Starting with the first-ever production of induced pluripotent stem cells (iPS cells) in 2006, cell reprogramming - the genetic conversion of cells from one type to another - has revolutionized stem cell research and opened the door to countless new medical applications. Inducing such reprogramming, however, is difficult, inefficient and time-consuming, involving a largely hit-or-miss process of selecting candidate genes.

In the current study, the OSC research team explored an alternative to iPS cells based on the use of transcriptional regulatory networks (TRNs), networks of transcription factors and the genes they regulate. Previous research by the team characterized the dynamic regulatory activities of such transcription factors during cellular differentiation from immature cell (monoblast) to developed (monocyte-like) cell using human acute monocytic leukemia cell lines (THP-1). Their findings led them to hypothesize that functional characteristics of the cell-type are maintained by its specific TRN.

Their new paper builds on this hypothesis, establishing a series of new methods for identifying transcription factors (TFs) for the monocyte network, which play a key role in inducing cell-specific functions. Four core TF genes of the monocyte TRN, identified using this approach, were introduced into human fibroblast cells, expression of which activated monocytic functions including phagocytosis, inflammatory response and chemotaxis. Genome-wide gene expression analysis of this reprogrammed cell showed monocyte-like gene expression profile, demonstrating that reconstruction of a functional TRN can be achieved by introducing core TRN elements into unrelated cell types.

Published in the journal PLoS ONE, the newly-developed methods open the door to a new form of direct cell reprogramming for clinical use which avoids the pitfalls of embryonic stem (ES) and induced pluripotent stem (iPS) cells, charting a course toward novel applications in regenerative medicine and drug discovery.

Provided by RIKEN (news : web)

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Study demonstrates cells can acquire new functions through transcriptional regulatory network

Doctor Wise Young in Hong Kong on February 22, 2012. Young, a leading researcher in spinal cord injuries, says China could hold the key to a cure that he has been searching for since he met late actor Christopher Reeve in the 1990s. AFP pic

US-based Doctor Wise Young first used the word cure in relation to his work after a conversation with Reeve, the Superman hero who became quadriplegic in an equestrian accident in 1995.

Reeve contacted him looking for help and the two became close friends. The actor died of heart failure in 2004 at the age of 52, having devoted his life to raising awareness about spinal cord injuries and stem-cell research.

But it was a star of a different sort, Chinese gymnast Sang Lan, who set Young on the path he believes has brought a cure closer than ever, thanks to ground-breaking clinical trials of stem-cell therapy he is conducting in China.

Everybody assumed that Im doing this in China because I wanted to escape George W. Bush, but thats not the case at all, Young said in an interview, recalling the former US presidents 2001 decision to effectively stop Federal funding of embryonic stem cell research.

I started the clinical trials in 2005 here in Hong Kong ... mainly because of a promise that I made to a young woman. Her name is Sang Lan.

Sang crushed her spine during a routine warm-up exercise at the Goodwill Games in New York in 1998. She met Young as she underwent treatment and rehabilitation in the United States over the next 12 months.

Her parents came to me and asked whether or not there would ever be a cure for her, and I said were working very hard on it, recalled Young, who was by then one of the leading US experts on spinal cord injuries.

When she went back to China after doing her rehabilitation in New York she cried and asked how would therapies go from the United States to China.

In those days China was still relatively poor and backward so she didnt think that any therapy would be coming from China. So I started in 1999 to talk to all the spinal cord doctors in China.

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Doctor looks to China for spinal injury ‘cure’

WASHINGTON, March 13, 2012 /PRNewswire/ -- TEDMED, http://www.TEDMED.com, the annual gathering where science, medical and technology leaders focus on "imagination, innovation and inspiration" to advance the art of health and medicine, today announced two new programs that will vastly increase the size and scope of its audience.

TEDMED is the world's only TED-licensed event focused solely on innovation and breakthrough thinking across all of health and medicine. It will be held at the John F. Kennedy Center for the Performing Arts in Washington, D.C., April 10 - 13.

Speakers, attendee-Delegates and participants will range from biologists (Dr. E.O. Wilson) and writers (Ben Goldacre), to physicists (Albert-Laszlo Barabasi) and public health leaders like the director of the National Institutes of Health (Dr. Francis Collins). Topics to be explored by TEDMED speakers will include neuroscience, microbiology, surgery, oncology, stem cell therapy, bad science, Alzheimer's, robotics, game science, wearable tech, disease evolution, patient choice, virtual anatomy models, the nature of imagination, and dozens more.

For the first time this year, TEDMED will offer a free simulcast, TEDMEDLive, to teaching hospitals, medical schools, research institutions, university life science departments, state and federal government agencies, health-oriented corporations and non-profits across the nation. Participants, forecasted at more than 50,000, will be able to view a high-definition live stream of each presentation and performance. Using the TEDMED Connect mobile app, remote participants can also ask questions of the speakers in real time, which may be answered directly from the TEDMED stage.

