Research Resources

Office of the Vice President for Research & Economic Development (OVPRED)

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

Integrated Research Administration Portal (IRAP)

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

UAB Institute for Innovation and Entrepreneurship

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

Funding Sources and Grant Opportunities

Presentations and general information related to effective grant writing.

Office of Postdoctoral Education

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

Study finds genetic risk factor can lead to hyperinflammatory disorder, death after viral infection
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

curcio lab 2CINCINNATI/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.

UAB study says Alzheimer’s plaques can also affect the brain’s blood vessels
UAB study says Alzheimer’s plaques can also affect the brain’s blood vessels
The Alzheimer’s plaques that accumulate around brain cells also congregate along the walls of blood vessels, according to UAB research, and that may contribute to cognitive issues.

Amyloid beta, the plaque that accumulates in the brains of people with Alzheimer’s disease, may also contribute to Alzheimer’s by interfering with normal blood flow in the brain, according to investigators at the University of Alabama at Birmingham.

In findings published Nov. 23 in the journal Brain, the team shows that when amyloid beta accumulates around blood vessels — where it is known as vascular amyloid — it appears to prevent the brain from properly regulating blood flow, which is essential to normal brain function.

“We have increasingly become aware that the disruption of blood flow in the brain can increase the risk of Alzheimer’s disease,” said Erik Roberson, M.D., Ph.D., associate professor in the UAB Department of Neurology. “While we have known that vascular amyloid built up around blood vessels, we did not fully understand its effects, and new technology now allows us to visualize how it affects the function of those vessels.”

Increased brain activity — remembering the lyrics to a song, for example — requires an increase in energy to the neurons responsible for memory. Neurons draw energy from glucose, which is transported by the blood stream. Cells called astrocytes regulate the diameter of blood vessels to increase or decrease blood flow and the corresponding glucose transportation. Astrocytes also tell the blood vessel to return to normal when the need has passed.

Astrocytes accomplish this signaling by means of projections called astrocytic endfeet, which wrap around the smooth muscle cells of the blood vessel wall. When a neuron calls for more glucose, the message is passed via the astrocytic endfeet, and the blood vessel expands and boosts blood volume.

The fate of astrocytic endfeet in a brain tumor study published last year at UAB led the research team to look more closely at vascular amyloid. UAB researchers led by Harald Sontheimer, Ph.D., then a professor in the Department of Neurobiology, published a paper in Nature Communications in June 2014 which showed that, in brain tumors, malignant astrocytes called glioma cells could travel along blood vessels and push astrocytic endfeet away, severing their connection to the vessel and interfering with their ability to regulate blood flow.

“We know vascular amyloid accumulates around the outside of blood vessels, and after seeing those research findings from the Sontheimer group, we wondered if these plaques could be doing the same thing,” Roberson said. “Working with Dr. Sontheimer and his laboratory, we used advanced imaging techniques — including high-resolution, 3-D image reconstructions from multiphoton laser scanning microscopes, and sophisticated labeling and experimental techniques — and were able to determine that, yes, vascular amyloid did push the astrocytic endfeet away and interfered with normal regulation of blood vessels.”

vascular slime3-D microscope image of blood vessels (in red) with surrounding vascular amyloid plaques (in green). Courtesy Ian Kimbrough.“In a live animal model of Alzheimer’s disease, we then activated the vascular smooth muscle cells with a pulsed laser, allowing us to mimic neuron-induced astrocyte-vascular signaling,” said Ian Kimbrough, a graduate research assistant in Neurobiology and a collaborator on the original brain tumor study. “In locations where no vascular amyloid was present, we saw a very dramatic and robust vessel response; however, on blood vessels that were surrounded by plaque, we saw a much diminished response.”

Kimbrough says that UAB is one of the few research centers in the Southeast with multiphoton laser-scanning microscopes, instruments capable of capturing images deep into a living brain. These images can then be used to create three-dimensional, volumetric representations of brain morphology.

“Using this 3-D model, which we can rotate and manipulate,” he said, “we can see the exact spatial relationship between the vasculature, the astrocytic endfeet and the vascular amyloid. This allows us to analyze how these elements interplay in a normal, healthy brain compared to an Alzheimer’s disease brain.”

Roberson and Kimbrough say that, as the plaque buildup worsens, the vascular amyloid forms rings around the blood vessels, with bridges eventually linking one ring to the next. These rings form a rigid exoskeleton on the vessels, restricting their ability to change in diameter when increased blood flow is demanded by neurons.

“The vessel has to be able to expand and contract, to dilate and constrict, if it’s going to regulate blood flow,” Roberson said. “If they have become rigid like a pipe, instead of having a flexible wall that can go back and forth, then they cannot do their job of regulating blood flow to the brain properly.”

“This was among the first studies to really attempt to understand the relationship between vascular amyloid and blood flow in the brain,” he said. “For the first time, using the amazing technology at our disposal, we can see what is happening in the vessel walls in real time, to better understand how the presence of vascular amyloid effects the function of that vessel.”

Funding for the study came from the National Institutes of Health.

Trial combining exercise and a drug may help seniors muscle up
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.

marcus bamman workoutA 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.

marcus bamman 2015Marcas 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

UAB engineers develop new method to repair elephant tusks
UAB engineers develop new method to repair elephant tusks
A resin developed at the Materials Processing and Applications Development center is replacing the metal ring typically used to prevent cracks from furthering down an elephant’s tusk.

When Birmingham Zoo veterinarians approached researchers from the University of Alabama at Birmingham School of Engineering to help them stop a crack from growing in their oldest elephant’s tusk, the engineers saw an opportunity to use their expertise in materials science to improve the industry standard for the repair process.

