OBJECTIVE: Laparoscopic radical prostatectomy (LRP) has been refined by experienced surgeons into a competitive treatment alternative for localized prostate cancer. Less is known, however, about the outcomes of "learning curve" cases from newly trained surgeons. We prospectively studied 100 cases of LRP performed by 2 senior and 2 junior surgeons and addressed the rates of positive margins-an important early endpoint of oncologic efficacy.

METHODS: 100 consecutive cases of LRP were performed by two senior (n=62) and two junior surgeons (n=38) by a 5-port transperitoneal route. Whole-mount step-section prostate specimens were examined by Stanford protocol.

RESULTS: Positive margins occured in 25% of cases: 18% for pT2a (2/11), 18% for pT2b (11/61), 45% for pT3a (10/22), and 50% for pT3b (2/4) (p=0.002 pT2 vs. pT3). By surgeon experience, the rates were 19% (12/62) for senior and 34% (13/38) for junior (p=0.04). However, in a multiple logistic regression analysis, only pathologic stage (p=0.083) and Gleason sum (p=0.0133) reached statistical significance, while surgeon experience did not (p=0.0992).

CONCLUSION: Positive margin rates after laparoscopic radical prostatectomy are significantly influenced by pathologic stage and Gleason score, and are within the range reported from open series. The higher positive margin rate from junior surgeons, although not statistically significant, suggests the need for further study and continued mentoring during surgery and/or video review of cases to improve oncologic results.

The present investigation focused on the possible hepatoprotective potential of captopril on carbon tetrachloride (CCl4)-induced acute liver injury in mice. Twenty-four hours after a single intraperitoneal injection of CCl4 (20 microl/Kg), hepatotoxicity was evidenced in the serum by elevated levels of aspartate transaminase (AST; EC: 2.6.1.1), alanine transaminase (ALT; EC: 2.6.1.2) and lactate dehydrogenase (LDH; EC: 1.1.1.27) and in the liver by depleted level of reduced glutathione (GSH), enhanced activity of glutathione peroxidase (GSH-Px; EC: 1I.11.1.9) and elevated level of lipid peroxides (LP). Captopril was given orally at three dose levels viz., 10, 25 and 50 mg/Kg/day for three consecutive days before subjecting the animals to the hepatotoxin. With the exception of the lowest dose namely, 10 mg/Kg/day, captopril afforded protection against CCl4-induced hepatotoxicity to different extents. Thus, the elevated activities of the enzymes AST, ALT, LDH and GSH-Px as well as the enhanced lipid peroxidation were markedly reduced below those elicited by the hepatotoxin, reaching values closer to the control, though still statistically higher. Captopril, however, did not ameliorate the depletion of GSH produced by CCl4. The data reported herein reveal a protective potential of captopril against the acute hepatotoxicity induced by CCl4 in mice. This hepatoprotection could be attributed, at least in part, to the free radical scavenging properties of the drug.

Several studies have indicated that wild type p53 plays an important role in controlling cell growth and acts as a cyclin modifier. Abnormalities in p53 induce the overexpression of proliferating cell nuclear antigen. The aim of this study is to correlate immunocytochemically the expression of mutant p53 and the proliferative index (PI) as indicated by image analysis of PCNA immunoreactivity in 81 cases of pleural and peritoneal effusions. There was a strong correlation (r = 73%) between p53 immunoreactivity and PCNA PIs. Forty-three (71%) cases indicated p53 immunostaining out of 61 cases with PCNA immunoreactivity, forty of which (93%) proved to have a diagnosis of malignancy using histological or clinical data. Furthermore, 7 malignant cases showed PCNA reactivity but no p53 immunostaining. An additional four malignant cases indicated no reactivity for either p53 or PCNA. Also, there was a significant difference in the PCNA PI between benign and malignant effusions (p < 0.001). These clinical observations confirm the function of wild p53 as a check point during cell cycling, and as a strong negative feedback effect on PCNA expression. Furthermore, such co-expression represents a significant indicator for malignancy.