Over 2,000 TEDMEDLive simulcast locations will participate, including institutions such as: Case Western Reserve University, Harvard University, University of California (Davis and Irvine), University of Pennsylvania, University of Washington, University of Virginia, Tulane University, Vanderbilt University and Yale University.

Another new TEDMED initiative is the Front-Line Scholarship Program, which offers up to $2 million in half- and full-fee scholarships to those leaders and innovators who are on the front lines of health and medicine. It assists those who would both contribute to the TEDMED conference as attendees, and would greatly benefit from joining the conference in Washington, D.C. in person as a Delegate. The Front-Line Scholarship Program is underwritten by the TEDMED Patron Fund, whose major contributors include Humana and The California Endowment.

"TEDMED is for everyone who is passionate about the future of health and medicine," said Jay Walker, curator of TEDMED."Accordingly, TEDMED is committed to bringing even more expertise and perspective to the table for a national discussion of health and medicine, regardless of ability to pay through our Front-Line Scholarship program. Front-Line Scholarships will permit the broadest possible group of healthcare providers, first responders and other contributors to attend so they can share even more ideas that will save lives."

More than 1,200 TEDMED onsite attendees including researchers, physicians, technologists and policy experts will foster cross-disciplinary collaboration and learning at the Kennedy Center this April. Institutions of excellence represented by speakers and attendees will include The American Cancer Society, The American Red Cross, Biodigital Systems, The Boulis Laboratory, Brandeis University, Brigham and Women's Hospital, The California Institute of Technology, Center for Complex Network Research, The Centers for Disease Control and Prevention, Duke University, Emory University, Harvard University, mc10, Methodist Institute for Technology, Innovation, and Education, The National Institutes of Health, New York University, Penn State University, Quest Diagnostics, The Center for Alzheimer Research and Treatment, Reuters Health, Children's Hospital Boston, The U.S. Department of Health and Human Services, and the Young Professionals Chronic Disease Network.

TEDMED Speaker List (as of 3/12/2012)

Additional speakers will be announced prior to the conference start date.

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TEDMED 2012 Conference Offers $2 Million in Scholarships to Health and Medicine Leaders and Innovators; Free National ...

Public release date: 13-Mar-2012 [ | E-mail | Share ]

Contact: David Sampson ajpmedia@elsevier.com 215-239-3171 Elsevier Health Sciences

Philadelphia, PA, March 13, 2012 A new study suggests that administering FTY720, an oral drug that has shown promise in trials for human multiple sclerosis, significantly improves locomotor recovery in mice with spinal cord injury (SCI). The research suggests a possible new avenue to counteract the degeneration of the spinal cord in human SCI. The study will be published in the April 2012 issue of The American Journal of Pathology.

Beyond the initial tissue damage, much of the degradation of the spinal cord in SCI is due to a cascade of secondary injuries, including neuronal and glial apoptosis, inflammation, glial scar formation, local edema and ischemia, and oxidative stress. The aim of current SCI treatment is to counteract the mechanisms of secondary injury and prevent their pathological consequences, because central nervous system (CNS) neurons have very limited capacity to self-repair and regenerate.

Researchers from the Jichi Medical University School of Medicine and the Graduate School of Medicine at the University of Tokyo had previously shown that the concentration of the lysophospholipid mediator, sphingosine 1-phosphate (S1P), was significantly increased in the location of a contusion injury, triggering the migration of neural progenitor/stem cells to the site of the injury. They hypothesized that targeting S1P receptors may become a candidate therapy for various refractory central nervous system disorders, including SCI.

FTY720 acts as a broad S1P receptor modulator. Its efficacy in central nervous system disorders is believed to derive from immunomodulation. Researchers found that orally administering FTY720 to mice shortly after contusion SCI significantly improved motor function recovery. Importantly, they found that the therapeutic effects of FTY720 were not solely dependent on immune modulation. The administration of FTY720 induced lymphopenia, clearing lymphocytes from the blood, and reduced T-cell infiltration in the spinal cord. But it did not affect the early infiltration of neutrophils and activation of microglia, and it did not reduce plasma levels and mRNA expression of inflammatory cytokines in the spinal cord. Tests in mice with severe combined immunodeficiency (SCID mice) with SCI found that FTY720 significantly improved recovery of hind limb motor function.

"These data clearly indicate the importance of immune-independent functions of FTY720 in the amelioration of functional deficits after SCI in mice," explains lead investigator Yoichi Sakata, MD, PhD, Research Division of Cell and Molecular Medicine, Center for Molecular Medicine, Jichi Medical University School of Medicine.

Dr. Sakata notes that S1P receptors exist in many types of cells and play a role in many cellular processes. "We observed that FTY720 decreased vascular permeability and astrocyte accumulation in injured spinal cord. These changes were also noted in SCID mice, suggesting they are not dependent on lymphocyte function. Increased vascular permeability can lead to destruction of the blood-brain barrier in spinal cord, and astrocyte accumulation is the main cellular component of glial scar after CNS injury. FTY720 might counteract these secondary injuries and thereby prevent their pathological consequences."

