Researchers Develop First Potential Medicine For Patients With Most Severe Form Of Congenital Hyperinsulinism

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Main Category: Diabetes
Also Included In: Pediatrics / Children's Health;  Genetics
Article Date: 04 Aug 2012 - 0:00 PDT Current ratings for:
Researchers Develop First Potential Medicine For Patients With Most Severe Form Of Congenital Hyperinsulinism

A pilot study in adolescents and adults has found that an investigational drug shows promise as the first potential medical treatment for children with the severest type of congenital hyperinsulinism, a rare but potentially devastating disease in which gene mutations cause insulin levels to become dangerously high.

"There is currently no effective medicine for children with the most common and most severe form of hyperinsulinism," said study leader Diva D. De Leon, M.D., a pediatric endocrinologist at The Children's Hospital of Philadelphia. "Our new research shows that this investigational drug, a peptide called exendin-(9-39), controls blood sugar levels in people, a very promising result."

The study appears online ahead of print in the journal Diabetes.

In congenital hyperinsulinism (HI), mutations disrupt the insulin-secreting beta cells in the pancreas. Uncontrolled, excessive insulin levels thus sharply reduce blood glucose levels, a condition called hypoglycemia. If untreated, hypoglycemia may cause irreversible brain damage or death in children. Congenital HI occurs in an estimated one in 50,000 U.S. children, with a higher incidence among Ashkenazic Jews and certain other groups.

The standard treatment for some forms of congenital HI is diazoxide, a drug that controls insulin secretion by opening potassium channels in beta cells. However, this drug does not work in the most common types of HI, in which mutations prevent these potassium channels from forming.

When abnormal beta cells occur only in a discrete portion of the pancreas, precise surgery on the tiny organ can remove the lesion and cure HI. The Congenital Hyperinsulinism Center at The Children's Hospital of Philadelphia is a world leader in diagnosing such lesions and performing the curative surgery on newborns.

However, in roughly half of congenital HI cases, abnormal cells are diffused through the pancreas, and surgeons must remove nearly the entire pancreas. This leaves the majority of patients at high risk of developing diabetes.

The current study, which builds on previous research by De Leon and colleagues in animals, uses exendin-(9-39), which blocks the action of a hormone receptor, glucagon-like peptide-1 (GLP-1), in beta cells. The GLP-1 receptor is currently the target of drugs that treat diabetes, using the opposite effect from that investigated in this HI study.

The current pilot study included nine subjects, aged 15 to 47 years old, who had hyperinsulinism caused by mutations in potassium channels. None were being treated for HI at the time of the study, but all were at risk of hypoglycemia during periods of fasting.

In all nine subjects, the drug controlled blood glucose levels during fasting. Exendin also controlled insulin secretion in cell studies of beta cells taken from newborns with HI. The current research did not focus on the biological mechanisms that occurred, but De Leon said the results are encouraging enough to progress to a clinical study in children with HI over the next year.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our diabetes section for the latest news on this subject. Financial support for this study came from the National Institutes of Health (grant 1R03DK07835), the Lester and Liesel Baker Foundation, and the Clifford and Katherine Goldsmith Foundation. De Leon's co-authors, all from Children's Hospital, were Charles A. Stanley, M.D., Andrew C. Calabria, M.D., Changhong Li, M.D., and Paul R. Gallagher In addition to their positions at Children's Hospital, De Leon, Stanley and Li also are in the Perelman School of Medicine at the University of Pennsylvania.
"The GLP-1 Receptor Antagonist Exendin-(9-39) Elevates Blood Fasting Glucose Levels in Congenital Hyperinsulinism due to Inactivating Mutations in the ATP-sensitive Potassium Channel," Diabetes, published online Aug.1, 2012, to appear in print, October 2012. doi: 10.2337/db12-0166.
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Potential Weapon In The Fight Against Cancer

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Main Category: Breast Cancer
Also Included In: Cancer / Oncology
Article Date: 03 Aug 2012 - 1:00 PDT
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Potential Weapon In The Fight Against Cancer

By identifying a key protein that tells certain breast cancer cells when and how to move, researchers at Michigan State University hope to better understand the process by which breast cancer spreads, or metastasizes.

When breast cancer metastasizes, cancer cells break away from a primary tumor and move to other organs in the body, including the lungs, liver and brain. In work published recently in the journal Cancer Research, MSU researchers Kathy Gallo and Jian Chen show a protein called MLK3 (mixed lineage kinase 3) is a critical driver of breast cancer cell migration and invasion.

