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Postdocs in UAB News

  • Allison elected fellow of the American Heart Association
    UAB’s David Allison, Ph.D., has been named to a prestigious fellowship with the American Heart Association for his work in nutrition and obesity.

    David B. Allison, Ph.D., Distinguished Professor in the School of Public Health and Quetelet Endowed Professor of Public Health at the University of Alabama at Birmingham, has been elected as a fellow of the American Heart Association, Council on Lifestyle and Cardiometabolic Health.

    Election as a fellow of AHA recognizes an individual’s scientific and professional accomplishments and volunteer leadership and service. Fellowship is open to scientists, physicians, clinical professionals and academicians with a major and productive interest in nutrition, physical activity, obesity or diabetes.

    Allison, who is also the associate dean for science in SOPH and the director of the Nutrition Obesity Research Center and Office of Energetics, received his Ph.D. from Hofstra University in 1990. He then completed a postdoctoral fellowship at the Johns Hopkins University School of Medicine and a second postdoctoral fellowship at the NIH-funded New York Obesity Research Center at St. Luke’s/Roosevelt Hospital Center. He joined the UAB faculty in 2001.

    He has written more than 500 scientific publications and edited five books. He has won several awards, including the 2002 Lilly Scientific Achievement Award from The Obesity Society, the 2002 Andre Mayer Award from the International Association for the Study of Obesity, and the National Science Foundation Administered 2006 Presidential Award for Excellence in Science, Mathematics and Engineering Mentoring.

    He was elected as a fellow of the American Statistical Association in 2007, the American Psychological Association in 2008, the American Association for the Advancement of Science in 2009, the NY Academy of Medicine in 2014 and the Gerontological Society of America in 2014, and was inducted into the Johns Hopkins Society of Scholars in 2013. He holds several NIH grants, including one of the Common Fund’s NIH Director’s Transformative Research Award titled “Energetics, Disparities & Lifespan: A unified hypothesis.”

  • U.S. biomedical postdoctoral fellow numbers decline, UAB researcher finds
    “A major issue facing biomedical research,” says Fran Lund, chair of UAB microbiology.

    The number of U.S. biomedical postdoctoral fellows has fallen for three years in a row, an unprecedented decline that University of Alabama at Birmingham researcher Louis Justement, Ph.D., and colleagues at the Federation of American Societies for Experimental Biology (FASEB) and Brown University call “an end to the era of expansion.”

    For 31 years since 1979, the number of biomedical postdocs had increased nearly every year, except for single-year dips in 1982, 1995 and 1999, according to analysis of data from the National Science Foundation Survey of Graduate Students and Postdoctorates in Science and Engineering. But in 2011, 2012 and 2013 — the most recent data available — that trend reversed. The number of biomedical postdocs fell each of those three years, with consecutively larger drops each year and an overall three-year decline of 5.5 percent, to a total of 38,719.

    “… unless we find some way to improve career prospects for early-career scientists, we risk losing the talent that will be essential for our future progress in the biologic and medical sciences,” Justement, first author Howard Garrison, Ph.D., and Susan Gerbi, Ph.D., wrote in a recent FASEB Journal paper. They conclude that a continued decline in the number of postdocs could diminish the quality and quantity of research because postdocs, along with graduate students, are the majority of the biomedical research workforce. Garrison is director of public affairs at FASEB, Justement is a UAB professor of microbiology, and Gerbi is a professor of biochemistry at Brown.

    “This is a major issue facing biomedical research,” commented Frances Lund, Ph.D., chair of the UAB Department of Microbiology. “It’s good to see that we have faculty at UAB who are working to influence science policy by providing data to support what is entirely obvious to those working in science but may not be evident to those responsible for setting the science budgets.”

    The authors say possible causes of the drop could include a decrease in qualified applicants, though data do not seem to support that; technical changes in employment titles from postdoc to something else; diminished demands for postdocs; or shifting patterns in the number of doctorate-holders willing to take postdoc positions. They note that the inflation-adjusted NIH budget lost 19 percent of its purchasing power from 2003 to 2012, and the number of RO1-like NIH grants fell by 11 percent in that same period.

    “… it may be that the declining purchasing power of grants and the rising cost of postdoctoral stipends and benefits reached critical threshold after 2010,” they wrote. “Postdocs are the most vulnerable part of the workforce, hired for short-duration, temporary positions. Therefore, as research budgets come under increased pressure, it would be expected that this group would be affected most.”

