Basic Research

Despite recent advances in our understanding of pain mechanisms, there has been little-to-no overall improvement in the clinical management of postoperative pain. It is now recognized that effective postoperative pain management depends on key predictors, especially patient sex. Preclinical and clinical data indicate that, while postoperative pain levels show little-to-no sex-dependent dimorphisms, there are significant sex-based differences in analgesic efficacy, safety profile and abuse/addiction potential of current drugs used to treat postoperative pain.

Public Service

Applied Research

Basic Research

Inorganic arsenic (iAs) is the highest-ranking toxin on the U.S. substance priority list. Chronic exposure through natural water sources is linked to a broad range of adverse health effects, including pathological changes in the urinary bladder. Due to the make up of the urothelial cell, iAs readily accumulates to elicit toxic effects. However the specific mechanisms of arsenic-induced urothelial injury are not fully characterized. Upon cell injury there is rapid influx of inflammatory mediators and increase in cellular inflammatory signaling.

Implantable cardioverter defibrillators (ICDs) are medical devices proven to prevent sudden cardiac death due to ventricular arrhythmias. Their decisions are based solely upon the intra--?cardiac ECG. This is incomplete information since up to 1/3 of patients experience an 'inappropriate' shock within the first 1-3 years of receiving the implant. Receiving a shock is associated with increased mortality as well as emotional trauma.

Basic Research

The proposed project asks fundamental and applied questions concerning the role that Mycoplasma pneumoniae (Mp) and its newly discovered ADP-ribosylating, vacuolating toxin, designated Community Acquired Respiratory Distress Syndrome (CARDS) toxin, play in the pathogenesis of airway disorders. CARDS toxin remarkably recapitulates the pro-inflammatory cytokine/chemokine profiles and histopathology that accompany Mp infection. In addition, inactivation of CARDS toxin significantly reduced the release of mature form interleukin-1(IL-1?) during Mp infection.