"Our data suggest that targeting S1P receptors with FTY720 is an attractive therapeutic approach for SCI," Dr. Sakata concludes. "However, further evaluation utilizing larger animals such as non-human primates will be necessary to confirm its efficacy in treating SCI. Further, strategies targeted at modulating the SIP concentration in injured CNS may lead to new therapeutic approaches towards repairing various CNS disorders."

###

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Research suggests new therapeutic approach for spinal cord injury

12-03-2012 20:48 by:www.medicaltourism.hk

Originally posted here:
Chia medical tourism--stroke--stem cell therapy 1.flv - Video

12-03-2012 21:11 by:www.medicaltourism.hk

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Chia medical tourism--stroke--stem cell therapy 3.flv - Video

LOS ANGELES Researchers at the UCLA stem cell center and the departments of chemistry and biochemistry and pathology and laboratory medicine have identified, for the first time, a generic way to correct mutations in human mitochondrial DNA by targeting corrective RNAs, a finding with implications for treating a host of mitochondrial diseases.

Mutations in the human mitochondrial genome are implicated in neuromuscular diseases, metabolic defects and aging. There currently are no methods to successfully repair or compensate for these mutations, said study co-senior author Dr. Michael Teitell, a professor of pathology and laboratory medicine and a researcher with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

Between 1,000 and 4,000 children per year in the United States are born with a mitochondrial disease and up to one in 4,000 children in the U.S. will develop a mitochondrial disease by the age of 10, according to Mito Action, a nonprofit organization supporting research into mitochondrial diseases. In adults, many diseases of aging have been associated with defects of mitochondrial function, including diabetes, Parkinson's disease, heart disease, stroke, Alzheimer's disease and cancer.

"I think this is a finding that could change the field," Teitell said. "We've been looking to do this for a long time and we had a very reasoned approach, but some key steps were missing. Now we have developed this method and the next step is to show that what we can do in human cell lines with mutant mitochondria can translate into animal models and, ultimately, into humans."

The study appears today in the peer-reviewed journal Proceedings of the National Academy of Sciences.

The current study builds on previous work published in 2010 in the peer-reviewed journal Cell, in which Teitell, Carla Koehler, a professor of chemistry and biochemistry and a Broad stem cell research center scientist, and their team uncovered a role for an essential protein that acts to shuttle RNA into the mitochondria, the energy-producing "power plant" of a cell.

Mitochondria are described as cellular power plants because they generate most of the energy supply within a cell. In addition to supplying energy, mitochondria also are involved in a broad range of other cellular processes including signaling, differentiation, death, control of the cell cycle and growth.

The import of nucleus-encoded small RNAs into mitochondria is essential for the replication, transcription and translation of the mitochondrial genome, but the mechanisms that deliver RNA into mitochondria have remained poorly understood.

The study in Cell outlined a new role for a protein called polynucleotide phosphorylase (PNPASE) in regulating the import of RNA into mitochondria. Reducing the expression or output of PNPASE decreased RNA import, which impaired the processing of mitochondrial genome-encoded RNAs. Reduced RNA processing inhibited the translation of proteins required to maintain the mitochondrial electron transport chain that consumes oxygen during cell respiration to produce energy. With reduced PNPASE, unprocessed mitochondrial-encoded RNAs accumulated, protein translation was inhibited and energy production was compromised, leading to stalled cell growth.

The findings from the current study provide a form of gene therapy for mitochondria by compensating for mutations that cause a wide range of diseases, said study co-senior author Koehler.

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Repairing mutations in human mitochondria

12-03-2012 17:41 Dr.Mark Newkirk is once again on the cutting edge of medicine. Newkirk Family Veterinarians now offer STEM CELL THERAPY for pets. Dr. Mark Newkirk combines traditional medicine and surgery with Holistic Alternatives to access the best of both worlds. As a Veterinarian, Dr. Newkirk has been serving Southern New Jersey for over 25 years. He is extensively trained in medicine and surgery and also is skilled in the care of exotic pets such as reptiles and birds. Dr. Newkirk is also one of only 5 doctors in the country currently undergoing training by the nationally renowned Dr. Martin Goldstein, the author of "The Nature of Animal Healing", and founder of immuno-augmentative therapy for animals, a true alternative cancer therapy. Dr. Newkirk is a member of American Holistic Veterinary Medical Society, the American Veterinary Medical Association, New Jersey Veterinary Medical Association and the Colorado Veterinary Medical Association. For more information check out Stem Cell Therapy on The Animal Planet's dogs 101 http://www.youtube.com

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Stem Cell Therapy at Newkirk Family Veterinarians - Hunter's Story - Video

Public release date: 12-Mar-2012 [ | E-mail | Share ]

