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February 6, 2012

In 2004, concerns about antidepressant drugs increasing suicidal thoughts and behaviors in young patients prompted the FDA to issue a rare “black box warning.” Now, a new analysis of clinical trial data finds that treatment with the antidepressant fluoxetine did not increase — or decrease — suicidality in children compared to placebo treatment.

An analysis built on data from 41 trials and more than 9,000 patients also found that two different popular antidepressant drugs were effective at reducing suicidal behavior and depressive symptoms in adult and geriatric patients. The findings are published online Feb. 6 in the journal Archives of General Psychiatry.

The failure to replicate the link between antidepressants and suicide should reassure doctors about prescribing these drugs to depressed patients, said first author Robert Gibbons, PhD, professor of medicine, health studies, and psychiatry at the University of Chicago Medicine.

“The key finding here, when we re-analyze all the patient-level longitudinal records in these studies, is that antidepressants neither increase nor decrease suicidal thoughts or behavior in children,” Gibbons said.

The FDA decision on the black box warning was based on retrospective data from 25 clinical trials of newer antidepressant medications, including the serotonin reuptake inhibitor drug fluoxetine, marketed as Prozac or Sarafem. A meta-analysis combining adverse event data (primarily based on self reports of suicidal thoughts) from the trials revealed a small, but significant, increase in suicidal thoughts and behavior in children and young adults up to the age of 25.

For the new analysis, Gibbons and colleagues from the University of Illinois at Chicago, the University of Miami and Columbia University obtained individual-level, longitudinal clinical trial data — some of it unpublished — from pharmaceutical producers and a large National Institute of Mental Health collaborative study of fluoxetine and venlafaxine. The data included weekly screening of each trial subject for depression and suicidal thoughts, allowing researchers to compare the effect of drug or placebo over time on these measures.

In the analysis of the adult and geriatric trials testing fluoxetine or venlafaxine, both antidepressants were found effective in reducing suicide risk and depression symptoms. These two effects were also found to be statistically associated, suggesting that the drugs reduced suicidality by alleviating depression. Therefore, Gibbons said, effective treatment of major depressive disorder is important for a patient’s safety.

“Basically, the results say that the mechanism by which the antidepressants affect suicide rates is by decreasing depression,” Gibbons said. “It follows that if a treatment is not working for an individual, the risk for suicidal behavior and perhaps worse remains high.”

To analyze the effects of antidepressants in children, the researchers used four trials of fluoxetine, which until recently was the only antidepressant approved for pediatric use. Once again, a reduction in depressive symptoms was observed in the drug-treated population compared to placebo. However, no significant change in suicide risk was detected between the two patient groups.

“I think that this paper supports the general idea that the effects of antidepressants in kids and adults are not really the same, since we don’t see anything but beneficial effects of antidepressants in adults and geriatrics,” Gibbons said. “In kids, we don’t see a harmful effect, but we do see a disassociation between the beneficial effects on depression and the potential beneficial effect on suicide.”

“This raises continued questions about what’s going on in children,” he continued. “Maybe children think about suicide in part because of depression, but also maybe due to other reasons not related to depression that are not affected by antidepressants.”

Gibbons, who sat on the Food and Drug Administration panel that considered placing the black box warning on antidepressants, said he hoped the new results would reassure clinicians about the safety of the drugs. Previous research by his group found that the addition of the warning significantly reduced antidepressant prescriptions to both children and adults and correlated with a spike in suicide rates.

“I hope that the warnings will not prevent depressed children and adults from getting treatment for depression,” Gibbons said. “The greatest cause of suicide is untreated or undiagnosed depression. It’s very important that this condition be recognized and appropriately treated and not discarded because doctors are afraid to be sued.”

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February 3, 2012

There are ways in which patients who leave the hospital against medical advice wind up paying for that decision. Being saddled with the full cost of their hospital stay, however, is not one of them.

Insurance companies know this. Patients who walk out may know this. But many physicians, according to a study published in the Journal of General Internal Medicine, do not.

A survey of general internal medicine doctors at the University of Chicago Medicine found that two-thirds of residents and almost half of attending physicians believe that when a patient leaves the hospital against medical advice, insurance companies will not pay for the patient’s hospitalization, leaving the patient liable for the full hospital bill.

“We have all heard this, and many physicians may have passed it on to their students, even to patients threatening to leave on their own,” said study author Vineet Arora, MD, associate professor of medicine at the University of Chicago Medicine. “But a closer look revealed this to be a myth, a medical urban legend, albeit a pervasive one.”

“This is a misconception that we need to correct,” she added. When patients leave the hospital against their doctor’s advice, “that indicates a breakdown in the doctor-patient relationship.”

Co-author Gabrielle Schaefer, a third-year medical student at the University of Chicago, said some physicians even will use the financial obligation angle as a threat to persuade a patient to stay. “But when a physician provides misinformation in order to influence a patient’s decisions — no matter how well intentioned — it compounds the loss of trust,” she said.

Every year, 1 to 2 percent of patients admitted to U.S. hospitals leave against medical advice. The number of patients who do this seems to be increasing: from 264,000 patients in 1997, to 368,000 in 2007, to nearly 500,000 in 2011. Studies demonstrate that those who leave against medical advice, or AMA, are much more likely to die or be readmitted within 30 days.

The researchers, all from the University of Chicago Medicine, combed through the records of more than 46,000 patients admitted to the general medicine service at the medical center’s adult hospital between July 2001 and March 2010. They found that 526 patients, about 1 percent, had left against doctor’s orders.

Consistent with previous studies, most of these patients had government-funded insurance, either Medicare or Medicaid (78 percent), or no insurance (14 percent). The average hospital charge was nearly $28,000, of which insurance paid on average almost $6,000. (Most patients also owe a minimal co-pay.) So leaving against medical advice brought no additional financial burden to the patient.

Of the 453 insured patients who left AMA, payment was initially denied in only 18 cases. All of those cases involved problems with the bill, not with the patient’s behavior. None of those patients were denied coverage for leaving against doctors’ orders.

A survey of internal medicine residents and attending physicians, however, found many did believe payment would be denied and warned patients that they could be held financially responsible if they left against medical advice.

An expanded survey found similar beliefs among residents at other Chicago-area hospitals, with more than 40 percent agreeing that they “often or always inform patients that they may be held financially responsible if they leave AMA.” Consent forms for patients leaving AMA from two area hospitals warned patients about possible financial consequences.

One member of the research team — John Schuman, MD, now at the University of Oklahoma School of Community Medicine — followed up the published study with a less formal survey.

“I thought it important to go to the source,” he wrote in GlassHospital, his health care blog. “I called the insurance companies themselves. I talked with VPs and media relations people from several of the nation’s largest private insurance carriers. Each of them told me that the idea of a patient leaving AMA and having to foot their bill is bunk.”

“They were glad to tell me so,” he added, “as this was a rare occasion of insurance companies looking magnanimous.”

The Agency for Healthcare Research and Quality and the National Institute on Aging funded this study. Additional authors include Heidi Matus, Keith Sauter, Ben Vekhter and David Meltzer.

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January 31, 2012

The current system for allocating donated lungs based on proximity and not on need appears to decrease the potential benefits of lung transplantation and increase the number of patients who die waiting, researchers said at an annual meeting of thoracic surgeons in Fort Lauderdale, Fla.

Using data provided by the United Network for Organ Sharing (UNOS), study author Mark J. Russo, MD, MS, and colleagues at the University of Chicago and Columbia University found that donor lungs were routinely allocated to less urgent, local candidates even when there were patients within the region but outside the local donor service who were in much greater need.

Among the 580 locally allocated double-lung transplants performed in 2009, 480 less needy candidates, or 83 percent of all double-lung transplants, received the organs even though a well-matched candidate in greater need existed in the region.

Twenty-four percent of such cases involved skipping over regional candidates with lung allocation scores — which range from 1 to 100, based on need and likely benefit — more than 10 points higher than the local recipient. More than 7 percent of the events involved a regional candidate with a lung allocation score (LAS) more than 25 points higher than the local recipient. Overall, 185 of the bypassed regional candidates ultimately died on the waitlist.

More than a decade ago, the U.S. Department of Health and Human Services issued the “Final Rule,” intended to ensure that organs were allocated “based on medical criteria, not accidents of geography.” The new data, however, show that where a transplant candidate lives continues to influence access to donated lungs.

“We found that too often, and to many patients’ detriment, organs are allocated according to geography rather than urgency,” said Russo, assistant professor of surgery at the University of Chicago Medicine. When lungs go to less needy candidates within the local Donor Service Area and never become available to sicker candidates at the regional or national level, “this decreases the overall benefits of a transplant,” he said.

One unfortunate but not unusual example was a 27-year-old man with cystic fibrosis who was in an intensive care unit awaiting a lung transplant. He had a lung allocation score of 91 out of 100, one of the highest of such scores in the U.S. at the time. He was expected to die within a week without a transplant.

