The role of acetate in alcohol-induced alterations of uterine glucose metabolism in the mouse during pregnancy

The acute exposure of mice to ethanol during post-implantation pregnancy has been reported to cause alterations in the levels of several glycolytic intermediates in the uterus, suggesting a possible indirect mechanism of alcohol embryo-toxicity. The present study was undertaken to assess whether the ethanol metabolite, acetate is implicated in this phenomenon. Blood and uterine alcohol concentrations in day 9--pregnant Quackenbush Swiss mice were maximal 15 minutes after the intraperitoneal injection of ethanol (3.5 g/kg body weight), and fell to almost negligible levels 6 hours later. In response to this treatment, the levels of blood and uterine acetate increased, liver glycogen decreased, plasma glucose increased, and uterine glucose, glucose-6-phosphate (G-6-P), fructose-6-phosphate (F-6-P), and citrate increased. When acetate was administered to pregnant mice in amounts approximating those generated by exposure to alcohol, the levels of uterine F-6-P and citrate increased while other metabolic parameters remained unaffected. The administration of 4-methylpyrazole to mice subsequently treated with alcohol produced conditions of alcohol exposure in the absence of ethanol-derived acetate and depressed the ethanol-induced rise in uterine G-6-P and citrate. The results support the notion that acetate contributes to the alcohol-induced alterations in metabolism, at least as far as the regulation of uterine citrate and hexose monophosphates are concerned. This, together with stress responses induced by exposure to the acute dose of alcohol, may present mechanisms underlying the fetal alcohol syndrome associated in particular with "binge" drinking.     

Coexistence of Competing Parasitoid Species on a Host with a Variable Life Cycle

Several special cases of a general model in which two parasitoid species attack different developmental stages of a single host species are presented. The inclusion of different mathematical forms of a maturation weighting function allows us to investigate the effect of several aspects of variation in immature stage durations on the outcome of competitition between the parasitoids. The two parasitoid species cannot coexist if the host developmental stages are fixed in duration. The outcome of competition depends in part on the relative duration of the two stages attacked by the parasitoid species. However, coexistence is possible if there is sufficient variation in the time that different host individuals remain in each stage. Distributed host developmental delays promote coexistence because they cause the host population to be composed of a mixture of host types with different relative egg versus larval stage durations. Each host type is thus largely available to only one of the parasitoid species.     

Temporal Association Between Pulmonary Inflammation and Antioxidant Induction Following Hyperoxic Exposure of the Preterm Guinea Pig

The time course and nature of the pulmonary inflammatory and antioxidant responses, both during and after hyperoxic-induced acute lung injury were studied in the preterm guinea pig. Three-day preterm (65 days gestation) guinea pigs were randomly exposed to either 21% O₂ (control) or 95% O₂ (hyperoxia) for 72 hours. All pups were then maintained in ambient conditions for up to a further 11 days, during which time lung damage was monitored. In animals exposed to hyperoxia, evidence of acute lung injury and inflammation was characterized by a marked increase in microvascular permeability and elevated numbers of neutrophils in bronchoalveolar lavage fluid. Protein concentration, elastase-like activity and elastase-inhibitory capacity in lavage fluid were at a maximum at the end of the 72 hours hyperoxic exposure. Four days later, all values had returned to control levels. In contrast, increased numbers of neutrophils, macrophages and lymphocytes were recovered in the lavage fluid during this early recovery period. Coinciding with the influx of inflammatory cells, there was a significant increase in glutathione peroxidase, manganese superoxide dismutase and catalase activities in immature lung. Lung copper/zinc superoxide dismutase activity remained unchanged during both experimental periods. The strong temporal relationship between the influx of inflammatory cells to the lung and the induction of pulmonary antioxidant enzyme defences suggests that a common mechanism underlies both responses. These findings have led us to regard inflammation in the hyperoxic-injured immature lung as a beneficial event and not, as previously suggested, as part of the injurious process.     

Immunolocalization of a gonadotropin-releasing hormone receptor site in murine endometrium that mediates apoptosis

Circumstantial evidence from a previous study indicated that antibodies generated against a synthetic N-terminal extracellular domain mouse pituitary gonadotropin-releasing hormone (GnRH) receptor peptide acted directly on the murine uterus affecting endometrial regression. Affinity-purified polyclonal sheep antibodies were used to assess tissue-specificity of antibody reactions in diestrous mice. Antibody binding was localized by immunofluorescence staining to anterior pituitary gland and endometrium. Ovary, brain, liver, kidneys, heart, lungs, spleen, gastrointestinal tract, adrenal glands, thymus, thyroid gland, muscle, and adipose were unreactive. Fragmented deoxyribonucleic acid, a marker of programmed cell death/apoptosis, was detected by digoxigenin labeling-immunoperoxidase in endometrial (but not pituitary) glands of animals injected with antipeptide antibodies or native ligand. It appears that luteal phase endometrium of mice expresses a GnRH receptor moiety that is coupled to a cell death (endonuclease) transduction pathway.     

Follicle-stimulating hormone pulse amplitude decreases with the onset of the breeding season in the mare

The relationship between daily mean FSH concentrations in serum and the pattern of FSH detected by frequent sampling for 12-h periods (samples every 15 min) was examined in five mares during the transition into the breeding season. The five mature anestrous mares were exposed to a natural increase in daylength. Blood samples were collected daily from February 1 until the first ovulation of the breeding season (April 14 +/- 3.7 days, Mean +/- SEM). Periods of frequent blood collection were performed every two weeks. Blood samples were obtained daily by jugular venipuncture or jugular cannula (frequent samples). Mean daily concentrations of FSH in serum determined by RIA decreased during seasonal transition. Patterns of FSH in serum detected by frequent sampling were pulsatile. FSH pulse amplitude decreased during seasonal transition, and the decrease in amplitude was associated with the decrease in mean serum FSH concentrations. This decrease in FSH pulse amplitude may reflect an involvement of a follicular product from developing follicles or a change in hypothalamic stimulation of pituitary FSH release.     

Clostridium difficile in association with sporadic diarrhoea.

A total of 154 patients admitted to an infectious diseases unit were included in a year''s prospective survey of sporadic diarrhoeal disease. Stools from 19 of them yielded Clostridium difficile, generally on more than one occasion. Twelve of these patients were assessed as having a severe or moderately severe gastrointestinal illness: Cl difficile was the only pathogen isolated from 10 of them, and two had an associated salmonella infection. Seven had had a recent course of antibiotics, but five had not taken antibiotics. Faeces from seven patients with moderate or mild gastrointestinal illness yielded Cl difficile, and two of these patients also had an associated salmonella infection. Two patients in this group had no antibiotic history. From these findings, the occurrence of C difficile in faeces could not be described as antibiotic-associated. Faecal Cl difficile cytotoxin was detected in only six patients, and generally at low levels. In such patients a more relevant pathogenic index might take account of the numbers of Cl difficile present and of their toxigenic potential.