OHSU is one of three recipients of the Circle of Life Award this year, along with two others that were awarded citations of honor. The Circle of Life Award celebrates programs across the nation that have made great strides in palliative and end-of-life care.

OHSU was specifically honored for its Palliative Medicine and Comfort Care Team. OHSU is considered a national leader in palliative care: treating those with life-threatening illnesses through caring for the whole person, alleviating suffering and promoting the quality of life.

OHSU was also honored for its focus on research and education which are integral to the success of the program. Team members, working with the Center for Ethics in Health Care and supported by The Kinsman Foundation, have provided more than 16,440 person-hours of continuing education in palliative care basics and program development to 2,740 health care practitioners throughout the state of Oregon

“This award honors not only the specific work of the Palliative Medicine and Comfort Care Team but it also reflects the commitment of the entire OHSU community, from top administration to bedside nurses, to provide compassionate care,” said Paul Bascom, M.D., OHSU Team Medical Director and an Associate Professor in the Division of Hematology/Medical Oncology and the Department of Internal Medicine, OHSU School of Medicine.

The awards are supported in part by the California Healthcare Foundation, based in Oakland, Calif., and Archstone Foundation. Major sponsors include the American Hospital Association, the American Association of Homes and Services for the Aging, the Catholic Health Association, the National Hospice and Palliative Care Organization and the National Hospice Foundation. The American Academy of Hospice and Palliative Medicine and the Hospice and Palliative Nurses Association are 2009 Circle of Life co-sponsors.

“Dealing with life-threatening illness and end-of-life decisions is difficult for all involved and today’s Circle of Life honorees understand that respect, compassion and honesty are vital aspects of palliative care,” said American Hospital Association President and CEO Rich Umbdenstock. “As our nation looks to true health reform, end-of-life and palliative care will be important components and these honorees are truly inspirational and help serve as models.”

OHSU was chosen by a selection committee made up of leaders from medicine, nursing, social work, ethics, and health administration. The committee focused on innovative programs that respect patient goals and preferences, provide comprehensive care, acknowledge and address the family or caregivers’ concerns and needs and build systems and mechanisms of support to continue the program for future patients and caregivers.

This is the tenth year for the Circle of Life Award. For more information on the Circle of Life Award, visit www.aha.org/circleoflife.

About OHSU

Oregon Health & Science University is the state’s only health and research university and Oregon’s only academic health center. OHSU is Portland’s largest employer and the fourth largest in Oregon (excluding government). OHSU’s size contributes to its ability to provide many services and community support activities not found anywhere else in the state. It serves patients from every corner of the state, and is a conduit for learning for more than 3,400 students and trainees. OHSU is the source of more than 200 community outreach programs that bring health and education services to every county in the state.

About the AHA

The AHA is a not-for-profit association of health care provider organizations and individuals that are committed to the improvement of health in their communities. The AHA is the national advocate for its members, which include almost 5,000 hospitals, health care systems, networks and other providers of care. Founded in 1898, the AHA provides education for health care leaders and is a source of information on health care issues and trends.

]]> http://usapharmacyonline.org/?feed=rss2&p=4 http://usapharmacyonline.org/?p=5 http://usapharmacyonline.org/?p=5#comments Thu, 30 Jul 2009 05:00:00 +0000 admin medicine health http://usapharmacyonline.org/?p=5 Janet Davison Rowley, MD, a pioneer in demonstrating that cancer is a genetic disease, will receive the 2009 Presidential Medal of Freedom the White House announced Thursday. President Barack Obama will award the Medal of Freedom, the nation’s highest civilian honor, to Rowley and 15 others at a ceremony Wednesday, August 12.

The Medal recognizes “an especially meritorious contribution to the security or national interests of the United States, world peace, cultural or other significant public or private endeavors.” First established in 1945, the medal was reinstated by President John Kennedy in 1963 to honor distinguished civilian service in peacetime. Among the ten previous recipients affiliated with the University of Chicago are scientist James Watson, economists Gary Becker and Milton Friedman, and historians Hanna Gray and John Hope Franklin.