An appropriately matched lung donor did became available less than 20 miles from the hospital where this man was waiting, but because the candidate was just outside of the donor’s local service area, two candidates from within the service area, each with an LAS in the 40s, took priority. One of these candidates received the organs. Five days later the 27-year-old patient died.

Such circumstances are not uncommon, Russo said.

“Ideally, a suitable donor organ would be available for every person who could benefit from transplantation,” he said. “Unfortunately, there remains a critical scarcity of donor organs. More efficient allocation of this scarce and precious resource could dramatically increase the overall benefit from lung transplantation.”

Russo and colleagues previously demonstrated that 82 percent of lung transplants went to patients with an LAS of less than 50. For patients in this low-priority group, five-year life expectancy even without transplant is good — better than 50 percent.

For these patients, early transplantation brings limited survival benefit, he said.

“At the same time,” Russo said, “candidates most in need and who could receive the greatest benefit are dying at high rates without the benefit of transplantation.” Most patients with high LAS are still alive after five years if they get transplanted quickly, but very few of those who do not get an organ survive more than a few months.

This study considered only double-lung candidates. It did not factor in the possibility of national matching or allow for blood groups to be crossed. As a result, “it likely underestimates the frequency of these events and lives lost,” Russo said. “Despite recent improvements in lung allocation, significant inefficiencies remain, resulting in diminished net benefit from transplantation and lost lives.”

The paper, “Local Allocation of Donor Lungs Results in Transplanting Lower Priority Lung Transplant Candidates,” by M. J. Russo, D. Meltzer, R. Gibbons, W. T. Vigneswaran of the University of Chicago and A. Iribarne and J. R. Sonett of Columbia University, is being presented at the annual meeting of the Society of Thoracic Surgeons on Tuesday, Jan. 31, 2012.

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January 25, 2012

Janet Davison Rowley, MD, the Blum-Riese Distinguished Service Professor of Medicine, Molecular Genetics & Cell Biology and Human Genetics at the University of Chicago, will share the 2012 Japan Prize for Healthcare and Medical Technology with Brian J. Druker, MD, from the Oregon Health and Science University, and Nicholas B. Lydon, PhD, formerly with Novartis. They were chosen for their roles in the development of the first precisely targeted anti-cancer drug, called imatinib (Gleevec^®).

The three recipients, according to the Japan Prize Foundation’s announcement on Jan. 25, “have made significant contributions to society by achieving momentous scientific and technological breakthroughs in creating and promoting new technologies for medical diagnosis and treatment.”

They each will receive a Certificate of Merit, a Japan Prize Medal and an equal share of 50 million Japanese yen (approximately $215,000 apiece).

“I am proud and humbled to join the previous winners who included the world’s most distinguished scientists.” Rowley said in her pre-recorded acceptance speech. “I am especially delighted to share this honor with eminent scientists who built on my discovery of the translocation and the work of others to develop a treatment that has turned this leukemia into a chronic disease for many patients.”

Imatinib is a highly effective leukemia medication with few side effects. Most conventional treatments for cancer have been based on their ability to kill rapidly dividing cells. The challenge has been finding a treatment that doesn’t harm healthy cells. A series of discoveries enabled the prize winners to develop a more focused medication, designed to interfere with the specific proteins that cause rapid multiplication of the cells that cause chronic myelogenous leukemia (CML), but without damaging healthy cells.

Rowley, Druker and Lydon were key players in a four-decade sequence of breakthroughs leading to the development of Gleevec. It began in the 1960s when two Philadelphia researchers — Peter Nowell and David Hungerford — found that patients with CML had an abnormally small chromosome 22 in their tumor cells, which was labeled the “Philadelphia” chromosome.

In 1973, using newly developed methods for visualizing segments of chromosomes, Rowley showed that chromosomes from CML cells did not lose genetic material, but rather they exchanged it, a phenomenon she has described in several types of leukemia.

The Philadelphia chromosome was the result of such 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 positions on the chromosome.

Other scientists used this discovery as a road map to narrow the search for specific genes that were disrupted by chromosome translocations. In 1993, Lydon — a medicinal chemist at Ciba-Geigy, later purchased by Novartis — began a collaboration with Druker, who had created cellular models of the genetic changes that drive CML. The two physicians developed the lead candidate drug from this program, then known as STI-571, and showed that Lydon’s drug exerted powerful effects against Druker’s CML cells.

In subsequent clinical trials, led by Druker, imatinib “shocked the world of clinical medicine,” according to the Japan Prize Foundation. It demonstrated dramatic clinical effectiveness in reducing leukemia cells, achieving long-term remissions in more than 90 percent of patients with CML. It was approved by the Food and Drug Administration in 2001 and has proved effective against several other cancers caused by similar genetic mechanisms.

“Before the development of the molecularly targeted drug imatinib, CML was a fatal disorder where patients progressed to blastic crisis within a few years and died due to a treatment-refractory acute leukemia,” notes the Foundation’s Award Citation. The molecular-targeting approach used to develop Imatinib, has given “great hopes for the future of cancer drug development.”

For this “extraordinary achievement, the development of a revolutionary therapy for cancers,” the Foundation has deemed Rowley, Druker and Lydon “most eminently deserving of the 2012 Japan Prize given to honor contributions in the field of Healthcare and Medical Technology.”

The Japan Prize Presentation Ceremony will be held in April in the presence of Their Majesties, the Emperor and Empress of Japan, with leaders “from every field of endeavor” in attendance.

Rowley, 86, has received many honors, including the Lasker Award, the National Medal of Science and the Presidential Medal of Freedom, the nation’s highest civilian honor. In December, the American Society of Hematology honored Rowley and Druker with its 2011 Ernest Beutler Lecture and Prize for their work on CML. Druker and Lydon received the Lasker Award in 2009.

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.

She continues to head an active laboratory at the University of Chicago that focuses on the connections between genetic changes and cancer. For further information regarding the Japan Prize, please visit www.japanprize.jp

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Janet Rowley, MD, to receive Japan Prize for her role in the development of targeted cancer therapy | Chicago Press Release Services - Chicago's leading press release newswire service; professional press release services, press release distribution and newswire services.

January 19, 2012

The impact of efforts by the U.S. Food and Drug Administration to notify the general public and health care providers about unanticipated risks from approved medications has been “varied and unpredictable,” according to a systematic review of published studies about FDA warnings and alerts over the last 20 years.

Although some communication efforts had a strong and immediate effect, many had little or no impact on drug use or health behaviors and several had unintended consequences, researchers report in the journal Medical Care.

“Communicating risk to large groups of people is a complex science,” said study director G. Caleb Alexander, MD, associate professor of medicine at the University of Chicago. “But success or failure at this can have significant consequences. As such efforts become more and more common — with the FDA’s mandate to establish a more active surveillance system — we will need a better understanding of how to make them work and where they can go wrong. And we need more and better studies of the successes and failures of this process.”

The FDA has several standard tools to disseminate new evidence about drug safety. These include “Dear Healthcare Provider” letters to prescribers, “public health advisories” and “Safety Alerts” targeting the general public, and “black box warnings” added to a label when a drug’s risks may be particularly severe or affect a large population. Despite numerous studies examining single alerts, advisories and label changes, no prior study has systematically examined the effect of these risk communications.

The researchers — from the University of Chicago Medical Center, North Shore University HealthSystem, Johns Hopkins Medicine and Harvard Medical School — combed through the literature on the topic. They screened 1,432 articles published between 1990 and 2010. Only 49 reports had a primary goal of assessing the consequences of FDA risk communications for prescription drugs. One-third of those articles focused on antidepressants.

The researchers sorted FDA risk communications into four categories: warnings about serious adverse events, recommendations against use in specific patient populations, preventing harmful drug-drug interactions, and calls for increased laboratory or clinical monitoring.

The most effective notices were those warning the public about potential serious adverse events, but even these varied in their impact. For example, several studies found that patients shifted away from the diabetes drug rosiglitazone after an FDA alert noted an increased risk of cardiovascular events with this drug. This led to decreased use of rosiglitazone and increased use of other, less risky anti-diabetes drugs.

A similar 2010 FDA warning for asthma patients, however, had little effect. It stressed that one class of asthma medications known as long-acting beta agonists should not be used without an asthma controller medication, such as inhaled corticosteroids. Rates of controller medication use with long-acting beta agonists were low before the FDA warning and did not significantly increase after the advisory was issued.

Recommendations that specific groups of patients avoid certain medications sometimes decreased use, but also produced unintended consequences. The most notable was a series of advisories about the use of antidepressants among children and adolescents. The widely publicized alerts significantly decreased use of these medications by adults as well as children, and one study suggested an unexpected increase in suicides among children and adolescents due to increases in untreated depression.

FDA warnings about harmful drug-drug interactions had some impact, although reductions in co-prescribing that occurred often required repeated risk advisories and took months to years. For example, initial messages to reduce the use of cisapride with contraindicated products were first sent in February 1995, but large changes in cisapride co-prescribing were not observed until after the third alert sent in June 1998.

A fourth category, recommendations to increase clinical or laboratory monitoring for patients taking certain drugs, produced “no evidence of a large or sustained impact of the FDA recommendations.” For example, recommendations to monitor patients using antipsychotic medications for hyperlipidemia and diabetes showed no changes in glucose testing following the FDA advisory.