More importantly, Chen and Gallo showed that in triple-negative breast tumor cells, which are more aggressive and for which targeted therapies are needed, it is possible to thwart that cell migration and invasion.

"While the classical approach to cancer drugs has been to find drugs that kill tumor cells, there recently also is an interest in finding drugs that interrupt metastasis," said Gallo, a professor in MSU's Department of Physiology. "The hope is that such drugs in combination with conventional therapies may lead to better outcomes in patients."

As part of their study, Gallo and Chen, a biochemistry graduate student, also found that eliminating MLK3 prevented tumors in animals from metastasizing to the lungs, providing the foundation for future research on targeting MLK3 pathways as an approach to preventing the spread of cancer.

The researchers identified how key cellular proteins were instructed by the MLK3 protein - through the addition of molecular tags called phosphates - to interact with one another, leading cancer cells to move. Specifically, MLK3 promotes the addition of phosphates to another protein called paxillin, which is known to control how cells move.

Gallo and Chen then stopped cell movement in breast cancer models by eliminating MLK3 altogether or using a drug called CEP-1347 to block MLK3's ability to add phosphates to other proteins. The experimental results indicate that when certain cancer cells lose MLK3, the ability to add phosphates is impaired, eventually crippling the cell migration machinery and diminishing cell movement.

"Our research suggests that the intracellular pathways involving MLK3 that control cell movement could provide new targets for the treatment of patients with metastatic cancer," Chen said. "Drugs developed for combating the MLK3 activity may be useful in reducing the spread of breast cancer."

Gallo added that MLK3 is a protein kinase, and these types of proteins have proven to be good drug targets in cancers and other diseases.

"While drugs such as chemotherapy kill all cells, research has shown drugs that inhibit kinases often can be effective with fewer side effects," she said.

The next step for the researchers is to test whether an MLK3 inhibitor can prevent cancer from metastasizing in animal models.

"Cancer is a very complex collection of diseases, but we believe that certain types of cancers may be sensitive to MLK inhibitors," Gallo said, "and targeting MLK3 may provide a very useful weapon in the fight against cancer."

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our breast cancer section for the latest news on this subject. The team’s research was supported by grants from the Department of Defense’s Breast Cancer Research Program and the Elsa U. Pardee Foundation. The MLK inhibitor, CEP-1347, was provided by Cephalon Inc., a wholly owned, indirect subsidiary of Teva Pharmaceuticals Industries Ltd.
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Potential Treatment For Macular Degeneration And Retinitis Pigmentosa Uses Nanoparticles To Deliver Steroids To Retina

Main Category: Eye Health / Blindness
Also Included In: Seniors / Aging
Article Date: 15 Dec 2011 - 0:00 PST

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Hitching a ride into the retina on nanoparticles called dendrimers offers a new way to treat age-related macular degeneration and retinitis pigmentosa. A collaborative research study among investigators at Wayne State University, the Mayo Clinic and Johns Hopkins Medicine shows that steroids attached to the dendrimers targeted the damage-causing cells associated with neuroinflammation, leaving the rest of the eye unaffected and preserving vision.

The principal authors of the study, Raymond Iezzi, M.D. (Mayo Clinic ophthalmologist) and Rangaramanujam Kannan, Ph.D. (faculty of ophthalmology at The Wilmer Eye Institute of Johns Hopkins) have developed a clinically relevant, targeted, sustained-release drug delivery system using a simple nanodevice construct. The experimental work in rat models was initiated and substantially conducted at Wayne State University, and showed that one intravitreal administration of the nanodevice in microgram quantities could offer neuroprotection at least for a month, and appears in the journal, Biomaterials (33(3), 979-988).

Both dry age-related macular degeneration and retinitis pigmentosa are caused by neuroinflammation, which progressively damages the retina and can lead to blindness. Macular degeneration is the primary cause of vision loss in older Americans, affecting more than 7 million people, according to the National Institutes of Health (NIH). Retinitis pigmentosa encompasses many genetic conditions affecting the retina and impacts 1 in 4,000 Americans, the NIH estimates.

