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Protein that repels immune cells protects transplanted pancreatic islets from rejection

Posted: March 10, 2015 at 2:54 am

Transplanting islets encapsulated with CXCL12 restores blood sugar control without immunosuppression in animal models of diabetes

An approach developed by Massachusetts General Hospital (MGH) investigators may provide a solution to the limitations that have kept pancreatic islet transplantation from meeting its promise as a cure for type 1 diabetes. In the March issue of the American Journal of Transplantation, the research team reports that encapsulating insulin-producing islets in gel capsules infused with a protein that repels key immune cells protected islets from attack by the recipient's immune system without the need for immunosuppressive drugs, restoring long-term blood sugar control in mouse models. The technique was effective both for islets from unrelated mice and for islets harvested from pigs.

"Protecting donor islets from the recipient's immune system is the next big hurdle toward making islet transplantation a true cure for type 1 diabetes," says Mark Poznansky, MD, PhD, director of the MGH Vaccine and Immunotherapy Center, who led the study. "The first was generating enough insulin-producing islets, which has been addressed by several groups using pig islets or - as announced last fall by Doug Melton's team at the Harvard Stem Cell Institute - with islet cells derived from human stem cells. Now our technology provides a way to protect islets or other stem-cell-derived insulin-producing cells from being destroyed as soon as they are implanted into a diabetic individual without the need for high-intensity immunosuppression, which has its own serious side effects."

While transplantation of pancreatic islets has been investigated for several decades as a treatment and potential cure for type 1 diabetes, its success has been limited. Along with the risk of rejection that accompanies all organ transplants - a risk that is even greater for cross-species transplants - donated islets are subject to the same autoimmune damage that produced diabetes in the first place. The immunosuppressive drugs used to prevent organ rejection significantly increase the risk of infections and some cancers, and they also can contribute directly to damaging the islets. Among the strategies investigated to protect transplanted islets are enclosing them in gel capsules and manipulating the immune environment around the implant. The MGH-developed approach includes aspects of both approaches.

Previous research from the MGH team demonstrated that elevated expression of a chemokine - a protein that induces the movement of other cells - called CXCL12 repels the effector T cells responsible for the rejection of foreign tissue while attracting and retaining regulatory T cells that suppress the immune response. For the current study they investigated how either coating islets with CXCL12 or enclosing them in CXCL12 gel capsules would protect islets transplanted into several different mouse models.

Their experiments revealed that islets from nondiabetic mice, either coated with CXCL12 or encapsulated in a CXCL12-containing gel, survived and restored long-term blood sugar control after transplantation into mice with diabetes that was either genetically determined or experimentally induced. CXCL12-encapsulated islets were even protected against rejection by recipient animals previously exposed to tissue genetically identical to that of the donor, which usually would sensitize the immune system against donor tissue. CXCL12-encapsulated pig islets successfully restored blood sugar control in diabetic mice without being rejected. The ability of CXCL12 - either as a coating or encapsulating gel - to repel effector T cells and attract regulatory T cells was also confirmed.

"While studying this procedure in larger animals is an essential next step, which is currently underway with the support of the Juvenile Diabetes Research Foundation, we expect that this relatively simple procedure could be readily translatable into clinical practice when combined with technologies such as stem-cell-derived islets or other insulin-producing cells and advanced encapsulation devices," says Poznansky, an associate professor of Medicine at Harvard Medical School. "We also hope that CXCL12 will have a role in protecting other transplanted organs, tissues and cells as well as implantable devices, a possibility we are actively investigating."

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Tao Chen, MD, of the MGH Vaccine and Immunotherapy Center (VIC) is lead author of the American Journal of Transplantation report. Additional co-authors include James Markmann, MD, PhD, and David Sachs, MD, of the MGH Center for Transplantation Sciences. The study was supported by grants from the Juvenile Diabetes Research Foundation and the Friends of VIC. A patent covering the approach described in this paper has been issued to the MGH and exclusively licensed to the biotech startup company VICapsys.

Massachusetts General Hospital, founded in 1811, is the original and largest teaching hospital of Harvard Medical School. The MGH conducts the largest hospital-based research program in the United States, with an annual research budget of more than $785 million and major research centers in AIDS, cardiovascular research, cancer, computational and integrative biology, cutaneous biology, human genetics, medical imaging, neurodegenerative disorders, regenerative medicine, reproductive biology, systems biology, transplantation biology and photomedicine.

