Stem Cell Therapy Network
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By: Stem Cell Therapy Network

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Stem Cell Therapy Network - Video

Lindsey Caldwell

Heart disease is the leading cause of death among Americans. Recently the bio-tech industry has been exploding with cardiac research like last week's heart attack preventing nanobots. New research by the team at the University of California, Berkley has created working human heart cells on a tiny chip designed to test the efficacy of new drugs in clinical trials. This heart-on-a-chip is officially known as a cardiac microphysiological system, or MPS. Using this heart-on-a-chip, scientists can measure the potential cardiac damage of a drug before it reaches expensive human trials.

Drug trials can take years, and to mitigate risk these drugs undergo testing in non-human subjects. Animals are often used in place of humans, but animal models can be problematic. Specifically, they are less effective at predicting cardiotoxicity, wherein a drug damages the heart. This is important because one-third of drugs withdrawn from testing are pulled due to cardiotoxic effects.

Drugs that are first tested in animal models can succeed to future testing stages without setting off alarms. After successful early stages more time and money is invested and the drugs progress to human trials, only to be stopped in their tracks because they are found to be toxic to human hearts.

The cells on this tiny MPS chip are human heart cells that were created from pluripotent stem cells. These cells react to drugs the same way as a human heart inside a living person. By creating a portable, low-risk, and accurate drug testing environment, scientists may be able to advance clinical trials of new drugs and bring them to market sooner.

Here is a video by the UC Berkley research team of their heart cells actually beating.

Source: Berkeley

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Heart-on-a-chip tests drugs cardiotoxicity with its real heartbeat

Orphan Designation Provides 7-Year Post Approval Marketing Exclusivity, Tax Credits and Elimination of FDA Prescription Drug User Fees

SAN DIEGO, CA--(Marketwired - February 10, 2015) - Targazyme Inc., a clinical-stage biopharmaceutical company developing enzyme technologies and products to improve efficacy outcomes for stem cell transplantation, immunotherapy, gene therapy and regenerative medicine, announced today that the U.S. Food and Drug Administration (FDA) has granted Orphan Drug designation to TZ101 to prevent and reduce the severity and incidence of graft vs. host disease (GVHD) in patients eligible for hematologic stem cell transplant.

GVHD is a serious, life-threating complication of stem cell transplantation.Orphan drug status confirms the importance of Targazyme's novel treatment approach to prevent and reduce the incidence and severity of GVHD in patients with blood cancers where stem cell transplant is prescribed.TZ101 could potentially transform hematopoietic stem cell transplantation by reducing patient morbidity and mortality from GVHD, which occurs in a large percentage of these patients and is very difficult to manage clinically.

"Our work with TZ101 demonstrates impressive increases in the persistence and activity of regulatory T cells in preclinical models of GVHD," said Dr. Elizabeth J. Shpall, Deputy Chair of the Department of Stem Cell Transplantation and Cellular Therapy at The University of Texas MD Anderson Cancer Center."We are looking forward to beginning clinical trials on this promising modality for preventing GVHD in our patients undergoing stem cell transplantation."

Orphan Drug Designation by FDA confers financial benefits and incentives, such as potential Orphan Drug grant funding to defray the cost of clinical testing, tax credits for the cost of clinical research, a 7 year period of exclusive marketing after Approval and a Waiver of Prescription Drug User Fee Act (PDUFA) filing fees which are now greater than $2 million.

"The granting of Orphan Drug status for TZ101 for prevention of GVHD in stem cell transplant patients, as well as our previous Orphan Drug designation of TZ101 for cord blood transplantation, provides additional validation of our innovative platform technologies," said Lynnet Koh, Chairman & Chief Executive Officer of Targazyme."TZ101 and our second product, TZ102 are enabling technologies for improving efficacy outcomes for multiple cell-based therapeutic approaches used to prevent and treat a variety of different diseases for which there is a high unmet medical need.In addition to initiating our registration trial with TZ101 in hematopoietic stem cell transplantation, we plan to embark on our cancer immunotherapy trial later this year."

About Targazyme, Inc.

Targazyme Inc. is a San Diego-based, clinical-stage biopharmaceutical company developing novel enzyme-based platform technologies and products to improve clinical efficacy outcomes for stem cell medicine, auto-immunotherapy, gene therapy and regenerative medicine.

The company's clinical-grade fucosyltransferase enzymes and small molecule products (TZ101 and TZ102) are off-the-shelf products used at the point-of-care to treat therapeutic cells immediately before infusion into the patient using a simple procedure that is easily incorporated into existing medical practice.The company has received a number of world-wide patents, multiple FDA orphan drug designations and major medical/scientific awards and grants.

Targazyme has partnerships and collaborations with Kyowa Hakko Kirin and Florida Biologix, as well as various medical research institutions including The University of Texas MD Anderson Cancer Center, Oklahoma Medical Research Foundation, Texas Transplant Institute, Case Western/University Hospitals, Scripps Hospitals, Fred Hutchinson Cancer Research Center, UCLA Medical Center, Stanford University Medical Center, University of Minnesota Medical Center, University of California San Diego, Sanford-Burnham Medical Research Institute, Indiana University, Memorial Sloan Kettering Cancer Center, and New York Blood Center.For more information please go to http://www.targazyme.com.