Part of the problem, the authors emphasize, is the challenge of communicating complex risk messages to a large, diverse audience. “The most effective communications were the simplest, those that were specific, where alternatives were available, and where the messaging was reinforced over time,” said Stacie Dusetzina, PhD, lead author from Harvard Medical School.

The study was funded by the Agency for Healthcare Research and Quality and an NIH Clinical and Translational Science Award to the University of Chicago. Additional authors include Haiden Huskamp from Harvard; Ashley Higashi, Rena Conti and Shu Zhu from the University of Chicago; Ray Dorsey from Johns Hopkins; and Craig Garfield from North Shore.

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January 23, 2012

The University of Chicago Medical Center, one of the leading academic medical institutions in the country, is introducing a new brand as it prepares to open a modern 10-story hospital on its South Side campus next January.

The launch of the University of Chicago Medicine marks a new era in the institution’s decades-long history as it seeks to strengthen the connection between the internationally renowned University of Chicago and its clinical programs. University of Chicago Medicine unifies the promise of compassionate, state-of-the-art patient care with a renewed commitment by its doctors, nurses, medical specialists, scientists, faculty and staff that medicine is at the core of the University’s clinical, educational and scientific missions.

“This brand allows us to signal to our patients, referring physicians, and the greater Chicago community the dramatic and exciting changes happening at the University of Chicago and its new state-of-the-art medical facility,” said Kenneth Polonsky, MD, dean and executive vice president for Medical Affairs.

The unveiling of the University of Chicago Medicine coincides with the one-year countdown to the opening of the New Hospital Pavilion, a 1.2-million-square-foot hospital that incorporates the latest in technology with in-patient and operating room design, allowing the hospital to continually modify for future technology. The New Hospital Pavilion is a bold symbol of the new brand and the commitment to technical sophistication in science and health care, coupled with impeccable standards of service, patient safety and clinical quality.

The new hospital will continue to foster collaboration with the best minds in medicine from across the University’s intellectual spectrum, with the most advanced technology and research to address the greatest challenges in the changing world of health care.

“Our new building is the embodiment of those changes,” said University of Chicago Medical Center President Sharon O’Keefe. “With Medicine as our main brand, we make it clear that medicine is what we do, it’s who we are and it’s where we continue to set the standards — at the forefront of medicine.”

The new hospital project has become an economic engine fueling minority- and women-owned businesses in the Chicago area. As of December 2011, $195.7 million had been awarded and paid in contracts to minority- and women-owned business enterprises, such as material suppliers, construction contractors and professional services firms, and paid in wages to minority and women laborers. The amount of money paid in contracts to minority- and women-owned businesses is more than 49 percent of the total spent for the project.

The University of Chicago Medicine will host a series of events throughout the year to highlight the new hospital leading up to the grand opening in January 2013, including a community open house and events with community leaders from the South Side and elsewhere, city and state legislators, business leaders and philanthropists.

The University of Chicago’s direct involvement in health care began in 1927 with the opening of Billings Hospital. The medical center is consistently recognized as a leading provider of sophisticated medical care. University of Chicago physician-scientists performed the first organ transplant and the first bone marrow transplant in animal models, the first successful living-donor liver transplant, the first hormone therapy for cancer and the first successful application of cancer chemotherapy. Its doctor-scientists also discovered REM sleep and were the first to describe many of the stages of sleep. Twelve of the 87 Nobel Prize winners who have been associated with the University of Chicago have won the prize for discoveries related to biology or medicine.

Frequently Asked Questions: University of Chicago Medicine Brand

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January 17, 2012

Four members of the faculty in the Biological Sciences Division — Habibul Ahsan, Peter Angelos, David Song and Jerrold Turner — have received named professorships.

Habibul Ahsan, MD, MMedSc, professor in the departments of health studies, human genetics and medicine, director of the Center for Cancer Epidemiology and Prevention at the University of Chicago Medical Center and associate director of the University of Chicago Comprehensive Cancer Center, has been named a Louis Block Professor.

Ahsan studies the relationships between environmental and genomic factors in cancer and other diseases to understand the pathogenesis, prognosis and prevention of diseases of broad public health significance. He has published extensively on the large-scale epidemiology, genetic susceptibility and prevention of health effects of arsenic exposure, from contaminated wells in parts of Bangladesh, and also on the molecular and genetic epidemiology of breast and other cancers.

Since 2000, Ahsan has led the Health Effects of Arsenic Longitudinal Study, or HEALS. This study examines the long-term consequences of arsenic exposure — a problem that affects nearly a third of the population of Bangladesh — on a sample of 20,000 men and women in Bangladesh. In 2010, his team showed that the risk of dying from a chronic disease was nearly 70 percent higher for those with high arsenic levels. Those with moderate exposures had a 20 to 30 percent increased risk. A follow-up study found that the combination of arsenic exposure with smoking multiplied the risk.

Based on the scientific leads from HEALS, Ahsan and colleagues are now testing whether inexpensive supplements of selenium and vitamin E can reduce rates of cancer, cardiovascular disease and death for those with elevated arsenic levels among 7,000 exposed individuals in a separate study called Bangladesh vitamin E and Selenium Trial (BEST).

He is also principal investigator of two genome-wide association studies to identify novel genes for breast cancer risk and prognosis among 7,000 young women from the United States, Germany, Canada and Australia.

Born in Bangladesh, Ahsan received his medical degree from Dhaka University in 1988, followed by a M.Med.Sc degree in epidemiology from the University of Western Australia in 1992 and post-doctoral training in molecular epidemiology at Columbia University from 1993-1995. He then served on the faculty at Columbia for 11 years before coming to Chicago in 2006.

Peter Angelos, MD, PhD, professor of surgery, section chief of endocrine surgery and associate director of the MacLean Center for Clinical Medical Ethics, has been named the Linda Kohler Anderson Professor at the University of Chicago.

A highly regarded physician with extensive experience in surgery of the thyroid, parathyroid and adrenal glands, Angelos is an expert in the use of minimally invasive surgical techniques in the treatment of endocrine cancers. He is also an authority on issues of medical professionalism, training new surgeons and surgical ethics.

A prolific author, Angelos has published more than 100 peer-reviewed journal articles and book chapters on improving outcomes of thyroid and parathyroid surgery, minimally invasive endocrine surgery, best practices for thyroid cancer treatment and ethical decision making in health care. He has edited the first and second editions of a book on Ethical Issues in Cancer Patient Care, delivered 150 invited lectures, primarily on surgical innovation and ethics, and was featured in a series of instructional surgical videos. He was chair of the ethics committee of the American College of Surgeons oncology group for 13 years and currently serves as Secretary-Treasurer of the American Association of Endocrine Surgeons and the U.S. chapter of the international Society of Surgery.

Angelos earned both his BA in medical science and philosophy and his MD in 1989 through a joint six-year program at Boston University. He completed his surgical residency at Northwestern University, with a year spent in an ethics fellowship at the University of Chicago, and his PhD in philosophy in 1995 at Boston University. After a second fellowship in endocrine surgery at the University of Michigan in 1996, he joined the faculty in surgery and medical ethics and humanities at Northwestern University, where he was chair of the ethics committee. He moved to the University of Chicago in 2006. Included in multiple lists of “top doctors,” he has received many honors for his clinical skills, emphasis on professionalism and devotion to teaching.

David H. Song, MD, MBA, professor of surgery, vice chair of the Department of Surgery, section chief of plastic and reconstructive surgery and director of the plastic surgery residency training program at the University of Chicago Medical Center, has been named the Cynthia Chow Professor.

An internationally recognized expert in plastic and reconstructive surgery, Song specializes in breast reconstruction and oncoplastic surgery — a multispecialty approach to tumor removal and tissue reconstruction. His research, including several current clinical trials, focuses on improving breast reconstruction after lumpectomy or mastectomy. He also has pioneered techniques for the repair of chest wall defects.

A fellow in the American College of Surgeons and past president of the Chicago Society of Plastic Surgeons, Song also has served as a board member of the American Society of Plastic Surgeons and the Association of Academic Chairmen of Plastic Surgery. He serves on the boards of the University of Chicago Laboratory Schools and the Medical Aid for Children of Latin America, which provides free surgical care for children with congenital deformities in the Dominican Republic. He organizes and staffs outreach efforts for this organization each year.

Song earned his BS in biomedical sciences from the University of California, Riverside, and his MD from the University of California, Los Angeles, in a joint seven-year program. He completed his general surgery residency and fellowships in plastic surgery and microsurgery at the University of Chicago Medical Center, then joined the faculty as an assistant professor in 2001. He was named section chief of plastic and reconstructive surgery at age 34 in 2004. In 2009, he completed an MBA at the University of Chicago’s Booth School of Business and was named vice chair for business and strategy for surgery.

