Activity of newer beta-lactam agents against clinical isolates of Bacteroides fragilis and other Bacteroides species.

The in vitro activities of beta-lactam antibiotics against Bacteroides fragilis and B. fragilis group isolates are presented. Clinical isolates from 1986 were compared with strains from 1979 to 1982. Imipenem, ticarcillin-clavulanic acid, and ceftizoxime were the most active agents. Cefotetan was equivalent to cefoxitin against B. fragilis but less active against B. fragilis group isolates. Enhancement of cefotaxime by its desacetyl metabolite was minimal.     

Platelet-binding immunoglobulins in pregnancy-induced hypertension I. Platelet-associated IgM on fetal platelets: evidence of a fetal autoimmune reaction?

Pregnancy-induced hypertension (PIH) can be complicated by maternal or fetal thrombocytopenia, or both. In order to investigate possible immunologic causes of these thrombocytopenias, platelet-associated IgG (PAIgG) and IgM (PAIgM) were measured in mothers with PIH and in their infants and compared with those from patients with autoimmune thrombocytopenic purpura (ATP), a known immunodestructive platelet disorder. Many PIH patients (33.3%) and most ATP patients (68.1%) had elevated levels of maternal PAIgG. In both diseases, the amount of PAIgG was directly proportional with the degree of thrombocytopenia (r = 0.446 in PIH and R = 0.668 for ATP). But in neither disease did the degree of maternal thrombocytopenia correlate with the degree of neonatal thrombocytopenia (r = 0.153 for PIH and R = 0.175 for ATP). Umbilical cord samples from PIH patients contained PAIgG (53.3%) and PAIgM (53.8%), whereas the umbilical cord samples from ATP patients had elevated amounts of PAIgG but not PAIgM. PAIgM in the umbilical cord blood could not be accounted for by IgM rheumatoid factors, IgM-containing immune complexes, or non-specific adsorption because of elevated total IgM levels. The umbilical cord blood PAIgM was probably not of maternal origin because it was observed even when the maternal blood contained no PAIgM and maternal IgM is not normally transported transplacentally. Therefore, the PAIgM appears to be of fetal origin. These results suggest that both maternal and fetal immunologic mechanisms may be involved in PIH-induced thrombocytopenia; if so, this is one of the first reported examples of a possible fetal autoimmune response.     

Endoscopic endonasal removal of an intra-suprasellar Rathke's cleft cyst: case report and surgical considerations.

An endoscopic endonasal approach was performed to remove an intra-suprasellar Rathke's cleft cyst. Rathke's cleft cyst are benign lesions, rarely diagnosed because they are often asymptomatic. To the best of our knowledge, at least 475 cases of Rathke's cleft cysts have been reported. They seem to arise from remnants of Rathke's pouch, an invagination of the stomodeum. A 52-year-old woman, complaining of bilateral frontal headaches, was operated on by using an endoscopic endonasal approach, for an intra-suprasellar tumor. The pre-operative diagnosis was non-functioning pituitary adenoma. Intra-operatively a creamy-coloured viscous tissue was found. After the removal of the cyst contents and of the capsule, the suprasellar structures were seen well. The chiasmatic cistern, the chiasm, the pituitary stalk and the pituitary gland were visualized with 0 and 30 degree endoscopes. The pathological findings showed a well-differentiated cuboidal epithelium. The diagnosis was Rathke's cleft cyst. No post-operative complications were observed. The endoscopic technique was particularly suitable in this case, both for the Rathke's cleft features and for an excellent outcome. The Rathke's cleft cyst was easily removed by suction and the cyst wall was entirely removed with curettes and pituitary punches. The hypophysis was distinguished from the cyst and was preserved. The surgical manoeuvres were all done under direct visual control. The absence of nasal packing and of breathing difficulties made comfortable the post-operative outcome. Thus, the endoscopic endonasal approach can be considered the favourite technique in case of either intra- and/or suprasellar Rathke's cleft cysts.     

No impact of repeated endoscopic screens on gastric cancer mortality in a prospectively followed Chinese population at high risk.

BACKGROUND: Gastric cancer (GC) is the leading cause of cancer deaths in China. Our study prospectively evaluated the impact of repeated endoscopic screens on GC mortality in a high-risk population in China. METHODS: Between 1989 and 1999, a population-based gastroscopic screening was conducted in 4,394 residents of Linqu County, China, a region with the highest rates of GC worldwide. Residents ages 35 to 64 years received initial gastroscopies with biopsies in 1989. Repeated endoscopies were performed in 1994 and 1999. Cancer occurrences and deaths were actively monitored throughout the entire period until July 2000. Mortality from GC was compared with expected values based on mortality rates obtained for Linqu in the 1990-1992 Chinese Cancer Mortality Survey. RESULTS: Between March 1989 and July 2000, 39,303 person-years were accumulated; 85 new GCs occurred, 29 (34.5%) were in early stage. Fifty-eight cases (68%) were identified at one of the screens. The number of observed deaths from GC (37) was close to the expected (36.8). The standardized mortality ratio was 1.01 (95% CI 0.72-1.37) for the entire cohort, 1.13 (95% CI 0.77-1.57) for males, and 0.65 (95% CI 0.26-1.32) for females. CONCLUSIONS: Despite high population coverage with repeated screens, no reduction in GC mortality was observed in this high-risk population in China.     

Postprandial induction of chaperone gene expression is rapid in mice.

Molecular chaperones assist in the biosynthesis and processing of proteins. Most chaperones are induced by physiological stresses. We have shown that dietary energy restriction decreases the mRNA and protein levels of many endoplasmic reticulum chaperones in the livers of mice. Here, we have investigated the response of chaperone mRNA to feeding. Control and 50% energy-restricted C3B10RF1 mice were deprived of food for 24 h, fed, and killed 0, 1.5, 5 or 12 h after feeding. Chaperone mRNAs were strongly induced as early as 1.5 h after feeding in control and energy-restricted mice. The integrated levels of these mRNA over 24 h were significantly lower in energy-restricted mice. The mRNA response to energy intake was mirrored over the course of days in the level of chaperone protein. A similar but smaller response to feeding was found in kidney and muscle. Puromycin and cycloheximide failed to inhibit the feeding response, suggesting that feeding releases chaperone expression from an unstable inhibitor. Studies with dibutyryl-cAMP- and glucagon-supplemented, normal and streptozotocin-diabetic mice suggest that glucagon and insulin may be mediators of the feeding response. Adrenalectomy enhanced the feeding induction, but dexamethasone administration had no effect. Thus, postprandial changes in insulin and glucagon may link chaperone gene expression to feeding, possibly in several tissues including liver.