Apolipoprotein M induces inhibition of inflammatory responses via the S1PR1 and DHCR24 pathways.

Apolipoprotein M (ApoM) is a type of apolipoprotein. It is well known that high­density lipoprotein (HDL) decreases inflammatory responses via the apoM­sphingosine­1­phosphate (S1P) pathway. The present study further investigated the importance of ApoM in the inhibitory effects of HDL on inflammation. Mice with an apoM gene deficiency (apoM­/­) were employed to investigate the effects of ApoM on the expression of interleukin­1ß (IL­1ß), monocyte chemotactic protein­1 (MCP­1), S1P receptor­1 (S1PR1) and 3ß­hydroxysterol Δ­24­reductase (DHCR24), as compared with in wild­type mice (apoM+/+). Furthermore, cell culture experiments were performed using a permanent human hybrid endothelial cell line (EA.hy926). Cells were cultured in the presence of recombinant human apoM (rec­apoM) or were induced to overexpress apoM (apoMTg); subsequently, cells were treated with tumor necrosis factor­α (TNF­α), in order to investigate the effects of ApoM on IL­1ß and MCP­1. The results demonstrated that the mRNA expression levels of IL­1ß and MCP­1 were significantly higher in the liver following administration of lipopolysaccharide in apoM­/­ mice compared with in apoM+/+ mice. In cell culture experiments, when cells were pre­cultured with rec­apoM or were engineered to overexpress apoM (apoMTg), they exhibited decreased expression levels of IL­1ß and MCP­1 following TNF­α treatment compared with in normal apoM­expressing cells (apoMTgN). Furthermore, the mRNA expression levels of IL­1ß and MCP­1 were significantly elevated following addition of the S1PR1 inhibitor W146, but not by the scavenger receptor class B type I inhibitor, block lipid transport­1 (BLT­1), in apoMTg cells prior to TNF­α treatment. Conversely, there were no differences in these inflammatory biomarkers under the same conditions in apoMTgN cells. The mRNA expression levels of DHCR24 were significantly reduced by the addition of BLT­1 prior to TNF­α treatment in apoMTg cells; however, there was no difference in the expression of this inflammatory biomarker in apoMTgN cells. In conclusion, ApoM displayed inhibitory effects against the inflammatory response in vivo and in vitro; these effects may be induced via the S1PR1 and DHCR24 pathways.

Emergent management of penetrating trauma of aortic arch in a countryside hospital.

According to the literature, only a small proportion of occurrences regarding penetrating trauma of the thoracic aorta can be treated successfully. Herein we reported our experience of a recent rescue of such a patient in a countryside hospital lacking advanced instruments for cardiopulmonary bypass operations. A 20-year-old male was admitted for a penetrating injury with disrupted innominate vein and right common carotid artery together with a 1.5-cm laceration on the aortic arch between the innominate artery and the left common carotid artery. The patient was successfully saved without the implementation of cardiopulmonary bypass. Presentation and management in this case were discussed.

Emergent treatment of patients with traumatic aorta ruptures.

OBJECTIVE: To discuss our experience on the diagnosis and treatment of thoracic aorta rupture (TAR) that is one of the main common causes of death in the victims under blunt chest trauma. METHODS: Between July 2001 and March 2006, 9 patients (6 men and 3 women, aged from 20 to 54 years) suffering from acute traumatic aorta rupture after motor vehicle accidents received emergent surgical treatments in our hospital. Based on our experience in the rescue of the first TAR patient we introduced a practical procedure on the diagnosis and treatment of TAR in our department. All the other patients generally followed this procedure. Eight patients received contrast material enhanced helical computerized tomography scan before the operation. The leakage of constrast medium from the aorta isthmus was found, and diagnosis of TAR was confirmed. Seven patients underwent immediate operation within 14 hours after accidents. One patient was treated on the 5th day of the accident because of delayed diagnosis of aortic rupture. All patients received general anesthesia with double lumen endotracheal tube and normothermic femoro-femoral partial cardiopulmonary bypass, with beating heart and aortic clamping. One patient received simple repair, and others received partial replacement of thoracic aorta with artificial vascular graft. RESULTS: Seven TAR patients were successfully salvaged. Three patients combined brain injury as well as extremitiy hemiplegia before operation. After treatments one was fully and two partially recovered without paraplegia. CONCLUSIONS: Proper practical protocol is emphasized for the surgical repair of TAR because it will reduce the mortality of severe blunt chest injury.