He and surgical colleagues developed a new technology that is now commercially available for closing the chest after open-heart surgery. He is the author or co-author of more than 50 research studies and multiple book chapters. He edited two textbooks and is associate editor for Plastic Surgery, 3rd Edition, the definitive textbook in the field, to be published in 2012.

Song has received many honors including recognition from the Korean Society of Plastic and Reconstructive Surgeons; the Distinguished Alumnus Award from the University of California, Riverside; and clinician of the year from Y-ME, a national breast cancer advocacy organization. In 2005, he was featured in Crain’s Chicago Business’ list of up-and-comers in its “40 Under 40.”

Jerrold R. Turner, MD, PhD, professor of pathology and medicine and associate chair of the Department of Pathology, has been named a Sara and Harold Lincoln Thompson Professor.

An active physician and scientist, Turner has primary clinical expertise in gastrointestinal pathology. His research interests relate to disorders associated with defective intestinal barrier function, including inflammatory bowel disease, celiac disease, and graft versus host disease. Turner’s research group integrates tools from diverse disciplines, including cell biology, electrophysiology, structural and molecular biology, and immunology to understand how barrier dysfunction drives disease.

Turner studies how the epithelial cells that line the digestive tract establish, maintain and regulate barriers to prevent uncontrolled exchange between the hostile environment of the gut lumen and the sterile internal tissues. His laboratory has focused the biology and pathobiology of tight junctions, the structures that seal and regulate flux across the space between adjacent epithelial cells.

Turner’s recent work has changed scientists’ understanding of how tight junctions function, replacing an older static model in which tight junction proteins are stably cross-linked with a more dynamic view in which the proteins actively bind to and release from one another. Ongoing efforts of his lab include molecular characterization of these interactions and their roles in barrier regulation. Application of these data to preclinical models has allowed Turner to develop novel therapeutic approaches that restore intestinal barrier function and limit or prevent disease.

The author of more than 190 original articles, reviews, and book chapters, Turner has been recognized with Outstanding Investigator awards from the American Society for Investigative Pathology and the American Physiological Society. He is presently associate editor of Gastroenterology, serves on several editorial boards and holds leadership positions in major pathology, physiology and gastroenterology societies.

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January 16, 2012

Hundreds of times during a baseball game, the home plate umpire must instantaneously categorize a fast-moving pitch as a ball or a strike. In new research from the University of Chicago, scientists have pinpointed an area in the brain where these kinds of visual categories are encoded.

While monkeys played a computer game in which they had to quickly determine the category of a moving visual stimulus, neural recordings revealed brain activity that encoded those categories. Surprisingly, a region of the brain known as the posterior parietal cortex demonstrated faster and stronger category-specific signals than the prefrontal cortex, an area that is typically associated with higher level cognitive functions.

“This is as close as we’ve come to the source of these abstract signals” said David Freedman, PhD, assistant professor of neurobiology at the University of Chicago. “One of the main points this study suggests is that the parietal cortex is more involved in the categorization process than we had expected.”

Organizing the chaos of the surrounding world into categories is one of the brain’s key functions. For instance, the brain can almost immediately classify a broad range of four-wheeled vehicles into the general category of “car,” allowing a person to quickly take the appropriate action. Neuroscientists such as Freedman and his laboratory team are searching for the brain areas responsible for storing and assigning these categories.

“The number of decisions we make per minute is remarkable,” Freedman said. “Understanding that process from a basic physiological perspective is bound to lead to ways to improve the process and to help people make better decisions. This is particularly important for patients suffering from neurological illnesses, brain injuries or mental illness that affect decision making.”

Ten years ago, experiments by Freedman and his colleagues found neurons were encoding category signals in the prefrontal cortex (PFC), a region thought to control important mental tasks such as decision making, rule learning and short-term memory. But in subsequent experiments, Freedman found a region of the parietal cortex called the lateral intraparietal area (LIP), thought to be primarily involved in basic visual and spatial processing, also encoded category information.

For the new study, to be published in the journal Nature Neuroscience, Freedman and graduate student Sruthi Swaminathan conducted the first direct comparison of prefrontal cortex and parietal cortex during categorization tasks. Monkeys were taught a simple game in which they classified dots moving in different directions into one of two categories. The subjects were shown two sets of moving dots one second apart, then held or released a joystick based on whether the two stimuli belonged to the same category or different categories.

During the task, scientists recorded neural activity in PFC and LIP. Neurons in both areas changed their activity according to the learned categories; for example, increasing firing for one category and decreasing for the other. However, category-specific neurons in LIP exhibited stronger and faster (by about 70 milliseconds) changes in activity during the task than those recorded from PFC.

“The relative timing of signals in the two brain areas gives us an important clue about their roles in solving the categorization task. Since category information appeared earlier in parietal cortex than prefrontal cortex, it suggests that parietal cortex might be more involved in the visual categorization process, at least during this task,” Freedman said.

More evidence for the primacy of parietal cortex was provided by an experiment where scientists threw their subjects a curveball. The monkeys were shown an ambiguous set of moving dots on the border between the two learned categories, then asked to compare them with a second set of non-ambiguous dots — a test with no correct answer. The subjects were required to make a decision about which category the ambiguous stimuli belonged to, and once again LIP neurons corresponded to that decision more closely than PFC.

“During the decision process, parietal cortex activity is not just correlated — it even predicts ahead of time what the monkey will tell you,” Swaminathan said. “You can record neuronal activity in parietal cortex and, in many cases, predict with great reliability what the monkey will report.”

In humans, the ambiguous stimuli would be similar to an umpire deciding whether a borderline pitch was a ball or a strike — a highly specialized real world example of the visual motion categorization task used in these experiments, Freedman said.

“In a lot of ways, that’s the process we hope to understand, this umpire calling balls and strikes,” he said. “It’s an interesting learned behavior that’s highly critical for an individual to perform with great reliability, and it’s a spatial categorization with a sharp boundary, so we think it’s the same process.”

Next, Freedman’s laboratory hopes to look at how the brain changes during the category-learning process, examining whether the category signals first arise in the parietal cortex or start in the prefrontal cortex before transferring to visual regions of the brain. The results may help scientists reverse engineer some of the brain’s most important tasks in daily life.

“Making effective decisions and evaluating every situation that you’re in moment by moment is critical for successful behavior,” Freedman said. “We’re really interested in what changes occur in the brain to allow you to recognize not just the features of a stimulus, but what it is and what it means.”

The paper, “Preferential encoding of visual categories in parietal cortex compared to prefrontal cortex,” will be published online Jan. 15 by the journal Nature Neuroscience [doi: 10.1038/nn.3016]. Funding for the study was provided by the National Institutes of Health, the National Science Foundation, the Alfred P. Sloan Foundation and the Brain Research Foundation.

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January 9, 2012

Yusuke Nakamura, MD, PhD, Secretary General in the Japanese Government’s Office of Medical Innovation and a professor of molecular medicine at Tokyo University’s Human Genome Center, has stepped down from his leadership position in the Japanese Cabinet Secretariat. He will join the faculty at the University of Chicago in April 2012.

Nakamura was actively recruited by the University of Chicago for a faculty position in the Department of Medicine to continue his innovative program in anticancer drug discovery and development, as well as his internationally recognized research in genomics and pharmacogenomics.

“Dr. Nakamura has made major contributions to modern genetics and genomics,” said Kenneth Polonsky, MD, Dean of the Biological Sciences Division and the Pritzker School of Medicine at the University of Chicago. “We are extremely gratified by his interest in continuing his illustrious career at the University of Chicago.”

“This was a wonderful opportunity for me,” said Nakamura. “I have long enjoyed a collaborative relationship with colleagues at the University of Chicago, which has very strong programs in cancer, pharmacogenomics and human genetics. I strongly wish to bring discoveries in basic medical science to the bedside, and improve the quality of life of cancer patients. I look forward to the opportunity to work closely with scientists as well as physicians there who take care of patients with cancer.”

Nakamura, 59, is a leading authority on using large-scale genomic research to understand various genetic diseases and cancer, and to develop cancer peptide vaccines and targeted anticancer drugs. He has done fundamental work on developing the tools for genetic mapping. He discovered genetic variations associated with common diseases or those related to drug responses as well as genes responsible for several inherited disorders. And he played an important role in the International HapMap Consortium, one of the most important biomedical achievements of the last decade because it laid the groundwork for modern genomic medicine.

Nakamura has also focused on applying genetic information to improve the care of cancer patients, working to bring his laboratory’s discoveries into the clinical arena. His cancer research at the University of Tokyo led to the formation of OncoTherapy Science in 2001, a highly successful public Japanese biotechnology company that concentrates on new cancer therapies.

“We are very excited to add such an internationally prominent scientist to our faculty,” said cancer specialist Everett Vokes, MD, chairman of the Department of Medicine. “We look forward to the profound impact Dr. Nakamura’s recruitment will make through his own work and by providing many collaborative opportunities.”

Nakamura began his career in 1977 as an abdominal surgeon. Frustrated by the shortcomings of available cancer treatments–he lost his mother to colon cancer–he entered a PhD program at Osaka University in molecular genetics in 1981. After completing his PhD, he spent five years as a research fellow and then as a faculty member at the Howard Hughes Medical Institute at the University of Utah, an international center for gene mapping.