Cracks in elephants’ tusks have historically been repaired by adhering a metal ring to the tusk in order to stabilize the crack and prevent it from growing any farther up the tusk.

The Birmingham Zoo asked the director of UAB’s Materials Processing and Applications Development Center, Brian Pillay, Ph.D., to do just that, for Bulwagi, a 35-year-old male African elephant in their care.

Pillay’s immediate response was to innovate the process, and apply some of the science the lab uses in other materials processes to create a new, more robust and seamless treatment for the crack.

“When the team at the Zoo asked me to create this metal ring, I thought, ‘we can do better,’” Pillay said. “We can use what we know about materials development to make something that will work better for the elephant.”

“This is something that’s bridging the gap between what Dr. Pillay’s lab does working with industrial settings and what we do working with a biologic situation,” said Richard Sim, DVM, associate veterinarian at the Zoo. “It’s a first of its kind in that way—combining engineering that would normally be used in structures like bridges and applying it to an elephant.”

elephant tusk brokenA cracked tusk can become infected and pose problems for an elephant. Tusks with cracks that are left untreated may ultimately have to be removed.A cracked tusk can become infected and pose problems for an elephant. Tusks with cracks that are left untreated may ultimately have to be removed.

“An open crack is a site for infection, as a tusk is basically a tooth,” Pillay said. “Imagine having a crack in your tooth—it’s rather painful for the elephants as well.”

The Zoo’s team of veterinarians, animal care specialists and curators worked with students and researchers from UAB to prepare, then apply, the composite fiberglass and carbon-fiber band and resin on Bulwagi’s tusk.

“We worked with Dr. Pillay’s lab to practice applying this product on a PVC pipe to start off with as a model,” Sim said. “I went down to the UAB lab on two occasions to really try to hammer out the details of how this was actually going to work. The first time I went down, we had a very successful practice session; but our idea of how we were going to apply it to a real-life setting was just not going to work for the elephant.”

Through training with MPAD staff engineer Ben Willis, Sim and Pillay’s team worked to perfect the process, and the end result was successful.

“We put a number of layers of carbon fiber and fiberglass around the tusk, and then used a vacuum pump to suck the resin, kind of like an epoxy, up into that product, and it set and became a really hard structure that is going to resist the forces that resulted in the crack,” Sim said. “No one has done this before, so it’s our hope that this will be a process that will stand the test of time.”

“It’s the latest in technology, and it’s a great deal lighter, stronger and tougher than steel,” Pillay said. “The standard ring that would have been traditionally used is four to five times heavier than what Bulwagi has now. This is a significantly better solution.”

Tusk cracks are fairly common in elephants, because a great deal of pressure is put on the tusk as the elephants use them to interact with their environment and other elephants, so the repair process is something that will always be in demand.

elephant tusk repaiThe Zoo’s team of veterinarians, animal care specialists and curators worked with students and researchers from UAB to prepare, then apply, the composite fiberglass and carbon-fiber band and resin on Bulwagi’s tusk.While Bulwagi may eventually lose his tusk because of the progression of this particular crack, UAB and the Zoo sought to use this development process as a way to help other elephants in the future.

“Our hope is that we came up with something that will help a lot of elephants moving forward,” Pillay said.

The team’s next step is to wait and see how, and whether, the crack continues to develop over time, to evaluate how their creation will work for other elephants.

“Right now it’s just a waiting game, but we feel good about what we created and are looking forward to seeing if it can help other elephants,” Pillay said. “We’re hopeful that when vets first observe cracks, they will be able to go in and replicate this procedure to prevent the cracks from growing any farther and save the elephants’ tusks.”

Regardless of the outcome, this project has served another purpose—fostering collaboration between two Birmingham organizations.

“Having a partnership with the Greater Birmingham area is a model we use in caring for our animals,” Sim said. “It can only benefit us by employing the expertise of our community to help with issues that are outside of the scope of what we can do here.”

“It’s a perfect partnership, with the Zoo’s environmental responsibility to protect and care for the animals,” Pillay said. “At UAB, we do a lot of work in terms of human care; but it’s great to be able to take some of that technology and apply it to the animal world.

“Working with the Zoo to innovate and create something that serves to benefit animals has been tremendously rewarding for our team of researchers and students. For our students, specifically, it’s opening their eyes to how diverse the engineering industry can be. Being able work on a project like this as undergraduate and graduate students has been invaluable for their career development.”

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

biological postdocsThe 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.”

postdoc researcher

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.

postdoc numbers

“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.”

Distinguished Faculty Lecturer Award

Nominations for the 2016 Distinguished Faculty Lecturer Award will open during the summer.

To be eligible for this prestigious annual award, an individual must be a full-time, part-time, or emeritus member with a primary or secondary appointment of the faculty of the Academic Health Center, or a University Professor who has:

  • Advanced the frontiers of science or otherwise made a significant contribution to the health of people, or
  • Made an outstanding contribution to the Academic Health Center through education, research, or public service.

Nominations for faculty in the Schools of Dentistry, Health Professions, Medicine, Nursing, Optometry, and Public Health, including Departments of the Joint Health Sciences, are welcome.

Nominations packets should include:
  1. a brief letter of nomination from the person submitting the nomination, and
  2. a current curriculum vitae of the nominee.
It is requested that nomination packets be in an electronic format and submitted via email to Linda Piteo, DFL Facilitator, at Hardcopy nominations may be submitted to Linda Piteo, AB 374, +0103.

The recipient will receive a $5,000 award and will be the keynote speaker at the DFL reception to be held in their honor in the fall.

Information related to the Distinguished Faculty Lecturer Award can be obtained by calling Linda Piteo at extension 4-9438 or by emailing her at

Past Recipients