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Leadership for all administrative research units serving the research enterprise at UAB. OVPRED oversees Core Facilities, Institutional Animal Care and Use Committee, and Institional Review Board.

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Electronic submission of funding applications and compliance forms for future research initiatives.

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The nexus for UAB innovation, entrepreneurial educational models, applied research, and management of intellectual property.

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Presentations and general information related to effective grant writing.

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UAB is committed to the development and success of outstanding postdoctoral scientists.

Conflict of Interest Review Board (CIRB)

Charged with the ongoing development of policies and procedures related to conflicts of interest in sponsored research, review of disclosures of financial interests submitted by investigators, and the development of conflict of interest management plans.

Research News

UAB study looks at racial disparity in deaths during childbirth
UAB study looks at racial disparity in deaths during childbirth
A UAB study of hospital deaths during childbirth suggests the high death rate of African-American women is likely associated with access to prenatal care.

pregnant ladyResearchers at the University of Alabama at Birmingham suggest barriers to care may be the primary cause of the high rate of black women who die during childbirth. National statistics show black women are nearly four times more likely to die in childbirth than are white women.

Statistics over 20 years showed the rate of death during childbirth at UAB Hospital is about the same for black women as it is for white women. The findings, published Nov. 5 in Anesthesia & Analgesia, looked at 77 maternal deaths occurring between 1990 and 2010.

The study authors report that there was insufficient evidence to suggest racial disparity in the incidence of death and that there was no association between mortality status and insurance status, income, body mass index, marital status or parity.

“Our findings suggest that the next step toward understanding racial differences in maternal deaths should be directed at health care delivery outside the tertiary-care hospital setting, particularly at eliminating access barriers to health care for all women,” said Michael Froelich, M.D., associate professor in the Department of Anesthesiology and lead author of the study.

Gestational age, fetal survival, duration of hospital stay, lack of prenatal care and cesarean delivery rate were factors associated with greater mortality. Obesity was not a factor in this study, although obesity has been implicated as a risk factor in other studies.

Froelich says gestational age, fetal survival, duration of hospital stay, lack of prenatal care and cesarean delivery rate were factors associated with greater mortality. He says that obesity was not a factor in this study, although obesity has been implicated as a risk factor in other studies.

“Women who lived farther away from the hospital were at greater risk of mortality, so proximity to appropriate health care may be a significant predictor of risk,” Froelich said., a supplement to Anesthesia & Analgesia, published a commentary on the study by section editor J. Lance Lichtor, M.D.

“We do not know if the results at the University of Alabama at Birmingham are representative of outcomes at all tertiary teaching hospitals,” wrote Lichtor, chief of Pediatric Anesthesiology at Yale University. “If this is a representative outcome, then our major teaching hospitals appear to provide equally excellent care to all patients, regardless of race. It follows that we need to look elsewhere to understand the racial differences in maternal mortality evident in U.S. national statistics.”

Novel theory connects mothers to childhood obesity: Evolution is the cause, moms are the cure
Novel theory connects mothers to childhood obesity: Evolution is the cause, moms are the cure

A UAB School of Public Health researcher has published a theory that suggests a mother’s activity and metabolism can influence her child’s likelihood of being obese.

obesitymomAs the waistlines of children in the United States continue to grow, scientists continue to seek causes of the childhood obesity epidemic. One University of Alabama at Birmingham School of Public Health researcher has published a new theory that he says explains why infants in the United States are being born heavier than at any time in our nation’s history.

According to the Centers for Disease Control and Prevention, obesity has more than doubled in children and quadrupled in adolescents in the past 30 years. In 2012, more than one-third of children and adolescents were overweight or obese.

“Childhood obesity is the major public health problem of the 21st century and will continue to be until we fully understand why children are becoming obese. My theory offers that understanding,” said Edward Archer, Ph.D., postdoctoral fellow in the Nutrition Obesity Research Center and Office of Energetics.