He returned to Japan in 1989 as head of the biochemistry department at the Cancer Institute, in Tokyo. In 1994, he was invited as a professor in the Institute of Medical Science, the University of Tokyo and named director of the newly created Human Genome Center at the University of Tokyo in 1995.

When the Japanese government launched its Millennium Genome Project in 2000, Nakamura was named group leader for the genetic diversity program at the renowned RIKEN Center for Genomic Medicine. He became the director for the RIKEN genomic center in 2005. In January 2011 he was appointed Special Adviser to the Cabinet and Secretary General of the Office of Medical Innovation by the Japanese Government.

Nakamura has received many awards for his work on cancer genetics, gene mapping and other projects, including the Princess Takamatsu Cancer Research Award in 1992, the Keio Medical Science Prize in 2000, the CHEN Award for Distinguished Academic Achievement in Human Genetic and Genomic Research in 2010, and the Japanese Medal with a Purple Ribbon, for contributions to education and culture.

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January 9, 2012

Much of what living cells do is carried out by “molecular machines” — physical complexes of specialized proteins working together to carry out some biological function. How the minute steps of evolution produced these constructions has long puzzled scientists, and provided a favorite target for creationists.

In a study published early online on Sunday, January 8, in Nature, a team of scientists from the University of Chicago and the University of Oregon demonstrate how just a few small, high-probability mutations increased the complexity of a molecular machine more than 800 million years ago. By biochemically resurrecting ancient genes and testing their functions in modern organisms, the researchers showed that a new component was incorporated into the machine due to selective losses of function rather than the sudden appearance of new capabilities.

“Our strategy was to use ‘molecular time travel’ to reconstruct and experimentally characterize all the proteins in this molecular machine just before and after it increased in complexity,” said the study’s senior author Joe Thornton, PhD, professor of human genetics and evolution & ecology at the University of Chicago, professor of biology at the University of Oregon, and an Early Career Scientist of the Howard Hughes Medical Institute.

“By reconstructing the machine’s components as they existed in the deep past,” Thornton said, “we were able to establish exactly how each protein’s function changed over time and identify the specific genetic mutations that caused the machine to become more elaborate.”

The study — a collaboration of Thornton’s molecular evolution laboratory with the biochemistry research group of the University of Oregon’s Tom Stevens, professor of chemistry and member of the Institute of Molecular Biology — focused on a molecular complex called the V-ATPase proton pump, which helps maintain the proper acidity of compartments within the cell.

One of the pump’s major components is a ring that transports hydrogen ions across membranes. In most species, the ring is made up of a total of six copies of two different proteins, but in fungi a third type of protein has been incorporated into the complex.

To understand how the ring increased in complexity, Thornton and his colleagues “resurrected” the ancestral versions of the ring proteins just before and just after the third subunit was incorporated. To do this, the researchers used a large cluster of computers to analyze the gene sequences of 139 modern-day ring proteins, tracing evolution backwards through time along the Tree of Life to identify the most likely ancestral sequences. They then used biochemical methods to synthesize those ancient genes and express them in modern yeast cells.

Thornton’s research group has helped to pioneer this molecular time-travel approach for single genes; this is the first time it has been applied to all the components in a molecular machine.

The group found that the third component of the ring in Fungi originated when a gene coding for one of the subunits of the older two-protein ring was duplicated, and the daughter genes then diverged on their own evolutionary paths.

The pre-duplication ancestor turned out to be more versatile than either of its descendants: expressing the ancestral gene rescued modern yeast that otherwise failed to grow because either or both of the descendant ring protein genes had been deleted. In contrast, each resurrected gene from after the duplication could only compensate for the loss of a single ring protein gene.

The researchers concluded that the functions of the ancestral protein were partitioned among the duplicate copies, and the increase in complexity was due to complementary loss of ancestral functions rather than gaining new ones.

By cleverly engineering a set of ancestral proteins fused to each other in specific orientations, the group showed that the duplicated proteins lost their capacity to interact with some of the other ring proteins. Whereas the pre-duplication ancestor could occupy five of the six possible positions within the ring, each duplicate gene lost the capacity to fill some of the slots occupied by the other, so both became obligate components for the complex to assemble and function.

“It’s counterintuitive but simple: complexity increased because protein functions were lost, not gained,” Thornton said. “Just as in society, complexity increases when individuals and institutions forget how to be generalists and come to depend on specialists with increasingly narrow capacities.”

The research team’s last goal was to identify the specific genetic mutations that caused the post-duplication descendants to functionally degenerate. By reintroducing historical mutations that occurred after the duplication into the ancestral protein, they found that it took only a single mutation from each of the two lineages to destroy the same specific functions and trigger the requirement for a three-protein ring.

“The mechanisms for this increase in complexity are incredibly simple, common occurrences,” Thornton said. “Gene duplications happen frequently in cells, and it’s easy for errors in copying to DNA to knock out a protein’s ability to interact with certain partners. It’s not as if evolution needed to happen upon some special combination of 100 mutations that created some complicated new function.”

Thornton proposes that the accumulation of simple, degenerative changes over long periods of times could have created many of the complex molecular machines present in organisms today. Such a mechanism argues against the intelligent design concept of “irreducible complexity,” the claim that molecular machines are too complicated to have formed stepwise through evolution.

“I expect that when more studies like this are done, a similar dynamic will be observed for the evolution of many molecular complexes,” Thornton said.

“These really aren’t like precision-engineered machines at all,” he added. “They’re groups of molecules that happen to stick to each other, cobbled together during evolution by tinkering, degradation, and good luck, and preserved because they helped our ancestors to survive.”

The paper, “Evolution of increased complexity in a molecular machine,” appears in the January 18, 2012, issue of Nature [doi: 10.1038/nature10724]. The work was a collaboration of Thornton’s molecular evolution lab with the research group of Tom Stevens, a yeast geneticist at the University of Oregon. Other authors include Gregory C. Finnigan and Victor Hanson-Smith, of the University of Oregon.

Funding for this work was provided by the National Institutes of Health, the National Science Foundation, and the Howard Hughes Medical Institute.

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January 9, 2012

A new study suggests that middle-aged adults recently diagnosed with diabetes and hypertension have time to try to learn how to control their high blood pressure without medications, but not too much time.

The consequences of delaying effective hypertension treatment for up to a year were small–a two-day reduction in quality-adjusted life expectancy–according to a study by University of Chicago researchers published online for the Journal of General Internal Medicine. But as the delay gets longer, the damages multiply. A ten-year delay decreased life expectancy by almost five months.

“For newly diagnosed patients, this means we have time,” said study author Neda Laiteerapong, MD, instructor of medicine at the University of Chicago. “Most patients would prefer to control their blood pressure through diet and exercise rather than with medications, and it can take months to learn how to change old habits and master new skills. Our results indicate that it’s OK to spend from six months to a year, perhaps even longer, to make the difficult lifestyle changes that are necessary and will pay off in the long run.”

High blood pressure is especially damaging for people with diabetes, raising their risk of stroke, coronary artery disease, kidney failure, vision loss and amputations. Both the American Diabetes Association (ADA) and the National Institutes of Health recommend a lower blood pressure target for patients with diabetes than for the general public, urging them to keep their pressures below 130/80 mmHg.

Two out of three adults with diabetes, however, never reach that goal. Many patients are hampered by limited access to health care. Others are delayed by what the authors call “clinical inertia,” a disinclination by patients to implement lifestyle changes or reluctance by their doctors to push additional medications. Among those who are prescribed blood pressure drugs, at least 20 percent of patients with diabetes do not stick to their treatments.

Until now, the implications of these delays on patients’ health had not been quantified. Laiteerapong and colleagues built computer models using published data to determine the magnitude of harm caused by different delays in controlling blood pressure in patients from 50-59 years of age with newly diagnosed type 2 diabetes. The damage caused by a one-year delay “may be small,” they concluded but delays of ten years or more were comparable to smoking in patients with cardiovascular disease.

Given time to learn how, many patients would prefer to control blood pressure through diet and exercise rather than with antihypertensive medications. Most guidelines, however, including those of the ADA, recommend at most a three-month trial of medication-free lifestyle therapy for patients with moderately elevated blood pressure. They call for immediate initiation of medication for those with blood pressure more than 10mmHg above the goal.

That is often not enough time for patients to learn the methods, develop good habits and demonstrate improvements.

“We ask patients with diabetes to do a billion things,” Laiteerapong said, “to test their blood sugars, to count carbohydrates, to spend 30 minutes a day doing exercise, including cardio and weight training. Most, if not all, of this is new to them. They need time to adapt. It’s important to do this right, but our results say it’s not that important to do it so fast.”

This study argues that caregivers should work with patients to help them gain the knowledge and develop the necessary skills gradually rather than rushing to drug treatment, especially if their blood pressure is only mildly elevated. It suggests that patients and providers “have more time,” the authors write, “at least up to one year, to focus on diabetes self-management and lifestyle modification.”

