UPMC Physician Resources

UPMC Inpatient Child and Adolescent Bipolar Services (In-CABS) Program Receives National Honor for Technological Initiatives

PITTSBURGH, April 6, 2015 – The Inpatient Child and Adolescent Bipolar Services (In-CABS) program at Western Psychiatric Institute and Clinic of UPMC has received a first prize National Council for Community Behavioral Healthcare 2015 Impact Award of Excellence in Health Information Technology. The award, which will be announced on April 21 at the Excellence Awards Dinner in conjunction with the National Council Conference in Orlando, recognizes In-CABS’ use of health IT interventions, comprehensive diagnostic assessments, state-of-the-art pharmacological treatment, and psychosocial interventions. The program also trains students and professionals from a broad range of disciplines in health IT.

Each year, the National Council’s Awards of Excellence honor individuals and organizations that are making large strides in fighting mental illness and addiction. Specifically, the awards celebrate the achievements of individuals who dedicate themselves to improving the lives of those with serious mental illnesses, and the accomplishments and efforts of those living with schizophrenia or bipolar disorder in improving their own lives and the lives of their peers.

“This award is important for In-CABS because it acknowledges our high-tech, innovative initiatives in our daily morning report and triage,” says Rasim Somer Diler, MD, assistant professor of psychiatry at the University of Pittsburgh School of Medicine and medical director of Inpatient Child and Adolescent Bipolar Services. “We’ve also implemented the Philips® Actiwatch to objectively measure sleep and arousal using neurocognitive measures, and we set up daily electronic mood and energy monitoring with an interactive projector through the Beckwith Institute’s Clinical Transformation Program.”

To learn more about In-CABS, please download the program brochure.

Geriatric Psychiatry Experts Present at AAGP 2015 Annual Meeting

PITTSBURGH, April 2, 2015 – UPMC and the University of Pittsburgh were well-represented at the recent American Association for Geriatric Psychiatry 2015 Annual Meeting in New Orleans. UPMC and the Department of Psychiatry hosted an alumni and friends cocktail reception during the meeting.

Faculty research also was featured in oral and poster presentations throughout the conference, including topics such as:

  • Non-Pharmacological Management of Behavioral Disturbance in Dementia
    Chair: Lalith Solai, MD
  • Research Update: Healthy Aging and Prevention of Late-Life Mood and Cognitive Disorders
    Faculty: Charles Reynolds III, MD
  • Update on Geriatric Sleep Disorders
    Faculty: Charles Reynolds III, MD
  • Neurocircuitry Dysfunction in Late-Life Depression: The Role of Negative Valence Systems and Cognitive Control Networks
    Faculty: Howard Aizenstein, MD, PhD
  • IPTci vs. PATH as Psychosocial Approaches to Cognitive Impairment: Clinical Perspectives, Advantages, and Limitations for Managing MCI to Moderate Dementia With Co-Morbid Depression
    Faculty: Mark Miller, MD
  • Recent Advances in Late Life Schizophrenia Research
    Session Chair: John Kasckow, MD, PhD
  • Opioids for Agitation in Advanced Alzheimer’s Disease
    Discussant: Crystal White, MD

For more information about the AAGP annual meeting, please visit the conference page.

A Strategy for Stimulating Heart Muscle Regeneration in Infants, Study Finds

PITTSBURGH, April 1, 2015 – Surgery often is life-saving for many infants born with heart defects, but one thing that doctors cannot do yet is replace heart muscle that is scarred and dysfunctional. Researchers from the Heart Institute at Children’s Hospital of Pittsburgh of UPMC and Boston Children’s Hospital hope to overcome the challenge by stimulating regeneration of heart tissue. The findings were described today in Science Translational Medicine.

Children born with congenital heart disease are at greater risk of developing heart failure even after surgical correction of the problem.

“It is not surprising that survivors often develop heart failure later on,” said lead author, Bernhard Kühn, M.D., director of research for the Division of Cardiology at Children’s Hospital, and associate professor of pediatrics at the University of Pittsburgh School of Medicine. “But when these patients were given adult medicines in clinical trials, it turned out that they were not effective. The need for pediatric-specific heart failure therapies is increasingly recognized.”

For the study, the research team examined the potential of recombinant growth factor neuregulin-1 (rNRG1), which stimulates heart regeneration by driving proliferation of heart muscle cells, called cardiomyocytes.