Archer says that previously there were no valid theories as to why children are becoming so obese so rapidly, and that the common notion of “moving too little and eating too much” is simplistic and leads to the stigmatization of a large portion of our population.

Through a meta-theoretic analysis, Archer unified ideas from a number of scientific fields and created a grand narrative, “The Childhood Obesity Epidemic As a Result of Non-Genetic Evolution: the Maternal Resources Hypothesis,” published in the November issue of the Mayo Clinic Proceedings.

“This paper is a significant advance in the theory and science of evolution, obesity and health,” Archer said. “It synthesizes a century of evidence from fields as diverse as pediatrics, evolutionary biology, anthropology and epidemiology to present a novel theory on the causes of the childhood obesity epidemic.”

There are three main findings:

  1. Obesity is the result of fat cells’ out-competing other tissues for the energy consumed through food.
  2. A woman’s physical activity and body composition before, during and after pregnancy have evolutionary consequences because both determine not only her metabolism and risk of disease but those of her children, grandchildren and great-grandchildren.
  3. Mothers in many subpopulations have evolved past a “metabolic tipping point” that makes obesity and poor physical fitness almost inevitable for their children and their children’s children.    

“My theory says that obesity is the result of nongenetic evolutionary forces, for example social/cultural evolution, that have led to the competitive dominance of fat cells,” Archer said. “Beginning in the 1960s, mothers became increasingly physically inactive, sedentary and heavier. This altered their bodies’ metabolism during pregnancy. With less competition between fat and muscle cells due to inactivity, more energy was available to increase the number of fat cells in their unborn children. The result was a dramatic increase in the risk of obesity and disease in infants and children.”

Archer says these findings demonstrate that the typically highlighted reasons for childhood obesity are not the root cause, and the issue began with earlier generations.

“My paper demonstrates that gluttony and sloth are not the primary determinants of obesity, and hopefully it will dispel the ignorance that causes good-hearted people to mistakenly think that a child is obese because of a lack of willpower, or because his or her mother does not care enough to provide proper food,” Archer said. “Willpower and good intentions cannot compete with evolution.”

To halt the continued evolution of obesity, Archer says would-be moms must be physically active throughout their lives — especially during puberty — to prepare their metabolisms for pregnancy and have metabolically healthy children. Archer thinks that clinicians must know that preconception and prenatal exercise are essential but underutilized tools in the struggle against obesity.

“Evolution is the cause, and active moms are the cure,” Archer said. “Only mothers have the power to change the evolution of obesity.”

In hopes of developing effective interventions based on his theory, Archer is building virtual humans — including pregnant women — via computational modeling.

“Science can improve the lives of mothers and children, and my theory is a productive first step,” Archer said.

$10 million UAB grant is probing control of viral infections
$10 million UAB grant is probing control of viral infections
The multi-project research targets key molecular steps of immune cell-fate decisions after virus infection.

troy randall webTroy RandallTo better understand the key molecular and cellular steps in the natural control of viral infections, the National Institute of Allergy and Infectious Diseases in late 2012 invited multi-project applications for U19 grants. The target theme was “Immune Mechanisms of Virus Control.” That has now led to a $10 million, five-year grant at the University of Alabama at Birmingham, awarded in late summer.

The grant includes three UAB labs working with mouse models and one lab at the University of California-Davis. It also includes a series of human experiments run at Emory University. The UAB grant focus — one of eight U19 grants funded — is viral-induced cell-fate decisions in anti-viral immunity.

The NIH grants are meant to help improve protective immunity after vaccination, or help tamp down the destructive, out-of-control immune response that sometimes follows a viral infection.

Researchers from UAB and the seven other U19 grants will hold their first yearly meeting in Washington next month, the start of what the NIH calls “a network of synergistic research teams.”

“The U19’s are a little different from a lot of grants,” said Troy Randall, Ph.D., principal investigator and a professor in the Department of Medicine’s Division of Clinical Immunology and Rheumatology. “The NIH decides ‘this is an underdeveloped area of science,’ and it calls for proposals. Given the expertise that we have, we put together a grant on adaptive immunity.”