"There is no cure for these diseases, said Iezzi. "An effective treatment could offer hope to hundreds of millions of patients worldwide. We tested the dendrimer delivery system in rats that develop neuroinflammation leading to retinal degeneration. The target was activated microglial cells, the immune cells in charge of cleaning up dead and dying material in the eye. When activated, these cells cause damage via neuroinflammation - a hallmark of each disease."

"Dendrimers are tree-like, non-cytotoxic polymeric drug delivery vehicles (~ 4 nm). Surprisingly, the activated microglia in the degenerating retina appeared to eat the dendrimer selectively and retain them for at least a month. The drug is released from the dendrimer in a sustained fashion inside these cells, offering targeted neuroprotection to the retina," said Kannan.

The treatment reduced neuroinflammation in the rat model and protected vision by preventing injury to photoreceptors in the retina. Although the steroid offers only temporary protection, the treatment as a whole provides sustained relief from neuroinflammation, the study found. The researchers believe that this patent-pending technology with significant translational potential will be advanced further, through this multi-university collaboration among Johns Hopkins, Mayo Clinic and Wayne State.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our eye health / blindness section for the latest news on this subject. The study was funded by grants from the Ligon Research Center of Vision at Wayne State University, the Ralph C. Wilson Medical Research Foundation, Office of the Vice President for Research at Wayne State University, and Research to Prevent Blindness.
The researchers declare no conflict of interest.
Co-authors include Bharath Raja Guru, Ph.D., Case Western Reserve University; Inna Glybina and Alexander Kennedy, Wayne State University; and Manoj Mishra, Ph.D., The Wilmer Eye Institute of Johns Hopkins.
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'Sleep Hormone' Discovery Leads To Novel Melatonin Drug With Potential To Treat Insomnia

Main Category: Sleep / Sleep Disorders / Insomnia
Also Included In: Endocrinology;  Depression
Article Date: 15 Dec 2011 - 0:00 PST

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A team from the Research Institute of the McGill University Health Centre (RI-MUHC) and McGill University has made a major breakthrough by unraveling the inner workings of melatonin, also known as the "sleep hormone." The research, conducted in collaboration with scientists in Italy, reveals the key role played by the melatonin receptor in the brain that promotes deep, restorative sleep. This discovery led the researchers to develop a novel drug called UCM765, which selectively activates this receptor. The results, published in The Journal of Neuroscience, may pave the way for the development of new and promising treatments for insomnia, a common public health problem that affects millions of people worldwide.

"We've spent many years develop medications that act selectively on a single melatonin receptor to specifically promote deep sleep, which we believe is the key to curing insomnia," says Dr. Gabriella Gobbi, a researcher in psychiatry at the RI-MUHC and the study's principal investigator. "Deep sleep has significant restorative effects, as well as the ability to increase memory and boost metabolism, while lowering blood pressure and slowing the heart rate." To date most treatments for insomnia, such as benzodiazepines, have not been selective for deep sleep, and can lead to dependence and cognitive impairment.

The researchers became interested in melatonin because of its effect on cerebral activity, and its involvement in sleep, depression and anxiety. Melatonin is a critical hormone produced by the pineal gland (located in the brain) in the absence of light stimulation. This hormone, present throughout the animal kingdom, is responsible for regulating sleep and circadian rhythms.

The research team discovered that two principal melatonin receptors, known as MT1 and MT2, played opposite roles in sleep regulation. "We discovered that MT1 receptors act on rapid eye movement (REM) sleep and block non-REM sleep, while MT2 receptors favour non-REM sleep, also known as deep sleep," explains Dr. Gobbi, who is also an associate professor of psychiatry in the Faculty of Medicine at McGill. "Specifying the role of MT2 receptors in melatonin represent a major scientific breakthrough that may designate them as a promising novel target for future treatments of insomnia. This discovery also explains the modest hypnotic effect of the over-the-counter melatonin pills, which act on both conflicting receptors."

Using a drug called UCM765, developed in collaboration with a group of chemists, under the leadership of Professor Tarzia in Urbino and Professor Mor in Parma, Italy which selectively binds to the MT2 receptor, the researchers observed an increase in the phases of deep sleep in rats and mice. Most importantly, UCM765 acts in a brain area called the reticular thalamus, which is the main driver of deep sleep. "This new molecule, contrary to traditional treatments for insomnia, increases deep sleep without destroying the "architecture" of sleep. In other words, it increases the duration of deep sleep while keeping the REM sleep episodes the same," says Dr. Gobbi.