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Gene regulatory path revealed as target for therapy of aggressive pediatric brain cancer

Posted: March 10, 2015 at 2:54 am

Laboratory studies suggest anticancer drug already in clinical trials in children may interrupt this gene pathway

Working with cells taken from children with a very rare but ferocious form of brain cancer, Johns Hopkins Kimmel Cancer Center scientists have identified a genetic pathway that acts as a master regulator of thousands of other genes and may spur cancer cell growth and resistance to anticancer treatment.

Their experiments with cells from patients with atypical teratoid/rhabdoid tumor (AT/RT) also found that selumetinib, an experimental anticancer drug currently in clinical trials for other childhood brain cancers, can disrupt part of the molecular pathway regulated by one of these factors, according to a research team led by Eric Raabe, M.D., Ph.D., an assistant professor of oncology at the Johns Hopkins University School of Medicine.

AT/RT mostly strikes children 6 and younger, and the survival rate is less than 50 percent even with aggressive surgery, radiation and chemotherapy, treatments that can also disrupt thinking, learning and growth. AT/RT accounts for 1 percent of more than 4,500 reported pediatric brain tumors in the U.S., but it is more common in very young children, and it represents 10 percent of all brain tumors in infants.

"What's exciting about this study is that it identifies new ways we can treat AT/RT with experimental drugs already being tested in pediatric patients," Raabe says. Because few outright genetic mutations -- and potential drug targets -- have been linked to AT/RT, Raabe and his colleagues turned their attention to genes that could regulate thousands of other genes in AT/RT cancer cells. Experiments in fruit flies had already suggested a gene known as LIN28 could be important in regulating other genes involved in the development of brain tumors. Specifically, the LIN28 protein helps regulate thousands of RNA molecules in normal stem cells, giving them the ability to grow, proliferate and resist damage.

"These factors provide stem cells with characteristics that cancer cells also have, such as resistance to environmental insults. These help tumor cells survive chemotherapy and radiation," says Raabe. "These proteins also help stem cells move around the body, an advantage cancer cells need to metastasize."

In a report on one of their studies, published Dec. 26 in the journal Oncotarget, the researchers examined cell lines derived from pediatric AT/RT patients and the tumors themselves. They found that the two members of the LIN28 family of genes were highly expressed in 78 percent of the samples, and that blocking LIN28 expression with specially targeted gene silencers called short hairpin RNAs curbed the tumor cells' growth and proliferation and triggered cell death. When Raabe and colleagues blocked LIN28A in AT/RT tumor cells transplanted into mice, they were able to more than double the mice's life span, from 48 to 115 days.

Using selumetinib in cell line experiments, the scientists cut AT/RT tumor cell proliferation in half and quadrupled the rate of cell death in some cell lines. Raabe says the drug appeared to be disrupting a key molecular pathway controlled by LIN28.

In a second study, described in the Journal of Neuropathology and Experimental Neurology, Raabe and his colleagues examined another factor in the LIN28 pathway, called HMGA2, which is also highly expressed in AT/RT tumors. They again used short pieces of RNA to "silence" HMGA2, which led to lower levels of cell growth and proliferation and increased cell death. Blocking HMGA2 also doubled the survival rate of mice implanted with tumors derived from pediatric AT/RT cell lines from 58 to 153 days.

Raabe says his team's work with LIN28 and HMGA2 should not only lead to understanding why cancers like AT/RT are so aggressive, but "also identify their Achilles' heels. We have shown that if we target these key proteins downstream of LIN28 in AT/RT, the tumors unravel."

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IUPUI biologist receives NIH grant to study how glaucoma develops in stem cells

Posted: March 10, 2015 at 2:53 am

IMAGE:This is Assistant Professor of Biology Jason Meyer, Ph.D. of the School of Science at Indiana University-Purdue University Indianapolis with graduate students Sarah Ohlemacher (left) and Akshaya Sridhar. view more

Credit: School of Science at Indiana University-Purdue University Indianapolis

INDIANAPOLIS -- Jason Meyer, Ph.D., assistant professor of biology in the School of Science at Indiana University-Purdue University Indianapolis, has received a National Institutes of Health grant to study how glaucoma develops in stem cells created from skin cells genetically predisposed to the disease. The five-year, $1.8 million grant is funded by the NIH's National Eye Institute.

Glaucoma is a group of degenerative diseases that damage the eye's optic nerve and can result in vision loss and blindness. It is the most common disease that affects retinal ganglion cells. These cells serve as the connection between the eye and the brain. Once these cells are damaged or severed, the brain cannot receive critical information, leading to blindness.