Contact: Sarah Jackson press_releases@the-jci.org 919-684-0620 Journal of Clinical Investigation

EDITOR'S PICK Restoring what's lost: uncovering how liver tissue regenerates

The liver is unique among mammalian organs in its ability to regenerate after significant tissue damage or even partial surgical removal. Laurie DeLeve and her colleagues at the University of Southern California in Los Angeles wanted to better understand which cells are specifically responsible for driving liver regeneration. A specialized cell type, known as liver sinusoidal endothelial cells, has generally been thought to promote regeneration of liver tissue. However, the DeLeve team suspected that stem cells and progenitor cells, which have the capacity to differentiate into mature cell types, might be responsible for stimulating liver regeneration by generating hepatocyte growth factor. Using a rat model system, they first identified the presence of stem and progenitor cells that give rise to liver sinusoidal endothelial cells in both the liver and the bone marrow. They next sought to determine which population of stem and progenitor cells are required for regeneration. DeLeve and colleagues found that the bone marrow-derived cells were not required for liver cell proliferation in the absence of damage. In contrast, following surgical removal of a portion of the rat liver, an infusion of bone marrow-derived progenitor cells was required for liver regeneration. These results improve our understanding of how liver tissue can regenerate following damage and may shed light on liver complications in patients with suppressed bone marrow tissue.

TITLE: Liver sinusoidal endothelial cell progenitor cells promote liver regeneration in rats

AUTHOR CONTACT: Laurie D. DeLeve University of Southern California Keck School of Medicine, Los Angeles, CA, USA Phone: 323-442-3248; Fax: 323-442-3238; E-mail: deleve@usc.edu

View this article at: http://www.jci.org/articles/view/58789?key=21e2857b21106f232595

ONCOLOGY New Determinant of Human Breast Cancer Metastasis Discovered

Researchers at the University of Kentucky's Markey Cancer Center in Lexington, KY have provided new insight as to why the most severe subtype of breast cancer in humans frequently metastasizes. Tumor cells can exploit a cellular program that promotes cell migration and reduces adhesion between cells to spread to distant sites in the body (metastasis). This cellular program, known as the epithelial-mesenchymal transition, is normally restricted to wound healing, tissue remodeling and embryonic development. Increasing cell motility requires a decrease in E-cadherin, which functions to promote cell-cell adhesion. Led by Binhua Zhou, the research team identified G9a as a major repressor of E-cadherin expression. They found that G9a interacts with Snail, which can repress gene expression, to modify the E-cadherin promoter and block expression of the E-cadherin gene. Their findings establish that G9a is an important determinant of metastasis in the most severe sub-type of breast cancer, and suggest the development of new therapeutics targeting this pathway could potentially disrupt the metastatic disease.

TITLE: G9a interacts with Snail and is critical for Snail-mediated E-cadherin repression in human breast cancer

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JCI early table of contents for March 12, 2012

Public release date: 12-Mar-2012 [ | E-mail | Share ]

Contact: Sarah Jackson sarah.jackson@the-jci.org 919-684-0620 Journal of Clinical Investigation

The liver is unique among mammalian organs in its ability to regenerate after significant tissue damage or even partial surgical removal. Laurie DeLeve and her colleagues at the University of Southern California in Los Angeles wanted to better understand which cells are specifically responsible for driving liver regeneration. A specialized cell type, known as liver sinusoidal endothelial cells, has generally been thought to promote regeneration of liver tissue. However, the DeLeve team suspected that stem cells and progenitor cells, which have the capacity to differentiate into mature cell types, might be responsible for stimulating liver regeneration by generating hepatocyte growth factor. Using a rat model system, they first identified the presence of stem and progenitor cells that give rise to liver sinusoidal endothelial cells in both the liver and the bone marrow. They next sought to determine which population of stem and progenitor cells are required for regeneration. DeLeve and colleagues found that the bone marrow-derived cells were not required for liver cell proliferation in the absence of damage. In contrast, following surgical removal of a portion of the rat liver, an infusion of bone marrow-derived progenitor cells was required for liver regeneration. These results improve our understanding of how liver tissue can regenerate following damage and may shed light on liver complications in patients with suppressed bone marrow tissue.

###

TITLE: Liver sinusoidal endothelial cell progenitor cells promote liver regeneration in rats

AUTHOR CONTACT: Laurie D. DeLeve University of Southern California Keck School of Medicine, Los Angeles, CA, USA Phone: 323-442-3248; Fax: 323-442-3238; E-mail: deleve@usc.edu View this article at: http://www.jci.org/articles/view/58789?key=21e2857b21106f232595

AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert! system.

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Restoring what's lost: Uncovering how liver tissue regenerates

Published: March 12, 2012

(NEW YORK, NY, March 11, 2012) A study by Columbia researchers suggests that cells in the patients intestine could be coaxed into making insulin, circumventing the need for a stem cell transplant. Until now, stem cell transplants have been seen by many researchers as the ideal way to replace cells lost in type I diabetes and to free patients from insulin injections.