They treated newborn mice with injections of rNRG1 at various times after heart injury and found that early treatment starting the first day after birth boosted cardiomyocyte cell division and heart function, and reduced scarring to a significantly greater degree compared to treatment that began at five days after birth. The growth factor also drove cardiomyocyte proliferation in lab tests of heart muscle samples obtained during surgery from human infants with congenital heart disease.

“These findings suggest that rNRG1 administration in infants with these birth defects might be a new therapeutic strategy for pediatric heart disease,” Dr. Kühn said. “Delivering agents early on that encourage the heart to make new cardiomyocytes could help the heart perform normally and reduce the risk of developing heart failure later in life.”

More research needs to be done before clinical testing of this strategy, the research team says. Dr. Kühn began the research while a member of the faculty at Boston Children’s Hospital.

Collaborators on the study were Balakrishnan Ganapathy, M.S., and Niyatie Ammanamanchi, M.S., both of Children’s Hospital of Pittsburgh of UPMC; Brian Polizzotti, Ph.D., Stuart Walsh, Ph.D., Sangita Choudhury, Ph.D., all of Boston Children’s Hospital; David Bennett, Ph.D., Beth Israel Deaconess Medical Center; Cristobal G. dos Remedios, Ph.D., Bosch Institute; Bernhard J. Haubner, M.D., and Josef M. Penninger, M.D., both with Institute of Molecular Biotechnology of the Austrian Academy of Sciences.

The research was supported by National Institutes of Health grants R01HL106302, K08HL085143, T32HL007572, and RR028792; Boston Children’s Hospital; and the Richard King Mellon Foundation Institute for Pediatric Research at Children’s Hospital of Pittsburgh of UPMC.

A Strategy for Stimulating Heart Muscle Regeneration in Infants, Study Finds

Surgery often is life-saving for many infants born with heart defects, but one thing that doctors cannot do yet is replace heart muscle that is scarred and dysfunctional. Researchers from the Heart Institute at Children’s Hospital of Pittsburgh of UPMC and Boston Children’s Hospital hope to overcome the challenge by stimulating regeneration of heart tissue. The findings were described today in Science Translational Medicine.

Children born with congenital heart disease are at greater risk of developing heart failure even after surgical correction of the problem.

“It is not surprising that survivors often develop heart failure later on,” said lead author, Bernhard Kühn, M.D., director of research for the Division of Cardiology at Children’s Hospital, and associate professor of pediatrics at the University of Pittsburgh School of Medicine. “But when these patients were given adult medicines in clinical trials, it turned out that they were not effective. The need for pediatric-specific heart failure therapies is increasingly recognized.”

For the study, the research team examined the potential of recombinant growth factor neuregulin-1 (rNRG1), which stimulates heart regeneration by driving proliferation of heart muscle cells, called cardiomyocytes.

They treated newborn mice with injections of rNRG1 at various times after heart injury and found that early treatment starting the first day after birth boosted cardiomyocyte cell division and heart function, and reduced scarring to a significantly greater degree compared to treatment that began at five days after birth. The growth factor also drove cardiomyocyte proliferation in lab tests of heart muscle samples obtained during surgery from human infants with congenital heart disease.

“These findings suggest that rNRG1 administration in infants with these birth defects might be a new therapeutic strategy for pediatric heart disease,” Dr. Kühn said. “Delivering agents early on that encourage the heart to make new cardiomyocytes could help the heart perform normally and reduce the risk of developing heart failure later in life.”

More research needs to be done before clinical testing of this strategy, the research team says. Dr. Kühn began the research while a member of the faculty at Boston Children’s Hospital.

Collaborators on the study were Balakrishnan Ganapathy, M.S., and Niyatie Ammanamanchi, M.S., both of Children’s Hospital of Pittsburgh of UPMC; Brian Polizzotti, Ph.D., Stuart Walsh, Ph.D., Sangita Choudhury, Ph.D., all of Boston Children’s Hospital; David Bennett, Ph.D., Beth Israel Deaconess Medical Center; Cristobal G. dos Remedios, Ph.D., Bosch Institute; Bernhard J. Haubner, M.D., and Josef M. Penninger, M.D., both with Institute of Molecular Biotechnology of the Austrian Academy of Sciences.

The research was supported by National Institutes of Health grants R01HL106302, K08HL085143, T32HL007572, and RR028792; Boston Children’s Hospital; and the Richard King Mellon Foundation Institute for Pediatric Research at Children’s Hospital of Pittsburgh of UPMC.

Renowned Expert in Viral Infections Named New Chief of Infectious Diseases at Children’s Hospital of Pittsburgh of UPMC

John V. Williams, M.D., an international authority on the epidemiology of respiratory viral infections, has been named chief of the Division of Pediatric Infectious Diseases at Children’s Hospital of Pittsburgh of UPMC.