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Targazyme Inc. Receives Orphan Drug Designation to TZ101 for Use With Regulatory T Cells to Prevent & Reduce the ...

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.

Microfluidic channels on either side of the cell area serve as models for blood vessels, mimicking the exchange by diffusion of nutrients and drugs with human tissue. In the future, this setup could also allow researchers to monitor the removal of metabolic waste products from the cells.

"This system is not a simple cell culture where tissue is being bathed in a static bath of liquid," said study lead author Anurag Mathur, a postdoctoral scholar in Healy's lab and a California Institute for Regenerative Medicine fellow. "We designed this system so that it is dynamic; it replicates how tissue in our bodies actually gets exposed to nutrients and drugs."

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Bioengineers put human hearts on a chip to aid drug screening

WATERTOWN, Conn. (AP) A year ago, Nancy Demers, 71, was diagnosed with myelodysplastic syndrome, a deficiency in the bone marrow. The disease can eventually become leukemia.

Its treated as if it were cancer but there is no cure for it, said her son, Scott Demers.

Now Nancy Demers has a new chance at life, thanks to advances in bone marrow stem cell transplants.

If I didnt do this, once I went out of remission its not if, its when I would go into acute leukemia and there will be nothing there to help me, Nancy Demers said. This will save my life and give me time.

Demers is one of a rapidly growing number of people looking to depend on strangers to donate marrow since she doesnt have a match within her family.

The rising number of patients seeking bone marrow has created new demands on registries that seek to match patient needs with willing donors.

Each sibling has a 25 percent chance of being a transplant match, according to Dr. Joseph Antin, chief and program director of the adult stem cell transplantation program at Dana Farber Brigham and Womens Hospital in Boston.

In the United States, about 30 percent of patients find a donor within their family, according to Be the Match. Those who dont must turn to international registries to find an unrelated donor.

Around 15 years ago, doctors couldnt do a transplant on anyone over the age of 50, according to Dr. Leslie Lehmann, clinical director of the Stem Cell Transplant Center at Dana Farber.

Its a big stress on the body, Lehmann said.

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Registries seek to match donors with rising marrow demand

Testing breast cancer cells for how closely they resemble stem cells could identify women with the most aggressive disease, a new study suggests.

Researchers found that breast cancers with a similar pattern of gene activity to that of adult stem cells had a high chance of spreading to other parts of the body.

Assessing a breast cancer's pattern of activity in these stem cell genes has the potential to identify women who might need intensive treatment to prevent their disease recurring or spreading, the researchers said.

Adult stem cells are healthy cells within the body which have not specialised into any particular type, and so retain the ability to keep on dividing and replacing worn out cells in parts of the body such as the gut, skin or breast.

A research team from The Institute of Cancer Research, London, King's College London and Cardiff University's European Cancer Stem Cell Research Institute identified a set of 323 genes whose activity was turned up to high levels in normal breast stem cells in mice.

The study is published today (Wednesday) in the journal Breast Cancer Research, and was funded by a range of organisations including the Medical Research Council, The Institute of Cancer Research (ICR), Breakthrough Breast Cancer and Cancer Research UK.

The scientists cross-referenced their panel of normal stem cell genes against the genetic profiles of tumours from 579 women with triple-negative breast cancer - a form of the disease which is particularly difficult to treat.

They split the tumour samples into two categories based on their 'score' for the activity of the stem cell genes.

Women with triple-negative tumours in the highest-scoring category were much less likely to stay free of breast cancer than those with the lowest-scoring tumours. Women with tumours from the higher-scoring group had around a 10 per cent chance of avoiding relapse after 10 years, while women from the low-scoring group had a chance of around 60 per cent of avoiding relapse.

The results show that the cells of aggressive triple-negative breast cancers are particularly 'stem-cell-like', taking on properties of stem cells such as self-renewal to help them grow and spread. They also suggest that some of the 323 genes could be promising targets for potential cancer drugs.

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'Stem cell' test could identify most aggressive breast cancers

IMAGE:Induced pluripotent stem cell-derived motor neurons from an ALS patient (left) compared with normal cells (right). The cells are being used to study the role of the genes TBK1 and... view more

NEW YORK, NY (February 19, 2015)--Using advanced DNA sequencing methods, researchers have identified a new gene that is associated with sporadic amyotrophic lateral sclerosis (ALS), or Lou Gehrig's disease. ALS is a devastating neurodegenerative disorder that results in the loss of all voluntary movement and is fatal in the majority of cases. The next-generation genetic sequencing of the exomes (protein-coding portions) of 2,874 ALS patients and 6,405 controls represents the largest number of ALS patients to have been sequenced in a single study to date.

