Effect of menopause on melatonin and alertness rhythms investigated in constant routine conditions

Although studies have reported the effects of the menstrual cycle on melatonin rhythmicity, none has investigated the effects of menopause on the melatonin rhythm. The circadian rhythm in melatonin and its relationship to subjective alertness was investigated in pre- and postmenopausal women under constant routine conditions (controlled posture, dim lighting, calorie intake, temperature, and prolonged wakefulness). Eleven healthy pre-menopausal (42+/-4 yr) and 10 postmenopausal women (55+/-2 yr) participated in the study. Salivary melatonin samples and subjective measures of alertness and sleepiness were assessed hourly during the 22 h constant routine protocol. Postmenopausal women had a significantly earlier melatonin acrophase (1.1+/-0.5 h clock time in decimal h; mean+/-SEM, p<0.05) compared to the pre-menopausal women (2.3+/-0.3 h). There was no significant difference between melatonin onset and amplitude between the pre-menopausal and postmenopausal women. Self-rated alertness declined in both study groups as the length of sleep deprivation increased. Melatonin onset preceded the onset of self-rated sleepiness in both groups. The time interval between melatonin onset and the onset of sleepiness and alertness offset was significantly greater in the postmenopausal women compared to the pre-menopausal women. In conclusion, under controlled experimental conditions the timing of the melatonin rhythm was advanced in postmenopausal women altering its phase relationship to subjective alertness and sleepiness.     

The dynamic ER: experimental approaches and current questions

The endoplasmic reticulum (ER) is an extremely plastic and dynamic organelle. Its size and shape can undergo drastic changes to meet changing demands for ER-related functions, or as a response to drugs or pathogens. Because of the ER's key functions in protein and lipid synthesis, this organelle is a hotbed of detailed molecular analysis.     

NADPH oxidase involvement in the pathology of Helicobacter pylori infection

Neutrophil oxidants are hypothesized to damage the gastric mucosa and promote carcinogenesis in people infected with Helicobacter pylori. To investigate this process we used wild-type and chronic granulomatous disease (CGD) mice with a targeted disruption of the gp91(phox) subunit of the NADPH oxidase. The mice were inoculated with a mouse-adapted strain of H. pylori and changes in gastric pathology were examined 12 and 30 weeks after infection. Glandular atrophy, a precursor lesion in the development of intestinal-type gastric carcinoma, and epithelial cell proliferation were both dramatically increased in the gastric body of CGD animals within 12 weeks. This correlated strongly with increased numbers of neutrophils in the mucosa (Pearson coefficient 0.97, P < 0.001). H. pylori is a noninvasive bacterium, and there was no increase in bacterial numbers in the CGD animals. Closer examination of the gastric tissue indicated the presence of degenerate neutrophils associated with atrophy. We hypothesize that the release of granule constituents from these neutrophils contributes to tissue damage. This is exacerbated by the absence of a functional NADPH oxidase, and is consistent with this enzyme complex having an important role in dampening the inflammatory response.     

The effects of selection,drift and genetic variation on life‐history trait divergence among insular populations of natterjack toad,Bufo calamita

Although loss of genetic variation is frequently assumed to be associated with loss of adaptive potential, only few studies have examined adaptation in populations with little genetic variation. On the Swedish west coast, the northern fringe populations of the natterjack toad Bufo calamita inhabit an atypical habitat consisting of offshore rock islands. There are strong among‐population differences in the amount of neutral genetic variation, making this system suitable for studies on mechanisms of trait divergence along a gradient of within‐population genetic variation. In this study, we examined the mechanisms of population divergence using Q_ST–F_ST comparisons and correlations between quantitative and neutral genetic variation. Our results suggest drift or weak stabilizing selection across the six populations included in this study, as indicated by low Q_ST–F_ST values, lack of significant population × temperature interactions and lack of significant differences among the islands in breeding pond size. The six populations included in this study differed in both neutral and quantitative genetic variation. Also, the correlations between neutral and quantitative genetic variation tended to be positive, however, the relatively small number of populations prevents any strong conclusions based on these correlations. Contrary to the majority of Q_ST–F_ST comparisons, our results suggest drift or weak stabilizing selection across the examined populations. Furthermore, the low heritability of fitness‐related traits may limit evolutionary responses in some of the populations.