Attenuation of myocardial injury by HMGB1 blockade during ischemia/reperfusion is toll-like receptor 2-dependent.

Genetic or pharmacological ablation of toll-like receptor 2 (TLR2) protects against myocardial ischemia/reperfusion injury (MI/R). However, the endogenous ligand responsible for TLR2 activation has not yet been detected. The objective of this study was to identify HMGB1 as an activator of TLR2 signalling during MI/R.

Akt or phosphoinositide-3-kinase inhibition reverses cardio-protection in Toll-like receptor 2 deficient mice.

Aim: Absence or inhibition of Toll-like receptor 2 (TLR2) signalling during murine myocardial ischaemia/reperfusion (MI/R) decreases myocardial necrosis and inflammation, thereby ameliorating cardiac dysfunction and improving survival. In the present study, we provide evidence for the involvement of the phosphoinositide-3-kinase/Akt pathway in TLR2-dependent reperfusion injury.

Methods: Adult male wild-type (WT) and TLR2(-/-) mice were subjected to myocardial ischaemia (30min) and reperfusion (4h).

Median arcuate ligament syndrome: vascular surgical therapy and follow-up of 18 patients.

Introduction: The median arcuate ligament syndrome (MALS) or celiac artery compression syndrome is a rare vascular disorder caused by an extrinsic compression of the celiac artery from the median arcuate ligament, prominent fibrous bands, and ganglionic periaortic tissue. Clinical symptoms are postprandial abdominal pain, nausea, vomiting, unintentional weight loss, and sometimes, abdominal pain during body exercise caused by an intermittent visceral ischemia. The aim of this study was to evaluate the operative management of patients with MALS in our institution, especially in consideration of various vascular reconstructive techniques.

Visceral artery aneurysms--follow-up of 23 patients with 31 aneurysms after surgical or interventional therapy.

Purpose: Visceral artery aneurysms (VAA) are rare forms of vascular pathology, with an incidence of 0.1% to 0.2% in routine autopsies.