Preoperative CT-based predictive factors for resectability and medium-term overall survival in patients with peritoneal carcinomatosis from colorectal cancer.

AIM: To determine preoperative radiological findings that may correlate with resectability and medium-term overall survival (OS) in patients with peritoneal carcinomatosis (PC) from colorectal cancer (CRC). MATERIALS AND METHODS: The study included 81 consecutive patients with PC scheduled for cytoreductive surgery (CRS) with hyperthermic intraperitoneal chemotherapy (HIPEC). PCI scores from preoperative computed tomography (CT) were compared with Peritoneal Cancer Index (PCI) scores at laparotomy. Odds ratio (OR), a Cox proportional hazards regression model, and Kaplan-Meier survival analyses were performed to evaluate resectability ("open and close procedure" [O&C]) and OS. RESULTS: A radiological PCI score ≥20 (OR; 20.61 p=0.001), involvement of the perihepatic region (OR; 3.63, p=0.047) and extensive small bowel involvement (OR; 9.90, p=0.019) were risk factors for O&C. Involvement of the left abdominal region correlated adversely to OS (HR; 6.86, p<0.001). CONCLUSIONS: The location of PC, in addition to the extent of PC as determined by preoperative CT, predicts resectability and medium-term survival.

Testicular steroid metabolism in juvenile bank voles (Clethrionomys glareolus Schreber) exposed to different photoperiods: an in vitro study.

Juvenile male bank voles (18-22 days of age) were either sacrificed immediately (Group C) or subjected first to a long (18L:6D, lights on 0600-2400; Group L) or a short (6L:18D, lights on 0800-1400; Group S) photoperiod for 1 week. The animal were killed by decapitation, the gonads were excised, and minced, and the conversion of [4-14C]pregnenolone (delta 3P) and [4-14C]dehydroepiandrosterone (DHA) to metabolites was studied in vitro. The radioactive steroids formed were separated and identified by thin-layer chromatography (TLC). The conversion of delta 3P to C19-steroids increased markedly from 35 (Group C) to 86% (Group L) during the first week in the long photoperiod whereas in the short photoperiod a decrease to 14.42% (Group S) was observed. The reduced production of C19-steroids in the more inactive testes was accompanied by the accumulation of progesterone (delta 4P) (52.98% Group S and 24.9% Group C) and small amounts of 17 alpha-hydroxyprogesterone (17 alpha-OH-delta 4P) (2.5 and 4.5%, respectively), whereas in Group L only trace amounts of these metabolites were encountered. No marked differences in the metabolism of [4-14C]DHA between the photoperiodic groups were observed. These results seem to indicate that at least in vitro marked changes in C17-C20-lyase and/or 17 alpha-hydroxylase activities occur in this seasonally breeding species during testicular maturation and photoperiodically induced regression.

Neuronal and liver protein synthesis in the developing offsprings following treatment of pregnant rats with ethanol or 1,3-butanediol.

Ethanol or 1,3-butanediol ingestion during pregnancy and lactation results in a marked inhibition of neuronal protein synthesis in the 18-day-old rat progeny, however the same treatment had a stimulatory effect on the amino acid incorporation by neuronal perikarya of 8-day-old pups. Liver protein synthesis in vitro, on the other hand, was enhanced in both 8-day and 18-day-old pups as a consequence of maternal ethanol consumption. This was attributable to increased amino-acylation in the liver pH 5 enzyme fraction.

Role of gastric emptying on ethanol poisoning in rats.

Intraperitoneal glucose was demonstrated to significantly inhibit the absorption of ethanol ( 2 g/kg) administered orally to rats. The effect was due to slowed emptying of the stomach, verified by analysis of the stomach contents and of blood enthanol levels. The observation agrees with previous findings, according to which the rate of stomach emptying is inversely related to the blood glucose level. However, when glucose was given intravenously 15 minutes after oral administration of a lethal dose of ethanol (12.5 g/kg) no significant inhibition of ethanol absorption could be observed. Intravenous propantheline, pyrithioxine and methylene blue were also unable to prolong the survival time or to influence the lethal blood ethanol concentration (about 170 mmol/l) of the enthanol-poisoned rats.

Ethanol-induced changes in cation-stimulated adenosine triphosphatase activity and lipid-proteolipid labeling of brain microsomes.

The experiments described are based on the hypothesis that prolongation of the depressant action of ethanol leads to compensatory changes in neuronal membrane structures involved in impulse conduction and transmission, and that these become manifest as increased tolerance and withdrawal hyperexcitability. Behavioral tolerance was tested by means of the tilted plane test in rats consuming 9-10 g ethanol/kg/day in a liquid diet fed ad lib., or given 5 g/kg every other day by stomach tube, or doses rising from 6 to 9 g/kg/day maintaining continuous intoxication. All treatments were continued for about three or four weeks before testing. Rats consuming ethanol at a self-regulated rate did not develop tolerance, evidently because sufficient alcohol levels were not built up. Prolonged intoxication induced a high degree of tolerance and withdrawal symptoms, whereas intoxication every other day induced an intermediate degree of tolerance. When no definite abstinence symptoms were associated with the behavioral tolerance, cation stimulated ATPase activity of the brain microsomal fraction was not changed. With increasing withdrawal excitability, there was a relative increase in Na+, K+-stimulated ATPase and an decrease in Mg2+-stimulated ATPase whereas total activity of the enzyme system was not altered. 14C-serine was used as a precursor in order to detect changes in the metabolism of membrane components. So far, only acute experiments have been carried out in vivo. Heavy intoxication (6 g ethanol/kg by stomach tube) inhibited labeling of brain microsomal lipids and proteolipids. In "hangover", proteolipid labeling had returned to the control level whereas lipid labeling was still depressed. Cerebral cortex slices from rats in a withdrawal state after prolonged intoxication, and from control rats, were incubated in vitro with 14C-serine. Unstimulated tissue showed no effect of the prior treatment. When electrical stimulation was applied, much more activity was recovered in microsomal lipids of slices from withdrawal animals than from controls.