Though much is known about the genetic underpinnings of familial ALS, only a handful of genes have been definitively linked to sporadic ALS, which accounts for about 90 percent of all ALS cases. The newly associated gene, called TBK1, plays a key role at the intersection of two essential cellular pathways: inflammation (a reaction to injury or infection) and autophagy (a cellular process involved in the removal of damaged cellular components). The study, conducted by an international ALS consortium that includes scientists and clinicians from Columbia University Medical Center (CUMC), Biogen Idec, and HudsonAlpha Institute for Biotechnology, was published today in the online edition of Science.

"The identification of TBK1 is exciting for understanding ALS pathogenesis, especially since the inflammatory and autophagy pathways have been previously implicated in the disease," said Lucie Bruijn, PhD, Chief Scientist for The ALS Association. "The fact that TBK1 accounts for one percent of ALS adds significantly to our growing understanding of the genetic underpinnings of the disease. This study, which combines the efforts of over two dozen laboratories in six countries, also highlights the global and collaborative nature of ALS research today.

"This study shows us that large-scale genetic studies not only can work very well in ALS, but that they can help pinpoint key biological pathways relevant to ALS that then become the focus of targeted drug development efforts," said study co-leader David B. Goldstein, PhD, professor of genetics and development and director of the new Institute for Genomic Medicine at CUMC. "ALS is an incredibly diverse disease, caused by dozens of different genetic mutations, which we're only beginning to discover. The more of these mutations we identify, the better we can decipher--and influence--the pathways that lead to disease." The other co-leaders of the study are Richard M. Myers, PhD, president and scientific director of HudsonAlpha, and Tim Harris, PhD, DSc, Senior Vice President, Technology and Translational Sciences, Biogen Idec.

"These findings demonstrate the power of exome sequencing in the search for rare variants that predispose individuals to disease and in identifying potential points of intervention. We are following up by looking at the function of this pathway so that one day this research may benefit the patients living with ALS," said Dr. Harris. "The speed with which we were able to identify this pathway and begin our next phase of research shows the potential of novel, focused collaborations with the best academic scientists to advance our understanding of the molecular pathology of disease. This synergy is vital for both industry and the academic community, especially in the context of precision medicine and whole-genome sequencing."

"Industry and academia often do things together, but this is a perfect example of a large, complex project that required many parts, with equal contributions from Biogen Idec. Dr. Tim Harris, our collaborator there, and his team, as well as David Goldstein and his team, now at Columbia University, as well as our teams here at HudsonAlpha, said Dr. Myers. "I love this research model because it doesn't happen very frequently, and it really shows how industry, nonprofits, and academic laboratories can all work together for the betterment of humankind. The combination of those groups with a large number of the clinical collaborators who have been seeing patients with this disease for many years and providing clinical information, recruiting patients, as well as collecting DNA samples for us to do this study, were all critical to get this done."

Searching through the enormous database generated in the ALS study, Dr. Goldstein and his colleagues found several genes that appear to contribute to ALS, most notably TBK1 (TANK-Binding Kinase 1), which had not been detected in previous, smaller-scale studies. TBK1 mutations appeared in about 1 percent of the ALS patients--a large proportion in the context of a complex disease with multiple genetic components, according to Dr. Goldstein. The study also found that a gene called OPTN, previously thought to play a minor role in ALS, may actually be a major player in the disease.

"Remarkably, the TBK1 protein and optineurin, which is encoded by the OPTN gene, interact physically and functionally. Both proteins are required for the normal function of inflammatory and autophagy pathways, and now we have shown that mutations in either gene are associated with ALS," said Dr. Goldstein. "Thus there seems to be no question that aberrations in the pathways that require TBK1 and OPTN are important in some ALS patients."

The researchers are currently using patient-derived induced pluripotent embryonic stem cells (iPS cells) and mouse models with mutations in TBK1 or OPTN to study ALS disease mechanisms and to screen for drug candidates. Several compounds that affect TBK1 signaling have already been developed for use in cancer, where the gene is thought to play a role in tumor-cell survival.

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New ALS gene and signaling pathways identified

Orthopedic Stem Cell Therapy From Bone Marrow
Stem Cell therapy derived from bone marrow is the latest in modern orthopedic medicine to help you alleviate severe joint pain, and avoid invasive joint repl...

By: Cross Bay Physical Medicine and Rehabilitation, P.C.

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Orthopedic Stem Cell Therapy From Bone Marrow - Video

Using Stem Cell Therapy to Repair Damaged Tissue from Shoulder Impingement Syndrome
Board Certified Orthopedic Surgeon, Dr. Wade McKenna discusses how Stemnexa stem cell therapy and amniotic tissue product can aid in healing frayed shoulder ...

By: Riordan-McKenna Institute

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Using Stem Cell Therapy to Repair Damaged Tissue from Shoulder Impingement Syndrome - Video

Contrasto/eyevine

Biologist Graziella Pellegrini has worked on stem-cell therapy at four different Italian institutions, including a hospital run by priests.

