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Fine Particulate Air Pollution Associated With Increased Risk of Childhood Autism

PITTSBURGH, May 21, 2015 – Exposure to fine particulate air pollution during pregnancy through the first two years of a child’s life may be associated with an increased risk of the child developing autism spectrum disorder (ASD), a condition that affects one in 68 children, according to a University of Pittsburgh Graduate School of Public Health investigation of children in southwestern Pennsylvania.

The research is funded by The Heinz Endowments and published in the July edition of Environmental Research.

“Autism spectrum disorders are lifelong conditions for which there is no cure and limited treatment options, so there is an urgent need to identify any risk factors that we could mitigate, such as pollution,” said lead author Evelyn Talbott, Dr.P.H., professor of epidemiology at Pitt Public Health. “Our findings reflect an association, but do not prove causality. Further investigation is needed to determine possible biological mechanisms for such an association.”

Dr. Talbott and her colleagues performed a population-based, case-control study of families with and without ASD living in six southwestern Pennsylvania counties. They obtained detailed information about where the mothers lived before, during and after pregnancy and, using a model developed by Pitt Public Health assistant professor and study co-author Jane Clougherty, Sc.D., were able to estimate individual exposure to a type of air pollution called PM2.5.

This type of pollution refers to particles found in the air that are less than 2.5 micrometers in diameter, or 1/30th the average width of a human hair. PM2.5 includes dust, dirt, soot and smoke. Because of its small size, PM2.5 can reach deeply into the lungs and get into the blood stream. Southwestern Pennsylvania has consistently ranked among the nation’s worst regions for PM2.5 levels, according to data collected by the American Lung Association.

“There is increasing and compelling evidence that points to associations between Pittsburgh’s poor air quality and health problems, especially those affecting our children and including issues such as autism spectrum disorder and asthma,” said Grant Oliphant, president of The Heinz Endowments. “While we recognize that further study is needed, we must remain vigilant about the need to improve our air quality and to protect the vulnerable. Our community deserves a healthy environment and clean air.”

Autism spectrum disorders are a range of conditions characterized by social deficits and communication difficulties that typically become apparent early in childhood. Reported cases of ASD have risen nearly eight-fold in the last two decades. While previous studies have shown the increase to be partially due to changes in diagnostic practices and greater public awareness of autism, this does not fully explain the increased prevalence. Both genetic and environmental factors are believed to be responsible.

Dr. Talbott and her team interviewed the families of 211 children with ASD and 219 children without ASD born between 2005 and 2009. The families lived in Allegheny, Armstrong, Beaver, Butler, Washington and Westmoreland counties. Estimated average exposure to PM2.5 before, during and after pregnancy was compared between children with and without ASD.

Based on the child’s exposure to concentrations of PM2.5 during the mother’s pregnancy and the first two years of life, the Pitt Public Health team found that children who fell into higher exposure groups were at an approximate 1.5-fold greater risk of ASD after accounting for other factors associated with the child’s risk for ASD – such as the mother’s age, education and smoking during pregnancy. This risk estimate is in agreement with several other recent investigations of PM2.5 and autism.

A previous Pitt Public Health analysis of the study population revealed an association between ASD and increased levels of air toxics, including chromium and styrene. Studies by other institutions using different populations also have associated pollutants with ASD.

“Air pollution levels have been declining since the 1990s; however, we know that pockets of increased levels of air pollution remain throughout our region and other areas,” said Dr. Talbott. “Our study builds on previous work in other regions showing that pollution exposures may be involved in ASD. Going forward, I would like to see studies that explore the biological mechanisms that may underlie this association.”

Additional co-authors of this study are Vincent C. Arena, Ph.D., Judith R. Rager, M.P.H., Drew R. Michanowicz, Dr.P.H., Ravi K. Sharma, Ph.D., and Shaina L. Stacy, Ph.D., all of Pitt Public Health.

Children’s Hospital of Pittsburgh of UPMC Lung Researcher Receives Prestigious Scientific Award

PITTSBURGH, May 18, 2015John F. Alcorn, Ph.D., assistant professor of pediatrics in the Division of Pulmonology at Children’s Hospital of Pittsburgh of UPMC, has been selected as the 2015 recipient of the Parker B. Francis Jo Rae Wright Award for Scientific Excellence. The award has been established by the Parker B. Francis Fellowship Program and the Francis Family Foundation to honor Jo Rae Wright, Ph.D.

The award will be presented to Dr. Alcorn today at the Parker B. Francis Fellowship Reception at the American Thoracic Society meeting.

“The Parker B. Francis Fellowship Program and the Francis Family Foundation has been instrumental in my early career development to independence,” said Dr. Alcorn, also assistant professor of pediatrics, University of Pittsburgh School of Medicine. “Receiving this award is exceptionally meaningful to me as I previously completed my Ph.D. training under Jo Rae’s mentorship at Duke University. I am honored to be the recipient Jo Rae Wright Award and I hope to continue on the path toward becoming a leader in pulmonary research.”

Dr. Alcorn’s research focuses on T-cell mediated immunity during influenza infections and secondary bacterial pneumonia, as well as the role of T-cells in severe, steroid-insensitive asthma.

