The Sean Leng Lab studies the biology of healthy aging. Specific projects focus on chronic infl...ammation in late-life decline; immunosenescence and its relationship to the basic biological and physiological changes related to aging and frailty in the human immune system; and T-cell repertoire analysis. view more

Dr. Menez and his laboratory are interested in clinical and translational acute kidney injury (...AKI) research, specifically with a focus on the transition between AKI and chronic kidney disease (CKD). Dr. Menez has investigated novel approaches to evaluate AKI using biomarkers of kidney injury, inflammation, and repair in the multi-center TRIBE-AKI and ASSESS-AKI Studies. Dr. Menez collaborates nationwide through the NIDDK-sponsored Kidney Precision Medicine Project, with a goal to improve the global understanding of kidney disease subgroups and identify new pathways and targets for novel therapies.



Since the start of the COVID-19 pandemic, he has additionally investigated the impact of COVID19 on kidney health, including short-term outcomes including need for dialysis or in-hospital mortality, as well as longer-term outcomes post-hospital discharge. view more

Chronic viral hepatitis (due to HBV and HCV) is a major cause of liver disease worldwide, and a...n increasing cause of death in persons living with HIV/AIDS. Our laboratory studies are aimed at better defining the host-pathogen interactions in these infections, with particular focus on humoral and cellular immune responses, viral evasion, inflammation, fibrosis progression, and drug resistance. We are engaged in synthetic biology approaches to rational vaccine development and understanding the limits on the extraordinary genetic variability of HCV. view more

The Systems Biology Lab applies methods of multiscale modeling to problems of cancer and cardio...vascular disease, and examines the systems biology of angiogenesis, breast cancer and peripheral artery disease (PAD).

Using coordinated computational and experimental approaches, the lab studies the mechanisms of breast cancer tumor growth and metastasis to find ways to inhibit those processes.

We use bioinformatics to discover novel agents that affect angiogenesis and perform in vitro and in vivo experiments to test these predictions. In addition we study protein networks that determine processes of angiogenesis, arteriogenesis and inflammation in PAD. The lab also investigates drug repurposing for potential applications as stimulators of therapeutic angiogenesis, examines signal transduction pathways and builds 3D models of angiogenesis.

The lab has discovered over a hundred novel anti-angiogenic peptides, and has undertaken in vitro and in vivo studies testing their activity under different conditions. We have investigated structure-activity relationship (SAR) doing point mutations and amino acid substitutions and constructed biomimetic peptides derived from their endogenous progenitors. They have demonstrated the efficacy of selected peptides in mouse models of breast, lung and brain cancers, and in age-related macular degeneration.

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Chronic rhinosinusitis (CRS) is a leading cause of morbidity globally and is the single most co...mmon self-reported chronic health condition and accounts for billions of dollars in health care costs and lost work days annually. Exposure to air pollutants is thought to be a critical modifier of CRS susceptibility. Despite marked reductions in air pollution levels in the United States, the fine particulate component of air pollution (PM2.5) and ultrafine pollutants secondary to traffic continue to remain a recalcitrant issue globally and in the United States. The Ramanathan Lab focuses on studying the role of air pollution (PM2.5) in CRS. In collaboration with scientists at the Bloomberg School of Public Health, we have utilized a state of the art air pollution exposure system to develop a novel mouse model of air pollution induced rhinosinusitis that mimics many of the features of CRS in humans. Our lab uses transgenic mouse models and novel immunologic/genomic techniques to study the mechanisms by which PM2.5 causes eosinophilic inflammation and sinonasal epithelial barrier dysfunction. We are also interested in the role of the antioxidant transcription factor, Nrf2, which has shown to stabilize the epithelial barrier and reduce eosinophilia in PM induced rhinosinusitis as a potential therapeutic target. view more

The Sfanos Lab studies the cellular and molecular pathology of prostate disease at the Johns Ho...pkins 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. view more

Vascular research led by Rafael Tamargo, M.D., the Walter E. Dandy Professor of Neurosurgery, e...xplores treatment of aneurysms, arteriovenous malformations, cavernous malformations, and arteriovenous fistulas of the brain and spinal cord. Basic science research has focused on endothelial cell-leukocyte interactions (inflammation) after subarachnoid hemorrhage and identifying drugs that might inhibit this inflammatory response as well as the narrowing of blood vessels. view more

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 the 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

Dr. Bhujwalla’s lab promotes preclinical and clinical multimodal imaging applications to unders...tand and effectively treat cancer. The lab’s work is dedicated to the applications of molecular imaging to understand cancer and the tumor environment. Significant research contributions include 1) developing ‘theranostic agents’ for image-guided targeting of cancer, including effective delivery of siRNA in combination with a prodrug enzyme 2) understanding the role of inflammation and cyclooxygenase-2 (COX-2) in cancer using molecular and functional imaging 3) developing noninvasive imaging techniques to detect COX-2 expressing in tumors 4) understanding the role of hypoxia and choline pathways to reduce the stem-like breast cancer cell burden in tumors 5) using molecular and functional imaging to understand the role of the tumor microenvironment including the extracellular matrix, hypoxia, vascularization, and choline phospholipid metabolism in prostate and breast cancer invasion and metastasis, with the ultimate goal of preventing cancer metastasis and 6) molecular and functional imaging characterization of cancer-induced cachexia to understand the cachexia-cascade and identify novel targets in the treatment of this condition. view more