Last month saw a major landmark for regenerative medicine: the first time that a stem-cell therapy beside the use of cells extracted from umbilical cords had been cleared for sale by any regulatory agency in the world. The European Commission approved Holoclar for use in cases of blindness caused by burning. The achievement is all the more remarkable because Holoclar was developed by a small laboratory in Italy, a country better known for its lack of support for life sciences and for its recent tolerance of an unproven stem-cell concoction, marketed by the Stamina Foundation, that claimed to be a panacea for many diseases. Nature talked to Graziella Pellegrini from the University of Modena about how she and her colleagues overcame the many obstacles to take the therapy from bench to bedside.

The surface of the cornea the transparent tissue that sits in front of the iris is constantly renewed in a healthy eye, to keep it smooth and clear. New corneal cells are generated from a niche of stem cells in the limbus, an area between the cornea and the white of the eye. But if the limbus is destroyed by burning, then the white of the eye grows over the cornea and becomes criss-crossed with blood vessels. This causes chronic pain and inflammation, as well as blindness.

I had seen patients who had starting seeing again after 20 years of blindness: how could I stop?

Holoclar treatment can help to reverse these symptoms by adding new stem cells to seed the regrowth of a transparent cornea. But there must be enough surviving limbus in one eye to allow 1 or 2 square millimetres of tissue to be extracted. This tissue is then cultivated on a support made from modified human fibrin (a biodegradable blood protein) under stringent clinical conditions until at least 3,000 stem cells have been generated. The culture, still on its fibrin scaffold, is transplanted into the injured eye, which has been scraped clear of the invading white, and from there stem cells seed the regrowth of a transparent cornea, free of blood vessels, within a year.

Only around 1,000 people annually in the whole of Europe will be eligible: burns victims who have become blind but whose eyes have not been too extensively destroyed.

It is always very hard to find research money in Italy. We had to uproot many times. I first started working on the concept of the therapy, with my colleague Michele De Luca, in 1990 when we were post-docs at the University of Genova studying the fundamental biology of epithelial cells the cells that form the sheets lining organs, and also the skin. In 1996, we moved to Rome to the Institute Dermopatico Immaculate, a hospital run by priests who were highly committed to research and who offered us wonderful facilities and access to patients. But in the end they did not want to support our eye work through to the clinic. So in 2002, we moved to the Veneto Eye Bank Foundation in Venice, which had an epithelial stem-cell laboratory. Then in 2008 we moved again, to the Centre for Regenerative Medicine Stefano Ferrari, which had been newly created at the University of Modena specifically to incubate such types of advanced therapy.

Italy is not supportive of biomedical research. Things might have been easier if we had not had to struggle so much. But I am Italian, and the best way to stimulate me to find a solution is to tell me I cant do something. And despite the problems, research into advanced therapies does have a history here. One of the worlds first gene-therapy trials on children with an immunodeficiency disorder was carried out in Milan.

We published the results of our first two patients both successes in 19971. That was proof of principle that the therapy could work. Our major clinical paper, on 112 patients, was published in 20102. Around 77% of the transplants were fully successful, and a further 13% partially successful.

Link:
Behind the scenes of the world's first commercial stem-cell therapy

THE contemporary age brings a lot of new things that leave people in awe, amazement, and sometimes, in disbelief and disagreement. One thing that the more advanced technology gave birth to is the controversial Stem Cell Therapy (SCT).

According to mayoclinic.org, SCT is the replacement of damaged or diseased stem cells by injecting or infusing healthy stems into your body.

An article from philstar.com also says that SCT replaces or supports ones degenerating tissues and organs. The stem cells used in this technology are capable of developing into different kinds of cells, thus, are also called master cells.

According to bethematch.org, the diseases that are treatable by SCT are leukemia, bone marrow diseases, inherited immune system disorders, and diseases with poorly functioning red blood cells.

SCT is also used as an anti-aging treatment. Some of the prominent Filipinos have used this therapy to maintain their youthful glow and energy.

In the Philippines, clinics offering SCT have sprouted like mushrooms due to its perceived benefits to the patients. In fact, Makati Medical Center has its Cellular Therapeutics Center, equipped with facilities from Germany, USA, and Japan.

In an article from makatimed.net, it was said that the center has an extensive range of services that boast the remarkable efficacy of stem cells.

Dr. Florencio Q. Lucero who started the use of adult SCT in the Philippines in 2006, was quoted in an article from inquirer.net saying that in the Philippines, most of the customers rich businessmen and public officials who are mostly males.

One of them is Manila Mayor Joseph Estrada. He had his SCT at a clinic in Germany called Villa Medica on April 2012. Another article from inquirer.net said that Estrada had 14 shots of blood from the donor animal, the unborn sheep, on his buttocks.

In the same article, Estrada was quoted saying he could sleep better, his knees are working better, and that his skin has shown its glow.

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Animal cells for a younger you

Albany, NewYork (PRWEB) February 27, 2015

ResearchMoz has announced the addition of a recent study that presents the analysis of the cell culture protein surface coating market across the globe. The research report discusses the current scenario and development prospects of the global cell culture protein surface coating industry for the period of 2015 to 2019.

