The Brendan Cormack Laboratory studies fungal pathogenesis, particularly the host-pathogen interaction for the yeast pathogen Candida glabrata. We are trying to identify virulence genes (genes that evolved in response to the host environment) by screening transposon mutants of C. glabrata for mutants that are specifically altered in adherence to epithelial cells, in survival in the presence of macrophages and PMNs. We also screen mutants directly in mice for those unable to colonize or persist in the normal target organs (liver, kidney and spleen). We also focus research on a family of genes--the EPA genes--that allow the organism to bind to host cells. Our research shows that a subset of them are able to mediate adherence to host epithelial cells. We are trying to understand the contribution of this family to virulence in C. glabrata by figuring out what the ligand specificity is of different family members, how genes are normally regulated during infection, and what mechanisms normally act to keep the genes transcriptionally silent and how that silence is regulated.

Research in the Brendan J. Canning Lab is focused on mechanistic studies of the cough reflex. Through our work, we identified the afferent nerves that play an essential role in regulating cough. We have also been characterizing the CNS pathways regulating the cough reflex and interactions amongst various afferent nerve subtypes in regulating cough. We have identified key sites of integration of airway afferent nerve input and mechanisms by which afferent nerve subtypes act synergistically to regulate cough. Our experimental approaches include electrophysiological recordings, CNS microinjection techniques, in vivo preparations for monitoring cough and reflex bronchospasm, neuronal tracing and immunohistochemistry.

The Brennen laboratory takes a rigorous, multi-disciplinary, team-based approach towards developing innovative therapeutic and prognostic strategies for prostate cancer with an emphasis on exploiting vulnerabilities within the tumor microenvironment towards this goal. To accomplish this goal, we are strategically pursuing novel therapeutic platforms, including stromal-targeted prodrugs, protoxins, and radiolabeled antibodies, in addition to cell-based therapy and drug delivery; all of which are designed to reduce toxicity to peripheral non-target tissue (i.e. side effects) while maximizing anti-tumor efficacy (i.e. therapeutic benefit). Currently, many of these strategies are focused on overcoming stromal barriers to anti-tumor immune responses such that men suffering from prostate cancer can share in the immense, revolutionary power of immunotherapy that is transforming care for many with advanced disease in other tumor types previously thought to be unmanageable using conventional approaches. Unfortunately, prostate cancer has largely proven refractory to these powerful approaches thus far and requires novel mono- or combinatorial treatment strategies to unleash the full potential of the immune system and generate personalized anti-tumor responses with the capability of producing long-term durable responses or even cures in these men.

Dr. Petty's laboratory interests focuses on antimicrobial chemotherapy, hospital-based medical practices, and internal medicine collaboration with ophthalmologic clinical trials.

Research in the Brian Garibaldi Lab focuses on acute lung injury (ALI) resolution. Recently, we evaluated the mechanisms underlying mobility therapy and found that therapeutic exercise reduces neutrophilic lung injury and skeletal muscle wasting in ALI mice.

The Brown Lab is focused on the function of the cerebral cortex in the brain, which underlies our ability to interact with our environment through sensory perception and voluntary movement. Our research takes a bottom-up approach to understanding how the circuits of this massively interconnected network of neurons are functionally organized, and how dysfunction in these circuits contributes to neurodegenerative diseases like amyotrophic lateral sclerosis and neuropsychiatric disorders, including autism and schizophrenia. By combining electrophysiological and optogenetic approaches with anatomical and genetic techniques for identifying cell populations and pathways, the Brown Lab is defining the synaptic interactions among different classes of cortical neurons and determining how long-range and local inputs are integrated within cortical circuits. In amyotrophic lateral sclerosis, corticospinal and spinal motor neurons progressively degenerate. The Brown Lab is examining how abnormal activity within cortical circuits contributes to the selective degeneration of corticospinal motor neurons in an effort to identify new mechanisms for treating this disease. Abnormalities in the organization of cortical circuits and synapses have been identified in genetic and anatomical studies of neuropsychiatric disease. We are interested in the impact these abnormalities have on cortical processing and their contribution to the disordered cognition typical of autism and schizophrenia.

Research interests in the Bruce Leff Lab include home hospital, guided care, medical education and long-term care.

The Bryan Lau Lab is interested in epidemiological and statistical methods for cohort studies and the application of these methods primarily to HIV cohort studies. We’re particularly interested in developing new methods and using approaches from other disciplines as novel solutions to specific epidemiologic issues.

Researchers in the C. David Mintz Lab seek to better understand the specific methods by which anesthesia can impair a patient’s brain development. Recent studies have investigated the ways in which anesthetics interfere with axon guidance in developing mouse neocortical neurons via a GABAA receptor mechanism, as well as the method by which anesthetics interfere with the polarization of developing cortical neurons.

Dr. Sperati’s group focuses on complement mediated kidney disorders, glomerular disease, and renal arterial disease secondary to fibromuscular dysplasia. His team has a particular interest in thrombotic microangiopathies involving the complement system.