On October 1, 2013 the UAB Research Foundation became a part of the UAB Institute for Innovation and Entrepreneurship (IIE). The IIE was approved by the UAB Board of Trustees in February 2013. The Research Foundation, which managed intellectual property created by the UAB community, will now have an expanded presence, and operate as the Institute for Innovation and Entrepreneurship. The Institute will serve to create and foster an entrepreneurial and innovative ecosystem integrating the UABRF’s existing strengths and capabilities, enhancing and facilitating service and technology commercialization. The mission will include engagement of faculty in creating new classroom and experiential learning opportunities for students across campus, as well as, encourage and cultivate interdisciplinary scholarly research and publication among faculty and clinicians, and serve as the resource center for UAB as it continues to advance its role in innovation and entrepreneurship. The Institute will provide an entry point for industries seeking to collaborate with this world class university. Read more about the IIE.


In The News at UAB

  • UAB senior Luke McClintock first-round finalist for highly competitive Hertz Fellowship
    Approximately 600 students apply for the Hertz Fellowship each year; only 15 percent are invited for a first-round interview.

    University of Alabama at Birmingham senior Luke McClintock has been selected as a first-round finalist for the Hertz Fellowship.

    The Hertz Fellowship provides financial support toward graduate education to exceptionally talented students in the applied physical, biological and engineering sciences. Through a rigorous application and interview process, the Hertz Foundation seeks to identify young scientists and engineers with the potential to change the world for the better, and support their research endeavors from an early stage.

    McClintock is UAB’s first finalist for this award in nearly a decade.

    “Luke’s selection to be interviewed for the Hertz Fellowship speaks highly of the rigorous undergraduate education he has received at UAB,” said Ashley Floyd Kuntz, Ph.D., director of national and international fellowships and scholarships at UAB. “Luke possesses the unique combination of technical expertise and creativity necessary to become an innovator in his field.”

    Each year the Fannie & John Hertz Foundation conducts a national search for new Hertz fellows. The foundation selects roughly 150 candidates from more than 600 written applications received. Of those, 50 are selected for a second-round interview. Only 15 to 20 students will be awarded a Hertz Fellowship.

    “I am extremely excited and equally nervous about my selection for an interview,” McClintock said. “My research mentor, Dr. Hilton, is doing all he can to help me prepare. There is no telling what the outcome of this interview will be; but win or lose, I am thrilled to have made it this far.”

    McClintock’s research interests include the use of high-powered magnets. Under the mentorship of UAB physics professor David Hilton, Ph.D., McClintock has spent time conducting research at the National High Magnetic Field Laboratory, the largest and highest-powered magnet lab in the world, as well as the Los Alamos National Laboratory.

    Upon graduating in the spring, McClintock intends to conduct materials research on the advancement of renewable energy technology, specifically in the area of photovoltaics and solar energy, and obtain a doctoral degree in physics.

    McClintock is a 2015 Goldwater Scholar and received honorable mention as a sophomore applicant in 2014. He is a student in the UAB Honors College’s University Honors Program and is pursuing a dual degree in physics and chemistry in the UAB College of Arts and Sciences.

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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 nicholas.miller@chmc.org
    Media Contact UAB: Bob Shepard 205-934-8934 or bshep@uab.edu

    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.

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