Read Complete Report With TOC @ http://www.researchmoz.us/global-cell-culture-protein-surface-coating-market-2015-2019-report.html

The research report, titled Global Cell Culture Protein Surface Coating Market, offers an analytical study, providing an in-depth assessment of the industry based on market trends, growth drivers as well as challenges. This is done taking various segments of the market into consideration. The report also forecasts that the worldwide cell culture protein surface coating industry will expand at a CAGR of 12.91% during the forecast period of 2014 to 2019.

Cell culture protein surface coating is defined as the coating process wherein cell culture surfaces are covered with extra-cellular matrix elements or with protein to improve in-vitro linkage and propagation in the cells.

The various kinds of proteins that are available in our surroundings are synthetic proteins, human-derived proteins, plant-derived proteins, and animal-derived proteins. Fibronectin, collagen, laminin, osteopontin, and vitronectin are some of the proteins that are utilized for cell culture protein surface coating. Cell culture protein surface coating assists in the development of several kinds of cells such as epithelial, endothelial, fibroblasts, muscle cells and myoblasts, leukocytes, CHO cell lines, and neurons.

The wide range of applications for cell culture protein surface coatings consist of enhanced adhesion of cells, better propagation and development of cells, cell matrix studies, morphogenesis studies, receptor-ligand binding studies, signal transduction studies, genetic engineering, differentiation of individual cell types, drug screening, and metabolic pathway studies.

Stem cells have high potential for the treatment of severe diseases such as cardiac ailments, neuro degenerative diseases, and even diabetes. This fact has resulted in the increase in demand for highly developed cell culture products for stem cell manufacturing and studies. Cell culture protein surface coating offers enhanced adhesion, propagation, and rapid development of cells during the period of isolation and cultivation.

The main factor that is adding to the growth of the global cell culture protein surface coating industry is increased focus of top market players towards stem cell research. However, the drawbacks of animal-derived protein surface coating is a factor that is soon becoming a matter of concern, hindering the growth of the cell culture protein surface coating market.

Top players of the cell culture protein surface coating industry are EMD Millipore, Thermo Fisher Scientific, Becton, Dickinson and Company, Corning, and Sigma-Aldrich.

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Global Cell Culture Protein Surface Coating Industry: Rising Focus towards Stem Cells Research to Trigger Market Growth

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Newswise STRATFORD Paola Leone, PhD, the director of the Cell and Gene Therapy Center and a professor of Cell Biology at the Rowan University School of Osteopathic Medicine (RowanSOM), has been awarded a three-year, $477,000 grant from the National Institute of Neurological Disorders and Stroke (NINDS) to develop a stem cell-based therapy for Canavan disease, a rare but devastating neurological disorder in children that typically takes a childs life by age 10.

Canavan disease is a fatal, inherited disease caused by a mutation in the aspartaocylase gene, Dr. Leone explained. The disease is characterized by progressive and severe brain atrophy that manifests in delayed development, developmental regression, microcephaly, spasticity, seizures, visual impairment and short life expectancy. There, currently, is no treatment or cure for Canavan disease.

Under Dr. Leones direction, a team of RowanSOM researchers and students will examine the potential of stem cells for the treatment of Canavan disease in an animal model. This new study will build on the research teams preliminary data that demonstrated the successful engraftment of stem cells in animal models.

Our project will generate pre-clinical data to support the development of a stem-cell based therapy for Canavan disease, Dr. Leone said. It will also provide an important opportunity for a new generation of clinical researchers. Both undergraduate and graduate students will participate in this project, providing them with valuable experience to work with an extremely promising therapeutic intervention.

The symptoms of Canavan disease usually appear within the first six months of a childs life. The disease is caused by a genetic mutation that stops cells, called oligodendrocytes, from developing myelin, the fatty substance that coats the nerves in the brain. Without the protective myelin covering, the nerves do not form properly, causing the brain to atrophy. The preliminary research that Dr. Leone conducted showed that the engraftment of stem cells promoted significant recovery of the myelin sheath surrounding the nerves.

Our research represents a significant departure from other studies that have focused solely on strategies to augment the loss of the aspartaocylase function that is highly reduced in the brains of these patients, Dr. Leone said. We believe that any strategy seeking to treat Canavan must include a way to restore the myelin development that is disrupted in children with this disease.

This research is supported by the NINDS of the National Institutes of Health, under grant number 1R15NS088763-01A1.

Journalists wishing to speak with Dr. Leone, should contact Jerry Carey, Rowan University Media and Public Relations at 856-566-6171 or at careyge@rowan.edu.

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Rowan Researcher Targets Stem Cell-Based Therapy for Rare Childhood Disease

A scientific breakthrough gets gay groups all excited about the possibility of creating egg and sperm cells from parents of the same sex.

CAMBRIDGE: Scientists at the University of Cambridge in collaboration with the Weitzmann Institute in Israel successfully used skin from five adults to artificially create germ cells or stem cells, responsible for making sperm and eggs in the body.

According to The Daily Mail UK, Jacob Hanna, the specialist leading the projects Israeli arm claimed that the technique could be developed to create a baby, in just two years time.

They also reported Cambridge Universitys Professor Azim Surani as saying:We have succeeded in the first and most important step of this process, which is to show we can make these very early human stem cells in a dish.

