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“Objective: Premenstrual symptoms affect the majority of healthy women. Premenstrual symptomatology has earlier been linked to stress and a state-like alteration in the perception of life events in the late-luteal phase of the menstrual cycle. We hypothesised that there is also
a trait-like negative bias in the perception of life events evident throughout the whole cycle which is associated with the likelihood to manifest more marked symptoms in the late-luteal phase of the cycle.
Methods: 88 healthy women completed the PRISM calendar for three consecutive cycles and the Objective and Subjective Event Checklist during the follicular phase of the first cycle. Association between PRISM score change from the follicular through the late-luteal phase and life event variables was investigated by Generalized Linear Model Analysis (GENMOD).
Results: The PRISM Cisplatin cost score change showed a significant negative association with the ratio of positive subjective life events and a significant positive association with the ratio of negative subjective life events. There were no significant results in case of the objective life events.
Conclusion: Our results indicate that women manifesting a more marked increase of symptoms from the late follicular through the late-luteal phase of the menstrual cycle are more likely to notice negative subjective life events and less likely to notice
positive subjective life events. This suggest a trait-like negative bias in the perception of life events present throughout the whole reproductive cycle which may play an important role in the emergence of premenstrual symptoms. (C) 2010 Elsevier Inc. click here All rights reserved.”
“The generation of
reactive oxygen species causes cellular oxidative damage, and has been implicated in the etiology many of Alzheimer’s disease (AD). L-NNNBP, a new chiral pyrrolyl alpha-nitronyl nitroxide radical synthesized in our department, shows potential antioxidant effects. The purpose of this study was to investigate the protective effects of L-NNNBP on beta-amyloid (A beta) deposition and memory deficits in an AD model of APP/PS1 mice. In cultured cortical neurons, L-NNNBP acted as an antioxidant by quenching reactive oxygen species, inhibiting lipid peroxidation, nitrosative stress, and stimulating cellular antioxidant defenses. L-NNNBP inhibited cell apoptosis induced by A beta exposure. In vivo treatment with L-NNNBP for 1 month induced a marked decrease in brain A beta deposition and tau phosphorylation in the blinded study on APP/PS1 transgenic mice (1 mM in drinking water, initiated when the mice were 6 months old). The L-NNNBP-treated APP/PS1 mice showed decreased astrocyte activation and improved spatial learning and memory compared with the vehicle-treated APP/PS1 mice. These actions were more potent compared with that of curcumin, a natural product, and TEMPO, a nitroxide radical, which are used as free radical scavengers in clinics.