Simply put, adaptive immunity is the response that follows a vaccination, where the body produces, not only antibodies that can recognize and neutralize a viral infection, but also “memory cells” that maintain watch against future infections by the same virus.

The response has many complex steps. Certain immune cells have to physically contact each other and also respond to specific cytokine signals in order to become activated. Activation provokes differentiation of the immune cells into new types of T and B cells that have complementary roles.

Unraveling details of those cell-fate decisions could help a clinician alter a patient’s immune response for the better — such as improving the response to vaccination, stimulating an “exhausted” immune system to resume the fight against cancer or HIV, or ratcheting down an auto-immune disease.

The U19 grants have one other intriguing feature — the chance to get additional funds for one-year pilot studies. “NIH set aside a pot of money that they call the Infrastructure and Opportunities Fund,” Randall said. “They want people to interact and cooperate…”

In the UAB grant, Randall’s lab is looking at CD4 T cells that develop into “T follicular helper cells” (Tfh). After they develop, the Tfh cells migrate into a lymph node follicle and stimulate rapid growth of the resident B cells (which creates those swollen lymph glands underneath the jaw). Based on a previous discovery that cytokine IL-2 prevents CD4 T cells from becoming Tfh cells, Randall will study how the IL-2 level is controlled during influenza infection in mice, and whether changes in that level will give better vaccination results.

The lab of Frances Lund, Ph.D., chair of the UAB Department of Microbiology, is looking at a cell-fate step in B cells after they have proliferated. She wants to understand the switch from rapid cell division to a cell that starts to manufacture antibody molecules. The cytokine interferon-gamma (IFN-gamma) has been implicated in that cell-fate decision, which leads to a fork in the road — most of the B cells make a lot of antibody and then die, but others become long-lived antibody-secreting cells that can produce protective antibodies for decades.

The lab of Allan Zajac, Ph.D., associate professor of microbiology at UAB, is looking at CD8 T cells, which can develop into the classic “killer” T cells that can destroy virus-infected cells. A cell-surface adhesion molecule called ICAM seems to direct the type of T cell produced after cell-to-cell interactions — some of the CD8 T cells become killer T cells, and others become long-lived memory T cells. Zajac believes that ICAM limits the amount of IL-2 experienced by some clustered T cells, and this helps produce memory cells rather than killer cells. Zajac has two versions of lymphocytic choriomeningitis virus that differ by only two nucleotides — one causes an acute infection in mice that is quelled in 10 days, while the other, faster-replicating virus gets out of control and exhausts the immune system, and the mice take months to recover.

Comparing those two infections may show how to control T cell differentiation to prevent immune response exhaustion or, conversely, how to “wake up” an exhausted immune response.

Nicole Baumgarth, DVM, Ph.D., University of California–Davis, studies early B cells that make IgM antibody right after influenza infection. This first-line defense is active during the week that it takes for the body to select, activate and proliferate B cells of the adaptive immune response that make the more potent IgG antibody. Though IgM binding to a virus is weaker, it activates the complement pathway that amplifies the immune response. Baumgarth wants to understand how those early B cells are controlled.

It is important to learn whether these human immune-response mechanisms mirror those of mice. So the UAB U19 grant includes several human experiments run by Frances Eun-Hyung Lee, M.D., assistant professor of pulmonary, allergy and critical care medicine, Emory University. She uses blood samples from volunteer patients or subjects for that work.

For the role of IL-2 in preventing Tfh cell differentiation, Lee will look at cancer patients who receive IL-2 as part of their treatment for multiple myeloma. She will test whether the IL-2 dampens their immune response to normal gut microflora.