"The development of this pharmacology by means of targeting deep sleep receptors to treat insomnia represents a major advancement in our ability to deal with this common health problem that affects people worldwide," concludes Dr. Vassilios Papadopoulos, Director of the Research Institute of the MUHC.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our sleep / sleep disorders / insomnia section for the latest news on this subject. About the study
This paper was co-authored by Rafael Ochoa-Sanchez, Stefano Comai, Francis Rodriguez Bambico and Sergio Dominguez-Lopez, Gabriella Gobbi (Dept. of Psychiatry, McGill University and Research Institute of the MUHC); Baptiste Lacoste, Laurent Descarries (Depts. of Pathology, Cell Biology, Physiology, Université de Montréal); Annalida Bedini, Gilberto Spadoni, Giorgio Tarzia (Institute of Medicinal Chemistry, University of Urbino, Italy); Marco Mor, Silvia Rivara (University of Parma, Italy); Debora Angeloni (Scuola Superiore Sant'Anna, Pisa, Italy), Franco Fraschini (Dept.of Pharmacology, Chemiotherapy and Medical Toxicology, University of Milan, Italy).
This work was supported by grants from the Fonds de la recherche en Santé du Québec (FRSQ), by the Canadian Institutes of Health Research (CIHR), by the Canadian Foundation for Innovation (CFI), MSBi Valorisation, the McGill University Health Centre (MUHC), and the Quebec Ministry of Economic Development, Innovation and Exportation (MDEIE).
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posted by Ann Jorn, Ph.D. on 15 Dec 2011 at 8:23 am

This breakthrough in understanding deep sleep and the role of the melatonin hormone provides great hope for the chronically sleep deprived chronic pain sufferer. Sleep is not simply disturbed by pain but when sleep does happen restorative sleep is minimal. This is especially true for those that suffer from fibromyalgia.

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Little-Studied Cellular Mechanism Elevated To Potential Drug Target

Main Category: Cancer / Oncology
Also Included In: Pharma Industry / Biotech Industry
Article Date: 13 Dec 2011 - 0:00 PST

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For years, science has generally considered the phosphorylation of proteins -- the insertion of a phosphorous group into a protein that turns it on or off -- as perhaps the factor regulating a range of cellular processes from cell metabolism to programmed cell death. Now, scientists from the Florida campus of The Scripps Research Institute have identified the importance of a novel protein-regulating mechanism -- called sulfenylation -- that is similar to phosphorylation and may, in fact, open up opportunities to develop new types of drugs for diseases such as cancer.

The study was published in an advance online edition of the journal Nature Chemical Biology.

"With this paper, we've elevated protein sulfenylation from a marker of oxidative stress to a bona fide reversible post translational modification that plays a key regulatory role during cell signaling," said Kate Carroll, a Scripps Research associate professor who led the study. "The sulfenyl modification is the new kid on the block."

During periods of cellular stress, caused by factors such as exposure to UV radiation or chronic disease states like cancer, the level of highly reactive oxygen-containing molecules can increase, resulting in inappropriate modification of proteins and cell damage. In sulfenylation, one oxidant, hydrogen peroxide, functions as a messenger that can activate cell proliferation through oxidation of cysteine residues in signaling proteins, producing sulfenic acid. Cysteine, an amino acid (natural protein building block), is highly oxidant sensitive.

Conventional wisdom has long held that if hydrogen peroxide does exist in the cell at any appreciable level, it represents a disease state, not a regulatory event. The new study shows that sulfenylation is actually a positive protein modification, and that it's required for signaling through the pathway, a validation of a long-held belief in some scientific circles that hydrogen peroxide functions as a general signaling molecule, not an oxidative "bad boy" to be eliminated at all costs.

A New Chemical Probe

To explore the process, Carroll and her colleagues developed a highly selective chemical probe -- known as DYn-2 -- with the ability to detect minute differences in sulfenylation rates within the cell.

With the new probe, the team was able to show that a key signaling protein, epidermal growth factor receptor (EGFR), is directly modified by hydrogen peroxide at a critical active site cysteine, stimulating its tyrosine kinase activity.

The technology described in the new paper is unique, Carroll said, because it allows scientists to trap and detect these modifications in situ, without interfering with the redox balance of the cell. "Probing cysteine oxidation in a cell lysate is like looking for a needle in a haystack," she said, "our new approach preserves labile sulfenyl modifications and avoids protein oxidation artifacts that arise during cell homogenization."