The Daily Nation, however, explained that what the Cambridge researchers did was identify the gene which determined which cells would become sperm and egg, and harvested them by culturing them with human embryonic stem cells, for five days.

When an egg is fertilised by a sperm, they develop into foetus or the placenta. Some become stem cells, while others become germ cells and subsequently sperm and eggs. But this isnt the same as artificial sperm and eggs.

For now, Surani said the process would contribute to scientists understanding human genetics and diseases related to aging, as they discovered that one of the occurrences in germ cells included epigenetic mutations, where cell mistakes that occur with age, were wiped out so the cell is regenerated and reset.

The views expressed in the contents are those of our users and do not necessarily reflect the views of FMT.

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Scientists claim they can create babies for gay couples

Hepatology. Author manuscript; available in PMC 2011 May 1.

Published in final edited form as:

PMCID: PMC2925460

NIHMSID: NIHMS221023

Recent advances in induced pluripotent stem (iPS) cell research significantly changed our perspective on regenerative medicine. Patient specific iPS cells have been derived not only for disease modeling but also as sources for cell replacement therapy. However, there have been insufficient data to prove that iPS cells are functionally equivalent to hES cells or safer than hES cells. There are several important issues which need to be addressed and foremost are the safety and efficacy of human iPS cells from different origins. Human iPS cells have been derived mostly from cells originated from mesoderm, with a few cases from ectoderm. So far there has been no report of endoderm derived human iPS cells, preventing comprehensive comparative investigations on the quality of human iPS cells from different origins.

Here we show for the first time reprogramming of human endoderm derived cells (i.e. primary hepatocytes) to pluripotency. Hepatocyte-derived iPS cells appear indistinguishable from human embryonic stem cells in colony morphology, growth properties, expression of pluripotency-associated transcription factors and surface markers, and differentiation potential in embryoid body formation and teratoma assays. In addition, these cells were able to directly differentiate into definitive endoderm, hepatic progenitors, and mature hepatocytes. The technology to develop endoderm derived human iPS cell lines, together with other established cell lines, will provide a foundation to elucidate the mechanisms of cellular reprogramming and to study the safety and efficacy of differentially originated human iPS cells for cell therapy. For studying liver disease pathogenesis, this technology also provides a potentially more amenable system to generate liver disease specific iPS cells.

Recent advances in induced pluripotent stem (iPS) cell research have provided great potential for these somatic cell-derived stem cells as sources for cell replacement therapy and for establishing disease models.114 Human iPS cells have been shown to be pluripotent in in vitro differentiation and in vivo teratoma assays, similar to human embryonic stem (hES) cells.914 Disease-specific iPS cell lines have been generated from fibroblasts and blood cells and some of the disease features have been recapitulated in tissue culture after directed differentiation of the iPS cells, demonstrating the power of this technology in disease modeling.13,15 However, several key issues have to be addressed in order for the iPS cells to be used for clinical purposes. First, although pluripotency has been demonstrated, it is premature to claim that iPS cells are functionally equivalent to hES cells. In fact, one study has suggested that iPS cells have distinct protein-coding and microRNA gene expression signatures from ES cells.1 These differences can not be completely explained by the reactivation of transgenes used in the reprogramming process since human iPS cells generated without viral or transgene integration also displayed a different transcriptional signature compared to hES cells.2 Secondly it was demonstrated that human iPS cells retained certain gene expression of the parent cells, suggesting that iPS cells from different origins may possess different capacity to differentiate.2 This issue is important not only for the purposes of generating functional cell types for therapy but also for safety implications. A comprehensive study using various mouse iPS cells has demonstrated that the origin of the iPS cells had a profound influence on the tumor-forming propensities in a cell transplantation therapy model.3 Mouse tail-tip fibroblast-iPS cells (mesoderm origin) showed the highest tumorigenic propensity, whereas gastric epithelial cell- and hepatocyte-iPS cells (both are endoderm) showed lower propensities.3 It is therefore extremely important to establish human iPS cell lines from multiple origins and thoroughly examine the source impact on both the safety issues and their differentiation potentials. In addition, the ability to reprogram human hepatocytes is crucial for developing liver disease models using iPS cells, especially for certain liver diseases carrying acquired somatic mutations which occur only in hepatocytes of patients, but not in other cell types.1620

In the mouse, iPS cells have been generated from derivatives of all three embryonic germ layers, including mesodermal fibroblasts,6 epithelial cells of endodermal origin7 and ectodermal keratinocytes,8 whereas human iPS cells have been produced mostly from mesoderm (fibroblasts and blood cells) or from ectoderm (keratinocytes and neural stem cells).913,21,22 Here we show reprogramming of human primary hepatocytes (endoderm) to pluripotency. Hepatocyte-derived iPS cells appear indistinguishable from human embryonic stem cells in colony morphology, growth properties, expression of pluripotency-associated transcription factors and surface markers, and differentiation potential in embryoid body (EB) formation as well as teratoma assays. In addition these cells were able to directly differentiate into definitive endoderm, hepatic progenitors, and mature hepatocytes.