For the role of IFN-gamma in creating long-lived B memory cells, Lee will compare two groups of people — veterinary school students at the University of Georgia who all get a rabies inoculation at the start of school and about 58 people of Thai descent, seen as patients at the NIH, who have an autoimmune disease that makes them deficient in IFN-gamma. The Thai patients also get a rabies inoculation as the normal standard of medical care before traveling to Thailand, where rabies-infected bats are common. Lee will look for differences in long-lived B cells between the two groups.

For the human correlate to the early B cells, Lee will look at people given measles vaccine, to see if such B cells appear in the early response and remain later.

About three-fourths of the UAB U19 grant money — more than $7 million — will be spent at UAB.

The U19 grants have one other intriguing feature — the chance to get additional funds for one-year pilot studies. “NIH set aside a pot of money that they call the Infrastructure and Opportunities Fund,” Randall said. “They want people to interact and cooperate. Hopefully, we will see, ‘Oh, they’re doing this neat thing. Let’s work with them to do something we can’t do alone.’ ”

The seven other U19 grants for immune mechanisms of virus control went to investigators at Mt. Sinai in New York (two separate grants at Mt. Sinai), the La Jolla Institute for Allergy and Immunology, the University of North Carolina, the University of Massachusetts Medical School, Washington University, and the University of Washington.

UAB Circulation Research paper is one of year’s top five
UAB Circulation Research paper is one of year’s top five
Research revealing new evidence about the role of the spleen following heart attack will be honored during the AHA scientific meeting Nov. 15-19.

circulation webClick to enlarge the letterTwo University of Alabama at Birmingham researchers will receive awards from the journal Circulation Research for writing one of the five most outstanding papers of the past year.

Ameen Ismahil, Ph.D., and Sumanth Prabhu, M.D., of the Division of Cardiovascular Disease in the UAB Department of Medicine are the first and last authors of an article — published last January — that showed splenocytes are intricately involved in the heart failure that follows an infarction in a mouse-model system. One of their lines of evidence was that adoptive transfer of the heart-failure splenocytes into healthy mice led to systolic dysfunction and heart “remodeling,” the cardiovascular disease term for deleterious changes in shape, size and function.

Ismahil and Prabhu provided, “… exciting new evidence implicating the spleen in the immunoinflammatory response after myocardial infarction,” said Nikolaos Frangogiannis, M.D., Albert Einstein College of Medicine, in the accompanying editorial in Circulation Research. But the significance of such mouse research ultimately will depend on “whether the spleen significantly contributes to the inflammatory and remodeling responses in human patients,” Frangogiannis wrote. Indeed, the UAB team is in the initial stages of expanding the observations in mice to humans with ischemic heart failure.

While people can live without their spleen, the organ has several important roles. It keeps a reserve supply of blood and helps remove old red blood cells, and in a surprising 2009 mouse-model study, the spleen was found to act as a reservoir for proinflammatory monocytes after myocardial infarction.

The judges for Circulation Research’s 2014 Best Manuscript Awards looked for “high standards of scientific excellence in terms of novelty, impact and methodology,” said Roberto Bolli, M.D., editor-in-chief, in a letter to Ismahil and Prabhu. They also looked at the number of online downloads. Papers published between July 2013 and June 2014 were eligible for consideration.

Ismahil is a research associate in Cardiovascular Disease and Prabhu is the division chair and director of UAB’s Comprehensive Cardiovascular Center. Other authors on the paper, titled “Remodeling of the Mononuclear Phagocyte Network Underlies Chronic Inflammation and Disease Progression in Heart Failure: Critical Importance of the Cardiosplenic Axis,” are Tariq Hamid, Ph.D., Shyam Bansal, Ph.D., and Bindiya Patel, all in UAB’s Division of Cardiovascular Disease, and Justin Kingery, M.D., Ph.D., of the Department of Medicine, University of Louisville.

The awards will be given at the American Heart Association Scientific Sessions 2014, which meets Nov. 15-19 in Chicago. Read a previous UAB News story about the article here.