As with phosphorylation, future studies on sulfenylation will delve into the exciting discovery of new enzymes, new signaling processes, and new mechanisms of regulation.

Another broad impact of these findings, Carroll said, is to open up an entirely new mechanism to exploit for the development of therapeutics, particularly in cancer. "It should influence the design of inhibitors that target oxidant-sensitive cysteine residues in the future," she said.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our cancer / oncology section for the latest news on this subject. The first author of the study, "Peroxide-dependent Sulfenylation of the EGFR Catalytic Site Enhances Kinase Activity," is Candice E. Paulsen of the University of Michigan. Other authors include Thu H. Truong and Stephen E. Leonard of the University of Michigan; and Francisco J. Garcia, Arne Homann and Vinayak Gupta of Scripps Research.
The study was supported by the Camille Henry Dreyfus Teacher Scholar Award and the American Heart Association.
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Potential Breast Cancer Prevention Agent Found To Lower Levels Of 'Good' Cholesterol Over Time

Main Category: Breast Cancer
Also Included In: Cholesterol
Article Date: 10 Dec 2011 - 0:00 PST

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Exemestane steadily lowered levels of "good" cholesterol in women taking the agent as part of a breast cancer prevention study, say researchers at Georgetown Lombardi Comprehensive Cancer Center. Exemestane, an aromatase inhibitor used to treat estrogen receptor-positive breast cancer, is being tested to prevent breast cancer in women at an increased risk of developing the disease.

Georgetown researchers say their findings, presented at the 2011 CTRC-AACR San Antonio Breast Cancer Symposium (SABCS), suggest that the effect this agent has on blood lipids may prove to be significant for women at high risk for heart disease due to elevated blood cholesterol, although no such effects have been seen yet in patients studied over two years of treatment.

There are two types of cholesterol transported in our blood - HDL and LDL. HDL cholesterol is known as "good" cholesterol, because high levels of it protect against heart attack. LDL cholesterol is known as "bad" cholesterol because it can buildup in the inner walls of the arteries that feed the heart and brain, and lead to atherosclerosis.

"Lower levels of the HDL, the good cholesterol, have been shown to increase the risk of heart attack and stroke. While we found that exemestane lowers good cholesterol levels, the clinical significance of this decrease is unknown," says a study investigator, Margaret Gatti-Mays, M.D. an intern in internal medicine at Georgetown.

The results come from a phase II multi-institutional study of women at increased risk for breast cancer that evaluated the safety and efficacy of exemestane over two years of therapy. The findings, from 31 patients, showed that the absolute change from the baseline HDL level at 3, 12, and 24 months were -8.0 mg/dL, -8.5 mg/dL, and -9.9 mg/dL, respectively. The rest of the lipid panel, including LDL (the bad cholesterol) was relatively unchanged.

"It is notable that both women taking and not taking lipid-lowering medication had decreases in HDL," Gatti-Mays says.

"Lower HDL levels are associated with an increased risk of heart disease, so if a patient has a low HDL level, exemestane may not be the best choice as a breast cancer prevention agent," says the study's senior investigator, Jennifer Eng-Wong, M.D., senior medical director of the Capital Breast Care Center at Georgetown Lombardi Comprehensive Cancer Center.

She adds that other anti-estrogen therapies designed to prevent breast cancer don't appear to lower HDL. "Less data is available on anastrozole and letrozole, which are other aromatase inhibitors, but they do not appear to lower HDL. Conversely, tamoxifen has an overall favorable effect on cholesterol."

"Exemestane has been shown to be an effective therapy in the prevention of breast cancer in postmenopausal women who have an increased risk of developing it. This study adds information that will help individualize care for these women though larger studies are needed to more fully evaluate the impact of exemestane on cholesterol and cardiovascular health," says Gatti-Mays.

The research was conducted at Georgetown and the National Cancer Institute (NCI), and was supported by both institutions, as well as the National Institutes of Health, and Pfizer Inc. (which supplied exemestane). (OVER)

A recipient of the ACCR Scholar-in-Training Award, Gatti-Mays' travel to the SABCS conference was funded by this award which is supported by Susan G. Komen for the Cure. She reports no personal financial interests related to the study.