Our study lays the ground work necessary to elucidate the mechanisms of cellular reprogramming and to study the safety and efficacy of differentially originated human iPS cells in cell therapy.

Primary human hepatocytes were obtained from Lonza plated on collagen 1 and matrigel coated dishes, and cultured in serum containing WEM (Willians' Medium E), Gentamicin, Dexamethasone 10 mM, FBS 5%, L-Glutamine, Hepes 15mM, Insulin 4 mg/ml with 50ng/ml of HGF and EGF. Medium for culturing hES cells and iPS cells is Knockout DMEM supplemented with 20% KOSR, NEAA, 2-ME, GlutaMAX, 6 ng/ml basic fibroblast growth factor (all Invitrogen). hESC lines WA09 (H9) and WA01 (H1) (WiCell) were cultured on irradiated MEF feeder layers in ES medium. This study was done in accordance with Johns Hopkins ESCRO regulations and following a protocol approved by the Johns Hopkins IRB.

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Researchers from Cambridge University have shown for the first time that it is possible to make human egg and sperm cells using skin from two adults of the same sex.

The scientific breakthrough may lead to a baby being made in a dish from the skin cells of two adults of the same sex, bringing hope to gay people.

The project, funded by the Wellcome Trust, was achieved at Cambridge University with Israels Weizmann Institute of Science.

The scientists used stem cell lines from embryos as well as from the skin of five different adults.

Ten different donor sources have been used so far and new germ-cell lines have been created from all of them, researchers said.

A gene called SOX1 has turned out to be critical in the process of reprogramming human cells, according to a report in a national newspaper.

The details of the technique were published in the journal Cell.

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Cambridge university researchers' breakthrough paves way for same sex couple babies

Beverly Hills, CA (PRWEB) February 17, 2015

The top stem cell clinic in Los Angeles and Beverly Hills is now achieving 80% success with stem cell therapy for all types of arthritis and soft tissue indications. This includes hip, knee, shoulder, elbow and ankle injections for helping patients achieve pain relief and avoid surgery. Call (310) 438-5343 for more information on the treatment options available and scheduling.

Dr. Raj, who was recently named a Super Doc Southern California for the 4th year in a row, has been performing stem cell therapy on patients for years. This includes athletes, weekend warriors, celebrities, executives, senior citizens and students as well.

There are two methods offered for the treatment, one of which is Bone Marrow derived. This includes harvesting bone marrow from the patient's hip area, and then the material is immediately processed to concentrate the stem cells and growth factors. the fluid is then injected into the problem area. An internal review at Beverly Hills Orthopedic Institute has shown that 80% of patients achieve excellent pain relief and increased functional abilities. This includes getting back to athletics, recreational activities and walking more.

The second method of treatment involves amniotic derived stem cell rich injections. The amniotic fluid is processed at an FDA regulated lab, with no fetal tissue being involved and no embryonic stem cells at all. Amniotic fluid has been used tens of thousands of times worldwide for many indications, and contains growth factors, hyaluronic acid and stem cells.

Indications for the treatment include tennis and golfer's elbow, plantar fasciitis, degenerative arthritis of the hip, knee, shoulder, elbow, ankle, ligament injuries, and tendonitis of the shoulder, knee, achilles and more.

Dr. Raj is a Double Board Certified orthopedic doctor in Los Angeles and serves as an ABC News Medical Correspondent and a WebMD expert. He is called frequently by networks for his opinion on orthopedic matters, and is on the Medical Advisory Board for R3 Stem Cell.

For more information and scheduling with the top stem cell clinic in Los Angeles and Beverly Hills, call (310) 438-5343.

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Dr. Raj at Beverly Hills Orthopedic Institute Achieving 80% Success with Stem Cell Therapy

Hip arthritis 3.5 years after stem cell therapy by Harry Adelson, N.D.
Bobby describes his outcome 3.5 years after stem cell therapy for his arthritic hip by Harry Adelson, N.D. http://www.docereclinics.com.

By: Harry Adelson, N.D.

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Hip arthritis 3.5 years after stem cell therapy by Harry Adelson, N.D. - Video

Gut. 2007 May; 56(5): 716724.

Y N Kallis, Department of Medicine, St Mary's Hospital Campus, Imperial College, London, UK

M R Alison, Institute of Cell and Molecular Science, Queen Mary School of Medicine and Dentistry, London, UK

S J Forbes, Tissue Fibrosis and Remodelling Laboratory, MRC/University of Edinburgh Centre for Inflammation Research, Edinburgh, UK

Correspondence to: Professor S J Forbes MRC/University of Edinburgh Centre for Inflammation Research, The Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, UK; stuart.forbes@ed.ac.uk

Stem cells are present in a variety of organs including the bone marrow (BM). Their role is to replenish multiple mature differentiated cell types and thereby achieve longterm tissue reconstitution. Stem cells retain the capacity to generate progeny and renew themselves throughout life. Haematopoietic stem cells (HSCs) are the main stem cell population within the BM and give rise to all mature blood lineages via erythroid, myelomonocytic and lymphoid precursors. A second type of bone marrow stem cell (BMSC), the mesenchymal stem cell (MSC), forms stromal tissue and can give rise to cells of mesodermal origin.

