A multi-centre UK-based survey on angioedema secondary to acquired C1 inhibitor deficiency.

Background: Acquired angioedema due to C1-inhibitor deficiency (AAE-C1-INH) is very rare compared to its prototype, hereditary angioedema. An updated characterisation of the AAE-C1-INH cohort in UK is required to inform management.

Objectives: To describe the disease burden of AAE-C1-INH, long-term prophylaxis (LTP) and the clinical, immunochemical and treatment profiles of AAE-associated diseases in UK.

Skin manifestations of inborn errors of NF-κB.

More than 400 single gene defects have been identified as inborn errors of immunity, including many arising from genes encoding proteins that affect NF-κB activity. We summarise the skin phenotypes in this subset of disorders and provide an overview of pathogenic mechanisms. NF-κB acts cell-intrinsically in basal epithelial cells during differentiation of skin appendages, influences keratinocyte proliferation and survival, and both responses to and amplification of inflammation, particularly TNF.

Incidence and predictors of left ventricular thrombus by cardiovascular magnetic resonance in acute ST-segment elevation myocardial infarction treated by primary percutaneous coronary intervention: a meta-analysis.

Introduction: The incidence of left ventricular (LV) thrombus formation in ST-segment elevation myocardial infarction (STEMI) patients in the current era of primary percutaneous coronary intervention (PCI) is not well established. We performed a meta-analysis to assess the actual incidence and predictors of LV thrombus by cardiovascular magnetic resonance (CMR) in STEMI treated by primary PCI.

Methods: We searched MEDLINE and EMBASE databases up to February 2018.

Promising strategies to minimize reperfusion injury in STEMI.

Morbidity in patients presenting with acute ST-segment elevation myocardial infarction remains significant despite prompt reperfusion by primary percutaneous coronary intervention. This has been partly attributed to "myocardial reperfusion injury" whereby the process of restoring coronary blood flow paradoxically induces myocardial injury and cardiomyocyte death, mitigating the full beneficial effects of reperfusion. A large number of cardioprotective therapies to reduce myocardial infarct size have been investigated in preclinical and small proof-of-concept clinical studies with mixed results.

Remote ischaemic preconditioning involves signalling through the SDF-1α/CXCR4 signalling axis.

Ischaemic preconditioning is one of the most potent experimental modalities known to decrease infarct size after ischaemia and reperfusion. Much interest has been stimulated by the phenomenon of remote ischaemic conditioning (RIC), in which the preconditioning stimulus is applied to a limb remote from the heart to stimulate cardioprotection via an unidentified humoral factor, believed to be a protein between 3.5 and 15 kDa.