The 2011 CTRC-AACR San Antonio Breast Cancer Symposium is presented by the Cancer Therapy & Research Center at UT Health Science Center San Antonio, the American Association for Cancer Research, and Baylor College of Medicine.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
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Potential New Therapies For People With Declining Sense Of Smell

Main Category: Ear, Nose and Throat
Also Included In: Seniors / Aging;  Neurology / Neuroscience;  Genetics
Article Date: 09 Dec 2011 - 1:00 PST

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University of California, Berkeley, neuroscientists have discovered a genetic trigger that makes the nose renew its smell sensors, providing hope for new therapies for people who have lost their sense of smell due to trauma or old age.

The gene tells olfactory stem cells the adult tissue stem cells in the nose to mature into the sensory neurons that detect odors and relay that information to the brain.

"Anosmia the absence of smell is a vastly underappreciated public health problem in our aging population. Many people lose the will to eat, which can lead to malnutrition, because the ability to taste depends on our sense of smell, which often declines with age," said lead researcher and campus neuroscientist John Ngai.

"One reason may be that as a person ages, the olfactory stem cells age and are less able to replace mature cells, or maybe they are just depleted," he said. "So, if we had a way to promote active stem cell self-renewal, we might be better able to replace these lost cells and maintain sensory function."

Gary K. Beauchamp, director of the Monell Chemical Senses Center in Philadelphia, who was not a member of the research team, noted that the olfactory system stands out for its ability to regenerate following injury or certain diseases

"This new paper ... presents an elegant analysis of some of the underlying genetic mechanisms regulating this regeneration," Beauchamp said. "It also provides important insights that should eventually allow clinicians to enhance regeneration, induce it in cases where, for currently unknown reasons, olfactory loss appears permanent, or even prevent functional loss as a person ages."

The discovery may also help scientists harness olfactory stem cells and stem cells found in other sensory systems more generally, to recover sensory function following injury or degenerative disease, said Ngai, the Coates Family Professor of Neuroscience in UC Berkeley's Department of Molecular and Cell Biology and director of the Helen Wills Neuroscience Institute and the QB3 Functional Genomics Laboratory.

Ngai, post-doctoral fellow Russell B. Fletcher and their UC Berkeley colleagues report their findings in the journal Neuron.

Self-renewal or differentiation

In the nose, smell sensory neurons live only about 30 days, then are replaced by new cells. The new cells are generated by adult stem cells in the olfactory epithelium. A key question, Ngai said, is what tells the stem cells to divide into new ones a process called self-renewal or to mature, or differentiate, into fully functional sensory nerve cells and other cells critical to maintaining olfactory function.

"These stem cells are capable of reconstituting the entire sensory epithelium of the nose following injury," Ngai said, "so understanding how these stem cells work is important for understanding the regeneration process that goes on in the nose."

Fletcher and Ngai screened nose epithelial cells for regulatory genes and discovered one, called p63, that was a previously known transcription factor that acts by controlling the transcription of other regulatory genes in epithelial stem cells, such as those in the skin, the lining of the airways and the prostate. By knocking out the p63 gene in mice, they showed that nasal olfactory stem cells rapidly differentiated into sensory neurons at the expense of the stem cells themselves.

"This gene produces a molecule that is like a brake on the stem cell," Fletcher said. "When the brake is on, stem cells self-renew. If you remove the brake, the stem cells go into differentiation."

A drug that regulates p63, or modulates one of the genes that p63, in turn, regulates, might be able to boost the number of nasal stem cells as well as the number that mature into smell neurons.

Because p63 is found in many epithelial tissues, Ngai noted, these findings could be applied to other adult tissue stem cells including stem cells in the skin and possibly lead to future therapeutic "cell replacement" strategies to take the place of damaged or dead cells not only in the nervous system but in other epihelial tissues in the body.

Article adapted by Medical News Today from original press release. Click 'references' tab above for source.
Visit our ear, nose and throat section for the latest news on this subject. Coauthors with Ngai and Russell are former graduate student Melanie S. Prasol, graduate student Jose Estrada, staff professionals Ariane Baudhuin and Yoon Gi Choi, and the late Karen Vranizan of UC Berkeley's Functional Genomics Laboratory.
The research is funded by the National Institute on Deafness and Other Communication Disorders of the National Institutes of Health, UC Berkeley's Siebel Stem Cell Institute, the California Institute of Regenerative Medicine and the National Science Foundation.
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