Meyer's research uses human induced pluripotent stem cells, which can be generated from any cell in the body. In this case, they are created from skin cells of patients predisposed to glaucoma. These cells are genetically reprogrammed and then given instructions to develop into cells of the eye's retina.

"Our hope is that because these cells have the genetic information to develop the disease, they will do so in our lab," Meyer said. "Hopefully, we can figure out what goes wrong in those cells and then develop new ways to fix that."

Meyer and two School of Science graduate students are now creating the stem cells and observing their features to determine what isn't going the way it should. They will determine whether they can identify the cause of damage or death of the retinal ganglion cells.

"This is a five-year award, so our hope is that toward the end of the award we can use the information we gather to start developing customized strategies to fix what's going wrong," Meyer said.

He sees this as an exciting approach to stem cell research. Often, stem cells are transplanted to replace cells damaged by disease. While that's a possibility, Meyer's research instead could lead to repairing the existing cells in the eye and restoring vision for patients.

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Graphene Shows Promise In Eradication Of Stem Cancer Cells

Posted: March 10, 2015 at 2:51 am

Graphene was made in a lab in 2003, but by 2014, it reportedly reached $9 million in sales predominately inelectronics, battery energy andsemiconductors.Graphene is100 times stronger than steel by weight and efficientlyconducts heat and electricity. Its a new material that can store bits of small energy or make battery terminals more efficient.

Scientistsat the University of Manchester, Englanddecided to use graphene in a completely different way: to neutralize cancer stemcells (CSC) and not harm other cells.

The scientistsused a modified version ofgraphene oxide flakes on six kinds of cancer cells where it hurts cancers the most, in the stem cells. They discovered that it acts as an anti-cancer agent that selectively targets stem cells. With cancer, stem cells are the origin for tumors, but they also withstand radiation, chemotherapy and surgery and typically are known to re-seed a tumor, even when it looks like it has been eradicated.

From the lab experiments, the scientistsreport the graphene oxide flakes inhibit the key signaling pathways active in the CSCs.

Cancer stem cells differentiate to form a small mass of cells known as a tumour-sphere. We saw that the graphene oxide flakes prevented CSCs from forming these, and instead forced them to differentiate into non-cancer stem-cells, saidDr.AravindVijayaraghavan, University of Manchester.

Researchers want to use the graphene oxide as a type of washing solution and after surgery, pump it into cancer area to destroy any stem cell survivors, so there is no chance of it returning or re-seeding.

According to the results of the study, the results showedthat graphene oxide had a non toxic effect on thecells which suggests thetreatment could havefewer side-effects asan anti-cancer therapy. The results of the study are found in the current issue ofOncotarget.

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Bioengineers put human hearts on a chip to aid drug screening

Posted: March 10, 2015 at 2:50 am

VIDEO:Shown is human heart tissue, derived from adult stem cells, before and after exposure to isoproterenol, a drug used to treat bradycardia (slow heart rate) and other heart problems. The... view more

Credit: Video by Dr. Anurag Mathur/Healy Lab

Berkeley -- When University of California, Berkeley, bioengineers say they are holding their hearts in the palms of their hands, they are not talking about emotional vulnerability.

Instead, the research team led by bioengineering professor Kevin Healy is presenting a network of pulsating cardiac muscle cells housed in an inch-long silicone device that effectively models human heart tissue, and they have demonstrated the viability of this system as a drug-screening tool by testing it with cardiovascular medications.

This organ-on-a-chip, reported in a study to be published Monday, March 9, in the journal Scientific Reports, represents a major step forward in the development of accurate, faster methods of testing for drug toxicity. The project is funded through the Tissue Chip for Drug Screening Initiative, an interagency collaboration launched by the National Institutes of Health to develop 3-D human tissue chips that model the structure and function of human organs.

"Ultimately, these chips could replace the use of animals to screen drugs for safety and efficacy," said Healy.

The study authors noted a high failure rate associated with the use of nonhuman animal models to predict human reactions to new drugs. Much of this is due to fundamental differences in biology between species, the researchers explained. For instance, the ion channels through which heart cells conduct electrical currents can vary in both number and type between humans and other animals.

"Many cardiovascular drugs target those channels, so these differences often result in inefficient and costly experiments that do not provide accurate answers about the toxicity of a drug in humans," said Healy. "It takes about $5 billion on average to develop a drug, and 60 percent of that figure comes from upfront costs in the research and development phase. Using a well-designed model of a human organ could significantly cut the cost and time of bringing a new drug to market."

