[Popliteal entrapment syndrome with distal embolization. Description of a clinical case]. / La sindrome da intrappolamento dell'arteria poplitea con embolizzazione distale. Descrizione di un caso clinico.

External compression of the popliteal artery is probably still underdiagnosed. Repeated minor trauma to the popliteal artery as it passes through anomalous fibrous bands, due to developmental defects, may lead to stenosis and occlusion, with consequent chronic or acute ischaemic symptoms, usually in young males without cardiovascular risk factors. Distal embolization to the tibial arteries, to the foot arch and digital vessels is common but is not emphasized in the literature. This distal embolization may compromise the results of surgical repair. Early repair of the anomaly fibrous band is advocated even in a still asymptomatic lower limb. One patient with bilateral popliteal artery entrapment, causing unilateral occlusion, with distal embolization, is reported.

[The rhabdomyolytic syndrome: a not uncommon occurrence]. / Sindrome rabdomiolitica: una evenienza non infrequente.

The paper examines one aspect of a medical pathology that is rather unusual and often wrongly diagnosed: rhabdomyolysis (RMC). The series examined suggests that the pathology is relatively common and arises in a wide variety of clinical conditions. In view of the fact that the consequences of rhabdomyolysis may be serious, emphasis is placed on the fact that correct diagnosis may be obtained by the careful consideration of simple clinical parameters such as subjective symptoms, urine colour, urine strip test and serum CPK assays.

Menadione-induced bleb formation in hepatocytes is associated with the oxidation of thiol groups in actin.

Incubation of isolated rat hepatocytes with menadione (2-methyl-1,4-naphthoquinone) or the thiol oxidant, diamide (azodicarboxylic acid bis(dimethylamide)), resulted in the appearance of numerous plasma membrane protrusions (blebs) preceding cell death. Analysis of the Triton X-100-insoluble fraction (cytoskeleton) extracted from treated cells revealed a dose- and time-dependent increase in the amount of cytoskeletal protein and a concomitant loss of protein thiols. These changes were associated with the disappearance of actin and formation of large-molecular-weight aggregates, when the cytoskeletal proteins were analyzed by polyacrylamide gel electrophoresis under nonreducing conditions. However, if the cytoskeletal proteins were treated with the thiol reductants, dithiothreitol or beta-mercaptoethanol, no changes in the relative abundance of actin or formation of large-molecular-weight aggregates were detected in the cytoskeletal preparations from treated cells. Moreover, addition of dithiothreitol to menadione- or diamide-treated hepatocytes protected the cells from both the appearance of surface blebs and the occurrence of alterations in cytoskeletal protein composition. Our findings show that oxidative stress induced by the metabolism of menadione in isolated hepatocytes causes cytoskeletal abnormalities, of which protein thiol oxidation seems to be intimately related to the appearance of surface blebs.

On the role of thiol groups in the inhibition of liver microsomal Ca2+ sequestration by toxic agents.

ATP-dependent Ca2+ sequestration by rat liver microsomes was assayed using three different methods, and characterized with regard to the effect of various inhibitors. When glucose and hexokinase were added in combination to deplete ATP in the incubation, Ca2+ uptake was followed by rapid release of Ca2+ from the microsomes. Ca2+ sequestration was inhibited by reagents that cause alkylation (e.g. p-chloromercuribenzoate) or oxidation (e.g. diamide) of protein sulfhydryl groups. Moreover, pretreatment of the microsomes with cystamine, which causes formation of mixed disulfides with protein thiols, also resulted in the inhibition of Ca2+ sequestration. It is concluded that microsomal Ca2+ sequestration is critically dependent on protein sulfhydryl groups, and that modification of protein thiols may be an important mechanism for the inhibition of microsomal Ca2+ sequestration by a variety of toxic agents.