Guidelines agree: Most patients with chronic kidney disease should take statins
Guidelines agree: Most patients with chronic kidney disease should take statins
UAB researchers compared two sets of guidelines to ascertain if people with chronic kidney disease should take statins to reduce high cholesterol levels linked to cardiovascular disease.

cholesterolA gradual loss of kidney function over time — or chronic kidney disease (CKD) — increases the risk of heart disease and stroke. Two sets of cholesterol-treatment guidelines published in 2013 inform the decision to use statins.

One set is specifically for patients with CKD, while the other is for the general population. University of Alabama at Birmingham experts compared them to find similarities and differences and to also determine if CKD patients are taking statins unnecessarily.

Around 26 million adults in the United States have CKD, according to the National Kidney Foundation, and heart disease and stroke are major causes of death among them.

In “Contrasting Cholesterol Management Guidelines for Adults with CKD,” published in the Journal of the American Society of Nephrology, UAB School of Public Health investigators compared the American College of Cardiology/American Heart Association cholesterol treatment guideline and the Kidney Disease Improving Global Outcomes Foundation Clinical Practice Guideline for Lipid Management in CKD.

Study lead author Lisandro Colantonio, M.D., doctoral candidate in the UAB Department of Epidemiology, said the two guidelines target different populations in treatment recommendations.

“The ACC/AHA guideline is aimed toward statin treatment decisions for the general population, while the KDIGO guideline is intended to guide treatment of patients with kidney disease,” Colantonio said.

The ACC/AHA guideline recommends statin treatment to individuals with a high risk of cardiovascular disease (CVD; heart disease or stroke) based on a history of CVD, diabetes or an estimated 10-year risk ≥7.5 percent using the Pooled Cohorts risk equations. The KDIGO guideline recommends statin therapy for all people ages 50-79 with CKD.

“While most patients with CKD are at high risk for CVD, we hypothesized that some patients with CKD are not at high risk and therefore may be unnecessarily recommended statins by the KDIGO guideline. Therefore, we felt it was important to understand in what ways the two cholesterol-treatment recommendations are similar and how they may be different.”

“While most patients with CKD are at high risk for CVD, we hypothesized that some patients with CKD are not at high risk and therefore may be unnecessarily recommended statins by the KDIGO guideline,” Colantonio said. “Therefore, we felt it was important to understand in what ways the two cholesterol-treatment recommendations are similar and how they may be different.”

Using data from the Reasons for Geographic and Racial Differences in Stroke (REGARDS) study, a cohort of more than 30,000 U.S. adults, the researchers found that 92 percent of people with CKD are recommended statin treatment by the 2013 general population ACC/AHA cholesterol treatment guideline versus 100 percent following the KDIGO guideline for patients with CKD.

“These results indicate that either guideline can be used to inform the decision to initiate statin therapy for people with CKD who are 50 to 79 years of age,” Colantonio said.

Study senior author Paul Muntner, Ph.D., professor in the UAB Department of Epidemiology, notes that while both the ACC/AHA and KDIGO guidelines recommend statins as the first therapy to prevent CVD among those with high risk, this treatment is not for all CKD patients.

“In contrast, prior studies on individuals with CKD who are on dialysis have shown no benefit of statins to prevent CVD,” Muntner said. “Both guidelines agree that statin therapy should not be initiated in those individuals on dialysis.”

Also discovered was that 50 percent of people with CKD who are recommended statins are not taking them.

“This represents an unmet treatment need, and there is a missed opportunity for lowering CVD risk among patients with CKD,” Colantonio said.

Colantonio adds that they did find that the Pooled Cohort risk equations were accurate among people with CKD, indicating that physicians have a valid tool available to accurately estimate CVD risk for their patients with CKD.

Both authors say an unanswered question is whether it is appropriate to initiate statins for people ages 80 and older; the KDIGO guideline recommends statins but the ACC/AHA guideline does not.

This study was supported by the National Institute of Neurological Disorders and Stroke of the National Institutes of Health.

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