Rowley receives the award for her discovery of recurring chromosomal abnormalities in leukemias and lymphomas—findings that have revolutionized how cancer is understood and treated.

“These outstanding men and women represent an incredible diversity of backgrounds,” said President Obama. “Yet they share one overarching trait: Each has been an agent of change. Each saw an imperfect world and set about improving it, often overcoming great obstacles along the way. Their relentless devotion to breaking down barriers and lifting up their fellow citizens sets a standard to which we all should strive.”

“Janet Rowley’s work established that cancer is a genetic disease,” said Mary-Claire King, PhD, a geneticist at the University of Washington. “She demonstrated that mutations in critical genes lead to specific forms of leukemia and lymphoma, and that one can determine the form of cancer present in a patient directly from the cancer’s genes. This changed the way cancer was understood, opened the door to development of drugs directed at the cancer-specific genetic abnormalities and created the paradigm that still drives cancer research.”

“By showing that unique genetic abnormalities are the root cause of cancer, Rowley laid the foundation for personalized cancer care and targeted therapy,” said Richard L. Schilsky, MD, professor of medicine at the University of Chicago and past president of the American Society for Clinical Oncology.

“Janet was a pioneer in what is now called ‘translational research,’ the direct application of laboratory studies to understanding and treating human disease,” added colleague, leukemia specialist Richard Larson, MD, professor of medicine at the University of Chicago. “She opened a window that allowed us to see the genetic basis of the leukemias and other cancers. She has also been a champion of international collaboration for the advancement of science.”

Rowley, 84, the Blum-Riese Distinguished Service Professor of Medicine, Molecular Genetics & Cell Biology and Human Genetics at the University of Chicago, has received many honors, including both the Lasker Award and the National Medal of Science in 1998 and, most recently, this year’s Genetics Prize from The Peter and Patricia Gruber Foundation. She continues to head an active laboratory that focuses on the connections between genetic changes and cancer, especially leukemia.

Despite the long list of previous honors, she said she was “flabbergasted” when the call came from the White House Monday afternoon. “I was in total disbelief. “When I tried to tell my family I couldn’t help crying. I was overwhelmed for 24 hours.”

Before Rowley, few scientists suspected that chromosomal aberrations caused tumors. The established view at the time was that abnormal chromosomes were manifestations of generalized chaos within leukemia and lymphoma cells. But Rowley wondered if something else might be going on with those damaged pieces of DNA, and continued to examine thousands of chromosomes from patients.

Her persistence bore fruit. Beginning in 1972, she made a number of remarkable discoveries, including the landmark finding that an abnormally short chromosome associated with chronic myelogenous leukemia (CML) was not a chromosome deletion, as many scientists had thought, but an exchange (known as a translocation) of segments between two chromosomes.

The next struggle was to convince fellow researchers. “I became a kind of missionary,” she said, saying that chromosome abnormalities were important and hematologists should know about them. I got sort of amused tolerance at the beginning,” before the field gained credence.

Prior to this discovery, Rowley had an unusual career path. In 1940, at age 15, she enrolled as an undergraduate at the Hutchins College at University of Chicago, which combined the last two years of high school with the first two years of college. In 1945, she was one of only seven women out of 65 students entering the University of Chicago School of Medicine. In 1948, the day after graduating from medical school, she married fellow student, Donald Rowley. They had four children, all boys. She stayed home to raise them while working part-time with mentally disabled children, including children with Down syndrome, caused by an extra chromosome.

