Congratulations to Dr Claudia McCarthy (Department of Pharmacology, Monash University) - winner of the Clinical Science Early Career Poster Prize at the 2013 Annual Scientific Meeting of the High Blood Pressure Research Council of Australia.

New Call For Papers

NADPH Oxidases in Health and Disease - we invite the submission of original papers by the deadline of 31 December 2014

Meeting Highlight

Experimental Biology 2014 - 26-30 April 2014 at the San Diego Convention Center, San Diego, CA, U.S.A.
>> Meeting website

EDITOR'S CHOICE: freely available throughout April 2014

Nalin Dayawansa, Xiao Ming Gao, David White, Anthony Dart and Xiao Jun Du (Baker IDI Heart and Diabetes Institute, Melbourne, Australia)

MIF (macrophage migration inhibitory factor) is a highly conserved molecule with pleiotropic actions and has been extensively studied for its pivotal role in a variety of inflammatory diseases. An area of increasing interest is the pathophysiological significance of MIF following myocardial infarction, and evidence is emerging that MIF possesses multiple and sometimes opposing actions depending on its cellular source, the severity of ischaemic injury and the time after acute myocardial infarction. In the present review, the authors summarize recent experimental and clinical studies examining the diverse functions of MIF across the spectrum of acute myocardial infarction from brief ischaemia to post-infarct healing.
Latest Papers
GLP-1 at physiological concentrations recruits skeletal and cardiac muscle microvasculature in healthy humans
GLP-1 increases microvascular perfusion in both skeletal and cardiac muscle, and brachial artery diameter and blood flow in humans. These vascular actions may contribute to the beneficial actions of the GLP-1 receptor analogues.
Thrombin induces ICAM-1 expression in human lung epithelial cells via c-Src/PDGFR/PI3K/Akt-dependent NF-ĸB/p300 activation
In the present study, we show that thrombin induced ICAM-1 expression and monocyte adherence via a c-Src/PDGFR/PI3K/Akt/NF-ĸB-dependent pathway in HPAEpiCs.
Smad7 inhibits AngII-mediated hypertensive nephropathy in a mouse model of hypertension
SMAD7 treatment inhibits AngII-induced hypertensive kidney disease. Inhibition of the Sp1/TGFβ/SMAD3/NF-ĸB/miR-29 regulatory network may be a mechanism by which SMAD7 protects kidney from hypertensive kidney injury. Thus SMAD7 may be a novel therapeutic agent for hypertensive kidney disease.