The heart cells were derived from human-induced pluripotent stem cells, the adult stem cells that can be coaxed to become many different types of tissue.

The researchers designed their cardiac microphysiological system, or heart-on-a-chip, so that its 3-D structure would be comparable to the geometry and spacing of connective tissue fiber in a human heart. They added the differentiated human heart cells into the loading area, a process that Healy likened to passengers boarding a subway train at rush hour. The system's confined geometry helps align the cells in multiple layers and in a single direction.

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"Big Brain" Gene Allowed for Evolutionary Expansion of Our Neocortex

Posted: March 10, 2015 at 2:49 am

The newly identified gene is found in modern-day humans, Neandertals and Denisovans, but not in chimps

New research suggests that a single gene may be responsible for the large number of neurons found uniquely in the human brain. When this gene was inserted in the brain of a mouse embryo (shown here), it induced the formation of many more neurons (stained red). The extra neurons led to the formation of characteristic convolutions that the human brain uses to pack so much brain tissue into a small space (convolutions shown on the right). Credit: Marta Florio and Wieland B. Huttner, Max Planck Institute of Molecular Cell Biology and Genetics

A single gene may have paved the way for the rise of human intelligence by dramatically increasing the number of brain cells found in a key brain region.

This gene seems to be uniquely human: It is found in modern-day humans, Neanderthals and another branch of extinct humans called Denisovans, but not in chimpanzees.

By allowing the brain region called the neocortex to contain many more neurons, the tiny snippet of DNA may have laid the foundation for the human brain's massive expansion.

"It is so cool that one tiny gene alone may suffice to affect the phenotype of the stem cells, which contributed the most to the expansion of the neocortex," said study lead author Marta Florio, a doctoral candidate in molecular and cellular biology and genetics at the Max Planck Institute of Molecular Cell Biology and Genetics in Dresden, Germany. Still, it's likely this gene is just one of many genetic changes that make human cognition special, Florio said.

An expanding brain

The evolution from primitive apes to humans with complex language and culture has taken millions of years. Some 3.8 million ago, Australopithecus afarensis, the species typified by the iconic early human ancestor fossil Lucy, had a brain that was less than 30 cubic inches (500 cubic centimeters) in volume, or about a third the size of the modern human brain. By about 1.8 million years ago, Homo erectus was equipped with a brain that was roughly twice as big as that of Australopithecus. H. erectus also showed evidence of tool and fire use and more complex social groups.

Once anatomically modern humans, and their lost cousins the Neanderthals and Denisovans, arrived on the scene, the brain had expanded to roughly 85 cubic inches (1.4 liters) in volume. Most of this growth occurred in a brain region called the neocortex.

"The neocortex is so interesting because that's the seat of cognitive abilities, which, in a way, make us human like language and logical thinking," Florio told Live Science.

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New insights into 3-D genome organization and genetic variability

Posted: March 10, 2015 at 2:49 am

Two NIH Roadmap Epigenomics studies answer longstanding questions about the differences between chromosome pairs and how chromosome folding influences gene expression

While genomics is the study of all of the genes in a cell or organism, epigenomics is the study of all the genomic add-ons and changes that influence gene expression but aren't encoded in the DNA sequence. A variety of new epigenomic information is now available in a collection of studies published Feb. 19 in Nature by the National Institutes of Health (NIH) Roadmap Epigenomics Program. This information provides a valuable baseline for future studies of the epigenome's role in human development and disease.

Two of these studies, led by researchers at University of California, San Diego School of Medicine and Ludwig Cancer Research, address the differences between chromosome pairs (one inherited from mom, the other from dad) and how chromosome folding influences gene expression.

"Both of these studies provide important considerations for clinicians and researchers who are developing personalized medicines based on a patient's genomic information," said Bing Ren, PhD, professor of cellular and molecular medicine at UC San Diego, Ludwig Cancer Research member and senior author of both studies.

The first paper by Ren's group takes a look at differences in our chromosome pairs. Each of us inherits one set from our mother and the other from our father. Chromosome pairs are often thought to be identical, one just a backup for the other. But this study found widespread differences in how genes are regulated (turned on and off) between the two chromosomes in a pair. It turns out that we all have "biases" in our chromosomes. In other words, different traits have a stronger contribution from one parent than the other. The study also suggests that these biases are rooted in inherited sequence variations and that they are not randomly distributed. These findings help explain why, for example, all kids in a family may have their father's hair but their mother's eyes.