The researchconducted in micewas published 11 March 2012 in the journal Nature Genetics.

Type I diabetes is an autoimmune disease that destroys insulin-producing cells in the pancreas. The pancreas cannot replace these cells, so once they are lost, people with type I diabetes must inject themselves with insulin to control their blood glucose. Blood glucose that is too high or too low can be life threatening, and patients must monitor their glucose several times a day.

Gut insulin cells express glucokinase, a key enzyme for glucose processing. Immunostaining detected insulin in red and glucokinase in green. Yellow marked merged colors.

A longstanding goal of type I diabetes research is to replace lost cells with new cells that release insulin into the bloodstream as needed. Though researchers can make insulin-producing cells in the laboratory from embryonic stem cells, such cells are not yet appropriate for transplant because they do not release insulin appropriately in response to glucose levels. If these cells were introduced into a patient, insulin would be secreted when not needed, potentially causing fatal hypoglycemia.

The study, conducted by Chutima Talchai, PhD, and Domenico Accili, MD, professor of medicine at Columbia University Medical Center, shows that certain progenitor cells in the intestine of mice have the surprising ability to make insulin-producing cells. Dr. Talchai, who works in Dr. Accilis lab, is a New York Stem Cell Foundation-Druckenmiller Fellow.

The gastrointestinal progenitor cells are normally responsible for producing a wide range of cells, including cells that produce serotonin, gastric inhibitory peptide, and other hormones secreted into the GI tract and bloodstream.

Inactivation of Foxo1, a gene important for metabolism generated insulin producing cells in small intestines of newborn mice, as detected by immunofluorescence in red.Drs. Talchai and Accili found that when they turned off a gene known to play a role in cell fate decisionsFoxo1the progenitor cells also generated insulin-producing cells. More cells were generated when Foxo1 was turned off early in development, but insulin-producing cells were also generated when the gene was turned off after the mice had reached adulthood.

Our results show that it could be possible to regrow insulin-producing cells in the GI tracts of our pediatric and adult patients, Dr. Accili says.

Excerpt from:
Columbia Researchers Find Potential Role for Gut Cells in Treating Type I Diabetes

Public release date: 12-Mar-2012 [ | E-mail | Share ]

Contact: Kim Irwin kirwin@mednet.ucla.edu 310-206-2805 University of California - Los Angeles Health Sciences

Researchers at the UCLA stem cell center and the departments of chemistry and biochemistry and pathology and laboratory medicine have identified, for the first time, a generic way to correct mutations in human mitochondrial DNA by targeting corrective RNAs, a finding with implications for treating a host of mitochondrial diseases.

Mutations in the human mitochondrial genome are implicated in neuromuscular diseases, metabolic defects and aging. There currently are no methods to successfully repair or compensate for these mutations, said study co-senior author Dr. Michael Teitell, a professor of pathology and laboratory medicine and a researcher with the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA.

Between 1,000 and 4,000 children per year in the United States are born with a mitochondrial disease and up to one in 4,000 children in the U.S. will develop a mitochondrial disease by the age of 10, according to Mito Action, a nonprofit organization supporting research into mitochondrial diseases. In adults, many diseases of aging have been associated with defects of mitochondrial function, including diabetes, Parkinson's disease, heart disease, stroke, Alzheimer's disease and cancer.

"I think this is a finding that could change the field," Teitell said. "We've been looking to do this for a long time and we had a very reasoned approach, but some key steps were missing. Now we have developed this method and the next step is to show that what we can do in human cell lines with mutant mitochondria can translate into animal models and, ultimately, into humans."

The study appears March 12, 2012 in the peer-reviewed journal Proceedings of the National Academy of Sciences.

The current study builds on previous work published in 2010 in the peer-reviewed journal Cell, in which Teitell, Carla Koehler, a professor of chemistry and biochemistry and a Broad Stem Cell Research Center scientist, and their team uncovered a role for an essential protein that acts to shuttle RNA into the mitochondria, the energy-producing "power plant" of a cell.

Mitochondria are described as cellular power plants because they generate most of the energy supply within a cell. In addition to supplying energy, mitochondria also are involved in a broad range of other cellular processes including signaling, differentiation, death, control of the cell cycle and growth.

The import of nucleus-encoded small RNAs into mitochondria is essential for the replication, transcription and translation of the mitochondrial genome, but the mechanisms that deliver RNA into mitochondria have remained poorly understood.

See the rest here:
Correcting human mitochondrial mutations

Public release date: 11-Mar-2012 [ | E-mail | Share ]

Contact: Kim Irwin kirwin@mednet.ucla.edu 310-206-2805 University of California - Los Angeles Health Sciences

UCLA stem cell researchers have shown that insulin and nutrition keep blood stem cells from differentiating into mature blood cells in Drosophila, the common fruit fly, a finding that has implications for studying inflammatory response and blood development in response to dietary changes in humans.

