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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.

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.

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.

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.

Pediatric Rehabilitation Chief Asked to Participate in CDC, AAP Activities

PITTSBURGH, March 5, 2015 – Amy Houtrow, MD, PhD, MPH, chief, Division of Pediatric Rehabilitation Medicine and a member of the Brain Care Institute at Children’s Hospital of Pittsburgh of UPMC, recently was invited by the Centers for Disease Control and Prevention (CDC) to participate in its National Center on Birth Defects and Developmental Disabilities (NCBDDD) and the Division of Human Development and Disability. Selected for her expertise in the area of disability and health, Dr. Houtrow also serves as associate professor and vice chair in the Department of Physical Medicine and Rehabilitation at the University of Pittsburgh. The group’s goal is to develop concrete recommendations to inform a current and innovative Disability and Health Branch roadmap over the next decade.

Dr. Houtrow also has been asked to serve on the American Academy of Pediatrics (AAP) National Conference & Exhibition Planning Group, a cross-section of more than two dozen practicing pediatricians, medical, and surgical pediatric subspecialists. The group reviews and accepts approximately 350 sessions — out of more than 500 proposals — that comprise the conference program.

Pitt Study Finds Popular YouTube Videos Drown Viewers with Positive Portrayals of Drunkenness

PITTSBURGH, Feb. 20, 2015 – The 70 most popular videos depicting drunkenness on YouTube account for more than 330 million views, with little portrayal of the negative outcomes of excessive alcohol consumption, according to an analysis led by the University of Pittsburgh Center for Research on Media, Technology, and Health (CRMTH).

The popularity of such videos on YouTube could be an opportunity for public health interventions aimed at educating teenagers and young adults of the negative consequences of intoxication, the researchers suggest in an article published in today’s issue of the journal Alcoholism: Clinical and Experimental Research.

“There has been little research examining Internet-based, alcohol-related messaging,” said lead author Brian A. Primack, M.D., Ph.D., director of CRMTH and assistant vice chancellor for health and society in Pitt’s Schools of the Health Sciences. “While we know that some viewers may be savvy enough to skeptically view music videos or advertisements portraying intoxication as fun, those same viewers may be less cynical when viewing user-generated YouTube videos portraying humorous and socially rewarding escapades of a group of intoxicated peers.”

Dr. Primack’s team mined YouTube for five terms synonymous with alcohol intoxication – drunk, buzzed, hammered, tipsy and trashed – winnowing their findings down to the most relevant.

There were a total of 333,246,875 views for all 70 videos combined.

  • Humor was juxtaposed with alcohol use in 79 percent of the videos.
  • Motor vehicle use was present in 24 percent.
  • Although 86 percent of the videos showed active intoxication, only 7 percent contained references to alcohol dependence.
  • An average of 23.2 “likes” were registered for every “dislike.”
  • While 89 percent of the videos involved males, only 49 percent involved females.
  • A specific brand of alcohol was referenced in 44 percent of the videos.

“This is the first comprehensive attempt to analyze YouTube data on intoxication, and these statistics should be valuable in guiding interventions,” said Dr. Primack, also a practicing physician. “For example, we know that men tend to report more frequent binge drinking than women and that alcohol use is perceived as more socially acceptable for men. Because they are portrayed more frequently in YouTube videos, it may be useful to target men with future interventions debunking alcohol-related myths propagated on social media.”

Dr. Primack found it concerning that nearly half the videos contained specific brand references. While this could indicate industry influence, the researchers did not note any clear indication of intentional advertising. Past research has linked exposure to brand references in popular media to encouraging alcohol consumption.

Additional authors on this research are Jason B. Colditz, M.Ed., and Kevin C. Pang, both of Pitt; and Kristina M. Jackson, Ph.D., of Brown University.

This research was funded by ABMRF/The Foundation for Alcohol Research.

Pitt Expert Talks Teenage Brain Development at American Association for the Advancement of Science Annual Meeting

PITTSBURGH, Feb. 14, 2015 – Teenage exploration and risk taking could be explained by dramatic changes in the brain that allow elaborate planning and are driven by the need for immediate reward, according to a University of Pittsburgh neuroscientist who will be talking about her research in a panel discussion and press briefing at the American Association for the Advancement of Science annual meeting, Feb. 13 to 16, in San Jose, Calif.

Using an elegant model in which eye movements, or saccades, reveal insight into executive brain function, Beatriz Luna, Ph.D., Staunton Professor of Psychiatry and Pediatrics, Pitt School of Medicine, has studied hundreds of young volunteers to examine brain development during the transition between childhood and adulthood.

“Our studies are beginning to challenge the traditional concept that the teenage brain can’t plan because of an immature prefrontal cortex,” Dr. Luna said. “Our findings indicate that the teen prefrontal cortex is not much different than in the adult, but it can be easily overruled by heightened motivation centers in the brain. You have this mixture of newly gained executive control plus extra reward that is pulling the teenager toward immediate gratification.”

In the experiments, volunteers are instructed to immediately look away from a small light that randomly appears on a screen in front of them. This “anti-saccade” test shows if the brain is able to engage the planning centers of the prefrontal cortex to overcome the impulse to look toward the light rather than away from it. Dr. Luna’s team has found in previous studies that children succeed in about half their tries, teens in about 70 percent of tries and adults in about 90 percent of tries. People with mental illnesses typically struggle with the task.

The study team had volunteers do the same tasks while scanning their brains with functional MRI. They found that much of the architecture of mature brain is in place by adolescence, but the ability of the networks to talk to one another and integrate information is still a work in progress.

“Further enhancement of this network integration is likely why adults can switch and very quickly adapt their behavior to changing circumstances, which is more difficult for adolescents,” Dr. Luna explained.

She added that while parents and teachers sometimes find bewildering the choices teens might make, their brains are perfectly adapted to explore and take some chances as they become independent adults.

“Across societies and species, we know that adolescence is a period of increased sensation seeking that can lead to risk taking, which increases mortality rate,” Dr. Luna said. “Also, we often see during this period the first signs of mental illnesses such as schizophrenia, depression and eating disorders. All of these have a neurobiological basis, so if we know how the brain is changing, we might be able to figure out a way to intervene earlier in life.”

Dr. Luna and researchers from the Children’s National Medical Center, Washington, D.C.; Columbia University Medical Center; and University of California, Berkeley, will present their work from 1:30 to 4:30 p.m., Saturday, Feb. 14, during a AAAS session called “From Womb to Tomb.”

They also will participate in a news briefing that day which will be webcast at 10 a.m. PT, 1 p.m. ET, at http://www.eurekalert.org/aaasnewsroom/2015/.

Watch a video of Dr. Luna describing her work.

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