“As chief, I am looking to expand the research capacity of the division, leveraging the strength in transplant medicine with my experience with viral immunology,” said Dr. Williams, also professor of pediatrics, University of Pittsburgh School of Medicine. “We will aim to develop an exceptional group of physicians and scientists to provide the best pediatric care for children with infections and conduct cutting-edge research relevant to pediatric infectious diseases.”

Prior to joining Children’s Hospital, Dr. Williams was at Vanderbilt University Medical Center where he was associate professor of pediatrics, pathology, microbiology and immunology. He is a graduate of the University of Virginia and completed medical school at the Medical College of Virginia/Virginia Commonwealth University. He trained in pediatrics at Children’s Hospital of Pittsburgh of UPMC and the University of Pittsburgh School of Medicine, and then in infectious diseases at Vanderbilt.

“The Division of Infectious Diseases has a long history of advancing knowledge in several areas, but in the clinical care of children who have undergone solid organ transplantation, it is particularly well established as an international force,” said David H. Perlmutter, M.D., physician-in-chief and scientific director, Children’s Hospital, and Distinguished Professor and Vira I. Heinz Endowed Chair, Department of Pediatrics, Pitt School of Medicine. “We are thrilled to have Dr. Williams take leadership of this program. With his expertise in the immunopathogenesis of viral infections, we believe this will be an exciting new direction for Children’s center of excellence in pediatric transplant care.”

During his fellowship at Vanderbilt, Dr. Williams began working on human metapneumovirus (MPV,) just after the virus was first discovered as a cause of acute respiratory infections. Over the years, his team has described the clinical features and epidemiology of MPV. His lab discovered that the major outer protein of MPV, the F protein, binds to cellular molecules called integrins to enter cells and initiate infection. His group also identified the MPV F protein as the target of antibodies that prevent infection, and showed that the F protein was an effective vaccine candidate.

In recent years, his lab has been responsible for identifying that MPV and other acute respiratory viral infections cause impairment of certain lung immune cells via a cellular signaling pathway that had previously only been associated with chronic infections and cancer. For this outstanding body of work on MPV, Dr. Williams was presented the 2014 E. Mead Johnson Award for Pediatric Research, the most prestigious research award in academic pediatrics.

Dr. Williams has extensive experience in other academic activities, including National Institutes of Health study sections and leadership in national and international academic societies. He is a member of the editorial boards of the Journal of Virology, Journal of Infectious Diseases, and Journal of the Pediatric Infectious Disease Society. He has been a very active mentor of students, residents and fellows, and in 2014 was elected to the Vanderbilt Academy for Excellence in Teaching. His wife, Stacey Swenn Williams, a general pediatrician and Pittsburgh native, will be joining Children’s Community Pediatrics at the CCP – GIL office.

For more information on Dr. Williams and the Division of Pediatric Infectious Diseases, visit www.chp.edu/infectiousdisease.

UPMC, Pitt Experts Present at AAOS 2015 Annual Meeting

PITTSBURGH, March 30, 2015 – UPMC and the University of Pittsburgh were well-represented at the recent American Academy of Orthopaedic Surgeons (AAOS) Annual Meeting in Las Vegas. UPMC and the Department of Orthopaedic Surgery hosted their annual cocktail reception during the meeting.

Faculty research also was featured in oral and poster presentations throughout the conference, including topics such as:

  • Positive Outcome Bias in the Total Joint Arthroplasty Literature
    Co-authors Carola Van Eck, MD (orthopaedic surgery resident), Adolph Yates Jr, MD
  • Increasing Women and Underrepresented Minorities in Orthopaedic Surgery: A Pipeline Initiative
    Co-author MaCalus Hogan, MD
  • Improving Orthopaedic Resident Surgical Skills Curricula Through Problem-Based Learning
    Co-contributors Adam Rothenberg, MD (orthopaedic surgery resident), MaCalus Hogan, MD, Vincent Deeney, MD, Freddie Fu, MD
  • The Use of Remnant in Individualized Anatomic ACL Reconstruction
    Co-contributor Freddie Fu, MD
  • Does Cross-sectional Area of the Median Nerve Correlate with Severity of Carpal Tunnel Syndrome?
    Co-authors Joseph Imbriglia, MD, William Hagberg, MD, John Fowler, MD
  • Degenerative Spondylolisthesis: An Evidence-Based Assessment of Treatment Options and Outcomes
    Faculty member James Kang, MD
  • Instructional Course: Surgical Management of Cervical Spondylotic Myelopathy
    Moderator James Kang, MD
  • Complications of Surgical Treatment
    Presenter James Kang, MD
  • Pro – Double Bundle Is Best
    Presenter Freddie Fu, MD

As part of the American Orthopaedic Society for Sports Medicine (AOSSM) Specialty Day, Dr. Fu also gave the John C. Kennedy, MD, Lecture entitled, “Anatomic ACL Reconstruction—A Changing Paradigm.”