Keeping blood stem cells, or progenitor cells, from differentiating into blood cells is important as they are needed to create the blood supply for the adult fruit fly.

The study found that the blood stem cells are receiving systemic signals from insulin and nutritional factors, in this case essential amino acids, that helped them to maintain their "stemness," said study senior author Utpal Banerjee, professor and chairman of the molecular, cell and developmental biology department in Life Sciences and a researcher with the Eli and Edythe Broad Center of Regenerative Medicine at UCLA.

"We expect that this study will promote further investigation of possible direct signal sensing mechanisms by mammalian blood stem cells," Banerjee said. "Such studies will probably yield insights into chronic inflammation and the myeloid cell accumulation seen in patients with type II diabetes and other metabolic disorders."

The study appears March 11, 2012 in the peer-reviewed journal Nature Cell Biology.

In the flies, the insulin signaling came from the brain, which is an organ similar to the human pancreas, which produces insulin. That insulin was taken up by the blood stem cells, as were amino acids found in the fly flood, said Ji Won Shim, a postdoctoral fellow in Banerjee's lab and first author of the study.

Shim studied the flies while in the larval stage of development. To see what would happen to the blood stem cells, Shim placed the larvae into a jar with no food - they usually eat yeast or cornmeal and left them for 24 hours. Afterward, she checked for the presence of blood stem cells using specific chemical markers that made them visible under a confocal microscope.

"Once the flies were starved and not receiving the insulin and nutritional signaling, all the blood stem cells were gone," Shim said. "All that were left were differentiated mature blood cells. This type of mechanism has not been identified in mammals or humans, and it will be intriguing to see if there are similar mechanisms at work there."

The rest is here:
UCLA scientists find insulin, nutrition prevent blood stem cell differentiation in fruit flies

Newswise UCLA stem cell researchers have shown that insulin and nutrition keep blood stem cells from differentiating into mature blood cells in Drosophila, the common fruit fly, a finding that has implications for studying inflammatory response and blood development in response to dietary changes in humans.

Keeping blood stem cells, or progenitor cells, from differentiating into blood cells is important as they are needed to create the blood supply for the adult fruit fly.

The study found that the blood stem cells are receiving systemic signals from insulin and nutritional factors, in this case essential amino acids, that helped them to maintain their stemness, said study senior author Utpal Banerjee, professor and chairman of the molecular, cell and developmental biology department in Life Sciences and a researcher with the Eli and Edythe Broad Center of Regenerative Medicine at UCLA.

We expect that this study will promote further investigation of possible direct signal sensing mechanisms by mammalian blood stem cells, Banerjee said. Such studies will probably yield insights into chronic inflammation and the myeloid cell accumulation seen in patients with type II diabetes and other metabolic disorders.

The study appears March 11, 2012 in the peer-reviewed journal Nature Cell Biology.

In the flies, the insulin signaling came from the brain, which is an organ similar to the human pancreas, which produces insulin. That insulin was taken up by the blood stem cells, as were amino acids found in the fly flood, said Ji Won Shim, a postdoctoral fellow in Banerjees lab and first author of the study.

Shim studied the flies while in the larval stage of development. To see what would happen to the blood stem cells, Shim placed the larvae into a jar with no food - they usually eat yeast or cornmeal and left them for 24 hours. Afterward, she checked for the presence of blood stem cells using specific chemical markers that made them visible under a confocal microscope.

Once the flies were starved and not receiving the insulin and nutritional signaling, all the blood stem cells were gone, Shim said. All that were left were differentiated mature blood cells. This type of mechanism has not been identified in mammals or humans, and it will be intriguing to see if there are similar mechanisms at work there.

In the fruit fly, the only mature blood cells present are myeloid cells, Shim said. Diabetic patients have many activated myeloid cells that could be causing disease symptoms. It may be that abnormal activation of myeloid cells and abnormal metabolism play a major role in diabetes.

Metabolic regulation and immune response are highly integrated in order to function properly dependent on each other. Type II diabetes and obesity, both metabolic diseases, are closely associated with chronic inflammation, which is induced by abnormal activation of blood cells, Shim said. However, no systemic study on a connection between blood stem cells and metabolic alterations had been done. Our study highlights the potential linkage between myeloid-lineage blood stem cells and metabolic disruptions.

Continue reading here:
Insulin, Nutrition Prevent Blood Stem Cell Differentiation in Fruit Flies

CLEARWATER, FL--(Marketwire -03/12/12)- Biostem U.S., Corporation (OTCQB: BOSM.PK - News) (Pinksheets: BOSM.PK - News) (Biostem, the Company), a fully reporting public company in the stem cell regenerative medicine sciences sector, announced today the addition of cardiothoracic surgeon Thomas W. Prendergast, M.D. to its Scientific and Medical Board of Advisors (SAMBA).

