Kaushik Parthasarathi

Mitochondrial reactive oxygen species regulate spatial profile of proinflammatory responses in lung venular capillaries.

High tidal volume ventilation induces proinflammatory signaling in rat lung endothelium.

Endothelial barrier strengthening by activation of focal adhesion kinase.

Mechano-oxidative coupling by mitochondria induces proinflammatory responses in lung venular capillaries.

Pressure-induced leukocyte margination in lung postcapillary venules.

IL-13 regulates the immune response to inhaled antigens.

Sequence of endothelial signaling during lung expansion.

Lung surfactant secretion by interalveolar Ca2+ signaling.

Connexin 43 mediates spread of Ca2+-dependent proinflammatory responses in lung capillaries.

Real-time lung microscopy.

Chloride-dependent secretion of alveolar wall liquid determined by optical-sectioning microscopy.

ITF1697, a stable Lys-Pro-containing peptide, inhibits weibel-palade body exocytosis induced by ischemia/reperfusion and pressure elevation.

Paracrine purinergic signaling determines lung endothelial nitric oxide production.

Preexposure to hyperoxia causes increased lung injury and epithelial apoptosis in mice ventilated with high tidal volumes.

Localized acid instillation by a wedged-catheter method reveals a role for vascular gap junctions in spatial expansion of acid injury.

Deletion of apoptosis signal-regulating kinase-1 prevents ventilator-induced lung injury in mice.

Real-time imaging reveals endothelium-mediated leukocyte retention in LPS-treated lung microvessels.

Endothelial connexin43 mediates acid-induced increases in pulmonary microvascular permeability.

Lipopolysaccharide induces endoplasmic store Ca2+-dependent inflammatory responses in lung microvessels.

Hyperoxia increases the elastic modulus of alveolar epithelial cells through Rho kinase.