[Swimming-induced pulmonary oedema].

Swimming-induced pulmonary oedema (SIPE) is a rare condition, where hemodynamic changes associated with immersion in water and swimming induces pulmonary oedema. Here, we report a case with a 57-year old very fit female triathlete experiencing critical lung edema during low intensity open water swimming. We speculate, that SIPE in this particular patient was caused by a combination of factors: 1) Stress-induced diastolic dysfunction, 2) tendency to vasoconstriction upon stress and 3) possibly paroxysmal atrial fibrillation induced by increased atrial pressure during the event.

Transformation-associated changes in sphingolipid metabolism sensitize cells to lysosomal cell death induced by inhibitors of acid sphingomyelinase.

Lysosomal membrane permeabilization and subsequent cell death may prove useful in cancer treatment, provided that cancer cell lysosomes can be specifically targeted. Here, we identify acid sphingomyelinase (ASM) inhibition as a selective means to destabilize cancer cell lysosomes. Lysosome-destabilizing experimental anticancer agent siramesine inhibits ASM by interfering with the binding of ASM to its essential lysosomal cofactor, bis(monoacylglycero)phosphate. Like siramesine, several clinically relevant ASM inhibitors trigger cancer-specific lysosomal cell death, reduce tumor growth in vivo, and revert multidrug resistance. Their cancer selectivity is associated with transformation-associated reduction in ASM expression and subsequent failure to maintain sphingomyelin hydrolysis during drug exposure. Taken together, these data identify ASM as an attractive target for cancer therapy.