Cholangiocarcinoma complicating primary sclerosing cholangitis: cholangiographic appearances

Cholangiograms from 104 patients (and serial cholangiograms in 66 patients) with primary sclerosing cholangitis (PSC) were reviewed. In 13 patients the additional diagnosis of cholangiocarcinoma was made at biopsy or autopsy. Cholangiograms from patients with both PSC and carcinoma were compared with cholangiograms from patients with PSC alone. Marked dilatation of ducts or ductal segments (100% vs. 24%) and the appearance of a polypoid mass (46% vs. 7%) were common findings in the group of patients whose disease was complicated by malignancy. In the malignant group, polypoid masses were larger, measuring 1 cm or greater in diameter. On serial cholangiograms, four of 15 patients with progressive stricture formation and four of five with progressive ductal dilatation proved to have carcinomas. The frequent occurrence of bile duct carcinoma as a complication of PSC in this group of patients indicates that PSC has a strong tendency to undergo malignant degeneration. Cholangiographic findings which suggest malignant degeneration include markedly dilated ducts or ductal segments, presence of a polypoid mass 1 cm or greater in diameter, and progressive stricture formation or ductal dilatation.     

吲满氨酯的磷光分析

吲满氨酯具有强的磷光,其水液激发波峰304 nm,发射波峰434 nm,磷光寿命为3.87s。在碱液中磷光比在酸液中强。重原子碘对吲满氨酯磷光有增强作用,而寿命变短。金属重原子Cu²⁺,Fe³⁺,Pb²⁺,Tl³⁺,Zn²⁺及钼酸铵等均无增强作用,Cu²⁺,Fe³⁺等反有猝灭作用。比较了9种吲满氨酯类似物的磷光性质,当2位亚甲基氧化为酮基后磷光明显下降。建立了吲满氨酯的磷光分析法,最小检出量为5ng。小鼠腹腔注入药物0.1 mg/kg后10 min其血药浓度为149 ng/ml。     

Factors affecting bioelectrical impedance measurements in humans

In several groups of young healthy subjects the effect of the ingestion of a meal, of drinking normal tea or beef tea, of exercise and of the menstrual cycle on body impedance was assessed. The day-to-day reproducibility of the method was also investigated under standardized conditions. Two to four hours after ingestion of a meal, body impedance had decreased by about 13-17 Ohms in comparison with body impedance in the fasting state. Drinking 200 ml of normal tea did not result in a change of body impedance, but drinking 200 ml beef tea lowered the body impedance significantly by 4 +/- 4 Ohms. Moderate exercise on a bicycle ergometer (90 min, 100 W) did not influence body impedance, but strenuous exercise (90 min, 175 W) resulted in a decrease of 9 +/- 11 Ohms in body impedance. In general, changes in body impedance during the menstrual cycle were small, and only the difference between measurements of body impedance 1 week before the onset of the menstruation and again 1 week after menstruation (8 +/- 9 Ohms) was statistically significant. Under standardized conditions (in the morning, in the fasting state after emptying the bladder) the within-person between-day variation was found to be 2.8 per cent (13 Ohms).     

Nutritional hazards of elimination diets in children with atopic eczema

The intake of nutrients over a five day period was studied in 23 children whose atopic eczema was being treated by the avoidance of multiple foods. The results were compared with those from 23 healthy control children not on a diet. Significantly low intakes of calcium were discovered in 13 patients but not in controls. Avoidance of multiple foods is potentially hazardous and requires continued paediatric and dietetic supervision.     

mdx muscle pathology is independent of nNOS perturbation

In skeletal muscle, neuronal nitric oxide synthase (nNOS) is anchored to the sarcolemma via the dystrophin-glycoprotein complex. When dystrophin is absent, as in Duchenne muscular dystrophy patients and in mdx mice, nNOS is mislocalized to the interior of the muscle fiber where it continues to produce nitric oxide. This has led to the hypothesis that free radical toxicity from mislocalized nNOS may contribute to mdx muscle pathology. To test this hypothesis directly, we generated mice devoid of both nNOS and dystrophin. Overall, the nNOS- dystrophin null mice maintained the dystrophic characteristics of mdx mice. We evaluated the mice for several features of the dystrophic phenotype, including membrane damage and muscle morphology. Removal of nNOS did not alter the extent of sarcolemma damage, which is a hallmark of the dystrophic phenotype. Furthermore, muscle from nNOS-dystrophin null mice maintain the histological features of mdx pathology. Our results demonstrate that relocalization of nNOS to the cytosol does not contribute significantly to mdx pathogenesis.