“Among middle-aged adults with diabetes, the harms of a one-year delay in managing blood pressure may be small,” the authors conclude. “Health care providers may wish to focus on diabetes management alone in the first year after diagnosis, to help patients establish effective self-management and lifestyle modification. However, after the first year, it is clear that achieving and maintaining tight blood pressure control among US middle-aged adults with diabetes has the potential to generate substantial population-level health benefits.”

The National Institutes of Health funded this study. Additional authors include Priya John, David Meltzer and Elbert Huang, all of the University of Chicago.

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January 4, 2012

An exact determination of expected body weight for adolescents based on age, height and gender is critical for diagnosis and management of eating disorders such as anorexia nervosa and bulimia. However, there are no clear guidelines regarding the appropriate method for calculating this weight in children with such disorders.

In a study to be published online Jan. 4, 2012, in the journal Pediatrics, researchers from the University of Chicago, the Harvard School of Public Health and the University of Rochester Medical Center compared three common methods for calculating expected body weight of adolescents with eating disorders and found that the body mass index (BMI) percentile method is recommended for clinical and research purposes.

“There are no clear guidelines in the adolescent field,” said study author Daniel Le Grange, PhD, professor of psychiatry and Director of the Eating Disorders Program at the University of Chicago. “We set out to do something that is relatively straightforward that hasn’t been done before, and that is look at some of the most frequently used methods of calculating weight in the pediatric and adolescent eating disorder populations, and see whether we can come up with a gold standard for clinical as well as for research purposes.”

Le Grange and his colleagues analyzed data from adolescents seeking treatment for eating disorders at the University of Chicago. They calculated expected body weights using the BMI method along with two other commonly used measures: the McClaren and Moore methods. The BMI method compares a patient’s current BMI to the 50th percentile BMI for a patient of the same age, height and gender according to charts published by the Centers for Disease Control and Prevention. That percentage can help determine whether a patient has an eating disorder.

Their analysis showed that of the three, the BMI method was the most useful for children and adolescents of all ages, heights and weights, and could account more accurately for very short and very tall patients as well.

By publishing their study in Pediatrics, the premier journal in the pediatric community, Le Grange hopes to reach a wider audience of pediatricians who may not be as familiar with eating disorders. “Pediatricians are at the forefront of making these diagnoses,” he said. “We wanted to make a clear statement to the pediatric and adolescent eating disorder community that we should all talk the same language and move forward in this way.”

The study also recommends that researchers cite the method used to calculate expected body weight in their research and stresses the importance of using the term “expected” instead of “ideal” to describe body weight to avoid unrealistic body image expectations in patients with eating disorders. “I think it’s a good clear clinical guide, and I hope pediatricians in the community feel they can pick it up and have a handy tool in their clinical practice,” Le Grange said.

The paper, “Calculation of Expected Body Weight in Adolescents with Eating Disorders,” appears as an early release online in Pediatrics [doi:10.1542/peds.2008-1536]. Other authors include Peter M. Doyle, Kali Ludwig and Catherine Glunz, University of Chicago; Sonja A. Swanson, Harvard School of Public Health; and Richard E. Kreipe, University of Rochester Medical Center.

Funding for this work was provided by the National Institutes of Health.

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These new results reaffirm the testing conducted before the batch was made available to retailers and consumers. Based on both sets of tests, Mead Johnson can say with confidence that Enfamil Premium Newborn formula, like every infant formula the company produces, is safe.

The company undertook the highly unusual retesting due to continuing misinformation and confusion in the marketplace. Mead Johnson recognizes that parents and health care professionals trust and rely on the Enfamil brand and takes that responsibility very seriously. The company wanted to reassure consumers – as quickly as possible and based on rigorous scientific data – of the safety and quality of all its products.

These results are consistent with independent media accounts from Reuters, CNN, the Associated Press and others, reporting that none of the formula samples relating to the case have tested positive.

The U.S. FDA and the U.S. Centers for Disease Control are seeking to determine the origin of the Cronobacter involved in the Missouri case and are expected to be testing a variety of possible environmental sources. The company has shared the results from its two tests with both authorities.

All Mead Johnson infant formulas undergo more than 2,300 quality tests and checks to ensure that they meet or exceed all standards set by regulatory bodies, including the World Health Organization and the U.S. FDA.

As always, Mead Johnson remains committed to its mission to nourish the world’s children for the best start in life.

About Mead Johnson

Mead Johnson, a global leader in pediatric nutrition, develops, manufactures, markets and distributes more than 70 products in over 50 markets worldwide. The company’s mission is to nourish the world’s children for the best start in life. The Mead Johnson name has been associated with science-based pediatric nutrition products for over 100 years. The company’s “Enfa” family of brands, including Enfamil(R) infant formula, is the world’s leading brand franchise in pediatric nutrition.

For more information on the company, go to meadjohnson.com.

SOURCE: Mead Johnson Nutrition

Mead Johnson Nutrition
Media: Christopher Perille, 847-224-9414
chris.perille@mjn.com

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December 21, 2011

The history of evolution is periodically marked by explosions in biodiversity, as groups of species try out a wide range of shapes and sizes. With a new analysis of two such adaptive radiations in the fossil record, researchers have discovered that these diversifications proceeded head-first.

By analyzing the physical features of fossil fish that diversified around the time of two separate extinction events, scientists from the University of Chicago and the University of Oxford found that head features diversified before body shapes and types. The discovery disputes previous models of adaptive radiations and suggests that feeding-related evolutionary pressures are the initial drivers of diversification.

“It seems like resources, feeding and diet are the most important factors at the initial stage,” said lead author Lauren Sallan, graduate student in the Department of Organismal Biology and Anatomy at the University of Chicago. “Strange heads show up first — crushing jaws, animals with big teeth, with long jaws — but they’re all pretty much attached to the same body.”

Adaptive radiations underlie the evolution of dominant and diverse groups. After a major disruption, such as an extinction event, surviving species diversify into a myriad variety of forms. Modern examples of this diversity are the fish family of cichlids, with more than 1,000 documented species, or “Darwin’s finches” of the Galapagos Islands, which exhibit many different beak types.

Evolutionary biologists have used these living species to propose at least two models of how adaptive radiations work. One model proposes a single “burst” of divergence followed by a long period of relative stability. Another, sometimes known as the “general vertebrate model,” introduced the idea of staged divergences, with habitat-driven changes in body type preceding diversification of head types.

However, these models had not yet been tested with the rich data sets available in the fossil record.

“There hadn’t been any tests of these things using fossils,” said Sallan, a graduate student in the laboratory of University of Chicago Professor Michael Coates. “You have all these analyses of diversification, yet not one of them goes back to the fossil record and says what’s happening at this time period, and the next time period, and the one after that.”

Sallan and co-author Matt Friedman, PhD, lecturer in paleobiology at the University of Oxford and a former member of Coates’ laboratory, looked at two different adaptive radiations in the fossil record. The first was the explosion of ray-finned fishes after the Hangenberg extinction, an event 360 million years ago that decimated ocean life on Earth. The second group was the acanthomorphs, a group of fish that exhibited a burst in diversity around the time of the end-Cretaceous extinction that ended the age of dinosaurs.

In both datasets, the researchers used a method called geometric morphometrics to quantify differences in features such as body depth, fin position and jaw shape between species. Crucially, Sallan and Friedman separated head features from body features in their analysis, to better detect the timing of when each compartment showed a burst of diversity in the record.

The results of the two analyses were in agreement: Diversification in cranial features preceded diversification in body types. Unusual head features such as jaws lined with sharp teeth or blunt teeth for crushing appeared before diverse body shapes on a spectrum from slender and eel-like to broad and disc-shaped.

“We have these two entirely separate radiations, and in both of them the pattern is heads first. So feeding might be more important to diversification than habitat use,” Sallan said. “It’s against both the adaptive radiation model and the proposed stage model.”

The pattern detected with the new analyses suggests that the appearance of new sources of food drives a burst of diversity before species begin to change to adapt to new habitats.

“Ecological limits are taken away,” Sallan said. “There’s more opportunity out there, more available resources, and they’re taking advantage of that. Later, they’re taking advantage of specializing to new habitats. So it’s not something within the animals themselves; it’s more opportunity that matters.”

While the new study offers two distinct examples of head-first diversification separated by hundreds of millions of years, the universality of the model remains to be conclusively proven.

“Evolution is really complex, and it’s not really clear that there should be only one model,” Sallan said. “It might be that this model might apply to fishes in certain time periods, or might apply to vertebrates, but a lot more investigation is needed to see whether that is actually true.”

The paper, “Heads or Tails: Staged Diversification in Vertebrate Evolutionary Radiations,” was published online Dec. 21 by the journal Proceedings of the Royal Society B.

Funding for the study was provided by the National Science Foundation, the Paleontological Association, the Paleontological Society, the American Society of Ichthyologists and Herpetologists, the Evolving Earth Foundation, the Natural Environment Research Council, the Fell Fund of the University of Oxford, the Environmental Protection Agency, and the Lerner-Grey Fund of the American Museum of Natural History.

