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Displaying 31 to 35 of 35 results for infections

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  • The Sfanos Lab

    The Sfanos Lab studies the cellular and molecular pathology of prostate disease at the Johns Hopkins University School of Medicine. We are specifically interested in agents that may lead to chronic inflammation in the prostate, such as bacterial infections and prostatic concretions called corpora amylacea. Our ongoing studies are aimed at understanding the influence of prostate infections and inflammation on prostate disease including prostate cancer and benign prostatic hyperplasia (BPH). The laboratory also focuses on the influence of the microbiome on prostate disease development, progression, and/or resistance to therapy.

    Research Areas: disease resistance, prostate cancer, prostate, benign prostatic hyperplasia, prostate disease, chronic inflammation

    Lab Website

    Principal Investigator

    Karen Sfanos, M.S., Ph.D.

    Department

    Pathology

  • The Transplant and Oncology Infectious Diseases (TOID) Center

    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.

    Research Areas: transplants, candidiasis, fungal infections, infectious disease, cancer, aspergillosis

    Lab Website

    Principal Investigator

    Kieren Marr, M.D.

    Department

    Medicine

  • 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.

    Research Areas: Sjogren's syndrome, antibodies, autoimmune diseases, self-molecules, systemic lupus erythematosus

    Principal Investigator

    Thomas Grader-Beck, M.D., Ph.D.

    Department

    Medicine

  • Todd Dorman Lab

    Research conducted in the Todd Dorman Lab examines the use of informatics in intensive care settings as it relates to remote patient monitoring, safety and management strategies. Specific areas of interest include the surgical stress response; aminoglycoside antibiotics; fungal infections; renal failure; pharmacokinetic models of drug administration; and ICU triage and its impact on disaster preparedness.

    Research Areas: fungal infections, patient safety, informatics, disaster preparedness, aminoglycoside antibiotics, surgical stress response, ICU, patient monitoring

  • William G. Nelson Laboratory

    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.
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    Research Areas: cellular biology, cancer, epigenetics, DNA

    Lab Website

    Principal Investigator

    William Nelson, M.D., Ph.D.

    Department

    Oncology

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