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.

More here:
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

The rest is here:
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

Read the original post:
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.

Here is the original post:
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.

View original post here:
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.

See more here:
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.

Read the rest here:
New approach to treating type 1 diabetes? Transforming gut cells into insulin factories

By Jonathan Benson

Food-borne illness outbreaks and the growing prevalence of antibiotic-resistant "superbugs" are two very serious societal problems for which researchers say they are actively looking for viable solutions. But one such solution found right in nature is coriander oil, which has been found to kill a number of different bacterial strains, as well as aid in digestion and treat the symptoms of food poisoning.

Dr. Fernanda Domingues and her colleagues from the University of Beira Interior in Portugal tested the effects of coriander oil, an essential oil extracted from the seeds of the coriander plant, also known as cilantro, on twelve different bacterial strains, including Escherichia coli (E. coli), Salmonella enterica, and methicillin-resistant Staphylococcus aureus (MRSA), the infamous hospital superbug. Read more...

AyurGold for Healthy Blood

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Scientific American

Seeing the invisible field: genetic engineering gives yeast the gift of ... SmartPlanet.com (blog) What all this means is that magnetism, that elusive sense that so many animals lack, could potentially be induced through some simple genetic engineering. Making cells magnetic could have uses for therapy and bioengineering. Magnetic YeastScientist all 11 news articles »

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Genetic Engineering News

Biopharma Will Need More than New Law to Embrace Crowdfunding Genetic Engineering News Genetic Engineering & Biotechnology News (GEN) has retained its position as the most widely read biotechnology publication around the globe since its launch in 1981. Published 21 times a year and with additional exclusive editorial content online, ... and more »

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Talk of the Sound

Iona Prep AP Biology Class Visits DNA Learning Center in Cold Spring Harbor Talk of the Sound By Talk of the Sou... on Tue, 03/06/2012 - 22:56 Iona Prep's AP biology class recently visited the DNA Learning Center in Cold Spring Harbor to perform a molecular genetics laboratory exercise called DNA Restriction Analysis. On Wednesday, February 29, ...

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MyHealthNewsDaily

Key to Making Egg Cells Mature Found, Researchers Say MyHealthNewsDaily 24 in the journal Human Molecular Genetics. Pass it on: By studying a protein called cdk1, researchers may gain a better insight into some cases of infertility in women. Follow MyHealthNewsDaily on Twitter @MyHealth_MHND. Find us on Facebook. woman ... Discovery of a molecule that initiates maturation of mammalian eggs can lead ...Science Daily (press release) all 6 news articles »

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Tweet 

http://www.celltherapyblog.com hosted by http://www.celltherapygroup.com

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During one such visit a senior executive noticed that two of my colleagues, sitting next to each other, supported their system (two different implementations of the same software) across two different geographies. They happened to have the name of the systems they support, pinned to a board at their desks. The executive wanted us to take a picture of the two cubicles and email to him. We were quite surprised at the request. Before moving on to speak to other people he asked a couple of questions and realized the guys were sharing each other’s experiences and leveraging the lessons learnt from one deployment for the other geography.  It turned out that this does not happen in their organization, in fact their internal teams hardly communicate as they are part of different business units and geographies

Read full article on at inPharmatics

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