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December 12, 2011
View video of the African lungfish using its thin pelvic limbs to lift its body off the bottom surface to propel itself forward.
The eel-like body and scrawny “limbs” of the African lungfish would appear to make it an unlikely innovator for locomotion. But its improbable walking behavior, newly described by University of Chicago scientists, redraws the evolutionary route of life on Earth from water to land.

Extensive video analysis, published in the Proceedings of the National Academy of Sciences, reveal that the African lungfish can use its thin pelvic limbs to not only lift its body off the bottom surface but also propel itself forward. Both abilities were previously thought to originate in early tetrapods, the limbed original land-dwellers that appeared later than the lungfish’s ancestors.

The observation reshuffles the order of evolutionary events leading up to terrestriality, the adaptation to living on land. It also suggests that fossil tracks long believed to be the work of early tetrapods could have been produced instead by lobe-finned ancestors of the lungfish.

“In a number of these trackways, the animals alternate their limbs, which suggested that they must have been made by tetrapods walking on a solid substrate,” said Melina Hale, PhD, associate professor of Organismal Biology and Anatomy. “We’ve found that aquatic animals with fundamentally different morphologies and that aren’t tetrapods could potentially make very similar track patterns.”

Lungfish are a popular pet in the paleontological community, treasured for their unique evolutionary heritage.

“The lungfish is in a really great and unique position in terms of how it is related to fishes and to tetrapods,” said Heather King, a graduate student and lead author of the study. “Lungfish are very closely related to the animals that were able to evolve and come out of the water and onto land, but that was so long ago that almost everything except the lungfish has gone extinct.”

While anecdotes and rumors circulated within the scientific community about the alleged walking behavior of these strange fish, nobody looked systematically at the biomechanics of their locomotion. An African lungfish (Protopterus annectens) kept in the laboratory of study co-author Michael Coates inspired King to study the species’ ability to walk on its unusually thin limbs.

King and her colleagues designed a special tank in which the motions of lungfish could be videotaped from the side and below for in-depth analysis. The videos revealed that lungfish commonly use their hind, or pelvic, limbs to elevate their body off the surface and propel themselves forward. Though the forelimbs look similar to the hindlimbs, they were not involved in locomotion, the authors found.

“This is all information we can only get from a living animal,” King said. “Because if you were just to look at the bones, like you would with a fossil, you might not ever know these motions could occur.”

Lungfish also demonstrated both “bounding” motions, where both limbs moved at once, and “walking,” marked by alternating limbs. Coupled with the ability of the lungfish to fully rotate the limb and place each subsequent footfall in front of the joint, the motion suggests that similar creatures would have been capable of producing some of the fossil tracks credited to tetrapods.

“It’s tempting to attribute alternating impressions to something like the footfalls of an early tetrapod with digits, and yet here we’ve got good evidence that living lungfish can leave similar sequences of similar gait,” said Coates, PhD, professor of Organismal Biology and Anatomy. “The fin or limb use thought to be unique to tetrapods is actually more general.”

The lungfish’s ability to use its thin limbs to support its body may be helped by the reduced demands of gravity underwater, the authors proposed. By filling its lungs with air, the lungfish may increase the buoyancy of its front end, enabling the scrawny hindlimbs to lift the entire body off the ground.

“If you showed me the skeleton of this creature and asked me to make a bet on whether it walks or not, I would have bet it couldn’t,” said co-author Neil Shubin, PhD, Robert R. Bensley Professor of Organismal Biology and Anatomy. “Their fins seem like the furthest thing from walking appendages possible. But it shows what’s possible in an aquatic medium where you don’t have to support yourself with gravity.”

The discovery suggests that many of the developments necessary for the transition from water to land could have occurred long before early tetrapods, such as Tiktaalik, took their first steps on shore. Lobe-finned ancestors of the lungfishes as well as tetrapods could have evolved hindlimb propulsion and the ability to walk on the substrate at the bottom of a lake or marsh millions of years before limbs with digits and land-dwelling animals appeared.

“This shows us — pardon the pun — the steps that are involved in the origin of walking,” Shubin said. “What we’re seeing in lungfish is a very nice example of how bottom-walking in fish living in water can easily come about in a very tetrapod-like pattern.”

The paper, “Behavioral evidence for the evolution of walking and bounding before terrestriality in sarcopterygian fishes,” will be published in the online Early Edition of Proceedings of National Academy of Sciences the week of December 12, 2011. Funding for this work was provided by the National Science Foundation.

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December 13, 2011

Molecular markers found in cancer cells that have spread from a primary tumor to a limited number of distant sites can help physicians predict which patients with metastatic cancer will benefit from aggressive, targeted radiation therapy.

In a study to be published online Dec. 13, 2011, in the journal PloS One, researchers from the University of Chicago and the University of Illinois at Chicago show that if cells from metastatic tumors have high levels of a particular type of microRNA — a tool cells use to silence certain genes– not even aggressive treatment of those tumors would help. But if the cells have lower levels of that biological marker, then focused local treatment could be effective, even curative.

“We previously demonstrated that we could provide lasting disease-free survival to a percentage of patients with metastatic disease,” said study author Ralph Weichselbaum, MD, professor and chair of radiation and cellular oncology and Director of the Ludwig Center for Metastasis Research at the University of Chicago. “This finding means we can have a pretty good sense in advance of which patients we can help. Patients unlikely to benefit from focused, local therapy can receive systemic treatment immediately.”

Yves Lussier, MD, professor of medicine at the University of Illinois at Chicago and co-senior author of the study, added that “the biological differences between locally curable metastases or potentially fatal widespread metastases can also be targeted for drug development.”

When patients die from cancer, it is usually caused by distant metastases, numerous cancer sites established by malignant cells that split off from the primary cancer and began growing in new settings. In 1994, Weichselbaum and colleague Samuel Hellman proposed that there was a potentially curable intermediate state between cancer that had not spread at all and cancer that had spread extensively. They named this phenomenon “oligometastasis,” meaning cancer that had spread to a few distant sites.

In 2004, they began a small clinical trial to test that theory. Patients with stage IV cancer with one to five distant metastases and no tumors bigger than 10 centimeters in diameter were enrolled. The results, published in 2008, showed that precisely targeted radiation therapy could eradicate all evidence of disease in about 20 percent of those patients.

“We were pleased to get such encouraging results in patients with stage IV cancers that had spread to distant sites,” Weichselbaum said. “This was proof of principle in patients who had already failed standard therapies.”

A follow-up study, published in October 2011, found that 18 percent of the patients in that initial trial had seen no progression of their cancers for the duration of the study and 27 percent developed no new tumor sites.

The next step was to determine in advance which patients were most likely to benefit from such targeted therapy and which ones should move on to whole-body treatments, such as chemotherapy. So they compared cells from secondary tumors from patients who did well in the original studies with those whose cancers went on to establish multiple metastatic sites.

They found that tumors that were highly proliferative, producing many metastases, had patterns of microRNA expression that differed from those that produced only a few. The tumors most likely to spread had high levels of a small nucleic acid known as microRNA-200c.

This came as a surprise. MicroRNA-200c was thought to suppress metastasis. But when the researchers boosted microRNA-200c levels in a mouse model of cancer, it significantly increased metastasis. The researchers subsequently showed that microRNA-200c reduced the activity of other genes that acted to prevent the spread of cancer.

Further tests in mouse models showed that boosting microRNA-200c levels significantly increased the metastatic potential of tumors that were not as prone to spread.

“Our findings are an initial step in discriminating between patients with a few treatable sites where the tumor has spread and those who will develop widespread metastasis, which is not curable with focused radiation therapy,” Weichselbaum said. “It is encouraging to find a common molecular basis for this treatable state across a broad variety of metastases from solid tumors.”

Oligometastases are “more common than generally recognized,” the authors note. “Potentially, 50 percent of patients with metastatic non-small cell lung cancer, the leading cause of cancer death in men and women, may be oligometastatic.”

When combined with other factors — the number and size of metastasis, the interval from treatment of a primary tumor to the appearance of metastasis, the microscopic structure and appearance of tumor tissue — the presence of microRNA-200c could become a key element of patient selection for targeted radiation therapy, Weichselbaum said, distinguishing between patients who have treatable tumors and those who have widespread metastasis, including many tumors too small to detect.

This project was collaborative effort by three research groups. Weichselbaum and colleagues Michael Hasselle, Renuka Malik, Kimberly Corbin, Mitchell C. Posner, Steven J. Chmura, and Samuel Hellman at the University of Chicago, with Joseph Salama of Duke University Medical Center, developed the idea and perfumed the clinical studies. Biological modeling was co-led by H. Rosie Xing, with Qingbei Zhang, and Hanli Fan, and Weichselbaum with Nikolai Khodarevi, Sajid Khan, Thomas Darga, Samantha Perakis and Matthew Filippo at the University of Chicago. The bioinformatics and genomic modeling was led by Lussier, with Yong Huang, Xinan Yang, and Younghee Lee at the University of Illinois at Chicago.