Her scientific career gained traction only in 1962. She traveled with her husband on his sabbatical to Oxford, where she learned newly developed techniques of chromosome analysis. Back in Chicago, at the request of her clinical colleagues, she used these techniques to study the chromosomes of patients with leukemia. For the next decade she labored over the microscope, searching amid the seeming genetic chaos of leukemic cells for consistent chromosome abnormalities. The first such abnormality had just been reported by Peter Nowell and colleague David Hungerford. They found that patients with chronic myelogenous leukemia had an abnormally small chromosome 22 in their tumor cells, which they labeled the “Philadelphia” chromosome.

The next step came in the early 1970’s when geneticists perfected the art of chromosome “banding,” a way of visualizing segments of chromosomes with more precision. Again, Rowley learned these techniques during a sabbatical in Oxford. They enabled her to discover that chromosomes from leukemic cells not only lost genetic material, they sometimes exchanged it. Early in 1972, Rowley discovered the first such “translocation,” an exchange of small pieces of DNA between chromosomes 8 and 21 in patients with acute myeloblastic leukemia. Later that same year, she found that the “Philadelphia” chromosome was also the result of a translocation. In patients with CML, a crucial segment of chromosome 22 broke off and moved to chromosome 9, where it did not belong. At the same time, a tiny piece of chromosome 9, which included an important cancer-causing gene, had moved to the breakpoint on chromosome 22. Because of this transfer from one chromosome to another, important genes that regulated cell growth and division were no longer located in their normal position on the chromosome. This provided critical evidence that cancer was a genetic disorder. Rowley and her colleagues subsequently identified several other chromosome translocations that were characteristic of specific malignancies, such as the 14;18 translocation seen in follicular lymphoma, and the 15;17 translocation that causes acute promyelocytic leukemia (APL). Quickly picking up on her lead that specific translocations defined specific forms of cancer, scientists around the world joined the search for chromosomes that either exchanged genetic material or in some cases lost it altogether in a process known as a “deletion.” Others used the translocations as road maps to narrow the search for specific genes that were disrupted by chromosome damage, thus opening up the current era of cancer genetics. Rowley’s contributions to identifying chromosomal abnormalities in leukemias and lymphomas have changed the way these diseases are diagnosed and treated. Today, newer techniques can identify the DNA damage within individual cells, offering a much more precise diagnosis of disease—and more effective treatments.

The research led to the development of the drug imatinib (Gleevec)—one of the most successful targeted cancer therapies to date—stems directly from Rowley’s work on the 9;22 translocation. Imatinib blocks the abnormal protein produced by that translocation.

She has also had an impact on the relationship between medical research and public policy. Rowley served on the President’s Council on Bioethics, established by President George Bush in 2001, where she advocated for fewer restrictions, including those placed on federally funded stem-cell research.”

Rowley’s research continues at her lab at the University of Chicago, where she has inspired and generously mentored countless students and postgraduate fellows. Cancer cytogenetics continues to fascinate her.

“We’re still working on the leukemias,” she says. “There’s a lot of evidence that translocations and other chromosome abnormalities aren’t sufficient to make a cell malignant. We’re looking for the other mechanisms involved.”

“I can’t think of anyone who deserved the award more or who would accept it more humbly,” said colleague Michelle Le Beau, PhD, director of the University of Chicago Cancer Research Center. “Janet has been a mentor for her colleagues as well as her trainees and an ongoing example of scientific wisdom and imagination combined with impeccable professional and personal style.”

The Medal of Freedom validates the enthusiasm that still inspires Rowley to bicycle from her Hyde Park home to her laboratory daily at the age of 84. “It’s a recognition not of me but of our research,” she said. “Our discoveries have had a major impact on the treatment and on the lives of patients with leukemia, especially those with CML.”

]]> http://usapharmacyonline.org/?feed=rss2&p=5 http://usapharmacyonline.org/?p=6 http://usapharmacyonline.org/?p=6#comments Thu, 30 Jul 2009 05:00:00 +0000 admin medicine health http://usapharmacyonline.org/?p=6 St. Louis, July 30, 2009 — Scientists at Washington University School of Medicine in St. Louis have identified a substance in the liver that helps process fat and glucose. That substance is a component of the common food additive lecithin, and researchers speculate it may one day be possible to use lecithin products to control blood lipids and reduce risk for diabetes, hypertension or cardiovascular disease using treatments delivered in food rather than medication.

