gene manipulation to specifically program an adult stem cell to become a new cell type, said Dr. Maria B. Grant, a professor of pharmacology and therapeutics at UFs College of Medicine. Although we used genes, we also suggest you can do the same thing with drugs but ultimately you would not give the drugs to the patient, you would give the drugs to their cells. Take the cells out, activate certain chemical pathways, and put the cells back into the patient.
In a paper slated to appear in the September issue of the journal Molecular Therapy, scientists describe how they used a virus carrying a gene that gently pushed cultured adult stem cells from mice toward a fate as retinal cells. Only after the stem cells were reintroduced into the mice did they completely transform into the desired type of vision cells, apparently taking environmental cues from the damaged retinas.
After studying the cell-transformation process, scientists were able to bypass the gene manipulation step entirely and instead use chemical compounds that mirrored environmental conditions in the body, thus pointing the stem cells toward their ultimate identities as vision cells.
First we were able to show you can overexpress a protein unique to a retinal cell type and trick the stem cell into thinking it is that kind of cell, said Grant, who collaborated with Edward Scott, the director of the Program in Stem Cell Biology and Regenerative Medicine at UFs McKnight Brain Institute. As we proceeded, we found we could activate the stem cells by mimicking the bodys natural signaling channels with chemicals. This implies a whole new field of stem cell research that uses drug manipulation rather than genetic manipulation to send these immature cells along new pathways.
Scientists chose to build retinal pigment epithelial cells, which form the outer barrier of the retina. In addition to being very specialized and easy to identify, RPE cells are faulty in many retinal diseases, including age-related macular degeneration, which affects nearly 2 million people in the United States, and some forms of blindness related to diabetes.
This work applies to 85 percent of patients who have age-related macular degeneration, Grant said. There are no therapies for this devastating disease.
The work was supported by the National Eye Institute. Researchers removed blood stem cells from the bone marrow of mice, modified the cells in cultures, and injected them back into the animals circulatory systems. From there, the stem cells were able to home in on the eye injury and become retinal cells.
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University of Florida Scientists Program Adult Stem Cells ...
Posted: November 6, 2014 at 11:52 pm
11 hours ago In this multiple confocal analysis of transverse sections from transgenic zebrafish embryos, vasculature is labeled by red fluorescence, NF-kB protein complex that regulates inflammation by green fluorescence and nuclei by blue fluorescence. The arrowhead indicates a potential hematopoietic stem cell emerging in the dorsal aorta with high expression of NF-kB. The image at bottom right combines all channels. Credit: UC San Diego School of Medicine
Hematopoietic stem cells (HSCs) give rise to all blood and immune cells throughout the life of vertebrate organisms, from zebrafish to humans. But details of their genesis remain elusive, hindering efforts to develop induced pluripotent stem cell (iPSC) replacements that might address a host of blood disorders.
In a paper published Nov. 20 in the journal Cell, researchers at the University of California, San Diego School of Medicine describe the surprising and crucial involvement of a pro-inflammatory signaling protein in the creation of HSCs during embryonic development, a finding that could help scientists to finally reproduce HSCs for therapeutic use.
"The recent breakthrough of induced pluripotency has made the concept of patient-specific regenerative medicine a reality," said principal investigator David Traver, PhD, professor in the Department of Cellular and Molecular Medicine. "The development of some mature cell lineages from iPSCs, such as cardiac and neural, has been reasonably straightforward, but not with HSCs. This is likely due, at least in part, to not fully understanding all of the factors used by the embryo to generate HSCs. We believe the discovery that pro-inflammatory cues are important in vivo will help us recapitulate instruction of HSC fate in vitro from iPSCs."
Traver and colleagues specifically looked at the role of a cytokine (a type of cell signaling protein) called tumor necrosis factor alpha or TNF, which plays a pivotal role in regulating systemic inflammation and immunity. The work extended previous research by Spanish biologist Victoriano Mulero, who had reported that TNF was important in the function of the embryonic vascular system and that in animal models where TNF function was absent, blood defects resulted.
The Cell paper's first author Raquel Espin-Palazon, a postdoctoral researcher in Traver's lab and a former colleague of Mulero's, determined that TNF was required for the emergence of hematopoietic stem cells during embryogenesis in zebrafish a common animal model.
Traver said the finding was completely unexpected because HSCs emerge relatively early in embryonic formation when the developing organism is considered to be largely sterile and devoid of infection.