The second paper by Ren's group tackles how the genome is organized and how it changes as stem cells differentiate (specialize). DNA strands in every cell are tightly wound and folded into chromosomes. Yet chromosomal structures, and how they influence gene expression, are not well understood. In this study, Ren and team mapped chromosomal structures in stem cells and several different differentiated cell types derived from stem cells. First, they induced differentiation in the stem cells. Then they used molecular tools to examine how the structure of the cells' chromosomes changed and how that change is associated with gene activity. The team found that chromosomes are partitioned into relatively stable structural units known as topologically associating domains (TADs), and that TAD boundaries remain constant in different cell types. What's more, the researchers found that the changes in chromosomal architecture mostly take place within the TADs in a way that correlates with changes in the epigenome.

"The epigenome -- chemical modifications to chromosomes and 3D chromosomal structure -- is not just a linear object," Ren said. "The epigenome is a 3D object, folded in a hierarchical way, and that should affect how we think about many aspects of human development, health and disease."

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Co-authors on the paper "Integrative Analysis of Haplotype-Resolved Epigenomes Across Human Tissues" include Danny Leung, Inkyung Jung, Nisha Rajagopal, Anthony Schmitt, Siddarth Selvaraj, Ah Young Lee, Chia-An Yen, Yunjiang Qiu, Samantha Kuan, Lee Edsall, Ludwig Cancer Research; Shin Lin, Yiing Lin, Stanford University and Washington University School of Medicine; Wei Xie, formerly at Ludwig Cancer Research and now at Tsinghua University; Feng Yue, formerly at Ludwig Cancer Research and now at Pennsylvania State University; Manoj Hariharan, Joseph R. Ecker, Howard Hughes Medical Institute and Salk Institute for Biological Studies; Pradipta Ray, University of Texas; Hongbo Yang, Neil C. Chi, UC San Diego; and Michael Q. Zhang, University of Texas, Dallas and Tsinghua University.

Co-authors on the paper "Chromatin Architecture Reorganization during Stem Cell Differentiation" include Jesse R. Dixon, Siddarth Selvaraj, Ludwig Cancer Research and UC San Diego; Inkyung Jung, Yin Shen, Ah Young Lee, Zhen Ye, Audrey Kim, Nisha Rajagopal, Yarui Diao, Ludwig Cancer Research; Jessica E. Antosiewicz-Bourget, Morgridge Institute for Research; Wei Xie, Tsinghua University; Jing Liang, Huimin Zhao, University of Illinois at Urbana-Champaign; Victor V. Lobanenkov, National Institute of Allergy and Infectious Diseases; Joseph R. Ecker, Howard Hughes Medical Institute and Salk Institute for Biological Studies; James Thomson, Morgridge Institute for Research, University of Wisconsin and University of California, Santa Barbara.

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Okyanos Stem Cell Therapy Launches Orthopedic Lifestyle Survey

Posted: March 10, 2015 at 2:40 am

Freeport, Grand Bahama (PRWEB) March 09, 2015

Okyanos, the leader in cell therapy, launched its next in a series of studies today to determine the emotional impact and lifestyle influence orthopedic conditions such as osteoarthritis and sports-related injuries have had on those affected. The survey focuses on people between the ages of 55 and 75 living with orthopedic health issues and is designed to examine the toll on those afflicted as well as their relationships.

According to Okyanos VP Marketing Carol Montgomery, Millions of people suffer disorders of the joints, bones, muscles and connective ligaments, tendons and cartilage debilitating conditions on a daily basis, ranging from reduced function to crippling pain but have exhausted available methods of treatment. These restrictions affect them in a variety of ways and our ongoing lifestyle surveys measure the effects such chronic conditions have on todays aging population. Many are turning to solutions like adult stem cell therapy for treatment with excellent results.

The Okyanos Lifestyle and Relationship Survey for Heart Disease, of nearly 700 adults, uncovered a staggering 93% were open to alternatives to their existing heart disease treatment plan showing a growing discontent with their current options. A majority 68% were emotionally impacted and felt they were saddled with restrictions imposed by their heart conditions such as chronic fatigue and shortness of breath.

Adult stem cell therapy has emerged as a new treatment alternative for those who are restricted in activities they can no longer do but are determined to live a more normal life. Okyanos cell therapy uses a unique blend of adult stem and regenerative cells derived from a patients own fat tissue, thereby utilizing the bodys own natural biology to heal itself.

