Inhibition of spleen tyrosine kinase signaling protects against acute lung injury through blockade of NADPH oxidase and IL-17A in neutrophils and γδ T cells respectively in mice.

Acute lung injury (ALI) is one of the most serious complications in critically ill patients which often leads to morbidity and mortality. ALI characterized by severe inflammation of lungs occurs due to uncontrolled inflammatory immune response. However, the immunological mechanism(s) are far from being understood.

Eugenol and carvone as relaxants of arsenic and mercury hypercontracted rat trachea.

Exposure to arsenic and mercury is known to cause respiratory problems in both humans and animals. In this study, we elicit and compare maximum contraction caused by As(III) and Hg(II) when the pollutants are fully equilibrated with contractile machinery in resting mode. Hypercontraction of 27% and 69% was obtained following exposure of tracheal rings to 25 µM As(III) and 6 nM Hg(II) for 40 min, respectively.

Modulation of Pb(II) caused aortal constriction by eugenol and carvacrol.

Exposure to lead is known to cause vasoconstriction, exact mechanism of which remains to be elucidated. In this study, we investigate contractile responses of rat aortal rings equilibrated with Pb(II) in organ bath system, explore pathways responsible for hypercontraction and examine two ameliorators of lead-induced hypercontraction. At 1 μmol L(-1) Pb(II), aortal rings showed an average increase of 50% in isometric contraction.

Inhibition of As(III) and Hg(II) caused aortic hypercontraction by eugenol, linalool and carvone.

Acute and chronic exposure to arsenic and mercury is known to produce vasoconstriction. There is, however, no clarity concerning the pathways leading to this increased contraction. In this study we elicit and compare maximum contractility of rat aortas under resting conditions in the presence of arsenic and mercury, and delineate pathways mediating this effect.