"Thus, there was no expectation that pro-inflammatory signaling would be active at this time or in the blood-forming regions," Traver said. "Equally surprising, we found that a population of embryonic myeloid cells, which are transient cells produced before HSCs arise, are the producers of the TNF needed to establish HSC fate. So it turns out that a small subset of myeloid cells that persist for only a few days in development are necessary to help generate the lineal precursors of the entire adult blood-forming system."
The newly discovered role of TNF in HSC development mirrors a parallel discovery regarding interferon gamma (INFg), another cytokine and major mediator of pro-inflammatory signaling, highlighting multiple inputs for inflammatory signaling in HSC emergence. Traver said the crucial roles of TNF and INFg in HSC emergence are likely similar in humans because of the highly conserved nature of HSC development across vertebrate evolution.
Explore further: New blood: Tracing the beginnings of hematopoietic stem cells
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Before there will be blood: Pro-inflammatory signaling plays surprising role in creation of hematopoietic stem cells
Posted: November 6, 2014 at 11:52 pm
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Newswise Hematopoietic stem cells (HSCs) give rise to all blood and immune cells throughout the life of vertebrate organisms, from zebrafish to humans. But details of their genesis remain elusive, hindering efforts to develop induced pluripotent stem cell (iPSC) replacements that might address a host of blood disorders.
In a paper published Nov. 20 in the journal Cell, researchers at the University of California, San Diego School of Medicine describe the surprising and crucial involvement of a pro-inflammatory signaling protein in the creation of HSCs during embryonic development, a finding that could help scientists to finally reproduce HSCs for therapeutic use.
The recent breakthrough of induced pluripotency has made the concept of patient-specific regenerative medicine a reality, said principal investigator David Traver, PhD, professor in the Department of Cellular and Molecular Medicine. The development of some mature cell lineages from iPSCs, such as cardiac and neural, has been reasonably straightforward, but not with HSCs. This is likely due, at least in part, to not fully understanding all of the factors used by the embryo to generate HSCs. We believe the discovery that pro-inflammatory cues are important in vivo will help us recapitulate instruction of HSC fate in vitro from iPSCs.
Traver and colleagues specifically looked at the role of a cytokine (a type of cell signaling protein) called tumor necrosis factor alpha or TNFa, which plays a pivotal role in regulating systemic inflammation and immunity. The work extended previous research by Spanish biologist Victoriano Mulero, who had reported that TNFa was important in the function of the embryonic vascular system and that in animal models where TNF function was absent, blood defects resulted.
The Cell papers first author Raquel Espin-Palazon, a postdoctoral researcher in Travers lab and a former colleague of Muleros, determined that TNFa was required for the emergence of hematopoietic stem cells during embryogenesis in zebrafish a common animal model.
Traver said the finding was completely unexpected because HSCs emerge relatively early in embryonic formation when the developing organism is considered to be largely sterile and devoid of infection.
Thus, there was no expectation that pro-inflammatory signaling would be active at this time or in the blood-forming regions, Traver said. Equally surprising, we found that a population of embryonic myeloid cells, which are transient cells produced before HSCs arise, are the producers of the TNFa needed to establish HSC fate. So it turns out that a small subset of myeloid cells that persist for only a few days in development are necessary to help generate the lineal precursors of the entire adult blood-forming system.
The newly discovered role of TNFa in HSC development mirrors a parallel discovery regarding interferon gamma (INFg), another cytokine and major mediator of pro-inflammatory signaling, highlighting multiple inputs for inflammatory signaling in HSC emergence. Traver said the crucial roles of TNFa and INFg in HSC emergence are likely similar in humans because of the highly conserved nature of HSC development across vertebrate evolution.
Posted: November 6, 2014 at 11:42 pm
New research from McLean Hospital and the Harvard Stem Cell Institute has shown that stem cell therapy reduces seizures in mice.
Researchers used an animal model to transplant seizure-inhibiting, human embryonic stem cell-derived neurons into the brains of mice that had a common form of epilepsy. Half of the mice that received the transplanted neurons no longer had seizures, while the other half experienced a significant drop in seizure frequency.
The transplanted neurons integrated into the mouse brains and began to receive neuronal activity. The neurons then released GABA, an inhibitory response that reversed the electrical hyperactivity that causes seizure.
Previous studies showed increasing inhibition in the epileptic brain can help control the seizure and also a lot of anti-epilepsy drugs are mimicking this GABA, so many of them worked by binding to the GABA receptors, researcher Sangmi Chung, assistant professor of psychiatry at Harvard, told FoxNews.com.