Biostem CEO, Dwight Brunoehler stated, "The Company is now positioned for growth and international expansion. Adding a world class team of clinical, laboratory, and regulatory experts for our Scientific and Medical Board of Advisors to guide our pursuits is essential. Dr. Prendergast brings a wealth of experience not only in the scientific aspects of stem cell use in regenerative medicine, but also in forging research and international economic development opportunities."

Dr. Prendergast is a busy clinical cardiothoracic surgeon, who performs 200-250 open-heart operations and 5 to 15 heart transplants each year. He is deeply involved in numerous clinical and research activities associated with stem cells and heart repair. He is presently Director of Cardiac Transplantation at Robert Wood Johnson University Hospital in New Brunswick, New Jersey where he holds an Associate Professorship of Surgery at the University of Medicine and Dentistry of New Jersey. In addition to being an active participant in stem cell research program development and teaching medical students and residents, his other interests include medical research funding and humanitarian development of programs for Disabled American Veterans.

Dr. Prendergast received his undergraduate degrees in biophysics and Psychology, as well as his medical degree, at Pennsylvania State University. His general surgery residency was for five years at the University of Massachusetts Medical School. His cardiothoracic surgery training was at the University of Southern California School of Medicine, including the Los Angeles County Medical Center. Subsequent fellowship training included pediatric cardiac surgery at Children's Hospital of LA, along with thoracic transplant fellowships at University of Southern California in Los Angeles and at Temple University Hospital in Philadelphia. He spent three years at the University of Kansas establishing thoracic transplant programs until returning to Temple University Hospital as one of their staff heart and lung transplant surgeons. Subsequent to his time at Temple, he joined up with Newark Beth Israel/St. Barnabas Hospitals, where he assumed directorship as the Chief of Cardiac Transplantation and Mechanical Assistance.

Regarding his appointment to the Biostem U.S. Scientific and Medical Board of Advisors, Dr. Prendergast said, "I am looking forward with excitement to working again with Dwight at Biostem. The expansion plan is sound, well paced, and will afford improved quality of life opportunities to many people around the world."

About Biostem U.S., Corporation

Biostem U.S., Corporation (OTCQB: BOSM.PK - News) (Pinksheets: BOSM.PK - News) is a fully reporting Nevada corporation with offices in Clearwater, Florida. Biostem is a technology licensing company with proprietary technology centered around providing hair re-growth using human stem cells. The company also intends to train and license selected physicians to provide Regenerative Cellular Therapy treatments to assist the body's natural approach to healing tendons, ligaments, joints and muscle injuries by using the patient's own stem cells. Biostem U.S. is seeking to expand its operations worldwide through licensing of its proprietary technology and acquisition of existing stem cell related facilities. The company's goal is to operate in the international biotech market, focusing on the rapidly growing regenerative medicine field, using ethically sourced adult stem cells to improve the quality and longevity of life for all mankind.

More information on Biostem U.S., Corporation can be obtained through http://www.biostemus.com, or by calling Kerry D'Amato, Marketing Director at 727-446-5000.

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Biostem U.S., Corporation Appoints Heart Surgeon, Thomas W. Prendergast, M.D. to Its Scientific and Medical Board of ...

Public release date: 11-Mar-2012 [ | E-mail | Share ]

Contact: Karin Eskenazi ket2116@columbia.edu 212-342-0508 Columbia University Medical Center

NEW YORK, NY -- A study by Columbia researchers suggests that cells in the patient's intestine could be coaxed into making insulin, circumventing the need for a stem cell transplant. Until now, stem cell transplants have been seen by many researchers as the ideal way to replace cells lost in type I diabetes and to free patients from insulin injections.

The researchconducted in micewas published 11 March 2012 in the journal Nature Genetics.

Type I diabetes is an autoimmune disease that destroys insulin-producing cells in the pancreas. The pancreas cannot replace these cells, so once they are lost, people with type I diabetes must inject themselves with insulin to control their blood glucose. Blood glucose that is too high or too low can be life threatening, and patients must monitor their glucose several times a day.

A longstanding goal of type I diabetes research is to replace lost cells with new cells that release insulin into the bloodstream as needed. Though researchers can make insulin-producing cells in the laboratory from embryonic stem cells, such cells are not yet appropriate for transplant because they do not release insulin appropriately in response to glucose levels. If these cells were introduced into a patient, insulin would be secreted when not needed, potentially causing fatal hypoglycemia.

The study, conducted by Chutima Talchai, PhD, and Domenico Accili, MD, professor of medicine at Columbia University Medical Center, shows that certain progenitor cells in the intestine of mice have the surprising ability to make insulin-producing cells. Dr. Talchai is a postdoctoral fellow in Dr. Accili's lab.

The gastrointestinal progenitor cells are normally responsible for producing a wide range of cells, including cells that produce serotonin, gastric inhibitory peptide, and other hormones secreted into the GI tract and bloodstream.

