Student Spotlight

Ryan Berry

Research Interests: Nutrition and Metabolic Disease
We are acdepting applications for Fall 2016! The priority deadline to apply is December 1, 2015 and the final deadline (for everyone) is January 15, 2016.

Welcome to the Cell, Molecular, and Developmental Biology (CMDB) PhD Theme, a part of the Graduate Biomedical Sciences program at the University of Alabama at Birmingham School of Medicine. The CMDB theme is designed to provide maximum flexibility that results in students who are prepared to launch into a career in the emerging biomedical science field. Our graduates have exciting careers in scientific research in both academic and industrial settings; scientific-related writing, business, law, bioterrorism, forensics, administration, and education. 

About Us: CMDB is a cross-disciplinary theme at a leading research University in the sunny south, consisting of a diverse group of scientists and physicians who have a collective interest in fundamental processes in cell, molecular, and developmental biology and how alterations in these processes result inhuman diseases and birth defects.

About UAB: We are consistently one of the top 25 NIH funded research institutions in the U.S. and with faculty from over 30 departments across campus there are many opportunities for you in new and exciting areas of biomedical research. And, UAB is a leader in innovative technology such as whole genome sequencing, electron microscopy, mass spectrometry, crystallography, flow cytometry, drug discovery and others.

Contact Us: We are always searching for the brightest and most dedicated students to join our highly competitive CMDB theme and experience firsthand our cutting edge science. This is your personal invitation to explore the many possible opportunities offered by CMDB at UAB. Please explore this web site and apply today!
  • 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

More Items

Epi Menu