“Currently, doctors use drugs called fibrates to treat problems with cholesterol and triglycerides,” says the study’s co-first author Irfan J. Lodhi, Ph.D., a post-doctoral fellow in endocrinology and metabolism. “By identifying this substance that occurs naturally in the body — and also happens to be used as a food additive — it may be possible to improve the treatment of lipid disorders and minimize drug side effects by adding particular varieties of lecithin to food.”

Lecithin is found at high concentrations in egg whites. It also is in soybeans, grains, fish, legumes, yeast and peanuts. Most commercially used lecithin comes from soybeans. Lecithin can alter food taste and texture and also can be mixed with water to disperse fats, making it a common additive in margarine, mayonnaise, chocolate and baked goods. Lecithin is a mixture of fatty compounds called phosphatidylcholines. Various types of phosphatidylcholines house different kinds of fatty molecules linked to a common core.

This new study demonstrates that in the liver, a specific type of lecithin binds with a protein called PPAR-alpha, allowing PPAR-alpha to regulate fat metabolism. Scientists long have known that PPAR-alpha is involved in lipid and glucose metabolism. When doctors prescribe fibrate drugs to lower triglycerides and elevate good cholesterol in the blood, those drugs work by activating PPAR-alpha.

Although fibrates activate the protein, no one previously had identified any naturally occurring substance that could perform that task. Reporting in the Aug. 7 issue of the journal Cell, the Washington University research team describes how it found the link between lecithin and PPAR-alpha.

They first created a strain of mice that could not make fatty acid synthase in the liver. When humans or animals eat, we take in sugars. Fatty acid synthase converts those sugars to fatty acids in the liver, where they play important roles in energy metabolism.

“To our surprise, animals missing fatty acid synthase in the liver were just like animals that couldn’t make PPAR-alpha. They had lower fasting insulin levels, and they were prone to develop fatty liver disease,” says senior investigator Clay F. Semenkovich, M.D., the Herbert S. Gasser Professor and chief of the Division of Endocrinology, Metabolism and Lipid Research. “When we gave the animals fibrate drugs that activated PPAR-alpha, the mice returned to normal, leading us to suspect that fatty acid synthase also was involved in the activation of PPAR-alpha. Although we knew that fibrate drugs would regulate PPAR-alpha, we also knew that our ability to regulate the metabolism of fats and sugars was in place long before humans started making drugs. But until now, no one had identified how it worked.”

Semenkovich, Lodhi, John Turk, M.D. Ph.D., professor of medicine and of pathology, and the rest of the team used mass spectrometry and gene expression studies to isolate the phosphatidylcholine, or lecithin compound, that activated PPAR-alpha in the liver.

One reason fatty acid synthase had never been connected to PPAR-alpha function was the distance of the two proteins from each other, according to Semenkovich. PPAR-alpha is a nuclear receptor. That is, it’s housed in the nucleus of the cell. Fatty acid synthase, on the other hand, lives out in the cell body, or cytoplasm.

“The neighborhoods where PPAR-alpha and fatty acid synthase live aren’t very close together,” says Semenkovich. “The synthase is way out in the cytoplasm — that’s like being in the suburbs — whereas the PPAR-alpha lives right in the middle of the ‘city.’ These are all microscopic distances, but to the cell, they’re worlds apart, so it’s amazing that the two are linked.”

It’s also fortunate, he says, that an extremely common compound like lecithin binds to a key drug target like PPAR-alpha.

“That information could be used to make better drugs or even to develop what people sometimes refer to as nutriceuticals — nutrients that have pharmaceutical-like properties,” Semenkovich says.