Drs. Talchai and Accili found that when they turned off a gene known to play a role in cell fate decisionsFoxo1the progenitor cells also generated insulin-producing cells. More cells were generated when Foxo1 was turned off early in development, but insulin-producing cells were also generated when the gene was turned off after the mice had reached adulthood.

"Our results show that it could be possible to regrow insulin-producing cells in the GI tracts of our pediatric and adult patients," Dr. Accili says.

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A new approach to treating type I diabetes? Gut cells transformed into insulin factories

London, Mar 12 (ANI): A new study conducted by scientists suggests a new approach that could give patients the ability to make their own insulin-producing cells without a stem cell transplant.

Until now, stem cell transplants have been seen by many researchers as the ideal way to replace cells lost in type I diabetes and to free patients from insulin injections.

Type I diabetes is an autoimmune disease that destroys insulin-producing cells in the pancreas. The pancreas cannot replace these cells, so once they are lost, people with type I diabetes must inject themselves with insulin to control their blood glucose.

Blood glucose that is too high or too low can be life threatening, and patients must monitor their glucose several times a day.

A longstanding goal of type I diabetes research is to replace lost cells with new cells that release insulin into the bloodstream as needed.

Though researchers can make insulin-producing cells in the laboratory from embryonic stem cells, such cells are not yet appropriate for transplant because they do not release insulin appropriately in response to glucose levels.

If these cells were introduced into a patient, insulin would be secreted when not needed, potentially causing fatal hypoglycemia.

The study, conducted by Chutima Talchai and Domenico Accili from Columbia University Medical Center, shows that certain progenitor cells in the intestine of mice have the surprising ability to make insulin-producing cells.

The gastrointestinal progenitor cells are normally responsible for producing a wide range of cells, including cells that produce serotonin, gastric inhibitory peptide, and other hormones secreted into the GI tract and bloodstream.

They found that when they turned off a gene known to play a role in cell fate decisions-Foxo1-the progenitor cells also generated insulin-producing cells. More cells were generated when Foxo1 was turned off early in development, but insulin-producing cells were also generated when the gene was turned off after the mice had reached adulthood.

Excerpt from:
Gut cells transformed into insulin factories 'could help to treat type I diabetes'

ScienceDaily (Mar. 11, 2012) A study by Columbia researchers suggests that cells in the patient's intestine could be coaxed into making insulin, circumventing the need for a stem cell transplant. Until now, stem cell transplants have been seen by many researchers as the ideal way to replace cells lost in type I diabetes and to free patients from insulin injections.

The research -- conducted in mice -- was published 11 March 2012 in the journal Nature Genetics.

Type I diabetes is an autoimmune disease that destroys insulin-producing cells in the pancreas. The pancreas cannot replace these cells, so once they are lost, people with type I diabetes must inject themselves with insulin to control their blood glucose. Blood glucose that is too high or too low can be life threatening, and patients must monitor their glucose several times a day.

A longstanding goal of type I diabetes research is to replace lost cells with new cells that release insulin into the bloodstream as needed. Though researchers can make insulin-producing cells in the laboratory from embryonic stem cells, such cells are not yet appropriate for transplant because they do not release insulin appropriately in response to glucose levels. If these cells were introduced into a patient, insulin would be secreted when not needed, potentially causing fatal hypoglycemia.

The study, conducted by Chutima Talchai, PhD, and Domenico Accili, MD, professor of medicine at Columbia University Medical Center, shows that certain progenitor cells in the intestine of mice have the surprising ability to make insulin-producing cells. Dr. Talchai is a postdoctoral fellow in Dr. Accili's lab.

The gastrointestinal progenitor cells are normally responsible for producing a wide range of cells, including cells that produce serotonin, gastric inhibitory peptide, and other hormones secreted into the GI tract and bloodstream.

Drs. Talchai and Accili found that when they turned off a gene known to play a role in cell fate decisions -- Foxo1 -- the progenitor cells also generated insulin-producing cells. More cells were generated when Foxo1 was turned off early in development, but insulin-producing cells were also generated when the gene was turned off after the mice had reached adulthood. "Our results show that it could be possible to regrow insulin-producing cells in the GI tracts of our pediatric and adult patients," Dr. Accili says.

"Nobody would have predicted this result," Dr. Accili adds. "Many things could have happened after we knocked out Foxo1. In the pancreas, when we knock out Foxo1, nothing happens. So why does something happen in the gut? Why don't we get a cell that produces some other hormone? We don't yet know."

Insulin-producing cells in the gut would be hazardous if they did not release insulin in response to blood glucose levels. But the researchers say that the new intestinal cells have glucose-sensing receptors and do exactly that.

The insulin made by the gut cells also was released into the bloodstream, worked as well as normal insulin, and was made in sufficient quantity to nearly normalize blood glucose levels in otherwise diabetic mice.

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New approach to treating type 1 diabetes? Transforming gut cells into insulin factories

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