For more information about the AAOS annual meeting, please visit the conference page.

Pitt Team Identifies Genes that Play Critical Role in the Development of Congenital Heart Disease

PITTSBURGH, March 25, 2015 – Fetal ultrasound exams on more than 87,000 mice that were exposed to chemicals that can induce random gene mutations enabled developmental biologists at the University of Pittsburgh School of Medicine to identify mutations associated with congenital heart disease in 61 genes, many not previously known to cause the disease. The study, published online today in Nature, indicates that the antenna-like cellular structures called cilia play a critical role in the development of these heart defects.

The findings are the culmination of an effort to find the genetic determinants of structural heart disease in the “Bench to Bassinet” program, launched six years ago by the National Heart, Lung, and Blood Institute (NHLBI), part of the National Institutes of Health, led at Pitt by principal investigator Cecilia Lo, Ph.D., professor and chair of the Department of Developmental Biology, Pitt School of Medicine.

“This project has given us new insights into the biological pathways involved in development of the heart,” Dr. Lo said. “The genes and pathways identified in our study will have clinical importance for interrogating the genetic causes of congenital heart disease in patients.”

For the study, Dr. Lo’s team mated mice exposed to chemicals that could create random genetic mutations, resulting in 87,355 pregnancies. They scanned each fetus using noninvasive ultrasound and recovered over 3,000 independent cases of congenital heart defects, all incompatible with life. They sequenced the genes of mutant animals and compared them to those of unaffected offspring to identify 91 recessive mutations in 61 genes.

“We were surprised to learn many of these genes were related to the cilia, or cilia-transduced cell signaling,” Dr. Lo said. “These findings suggest cilia play a central role in the regulation of heart development, including patterning left-right asymmetry in the cardiovascular system critical for efficient oxygenation of blood.”

She added that pathways recovered in the mouse study show overlap with those associated with de novo, or spontaneous, mutations identified in congenital heart disease patients. Co-investigators of the project include other researchers from the University of Pittsburgh; the University of Massachusetts Medical School; the Jackson Laboratory; and Children’s National Medical Center.

The project was funded NHLBI grants HL098180 and HL098188; National Institute of Mental Health grant MH094564; National Human Genome Research Institute grant HG000330; and the University of Pittsburgh School of Medicine.

Rebooting Cell Programming Can Reverse Liver Failure, Says Children’s Hospital/Pitt Study

PITTSBURGH, March 16, 2015 – It might be possible to heal cirrhotic liver disease by rebooting the genes that control liver cell function, according to researchers at Children’s Hospital of Pittsburgh of UPMC and the University of Pittsburgh School of Medicine. If validated in human studies, the game-changing strategy, described today in the online version of the Journal of Clinical Investigation, could potentially treat patients who are too sick for liver transplantation and, in the future, reduce the need for transplants.

The project grew out of the observation that not everyone who develops cirrhosis, or scarring of the liver, progresses to liver failure and its life threatening complications, explained Ira Fox, M.D., professor of surgery, Pitt School of Medicine, and director of the Center for Innovative Regenerative Therapies at Children’s Hospital and the McGowan Institute for Regenerative Medicine.

“Even with the large amount of scar tissue that comes with cirrhosis, there should be enough cells left to carry out the normal functions of the liver,” Dr. Fox said. “So when the liver fails, it is the liver cells themselves that aren’t working properly. In this study, we demonstrate what has caused the problem, and more importantly, a way to repair it.”

His team developed a rat model of liver disease that mimics the form of human cirrhosis that progresses to organ failure. In previous work, they found that liver cells taken from animals with cirrhosis, but no liver failure, immediately functioned properly when transplanted into another animal. But cells transplanted from animals with both cirrhosis and liver failure did not function normally at first, indicating that both the liver cells and the liver tissue environment were damaged.

The researchers then compared the genes in the liver cells of the two groups of cirrhotic rats and found unusually low activity levels of the genes that control proteins which play a central role in liver cell function, the most important being a factor called HNF4.

