[Fatal chest injury from a shotgun slug: homicide, accident or suicide?]. / Tödlicher Brustschuss mit Flintenlaufgeschoss--Tötungsdelikt, Unfall oder Suizid?

A 78-year-old hunter was found dead beside his raised hide with a gunshot wound to his chest. In the present case, the reconstruction of the shooting event revealed an accident. Disregarding all safety rules, the hunter had placed his superposed rifle-shotgun on the chair and pulled the barrels of the cocked gun towards his body. One of the triggers interlocked with the button of a camping chair's cushion and a shot was fired. Furthermore the morphology of wounds from shotgun slugs is discussed on the basis of the autopsy findngs.

[Delayed pericardial tamponade following a stab wound to a branch of the right coronary artery]. / Aussergewöhnlicher Verlauf einer Herzbeuteltamponade nach Stichverletzung eines Astes der rechten Koronararterie.

A 45-year-old man was attacked with a knife and suffered multiple stab wounds to the chest and abdomen. After surgical treatment and hospitalization for 9 days he was discharged in a stable condition. The following day he was found dead in his apartment. The autopsy revealed a pericardial tamponade caused by acute bleeding from an injured branch of the right coronary artery. This case shows that life-threatening late complications in patients with penetrating cardiac wounds may occur despite an initially uneventful course.

Lipoprotein lipase-facilitated uptake of LDL is mediated by the LDL receptor.

LPL mediates the uptake of lipoproteins into different cell types independent of its catalytic activity. The mechanism of this process and its physiological relevance are not clear. Taking into account the importance of the endothelial barrier for lipoprotein uptake, in vitro studies with primary aortic endothelial cells from wild-type and low density lipoprotein receptor (LDLR)-deficient (LDLR(-/-)) mice were performed. Addition of LPL almost doubled the uptake of LDL into wild-type cells. However, there was virtually no LPL-mediated change of LDL uptake into LDLR(-/-) cells. Upregulation of LDLR by lipoprotein-deficient serum/lovastatin in wild-type cells resulted in a 7-fold increase of LPL-mediated LDL uptake. Uptake of chylomicron remnants was not affected by LDLR expression. In proteoglycan-deficient cells, LPL did not increase the uptake of lipoproteins. The physiological relevance of this pathway was studied in mice that were both LDLR(-/-) and transgenic for catalytically inactive LPL in muscle. In the presence of LDLR, inactive LPL reduced LDL cholesterol significantly (13-24%). In the absence of LDLR, LDL cholesterol was not affected by transgenic LPL. Metabolic studies showed that in the presence of LDLR, LPL increased the muscular uptake of LDL by 77%. In the absence of LDLR, transgenic LPL did not augment LDL uptake. Chylomicron uptake was not affected by the LDLR genotype. We conclude that LPL-mediated cellular uptake of LDL, but not of chylomicrons, is dependent on the presence of both LDLR and proteoglycans.