Brian J. Hawkins

Adaptation of pulmonary oxygen consumption slow component following 6 weeks of exercise training above and below the lactate threshold in untrained men.

Selective role for superoxide in InsP3 receptor-mediated mitochondrial dysfunction and endothelial apoptosis.

Unique cardiopulmonary exercise test responses in overweight middle-aged adults with obstructive sleep apnea.

Superoxide flux in endothelial cells via the chloride channel-3 mediates intracellular signaling.

The proapoptotic factors Bax and Bak regulate T Cell proliferation through control of endoplasmic reticulum Ca(2+) homeostasis.

G protein-coupled receptor Ca2+-linked mitochondrial reactive oxygen species are essential for endothelial/leukocyte adherence.

Simultaneous detection of apoptosis and mitochondrial superoxide production in live cells by flow cytometry and confocal microscopy.

Endothelial targeting of semi-permeable polymer nanocarriers for enzyme therapies.

Caveolae are an essential component of the pathway for endothelial cell signaling associated with abrupt reduction of shear stress.

Inhalational anesthetics induce cell damage by disruption of intracellular calcium homeostasis with different potencies.

Execution of superoxide-induced cell death by the proapoptotic Bcl-2-related proteins Bid and Bak.

Melanocyte-like cells in the heart and pulmonary veins contribute to atrial arrhythmia triggers.

Nitration of the mitochondrial complex I subunit NDUFB8 elicits RIP1- and RIP3-mediated necrosis.

Mitochondrial complex II prevents hypoxic but not calcium- and proapoptotic Bcl-2 protein-induced mitochondrial membrane potential loss.

Methamphetamine causes mitrochondrial oxidative damage in human T lymphocytes leading to functional impairment.

S-glutathionylation activates STIM1 and alters mitochondrial homeostasis.

PECAM-targeted delivery of SOD inhibits endothelial inflammatory response.

Deregulation of microRNAs by HIV-1 Vpr protein leads to the development of neurocognitive disorders.

HIV-1 Tat protein promotes neuronal dysfunction through disruption of microRNAs.