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David Hackam’s laboratory focuses on necrotizing enterocolitis (NEC), a devastating disease of premature infants and the leading cause of death and disability from gastrointestinal disease in newborns.
The disease strikes acutely and without warning, causing sudden death of the small and large intestines. In severe cases, tiny patients with the disease are either dying or dead from overwhelming sepsis within 24 hours. Surgical treatment to remove most of the affected gut results in lifelong short gut (short bowel) syndrome.
The Hackam Lab has identified a critical role for the innate immune receptor toll-like receptor 4 (TLR4) in the pathogenesis of necrotizing enterocolitis. The lab has shown that TLR4 regulates the development of the disease by tipping the balance between injury and repair in the stressed intestine of the premature infant. Developing an Artificial Intestine A key goal is to create, in the laboratory, new intestines made from patients’ own cells, which can then ...be implanted into the patient to restore normal digestive function. This innovative design could transform child development and quality of life in necrotizing enterocolitis survivors without the risks of conventional donor transplant. view more
The mission of the Transplant and Oncology Infectious Diseases (TOID) Center is to expand institutional expertise in clinical and academic activities focused on infectious complications in transplant (solid organ and stem cell) and oncology patients at Johns Hopkins medical institutions. Key efforts include developing standardized algorithms for the prevention and treatment of infections in these vulnerable patients and to establish an expanded infrastructure to facilitate clinical and translational studies at TOID. Current research projects focus on diagnostics for invasive fungal infections and specialized studies of the pathogenesis of candidiasis and aspergillosis.
Thomas Grader-Beck Lab
Research in the Thomas Grader-Beck Lab aims to understand the pathogenesis of systemic autoimmune diseases—particularly systemic lupus erythematosus (SLE) and Sjögren’s syndrome—by taking a translational approach. Autoantibodies (antibodies that target self-molecules) are believed to contribute significantly to the disease process. We are studying mechanisms that may make self-structures immunogenic. We theorize that certain post-translational antigen modifications, which can occur in infections or malignant transformation, result in the expression of neoepitopes that spread autoimmunity in the proper setting. The team has combined studies that employ a number of mouse strains, certain gene-deficient mice and human biological specimens.
Thomas Quinn Lab
Research in the Thomas Quinn Lab encompasses epidemiology, pathogenesis and clinical features of HIV/AIDS internationally, which includes the interaction between STDs and tropical diseases on the natural history and spread of HIV/AIDS in developing countries. Our recent research has examined the viral kinetics and transmission probabilities of HIV among discordant couples with the subsequent design and application of interventions, including therapy to prevent transmission of HIV. Molecular studies have mapped the molecular epidemic of HIV on a global basis, linking virologic changes to the spread of HIV and measuring the demographic impact of the epidemic.
The goals of the Translational neurobiology Laboratory are to understand the pathogenesis and cell death pathways in neurodegenerative disorders to reveal potential therapeutic targets for pharmaceutical intervention; to investigate endogenous survival pathways and try to induce these pathways to restore full function or replace lost neurons; and to identify biomarkers to mark disease function or replace lost neurons; and to identify biomarkers to mark disease progression and evaluate therapeutics. Our research projects focus on models of Huntington's disease and Parkinson's disease. We use a combination of cell biology and transgenic animal models of these diseases.
The William Bishai Laboratory studies the molecular pathogenesis of tuberculosis. The overall goal of our laboratory is to better understand tuberculosis pathogenesis and then to employ this understanding toward improved drugs, vaccines and diagnostics. Since Mycobacterium tuberculosis senses and adapts to a wide array of conditions during the disease process, it is clear that the regulation of expression of virulence factors plays an important role in pathogenesis. As a result, a theme of our research is to assess mycobacterial genes important in gene regulation. We are also interested in cell division in mycobacteria and the pathogenesis of caseation and cavitation.
Normal and neoplastic cells respond to genome integrity threats in a variety of different ways. Furthermore, the nature of these responses are critical both for cancer pathogenesis and for cancer treatment. DNA damaging agents activate several signal transduction pathways in damaged cells which trigger cell fate decisions such as proliferation, genomic repair, differentiation, and cell death. For normal cells, failure of a DNA damaging agent (i.e., a carcinogen) to activate processes culminating in DNA repair or in cell death might promote neoplastic transformation. For cancer cells, failure of a DNA damaging agent (i.e., an antineoplastic drug) to promote differentiation or cell death might undermine cancer treatment.
Our laboratory has discovered the most common known somatic genome alteration in human prostatic carcinoma cells. The DNA lesion, hypermethylation of deoxycytidine nucleotides in the promoter of a carcinogen-defense enzyme gene, appears to result in inactivation of th...e gene and a resultant increased vulnerability of prostatic cells to carcinogens.
Studies underway in the laboratory have been directed at characterizing the genomic abnormality further, and at developing methods to restore expression of epigenetically silenced genes and/or to augment expression of other carcinogen-defense enzymes in prostate cells as prostate cancer prevention strategies.
Another major interest pursued in the laboratory is the role of chronic or recurrent inflammation as a cause of prostate cancer. Genetic studies of familial prostate cancer have identified defects in genes regulating host inflammatory responses to infections.
A newly described prostate lesion, proliferative inflammatory atrophy (PIA), appears to be an early prostate cancer precursor. Current experimental approaches feature induction of chronic prostate inflammation in laboratory mice and rats, and monitoring the consequences on the development of PIA and prostate cancer. view more