The National Institutes of Health, the Ludwig Center for Metastasis Research, the University of Chicago Center for Radiation Therapy, the Chicago Tumor Institute, Dr. Lloyd Old, Mr. and Mrs. Vincent Foglia and the Foglia Foundation, the Lung Cancer Research Foundation, the University of Chicago Cancer Research Foundation, the University of Chicago Comprehensive Cancer Center and the National Center for the Multi Scale Analysis of Genomic and Cellular Networks supported this study.

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December 15, 2011

Sharon O’Keefe, President of the University of Chicago Medical Center, has been elected to the Illinois Hospital Association’s Board of Trustees. O’Keefe will begin serving a three-year term on the IHA board on Jan. 1, 2012.

O’Keefe is a nationally recognized authority on hospital operations, health care quality, patient satisfaction and employee engagement. She has served as President of the University of Chicago Medical Center since January 2011.

“This is both a genuine honor and a significant responsibility,” O’Keefe said. “The ongoing economic challenge, the state’s fiscal situation and the mounting pressures on hospitals to provide more care and outreach despite decreasing resources have made strong leadership from the IHA more and more important. I look forward to the opportunity to contribute in this new role.”

A Chicago native, O’Keefe, 59, began her health care career as a critical care nurse. She soon advanced into more administrative roles, where she focused on improving hospital operations and performance, enhancing health care quality and safety, and increasing patient and employee satisfaction. Her quality-improvement efforts led to national recognition. She was appointed to be an examiner for the U.S. Department of Commerce’s Malcolm Baldrige National Quality Award in 2005. She currently serves on the National Institutes of Health Advisory Board for Clinical Research.

She has held administrative roles as the director of nursing for surgical services at Johns Hopkins Hospital, an associate hospital director at Montefiore Hospital in New York, a senior manager for health care at the Ernst & Whinney accounting firm and senior vice president for operations at the University of Maryland Medical System in Baltimore.

Before coming to the University of Chicago Medical Center, she was executive vice president and chief operating officer from 1999 to 2002 at Boston’s Beth Israel Hospital. She also served as chief operating officer at Barnes-Jewish Hospital in St. Louis from 2002 to 2009 and president of Loyola University Medical Center from 2009 to 2011.

The IHA Board of Trustees is the Association’s policymaking body. The Board is made up of 32 trustees, including 14 at-large trustees elected by the voting members of the Association, nine regional trustees elected directly by the regions, six elected officers (chairman, chairman-elect, immediate past chairman, immediate past, past chairman, treasurer, and secretary), and the Association’s president ex officio. Constituency sections, councils and ad hoc task forces provide members with opportunities to participate in the Association’s policy development process.

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December 8, 2011

Neil Shubin’s 2004 discovery of the pivotal fossil Tiktaalik roseae, a transitional species between ancient fish and the first limbed animals, is among 10 projects selected for their historical significance as part of the National Geographic celebration of the magazine’s first 10,000 grants.

Since 1890, the National Geographic Society has funded grants to every corner of the planet –unlocking many of its secrets, sometimes in spectacular ways. The total number of National Geographic grants reached 10,000 in late 2011, representing a combined value of $153 million.

To celebrate the landmark, National Geographic chose 10 grants that “have made the greatest difference in understanding the Earth.” The most recent grant on the list is the 2004 expedition to the Canadian Arctic co-led by Shubin, PhD, the Robert R. Bensley Professor in the Department of Organismal Biology and Anatomy at the University of Chicago, which discovered the first fossils of Tiktaalik on Ellsmere Island.

The species, which mixed fish-like features with shoulder, elbow and wrist-like limb joints, provided the missing evolutionary link between fish and the first animals that walked out of water onto land about 375 million years ago. The discovery inspired Shubin’s 2008 book, “Your Inner Fish: A Journey Through the 3.5-Billion-Year History of the Human Body,” which won science-writing awards from Phi Beta Kappa, the Library Journal and the National Academy of Sciences.

Shubin’s work is featured alongside notable research by scientists such as Jacques-Yves Cousteau and Jane Goodall. Paleontologist Paul Sereno, PhD, Professor of Organismal Biology and Anatomy at the University of Chicago, is also mentioned for “the discovery of new dinosaur species on nearly every continent” as a grantee of National Geographic.

“The impact and results of these 10,000 grants are beyond calculation — they have filled countless gaps in our knowledge of the Earth and all that lives on it,” said John Francis, vice president for research, conservation and exploration at National Geographic. “The urgent need for solutions to the planet’s pressing problems means that the next 10,000 grants will be even more critical.”

Tiktaalik discovery among National Geographic’s top grants | Chicago Press Release Services - Chicago's leading press release newswire service; professional press release services, press release distribution and newswire services.

December 6, 2011

A three-drug combination treatment for the blood cancer multiple myeloma compares favorably to the best established therapy for newly diagnosed patients, according to a multi-center study led by Andrzej Jakubowiak, MD, PhD, professor of medicine and director of the multiple myeloma program at the University of Chicago Medical Center.

Jakubowiak will present final results of the phase I-II study on Dec. 12, 2011, at the American Society of Hematology (ASH) Annual Meeting and Exposition in San Diego, Calif. The initial results from phase I of this study were presented at the ASH Meeting 2010 and were selected for the Best of ASH 2010 session.

The combination includes a newer investigational medicine called carfilzomib combined with two standard medications: lenalidomide, an analogue of thalidomide, and low-dose dexamethasone, an anti-inflammatory with anti-cancer properties.

“This combination appears to deliver everything we expected and more,” said Jakubowiak, who came to the University of Chicago this fall from the University of Michigan. “We have seen excellent efficacy — the best reported to date — without the neurotoxicity that has been problematic with other drug combinations.”

Multiple myeloma is a type of cancer that arises in plasma cells, the bone marrow component that produces antibodies. The American Cancer Society estimates that about 20,520 Americans will be diagnosed with multiple myeloma in 2011 and 10,610 will die from the disease.

The research team enrolled 53 people at three different carfilzomib dose levels. Most patients responded quickly to the combination and continued to improve with additional treatment cycles.

After at least one 28-day cycle, 94 percent had a partial response — at least a 50 percent reduction of the disease. After at least four cycles, all patients had a partial response. After 12 cycles or more, 100 percent of patients had a “very-good partial response,” defined as a 90 percent reduction of disease, and four out of five patients showed little or no sign of cancer.

“These response rates are higher than those achieved by the best established regimens for newly diagnosed multiple myeloma,” Jakubowiak said.

After a median follow-up of nine and a half months, all patients were alive and only one patient’s cancer had progressed. The three-drug combination was overall well-tolerated, with few serious side effects. The side effect that typically limits extended treatment for multiple myeloma — peripheral neuropathy, numbness or tingling of the fingers and toes that can progress to significant pain — was infrequent and mild.

The study included patients who were eligible for a bone marrow transplant using their own stem cells, but it offered a deferred-transplant approach and only two patients chose that option. Most patients remained on the three-drug treatment and achieved responses similar to or better than those observed after a stem cell transplant. They are still eligible for a stem cell transplant if their disease becomes resistant to the drug combination.

“Newly diagnosed myeloma is most sensitive to treatment,” Jakubowiak said. “A great and sustained response in the initial phase of treatment, as is the case in this study, typically projects longer remission, and possibly longer overall survival.”

Carfilzomib has recently emerged as an important experimental medicine in the treatment of multiple myeloma. It is a proteasome inhibitor, a drug that interferes with the mechanism that cells use to get rid of unneeded or defective proteins. Because myeloma cells develop from antibody-producing white blood cells, they are “protein factories.” Blocking their efforts to get rid of dysfunctional proteins can lead to cell death.

The Multiple Myeloma Research Consortium, Onyx Pharmaceuticals Inc., Celgene Corp. and the University of Michigan funded the study.

Additional authors include Dominik Dytfeld, Tara B. Anderson, Brian Nordgren, Daniel Lebovic, Kent Griffith, K Detweiler-Short, Terri Jobkar, Diane Durecki, Ammar Al-Zoubi, Daniel Couriel, and Melissa Mietzel from the University of Michigan; Sundar Jagannath from Mt. Sinai Medical Center, New York; David H. Vesole from Hackensack University Medical Center; Keith Stockerl-Goldstein and Ravi Vij from Washington University School of Medicine; Robert Ott and Sandra Wear from the Multiple Myeloma Research Consortium; Mohamad Hussain from Celgene Corp.; and Homa Yeganegi from Onyx Pharmaceuticals Inc.

Presentation: 53nd American Society of Hematology Annual Meeting and Exposition, Dec. 10-13, 2010, Orlando, Fla. 631 – Final Results of a Frontline Phase 1/2 Study of Carfilzomib, Lenalidomide, and Low-Dose Dexamethasone (CRd) in Multiple Myeloma (MM). Monday, December 12, 2011: 2:45 PM, Ballroom 20D (San Diego Convention Center).

Drug combination highly effective for newly diagnosed myeloma patients, study finds | Chicago Press Release Services - Chicago's leading press release newswire service; professional press release services, press release distribution and newswire services.