    Also, they say, Ph.D. recipients may be deciding to forgo a postdoctoral position for different career options, in the face of a tight academic labor market and uncertain prospects for success. The loss of talented research personnel threatens biomedical research.

    “A continued loss of postdocs without an alternative source of talented research personnel will slow our rate of progress,” they concluded. “We need to develop a steady-state model for the biomedical research workforce while maintaining the vitality and excellence of the enterprise.”

    UAB has also seen a decline in postdocs.

    “Looking at numbers from over the past nine years, we have seen a decline of approximately 20 percent in the total number of Ph.D. postdocs here at UAB,” said Lisa Schwiebert, the UAB associate dean for Graduate and Postdoctoral Affairs, and a professor in the Department of Cell, Developmental and Integrative Biology. “As discussed in Dr. Justement’s paper, this is likely the result of several concurrent forces, including but not limited to a decrease in NIH funding, coupled with increased awareness of career options that don’t require a postdoc. Despite this trend, we continue to actively recruit postdocs, as they represent a critical part of the research program here at UAB. We work diligently to provide them with opportunities to broaden their professional skills and development, so that they are able to pursue the career of their choice.”

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UAB Research News

  • Study finds genetic risk factor can lead to hyperinflammatory disorder, death after viral infection
    A UAB/Children’s of Alabama/Cincinnati Children’s study finds genetic risk for fatal inflammatory disorder linked to viral infection.
    Media Contact Cincinnati Children’s: Nick Miller 513-803-6035 or
    Media Contact UAB: Bob Shepard 205-934-8934 or

    CINCINNATI/BIRMINGHAM, Ala. – A group of people with fatal H1N1 flu died after their viral infections triggered a deadly hyperinflammatory disorder in susceptible individuals with gene mutations linked to the overactive immune response, according to a study in The Journal of Infectious Diseases.

    Researchers at Cincinnati Children’s Hospital Medical Center, the University of Alabama Birmingham and Children’s of Alabama led the study, published online Nov. 23. They suggest people with other types of infections and identical gene mutations also may be prone to the disorder, known as reactive HLH (rHLH), or hemophagocytic lymphohistiocytosis.

    HLH causes the immune system to essentially overwhelm the body with inflammation that attacks vital organs, often leading to death. Study authors raise the possibility of screening children for HLH genes to identify those who may be at risk during a viral infection.

    “Viruses that cause robust immune responses may be more likely to trigger rHLH in genetically susceptible people,” said Randy Cron, M.D., Ph.D., a senior investigator on the study and physician in pediatric rheumatology at UAB and Children’s of Alabama. “Prenatal screening for mutations in common HLH-associated genes may find as much as 10 percent of the general population who are at risk for HLH when an inflammation threshold is reached from H1N1 or other infection triggers.”

    This study is the first to identify mutations of HLH-associated genes in H1N1 cases where patients had clinical symptoms of rHLH and a related condition called macrophage activation syndrome, or MAS. An outbreak of H1N1 in 2009 turned into a global pandemic. H1N1 has since become part of the viral mix for the annual flu season and preventive vaccine, the authors note.

    Collaborating on the study were co-senior investigator Alexei Grom, M.D., and first author Grant Schulert, M.D., Ph.D., both physicians in the Division of Rheumatology at Cincinnati Children’s.

    Cron and Grom have published articles linking clinical signs of rHLH to patients with hemorrhagic fever and systemic juvenile idiopathic arthritis, an inflammatory condition in which the body thinks it has an infection and attacks vital organs and joints. The precise reasons these patients have clinical signs of rHLH have not been clear, although some juvenile arthritis patients who develop MAS also have HLH-linked gene mutations, according to the authors.

    This study is the first to identify mutations of HLH-associated genes in H1N1 cases where patients had clinical symptoms of rHLH and a related condition called macrophage activation syndrome, or MAS. An outbreak of H1N1 in 2009 turned into a global pandemic. H1N1 has since become part of the viral mix for the annual flu season and preventive vaccine, the authors note.

    There are two types of HLH, hereditary and the reactive form focused on in the current study. Both share common physical traits that involve the body’s immune system’s overheating, excessive proliferation of immune cells called macrophages and severe inflammation. The only curative treatment at present is a bone marrow transplant, a risky procedure that is not always successful.