Chakravarthy MV, Lodhi IJ, Malapaka RV, Xu HE, Turk J, Semenkovich CF. Identification of a physiologically relevant endogenous ligand for PPARα in liver. Cell, vol. 138, pp. 1-13, Aug. 7. 2009

This work was funded by grants from the National Institutes of Health, the Jay and Betty Van Andel Foundation and the American Diabetes Association.

Washington University School of Medicine’s 2,100 employed and volunteer faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Children’s hospitals. The School of Medicine is one of the leading medical research, teaching and patient care institutions in the nation, currently ranked third in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Children’s hospitals, the School of Medicine is linked to BJC HealthCare.

The findings appear in the January issue of Neuropsychology, which is published by the American Psychological Association (APA).

The study may help rule out the possibility of very early Alzheimer’s as the cause of the declines among carriers before they reach old age. Write the authors, “[Alzheimer’s disease] processes may occur later in the lifespan and add to normal cognitive aging to produce a dementia syndrome.”

The study confirmed that carriers of the APOE4 gene type (allele), which confers higher risk for Alzheimer’s, are just like other people their age throughout most of adult life in terms of core mental functions. Previous findings had been unclear. Lead author Anthony Jorm, PhD, DSc, explains, “Although some areas of cognitive decline begin from early adulthood onwards, this is not due – as some have speculated — to very early Alzheimer’s changes in the brain.”

The APOE gene helps to transport cholesterol through the production of apolipoprotein E. People carry two copies of APOE, each being one of four APOE alleles. APOE4 raises Alzheimer’s risk. In this study, researchers at the University of Melbourne and Australian National University assessed whether the small percentage (varying by ethnicity) of the population that carries at least one copy of APOE4 are cognitively different from non-carriers long before anyone shows signs of dementia.

The authors studied 6,560 people living in Canberra or neighboring Queanbeyan enrolled in the PATH Through Life Project, a long-term study of aging that assesses people in the age groups of 20-24, 40-44, and 60-64 years every four years for a period of 20 years. Jorm and his colleagues evaluated whether, in each age group, carriers of APOE4 (27 percent in their sample) were significantly different from non-carriers on tests of functions affected by Alzheimer’s: episodic memory, working memory, mental speed, reaction time, and reading vocabulary.

Performance on all tests (except for reading vocabulary, which tends to hold up with age) declined across age groups, a sign of normal cognitive aging. However, APOE4 did not affect performance at any age. Thus the researchers conclude that at least between ages 20 and 64, people with APOE4 age normally in those central cognitive functions.

This finding suggests that APOE4 heightens the risk for Alzheimer’s in old age through an additional, as-yet-unknown process that accelerates or intensifies normal changes, pushing them into the range of disease. Jorm provides an analogy. “In general, hair becomes thinner with age,” he says. “However, there are some people who have an additional hereditary factor that makes them bald at an early age.”

Article: “APOE Genotype and Cognitive Functioning in a Large Age-Stratified Population Sample;” Anthony F. Jorm, PhD, DSc, University of Melbourne and Australian National University, and Karen A. Mather, PhD, Peter Butterworth, PhD, Kaarin J. Ansley, PhD, Helen Christensen, PhD, and Simon Easteal, PhD, Australian National University; Neuropsychology, Vol 21. No. 1.

(Full text of the article is available from the APA Public Affairs Office and at http://www.apa.org/journals/releases/neu2111.pdf )

Anthony Jorm can be reached by email at ajorm@unimelb.edu.au or by phone at 44 (0) 613 93423747.

The American Psychological Association (APA), in Washington, DC, is the largest scientific and professional organization representing psychology in the United States and is the world’s largest association of psychologists. APA’s membership includes more than 150,000 researchers, educators, clinicians, consultants and students. Through its divisions in 54 subfields of psychology and affiliations with 60 state, territorial and Canadian provincial associations, APA works to advance psychology as a science, as a profession and as a means of promoting human welfare.

