These results support the concept of a genetic predisposition in pemphigus. The non-complement-fixing PV-IgG4 and at least one complement-fixing PV-IgG subclass appear to be involved in the pathogenesis of the disease. The absence of PV-IgG4 among relatives who were PV-IgG carriers seems to be linked to the fact that they do not develop pemphigus. The exact nature of this linkage is still unclear.

A pre-endoscopy patient education program apparently increase patient compliance, thereby decreasing both the need for repeated examinations and their attendant costs.

A sterile urine culture does not rule out the stent itself being colonized. Therefore, patients with indwelling ureteral stents and a sterile urine culture may benefit from prophylactic antibiotic treatment prior to endourologic procedures. The prophylactic regimen must provide coverage for common gram-negative uropathogens as well as gram-positive bacteria, including enterococci.

Apoptosis appears to be a central mechanism of cell death following reperfusion of the ischemic liver. The aim of this study was to determine the effect of decreased expression of the proapoptotic Bax gene on hepatic apoptotic warm ischemia/reperfusion (I/R) injury. Three groups of mice were studied: homozygotic knockout mice (Bax Ϫ/Ϫ ); heterozygotic (Bax ϩ/Ϫ ); and wild type (Bax ϩ/ϩ ). Isolated mouse livers were subjected to 90 minutes of ischemia (37°C) followed by 15 minutes of reperfusion. Bax and Bcl-2 expression in liver tissue homogenates was measured by Western blot. Serum liver enzyme levels were measured and intrahepatic caspase-3 activity was determined by fluorimetric assay. Oil red O (ORO) staining was performed for fat detection. Apoptotic cells were identified by morphological criteria, immunohistochemistry for caspase-3, and terminal deoxynucleotidyl transferase-mediated 2Ј-deoxyuridine 5Ј-triphosphate nick-end labeling (TUNEL) assay. At 1 minute of reperfusion, the ischemic (Bax Ϫ/Ϫ ) livers were characterized by statistically significantly lower liver enzyme levels and lower caspase-3 activity than the ischemic (Bax ϩ/ϩ ) livers (P Ͻ 0.05 for both). The reduction in postischemic apoptotic hepatic injury in the ischemic Bax Ϫ/Ϫ livers group was confirmed morphologically, by the significantly reduced microvesicular steatosis as determined by ORO staining, fewer apoptotic hepatocyte cells detected (P Ͻ 0.05); immunohistochemically, by the significantly weaker activation of caspase-3 compared to the ischemic group (P Ͻ 0.05); and by TUNEL assay (P Ͻ 0.05). Similar levels of antiapoptotic Bcl-2 protein expression were detected in all 3 groups of ischemic livers on Western blots. Bax protein was not expressed in Bax-deficient livers and was detected in Bax ϩ/ϩ normal livers. In the Bax ϩ/Ϫ livers, levels of the damage markers were moderate. In conclusion, The better tolerance of Bax knockout livers to I/R injury suggests that the Bax gene may serve as a potential target for therapeutic intervention in hepatic I/R injury.

No abstract