Urocortin protects chondrocytes from NO-induced apoptosis: a future therapy for osteoarthritis?

Osteoarthritis (OA) is characterized by a loss of joint mobility and pain resulting from progressive destruction and loss of articular cartilage secondary to chondrocyte death and/ or senescence. Certain stimuli including nitric oxide (NO) and the pro-inflammatory cytokine tumor necrosis factor α (TNF-α have been implicated in this chondrocyte death and the subsequent accelerated damage to cartilage. In this study, we demonstrate that a corticotrophin releasing factor (CRF) family peptide, urocortin (Ucn), is produced by a human chondrocyte cell line, C-20/A4, and acts both as an endogenous survival signal and as a cytoprotective agent reducing the induction of apoptosis by NO but not TNF-α when added exogenously. Furthermore, treatment with the NO donor S-nitroso-N-acetyl-D-L-penicillamine upregulates chondrocyte Ucn expression, whereas treatment with TNF-α does not. The chondroprotective effects of Ucn are abolished by both specific ligand depletion (with an anti-Ucn antibody) and by CRF receptor blockade with the pan-CRFR antagonist α-helical CRH(9-41). CRFR expression was confirmed by reverse transcription-PCR with subsequent amplicon sequence analysis and demonstrates that C-20/A4 cells express both CRFR1 and CRFR2, specifically CRFR1α and CRFR2ß. Protein expression of these receptors was confirmed by western blotting. The presence of both Ucn and its receptors in these cells, coupled with the induction of Ucn by NO, suggests the existence of an endogenous autocrine/paracrine chondroprotective mechanism against stimuli inducing chondrocyte apoptosis via the intrinsic/mitochondrial pathway.

Innominate truncal dissection and rupture into right pleural cavity following acute type A dissection of the aorta with right coronary ostial avulsion and inferior STEMI.

An innominate truncal dissection and rupture into the right pleural cavity with massive hemothorax is the initial presentation in this 66-year-old lady with type A dissection of the aorta complicated by right coronary ostial avulsion and inferior STEMI. She underwent supracoronary interposition graft replacement of the ascending aorta and hemiarch, interposition graft replacement of the innominate trunk and saphenous vein bypass grafting of the right coronary artery successfully. Innominate truncal rupture following aortic dissection is practically unknown and has not been described before in the absence of aortic rupture. Innominate truncal rupture secondary to other pathologies presents with supraaortic and mediastinal hematomas, but almost never with right hemothorax. On the backdrop of this unusual presentation with no neurological injury, we review the literature for innominate truncal dissection and rupture, other etiologies for innominate truncal rupture, the complex interplay of factors determining neurological injury and discuss the changes in the strategies and conduct of arterial return during cardiopulmonary bypass and selective antegrade perfusion imposed by this previously undescribed instance of innominate truncal rupture due to dissection.

Prevalence of antibodies to hepatitis A among children and adolescents in Larnaca area, Cyprus.

The prevalence of antibodies to hepatitis A virus was investigated in 385 children and adolescents (52.2% males), aged 6 to 18, in the Larnaca area of Cyprus. This is the first study investigating the prevalence of hepatitis A in Cyprus for this age group. The population was stratified into two groups: 6 to 12 years old and 13 to 18 years old. None of the subjects in the first group were positive. The prevalence of hepatitis A in the age of group 13 tol8 was 1.6%. In conclusion, the low prevalence of anti-HAV demonstrates the susceptibility of young Cypriots to hepatitis A. This is a cause for concern as these unprotected young adults are frequently exposed to potentially infected individuals.