The test may provide physicians with a tool to guide patient treatment by predicting if a patient is likely to become resistant to a particular HIV drug, said one of its developers, Feng Gao, M.D., associate professor of medicine. Drug resistance is one of the most common reasons why therapy for HIV, the virus that causes AIDS, fails.

The test, which detects genetic changes, or mutations, in HIV, also may help scientists understand how the constantly evolving virus develops drug resistance, Gao said. He said such knowledge ultimately may result in the development of new treatments designed to evade resistance.

The findings will appear online on Sunday, Jan. 7, 2007, in the journal Nature Methods, as well as in the journal’s February 2007 print edition. The work was supported by the National Institutes of Health and the Duke Center for AIDS Research.

Duke has filed for a provisional patent on the technology, and the researchers are considering ways to establish a new company to pursue its development or to license the technology to an existing company, Gao said.

Because HIV genes mutate so easily and the virus reproduces so rapidly, most people who are infected have many different forms of the virus in their bodies. In some cases, mutated strains take on new properties that make them more resistant to the drugs used in antiretroviral therapy, the primary means of treatment for HIV infection.

During antiretroviral therapy that does not fully suppress the virus, a strain that develops drug resistance will grow more quickly than strains lacking such resistance, and the resistant strain will replicate to become the most prominent virus in the person’s body.

“The viral populations found in the blood of one patient can be very different from the populations present in another,” Gao said. “Which resistant viruses are at hand can have important implications for the successful treatment of that patient.”

More than 20 drugs currently are available for treating HIV infection. All but one of the drugs target two of the genes that serve as blueprints for vital protein components of HIV: reverse transcriptase and protease.

The Duke test examines the genes of HIV strains for mutations at certain positions that are known to be linked to drug resistance. For example, a change at a specific spot along the genetic code — position 46 — of the protease gene results in resistance to the drug indinavir.

To assess the test, the researchers analyzed blood samples from three different groups of HIV patients: those who had never received antiretroviral treatment, those who had received treatment but were not currently being treated and those who were receiving treatment but the treatment was not completely successful.

After processing the blood samples and isolating the genetic material in each of them, the researchers added tiny fluorescent tags designed to stick to HIV genes in particular ways. Tags designed to stick to mutated gene locations known to produce drug resistance were labeled to appear green, while tags designed to stick to the same gene locations but where the genes had not mutated were labeled to appear red.

The researchers used a sophisticated computer program to count the number of molecules with green or red fluorescent tags in each sample. The test proved sensitive enough to detect a single mutated virus out of 10,000 nonmutated viruses in the patient samples, Gao said.

“This level of sensitivity makes the assay about 1,000 times more sensitive than the most widely used assays on the market for detecting drug-resistant HIV viruses” Gao said. “Thus, the assay may permit more accurate prediction of treatment outcomes.”

The test also can detect when a virus molecule has more than one mutation, a capability that no commercially available test has achieved, Gao said. This capability may prove critical for detecting HIV strains that have become resistant to multiple drugs, a condition that occurs often as many patients are treated with many drugs at the same time.

The test may find broader medical application as well, Gao said. He said it has the potential to detect mutations that confer drug resistance in infectious agents that cause other diseases besides HIV, such as hepatitis B, hepatitis C and tuberculosis.

Other researchers participating in the study were Fangping Cai, Haifeng Chen, Charles B. Hicks, John A. Bartlett and Jun Zhu.

“Our hope is that these cells will provide a valuable resource for tissue repair and for engineered organs as well,” said Anthony Atala, M.D., senior researcher and director of the Institute for Regenerative Medicine at Wake Forest University School of Medicine.

Atala announced the breakthrough with colleagues from Wake Forest University School of Medicine and Harvard Medical School.

“It has been known for decades that both the placenta and amniotic fluid contain multiple progenitor cell types from the developing embryo, including fat, bone, and muscle,” said Atala. “We asked the question, ‘Is there a possibility that within this cell population we can capture true stem cells?’ The answer is yes.”