Researchers initially set out to test the functionality of human neurons, but later decided to test their effect on epilepsy because it is such a devastating disease. About 30 percent of people do not respond to seizure drugs and one out of 26 people will be affected by seizures in their lifetime, Chung said.
Over 65 million people worldwide are affected by epileptic seizures, which can cause convulsions, loss of consciousness and other neurological symptoms. Patients are treated with anti-seizure drugs, and may choose to have a portion of their brain removed.
Because mouse cells mature more quickly than human cells within weeks instead of years it was unclear how long a stem cell transplant in a human would take before becoming effective, Chung noted.
If we compare it with the mouse [model], we believe it will be years, not weeks, she said.
However, the study found that, even without full maturation, the cells integrated into the epileptic mouse brains, receive signals and release GABA, therefore preventing seizures.
I think its really good news in terms of transplantation even maturing, not fully mature [cells] still work, Chung said.
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Stem cell transplants may help reduce seizures, study says
Posted: November 6, 2014 at 11:42 pm
PUBLIC RELEASE DATE:
6-Nov-2014
Contact: David McKeon dmckeon@nyscf.org 212-365-7440 New York Stem Cell Foundation @nyscf
New York, NY (November 6, 2014) - A team of scientists led by The New York Stem Cell Foundation (NYSCF) Research Institute successfully created a human stem cell disease model of Parkinson's disease in a dish. Studying a pair of identical (monozygotic) twins, one affected and one unaffected with Parkinson's disease, another unrelated Parkinson's patient, and four healthy control subjects, the scientists were able to observe key features of the disease in the laboratory, specifically differences in the patients' neurons' ability to produce dopamine, the molecule that is deficient in Parkinson's disease. In addition, the scientists also identified a potential strategy for developing novel therapies for Parkinson's disease.
Attributed to a combination of genetic and nongenetic factors, Parkinson's disease has no completely effective therapy or cure. Parkinson's disease is moderately heritable, but the mechanisms of this inheritance are not well understood. While genetic forms of the disease exist, sporadic forms are far more common.
"The unique scenario of identical twins, one with this disease and one without, allowed our scientists an unprecedented look into the mechanisms of Parkinson's disease," said Susan L. Solomon, NYSCF Chief Executive Officer. "Advanced stem cell research techniques allow us to push the boundaries of science and see what actually goes wrong at the cellular level, step by step during the disease process."
DNA mutations resulting in the production of a specific enzyme called glucocerebrosidase (GBA) have been linked to a five-fold greater risk of developing Parkinson's disease; however, only 30% of individuals with this mutation have been shown to develop Parkinson's disease by the age of 80. This discordance suggests that multiple factors contribute to the development of Parkinson's disease, including both genetic and non-genetic factors. To date, there has been no appropriate model to identify and test multiple triggers leading to the onset of the disease.
In this study, published today in Cell Reports, a set of identical twins, both with a GBA mutation, provided a unique opportunity to evaluate and dissect the genetic and non-genetic contributions to the development of Parkinson's disease in one twin, and the lack of disease in the other. The scientists made induced pluripotent stem (iPS) cells from skin samples from both twins to generate a cellular model of Parkinson's in a dish, recapitulating key features of the disease, specifically the accumulation of -synuclein and dopamine deficiency.
Upon analyzing the cell models, the scientists found that the dopamine-producing neurons from both twins had reduced GBA enzymatic activity, elevated -synuclein protein levels, and a reduced capacity to synthesize and release dopamine. In comparison to his unaffected brother, the neurons generated from the affected twin produced less dopamine, had higher levels of an enzyme called monoamine oxidase B (MAO-B), and poor ability to connect with each other. Treating the neurons with molecules that lowered the activity of MAO-B together with overexpressed GBA normalized -synuclein and dopamine levels in the cell models. This suggests that a combination therapy for the affected twin may be possible by simultaneously targeting these two enzymes.
"The subject of Parkinson's disease discordant twins gave us an incredible opportunity to utilize stem cell models of disease in a dish to unlock some of the biological mechanisms of disease," said Dr. Scott Noggle, NYSCF Vice President, Stem Cell Research and The NYSCF - Charles Evans Senior Research Fellow for Alzheimer's Disease. "Working with these various different groups and scientists added to the depth and value of the research and we hope our findings will be applicable to other Parkinson's disease patients and other neurodegenerative disorders."