Just 50 miles from US shore, Okyanos cell therapy is available to patients suffering with the daily discomfort of orthopedic conditions including osteoarthritis, rheumatoid arthritis, sports-related injuries and spine disease.

Patients with a severe orthopedic condition, interested in participating in the study can go to: https://www.surveymonkey.com/s/ortho_Okyanos

For a copy of the Okyanos Heart Disease Lifestyle Report that reveals the emotional toll and lifestyle impact heart disease has on patients in the United States, visit: Heart Disease Lifestyle Report

Patients can contact Okyanos to learn more and request a free consultation at http://www.Okyanos.com or by calling 1-855-659-2667.

About Okyanos: (Oh key AH nos) Based in Freeport, Grand Bahama, Okyanos brings a new standard of care and a better quality of life to patients with coronary artery disease, tissue ischemia, autoimmune diseases, and other chronic neurological and orthopedic conditions. Okyanos Cell Therapy utilizes a unique blend of stem and regenerative cells derived from patients own adipose (fat) tissue which helps improve blood flow, moderate destructive immune response and prevent further cell death. Okyanos is fully licensed under the Bahamas Stem Cell Therapy and Research Act and adheres to U.S. surgical center standards. The literary name Okyanos, the Greek god of the river Okyanos, symbolizes restoration of blood flow.

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Okyanos Stem Cell Therapy Launches Orthopedic Lifestyle Survey

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The International Society for Stem Cell Research announces annual meeting details

Posted: March 10, 2015 at 2:40 am

CHICAGO -- The International Society for Stem Cell Research's 13th annual meeting will take place June 24-27, 2015 at the Stockholmsmssan Exhibition and Convention Center in Stockholm, Sweden. The meeting will bring together approximately 4,000 stem cell scientists, bioethicists, clinicians and industry professionals from over 50 countries to present and discuss the latest discoveries and technologies within the field.

"The ISSCR is excited to bring its annual meeting to Stockholm, a city that shares our passion and reputation for great scientific research and collaboration," said ISSCR President Rudolf Jaenisch, M.D., Whitehead Institute for Biomedical Research. "We look forward to learning more about the strong work being done in Sweden and across Europe."

The meeting will open with the Presidential Symposium on June 24 from 1:15-3:15 p.m. local time. The symposium sets the stage for the meeting with world renowned speakers, including Nobel Prize winner Shinya Yamanaka. It is also the platform for the formal recognition of the 2015 recipients of the McEwen Award for Innovation and the ISSCR Public Service Award. Another prestigious award, the ISSCR-BD Biosciences Outstanding Young Investigator Award, will be presented during Plenary VI on June 27 from 9-11:20 a.m. and followed by an award lecture.

"I look forward to the Presidential Symposium setting the tone for the entire program," Jaenisch said. "A thread throughout will be the use of stem cells to drive our understanding of development and disease, as we explore disease modeling, gene and tissue engineering technologies and other important advances that are bringing stem cells into the clinic."

Presidential Symposium speakers will include:

Fred H. Gage, Ph.D., Salk Institute for Biological Sciences, U.S.

Jrgen Knoblich, Ph.D., Institute of Molecular Biotechnology, Austria

Shinya Yamanaka, M.D., Ph.D., Center for iPS Cell Research & Application, Japan

Jeannie Lee, M.D., Ph.D., Massachusetts General Hospital, U.S.

The McEwen Award for Innovation award winners (Presidential Symposium):

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MS stem cell treatment hailed 'miraculous' as patients make dramatic recovery

Posted: March 10, 2015 at 2:40 am

Pioneering treatment has allowed wheelchair-bound patients to run again Patient given high dose of chemotherapy to wipe out faulty immune system Therapy then uses person's own stem cells to fight the devastating disease It may be the first ever treatment tosuccessfullyreverse symptoms of MS

By Fiona Macrae for the Daily Mail

Published: 13:27 EST, 1 March 2015 | Updated: 02:54 EST, 2 March 2015

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Britons left wheelchair-bound by multiple sclerosis can walk, run and even dance again after being given a pioneering stem cell treatment.

Doctors have described the recoveries as miraculous, while patients say they have been given their lives back.

The treatment uses a patients own stem cells the bodys master cells to fight the disease.

Recovery: MS sufferer Holly Drewerybecame wheelchair-bound after the birth of daughter Isla, but thanks tothe stem cell transplant shecan dance, run and chase after Isla in the park

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