    “There are no widely accepted and validated diagnostic criteria for reactive HLH, and criteria for familial HLH are not considered effective for rHLH or MAS,” said Schulert. “Regardless, it seems clear that a sizeable number of patients with fatal H1N1 infection develop rHLH. Our data suggest some people may have a genetic predisposition to develop severe H1N1 influenza, and critically ill H1N1 patients should be carefully evaluated for rHLH and MAS. The question is whether immunosuppressive therapy may benefit some patients with life-threatening influenza infection."

    The current study examined the medical records of 16 adult patients ages 23 and 61 who died between 2009 and 2014 while infected with H1N1. The patients and their HLH-like symptoms initially were identified through the Michigan Hospital Department of Pathology Database by study collaborator Paul Harms, M.D., and his team at Michigan Center for Translational Pathology, University of Michigan Medical School.

    Processed tissue samples from the patients were examined using whole exome genetic sequencing, which reads an individual’s entire genetic code of every gene.

    Forty-four percent of the H1N1 cases met the clinical criteria for HLH and 81 percent for the related condition MAS. Five patients carried one of three different gene mutations in the commonly identified HLH gene LYST. Two of those same five patients also had a specific mutation in the gene PRF1, which decreases the function of immune system natural killer cells and aids the overproliferation of macrophage cells. Several patients in the study also carried variants of other genes linked to observed cases of MAS.

    The current study involved a small patient population in a single state and was retrospective in design, looking at records from past cases. The authors recommend conducting a larger prospective study to determine whether genomic testing can predict the course of disease progression during influenza and other types of infections. Researchers also want to conduct further genomic and biological testing of children with juvenile arthritis to solidify potential links between gene mutations and secondary autoimmune disease.

    Funding support for the study came in part from the National Institutes of Health (R01-AR059049, K12-HL119986), the Kaul Pediatric Research Institute and a Scientist Development Award from the American College of Rheumatology’s Rheumatology Research Foundation.

  • Trial combining exercise and a drug may help seniors muscle up
    A diabetes drug combined with exercise may help older adults regrow muscle, and UAB’s Center for Exercise Medicine is investigating.

    A participant in the Master's trial exercises under the supervision of Marcas Bamman and Craig Tuggle.A drug that might help older adults regrow muscle is under investigation at the University of Alabama at Birmingham. UAB is recruiting healthy adults age 65 and older for a study combining strength training exercise with the anti-diabetes drug metformin.

    The investigators have reason to suspect that metformin might improve the effectiveness of exercise in rebuilding muscle tissue.

    “Muscles atrophy as we age, and inflammation is one of the suspected causes,” said Marcas Bamman, Ph.D., director of the UAB Center for Exercise Medicine in the School of Medicine. “We have evidence from previous studies in our laboratory that metformin can play an important role in reducing inflammation in the muscles, and we are launching this study to confirm those preliminary findings.”

    The key, Bamman says, are cells called macrophages, which are some of the body’s trash collectors. Macrophages surround and digest rogue cells or cellular debris that has been identified by the body as not belonging to a healthy cell. As part of this process, macrophages promote inflammation, which stimulates the immune system to respond to the threatened area.

    However, when the crisis has been managed, and it is time for the immune system to ramp down, some macrophages transition from an inflammatory to an anti-inflammatory role. Through a process called polarization, M1 macrophages, which cause inflammation, transition to M2 macrophages, which decrease inflammation and encourage tissue repair.

    Marcas Bamman, Ph.D., director of the UAB Center for Exercise MedicineThe team’s preliminary studies suggest metformin may promote the polarization from M1 to M2.

    “Reducing inflammation in muscle of older adults should create a pro-growth environment and help these individuals build new muscle,” said Bamman, who is also a professor in the Department of Cell, Developmental and Integrative Biology. “We’re intrigued to see whether metformin’s effect on macrophages contributes to this regrowth. The overall goal is to establish a low-cost, personalized approach to prevent frailty in the elderly.”

    The MASTERS trial is being conducted in collaboration with investigators at the University of Kentucky. The two institutions are looking for 100 adults 65 or older who do not have diabetes. Participants will exercise three times a week for 14 weeks with certified trainers and receive either metformin or a placebo. Participants will also get a physical examination, along with DEXA scans, CT imaging and other tests.

    The study is funded by the National Institutes of Health. For more information, or to enroll in the study, go to Current Research at

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