In the new paper, they showed that restoring production of HNF4 by gene therapy reboots the liver cells to normal function. The team first showed this in lab tests and then in rats with liver failure.

“We were pleased to see that the animals got better almost immediately. Remarkably, our tests indicated that it wasn’t stem cells, regeneration or growth of new liver cells that caused improvement. Instead, the diseased cells had healed,” Dr. Fox said. “It seems that in at least some forms of cirrhosis, chronic injury reprograms the liver cells to shut down HNF4 production, a dysfunction that eventually causes liver failure.”

HNF4 gene therapy provided unique insight into the cause of liver failure and has significant potential for human therapy, but the investigators are now looking for other gene targets to develop simpler therapies, such as drugs that block the pathways that mediate failure. The team also is confirming their results with human liver cells.

Co-investigators include Alejandro Soto-Gutierrez, M.D., Ph.D., Joseph Locker, M.D., Ph.D., and other researchers from Children’s Hospital, Pitt School of Medicine and the McGowan Institute; Kyoto Prefectural University of Medicine, Japan; and the University of Pennsylvania.

The project was funded by National Institutes of Health grants DK48794, DK099320 and DK099257, as well as grants from the U.S. Department of Defense.

Pitt Experts Present at AAP Annual Meeting

SAN ANTONIO, March 16, 2015 – The University of Pittsburgh was well-represented at the recent Association of Academic Physiatrists (AAP) Annual Meeting in San Antonio. Faculty research was featured in oral and poster presentations throughout the conference, including:

Two physical medicine and rehabilitation residents also received awards for the following presentations:

For more information, or to view a complete list of presentations at the AAP Annual Meeting, please visit the conference page.

 

Rebooting Cell Programming Can Reverse Liver Failure, Says Children’s Hospital/Pitt Study

It might be possible to heal cirrhotic liver disease by rebooting the genes that control liver cell function, according to researchers at Children’s Hospital of Pittsburgh of UPMC and the University of Pittsburgh School of Medicine. If validated in human studies, the game-changing strategy, described today in the online version of the Journal of Clinical Investigation, could potentially treat patients who are too sick for liver transplantation and, in the future, reduce the need for transplants.

The project grew out of the observation that not everyone who develops cirrhosis, or scarring of the liver, progresses to liver failure and its life threatening complications, explained Ira Fox, M.D., professor of surgery, Pitt School of Medicine, and director of the Center for Innovative Regenerative Therapies at Children’s Hospital and the McGowan Institute for Regenerative Medicine.

“Even with the large amount of scar tissue that comes with cirrhosis, there should be enough cells left to carry out the normal functions of the liver,” Dr. Fox said. “So when the liver fails, it is the liver cells themselves that aren’t working properly. In this study, we demonstrate what has caused the problem, and more importantly, a way to repair it.”

His team developed a rat model of liver disease that mimics the form of human cirrhosis that progresses to organ failure. In previous work, they found that liver cells taken from animals with cirrhosis, but no liver failure, immediately functioned properly when transplanted into another animal. But cells transplanted from animals with both cirrhosis and liver failure did not function normally at first, indicating that both the liver cells and the liver tissue environment were damaged.

The researchers then compared the genes in the liver cells of the two groups of cirrhotic rats and found unusually low activity levels of the genes that control proteins which play a central role in liver cell function, the most important being a factor called HNF4.

In the new paper, they showed that restoring production of HNF4 by gene therapy reboots the liver cells to normal function. The team first showed this in lab tests and then in rats with liver failure.

“We were pleased to see that the animals got better almost immediately. Remarkably, our tests indicated that it wasn’t stem cells, regeneration or growth of new liver cells that caused improvement. Instead, the diseased cells had healed,” Dr. Fox said. “It seems that in at least some forms of cirrhosis, chronic injury reprograms the liver cells to shut down HNF4 production, a dysfunction that eventually causes liver failure.”

HNF4 gene therapy provided unique insight into the cause of liver failure and has significant potential for human therapy, but the investigators are now looking for other gene targets to develop simpler therapies, such as drugs that block the pathways that mediate failure. The team also is confirming their results with human liver cells.

Co-investigators include Alejandro Soto-Gutierrez, M.D., Ph.D., Joseph Locker, M.D., Ph.D., and other researchers from Children’s Hospital, Pitt School of Medicine and the McGowan Institute; Kyoto Prefectural University of Medicine, Japan; and the University of Pennsylvania.

The project was funded by National Institutes of Health grants DK48794, DK099320 and DK099257, as well as grants from the U.S. Department of Defense.

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