The Parker B. Francis Jo Rae Wright Award for Scientific Excellence is given annually to a recent graduate of the Fellowship Program whose research shows outstanding creativity and promise and who has demonstrated outstanding mentoring and professional leadership qualities. Dr. Alcorn will receive a one-time award of $5,000 to be used to support research costs.

Dr. Jo Rae Wright was a world-renowned scientist, devoted teacher and mentor, and a leader in academia and professional organizations. She served as dean of the Graduate School of Duke University and was president of the American Thoracic Society in 2008. She received the American Physiological Society’s Walter B. Cannon Award for lifetime achievements in research in 2005. She served as a member of the Parker B. Francis Fellowship Program Council of Scientific Advisors from 2004 through 2007 and was a mentor to Parker B. Francis Fellows.

For more information on Dr. Alcorn, visit www.chp.edu.

Children’s Pulmonologist Honored By Association of American Physicians and American Thoracic Society

PITTSBURGH, May 6, 2015 – Juan Celedón, MD, DrPH, Chief of Service in the Division of Pediatric Pulmonology, Allergy, and Immunology at Children’s Hospital of Pittsburgh of UPMC recently was elected to the Association of American Physicians. Dr. Celedón also was chosen for the Innovations in Health Equality — Lifetime Achievement Award from the American Thoracic Society’s Clinicians Advisory Committee and its Health Equality Subcommittee.

Dr. Celedón’s research is focused on the genetics and epidemiology of asthma in Puerto Rican and black children. He also is leading a study of chronic obstructive pulmonary disease (COPD) genetics in Costa Rica.

For more information on Dr. Celedón’s work, please visit the Division of Pulmonary, Allergy, and Critical Care Medicine page.

Pitt, Children’s Research Papers Receive Top 10 Awards from Clinical Research Forum

PrintPITTSBURGH, April 20, 2015 – Three scientific papers published in 2014 by research teams from the University of Pittsburgh School of Medicine and Children’s Hospital of Pittsburgh of UPMC have each been selected to receive a Clinical Research Forum Annual Top 10 Clinical Research Achievement Award. The awards were announced last night at the Forum’s annual meeting in Washington, D.C. The winning papers from Pitt and UPMC were chosen based on their degree of innovation from a pool of more than 50 nominations from 30 research and academic health centers nationwide. The Forum and its supporters believe these and other top ten papers represent the best and brightest work in the field, and will lead to advancements in medicine that will change lives and patient outcomes worldwide. “It is extraordinary to have three University of Pittsburgh projects in a variety of disciplines recognized by the Forum for their clinical impact and rigorous science,” said Arthur S. Levine, M.D., Pitt’s senior vice chancellor for the health sciences and the John and Gertrude Petersen Dean of Medicine. “This impressive showing reflects the commitment and caliber of the researchers on our campus, and is a tribute to the University’s Clinical and Translational Science Institute, which facilitates and supports these endeavors.” The three winners are:

  • “Upper-Airway Stimulation for Obstructive Sleep Apnea,” published Jan. 9, 2014, in the New England Journal of Medicine, showed implanting a device called Inspire® Upper Airway Stimulation led to a 70 percent reduction of severe obstructive sleep apnea symptoms. Project investigators included lead author Patrick Strollo, M.D., professor of medicine and clinical and translational science, Pitt School of Medicine, and medical director of the UPMC Sleep Medicine Center, and Ryan Soose, MD.
  • A Randomized Trial of Protocol-Based Care for Early Septic Shock,” published May 1, 2014, in the New England Journal of Medicine, showed that a structured, standardized approach to diagnose and treat sepsis in its early stages did not change patient survival rates. Project investigators included Derek Angus, M.D., M.P.H., distinguished professor and Mitchell P. Fink Chair, Department of Critical Care Medicine, Pitt School of Medicine, and Donald M. Yealy, M.D., professor and chair of Pitt’s Department of Emergency Medicine.
  • Antimicrobial Prophylaxis for Children with Vesicoureteral Reflux,” published June 19, 2014, in the New England Journal of Medicine, showed that children with abnormal flow of urine from the bladder to the upper urinary tract, called vesicoureteral reflux (VUR), can avoid recurrent urinary tract infections by taking daily low-dose antibiotics. Project investigators included senior author Alejandro Hoberman, M.D., chief, Division of General Academic Pediatrics at Children’s Hospital, and professor of pediatrics, Pitt School of Medicine.

“I applaud the researchers recognized for their groundbreaking clinical research that will advance new treatments to reduce suffering and bring hope to millions of people,” said National Institutes of Health director, Francis S. Collins, M.D., Ph.D. “And I’m especially proud that NIH funding makes these advances possible.” Other awardees include scientists from Harvard Medical School, Yale University, the University of Pennsylvania, UCLA and other leading institutions. The Clinical Research Forum was formed in 1996 to discuss the unique and complex challenges to clinical research in academic health centers. The mission of the Forum is to provide leadership to the national clinical and translational research enterprise and promote understanding and support for clinical research and its impact on health and health care.

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

PrintSurgery 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

PrintJohn 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.

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