A longstanding principle of cell biology has been that cell loss is reconstituted via stem cells resident within and specific to an organ. However, recent work suggests that this paradigm may not hold for all organs or all types of injury, and tissue damage may attract migratory stem cell populations, particularly those from the BM. This observation has caused considerable interest in the field of liver disease, where new strategies to restore hepatocyte number, augment liver function and counteract progressive organ fibrosis are required. This article will focus on the various relationships between BMSCs and liver disease. It will concentrate on the evidence from animal models and human studies that BMSCs may aid in the regeneration of liver cell populations and may also contribute to the pathogenesis of liver damage. It will discuss the potential to use BMSCs for therapeutic application and review the current status of clinical trials in patients with liver disorders.

The hepatic parenchyma is made up of hepatocytes and cholangiocytes. Unlike other organs such as the gut, liver cell mass is restored primarily through division of the majority of mature hepatocytes and not via a dedicated stem cell population. After a regenerative stimulus, such as a twothirds partial hepatectomy, most hepatocytes rapidly enter the cell cycle and undergo symmetrical mitosis. Liver cell mass can be restored via an average of less than two cell division cycles, albeit individual hepatocytes seem to have an intrinsic capacity for up to 70 doublings in serial transplantation experiments.1 At times of overwhelming cell loss, with longstanding iterative injury (eg, chronic viral hepatitis), or when hepatocyte replication is impeded (eg, replicative senescence of steatohepatitis), regeneration seems to occur via a second cell compartment.2,3 This compartment remains poorly defined and seems to arise from a less differentiated cell population within the terminal branches of the intralobular biliary tree the canals of Hering.4 In rodents these cells are called oval cells, but in humans they are more aptly named hepatic progenitor cells.5 Attempts to identify the originating stem cell are hampered by a paucity of specific cell surface markers.

Initial studies in humans suggested that some hepatocytes have a BM origin. Using Y chromosome tracking, a sparse number of hepatocytes seemed to be originating from the BM in male recipients of female orthotopic liver transplants, and in females who had received bone marrow transplantation (BMT) from male donors and thereafter developed liver disease.6,7 Similarly, other epithelial tissues, such as gut and skin, seemed to harbour cells of BM origin.8 Investigators then turned to an animal model of hereditary type I tryosinaemia, the fumarylacetoacetate hydrolase knockout mouse (FAH(/)), in which it seemed that this potentially fatal enzyme deficiency could be rescued through repopulation of the abnormal liver by BM cells derived from wildtype donors. The implication was that stem cells could cross conventionally demarcated lineage boundaries through a process termed transdifferentiation or stem cell plasticity, leading researchers to question the longheld tenets of cell biology. With time, it became apparent that these initial observations were difficult to reproduce, and later elegant studies in the same FAH(/) mouse model conclusively showed that monocytehepatocyte fusion was the explanation for the restored normal phenotype to the FAHdeficient liver, in which hepatocytes formed by fusion expanded rapidly owing to a considerable survival advantage.9,10

Unfortunately, in the absence of a strong selective pressure, it seems that stable longterm engraftment of BMderived parenchymal cells is unusual. In rats given inhibitors of hepatocyte replication (eg, dgalactosamine, retrorsine or 2acetylaminofluorene), if subjected to a regenerative stimulus such as a partial hepatectomy, BMderived oval cell engraftment can rapidly decrease with time to <1%.11 In the hepatitis B surface antigen transgenic mouse, the BM contributed to hepatocyte repopulation through cell fusion, but only at a very modest rate. In this model, constitutive HBsAg expression induces chronic lowgrade hepatocyte turnover with nodule formation, and inhibition of hepatocyte replication with retrorsine provokes an oval cell response. Here, the contribution from BMderived cells to hepatocyte repopulation waned to just 1.6% by 6months, presumably owing to lack of a sustained selection advantage.12 Likewise, when human HSCs were transplanted into carbon tetrachloride (CCl4)damaged nonobese diabetes/severe combined immune deficiency (NOD/SCID) mice, donorderived hepatocytes expressing mRNA for human albumin and 1 antitrypsin were found in the liver. These hepatocytes occurred through cell fusion, but the phenotype of the chimaeric cells was variable and donorderived genetic material was lost over time.13 When human cord blood, a rich source of progenitor cells, was transplanted into sublethally irradiated NOD/SCID mice, a contribution to the hepatocyte population of only 0.01% was found in the undamaged liver, reportedly through transdifferentiation.14 However, a subsequent study using human cord blood cells again demonstrated only low levels of hepatocyte repopulation even after CCl4induced or hepatocyte growth factor (HGF)induced regeneration. Here the cells were chimaeric for both human and mouse antigens, suggesting that cell fusion rather than transdifferentiation had occurred.15

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Bone marrow stem cells and liver disease - National Center ...

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...

By: MSSocietyCanada

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FAQ Part 1: MEsenchymal Stem cell therapy for CAnadian MS patients (MESCAMS) - Video