Atala and colleagues discovered a small number of stem cells in amniotic fluid –
estimated at 1 percent – that can give rise to many of the specialized cell types found in the human body. The scientists believe the newly discovered stem cells, which they have named amniotic fluid-derived stem (AFS) cells, may represent an intermediate stage between embryonic stem cells and adult stem cells. They have markers consistent with both cell types.

“It took this long to verify that we had a true stem cell,” said Atala, who began the work seven years ago. “These cells are capable of extensive self-renewal, a defining property of stem cells. They also can be used to produce a broad range of cells that may be valuable for therapy.”

An advantage of the AFS cells for potential medical applications is their ready availability. The report describes how the cells were harvested from backup amniotic fluid specimens obtained for amniocentesis, a procedure that examines cells in this fluid for prenatal diagnosis of certain genetic disorders. Similar stem cells were isolated from “afterbirth,” the placenta and other membranes that are expelled after delivery.

Atala said a bank with 100,000 specimens theoretically could supply 99 percent of the U.S. population with perfect genetic matches for transplantation. There are more than 4 million live births each year in the United States.

In addition to being easily obtainable, the AFS cells can be grown in large quantities because they typically double every 36 hours. They also do not require guidance from other cells (termed “feeders”) and they do not produce tumors, which can occur with certain other types of stem cells. The scientists noted that specialized cells generated from the AFS cells included all three classes of cells found in the developing embryo - termed ectoderm, mesoderm, and endoderm. In their high degree of flexibility and growth potential, the AFS cells resemble human embryonic stem cells, which are believed capable of generating every type of adult cell.

“The full range of cells that AFS cells can give rise to remains to be determined,” said Atala. “So far, we’ve been successful with every cell type we’ve attempted to produce from these stem cells. The AFS cells can also produce mature cells that meet tests of function, which suggests their therapeutic value.”

The functional tests included implanting neural cells created from AFS cells into mice with a degenerative brain disease. The cells grew and “re-populated” the diseased areas. In addition, bone cells produced from the stem cells were successfully used to grow bony tissue in mice, and liver cells were able to secrete urea, which the liver produces from ammonia.

The potential to generate a broad range of mature cell types is why many scientists believe stem cells have promise to replace damaged cells and tissue in conditions such as spinal cord injuries, diabetes, Alzheimer’s disease and stroke.

Embargoed for Release at 1 p.m. ET on Sunday, Jan. 7, 2007

Co-researchers were Paolo De Coppi, M.D., Georg Bartsch Jr., M.D., M. Minhaj Siddiqui, M.D., Tao Xu, Ph.D., Cesar C. Santos, M.D., Laura Perin, Ph.D., James J. Yoo, M.D., Ph.D., Mark E. Furth, Ph.D., and Shay Soker, Ph.D., all with Wake Forest University, and Gustavo Mostoslavsky, Ph.D., Evan Y. Snyder M.D., and Angéline C. Serre, all with Harvard Medical School.

Media Contact: Shannon Koontz, shkoontz@wfubmc.edu, at 336-716-4587.

Interviews: Requests for individual interviews are welcome. In addition, a one-hour teleconference will be held from 2:30 to 3:30 p.m. EST on Friday, Jan. 5. To join the conference, dial (800) 230-1951 (USA), or (612) 332-1213 (International calls.) Ask for the “Dr. Atala Briefing.” Digitized replay of the conference will be available at 6 p.m. EST by dialing (800) 475-6701 (USA) or (320) 365-3844 (International) and using Access Code: 857490.

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Wake Forest University Baptist Medical Center is an academic health system comprised of North Carolina Baptist Hospital and Wake Forest University Health Sciences, which operates the university’s School of Medicine. Wake Forest University School of Medicine ranks 35th in research funding by the National Institutes of Health. Almost 150 members of the medical school faculty are listed in Best Doctors in America.