Thrombomodulin's lectin-like domain reduces myocardial damage by interfering with HMGB1-mediated TLR2 signalling.

Aims: Thrombomodulin (TM), via its lectin-like domain (LLD), exhibits anti-inflammatory properties partly by sequestering the pro-inflammatory cytokine, high-mobility group box 1 (HMGB1). Since myocardial damage after ischaemia and reperfusion is mediated by inflammation, we evaluated the cardioprotective effects of the LLD of TM. Using an in vivo mouse model of transient ischaemia and in vitro models of cardiomyocyte hypoxia, we assessed the ability of the LLD to suppress HMGB1-mediated activation of the receptors, receptor for advanced glycation endproducts (RAGEs) and Toll-like receptors (TLRs) 2 and 4.

Paediatric airway management in mucopolysaccharidosis 1: a retrospective case review.

Context: Airway management in children suffering from mucopolysaccharidosis 1 (Hurler syndrome) remains challenging despite advances in both treatment and airway management techniques.

Objectives: Forty-one anaesthetic charts following ten children over a 6-year period (2004-2010) were reviewed with emphasis on airway problems.

Results: All children had early stem cell transplantation at the age of 2 years or earlier.

Syndecan-4 signalling inhibits apoptosis and controls NFAT activity during myocardial damage and remodelling.

Aims: Myocardial infarction (MI) results in acute impairment of left ventricular (LV) function through the initial development of cardiomyocyte death and subsequent progression of LV remodelling. The expression of syndecan-4 (Sdc4), a transmembrane proteoglycan, is up-regulated after MI, but its function in the heart remains unknown. Here, we characterize the effects of Sdc4 deficiency in murine myocardial ischaemia and permanent infarction.

In vivo fluorescence-mediated tomography for quantification of urokinase receptor-dependent leukocyte trafficking in inflammation.

Background: Inflammation is characterized by leukocyte recruitment. Macrophages and neutrophils contribute to tissue damage and organ dysfunction. Modulating leukocyte invasion can protect from these adverse effects.

Lidocaine protects from myocardial damage due to ischemia and reperfusion in mice by its antiapoptotic effects.

Background: Perioperative myocardial ischemia poses a vital threat to surgical patients. Means to protect postischemic myocardium are clinically not available. Lidocaine has been demonstrated to exert antiinflammatory pleiotropic effects.