Both ST and sub-ST were significant diurnal fluctuations with the peak in the early morning (9 h after dim-light melatonin onset time, 2 h after nadir time of core body temperature rhythm), and subjective
sleep duration was estimated to be longer than actual times in all nap intervals (sub-ST>ST). There were significant diurnal fluctuations in discrepancy (sub-ST ST) of TEA during sleep, and the degree of discrepancy correlated positively with increase in the amount of REM sleep and decrease in the amount of slow-wave sleep. These findings suggest that human TEA operates at a certain level of discrepancy during sleep, and that this discrepancy PF299804 nmr might be related to the biological clock and its associated sleep architecture. (C) 2010 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.”
“For infections for which the perceived risk of serious disease is steadily low, the perceived
risk of suffering some vaccine side effects might become the driving force of the vaccine demand. We investigate the dynamics of SIR infections in homogeneously mixing populations where the vaccine uptake is a decreasing function of the current (or past) incidence, or prevalence, of vaccine side effects. We define an appropriate model where vaccine side-effects are modelled as functions of the age since vaccination.
It happens that the vaccine uptake follows its own dynamics independent of epidemiological variables. We show the conditions
under which the vaccine uptake lands on a globally MK-0518 in vitro stable equilibrium, or steadily oscillates, and the implications of such behaviour for the dynamics of epidemiological variables. We finally report some unexpected scenarios caused by trends in vaccine side effects. (C) 2010 Elsevier Ltd. All rights reserved.”
“The neurotoxicity of carbon monoxide (CO) poisoning Selleckchem AG14699 is a significant clinical problem, but its mechanisms remain unclear. Previous studies of CO-exposed rats showed spatial memory disturbances and degradation of myelin basic protein (MBP) in the brain; however, regional localization of the degradation was not analyzed. In the present study, we histologically determined the foci of CO effects in the hippocampus. Wistar rats were exposed to CO for 60 min (1000 ppm for 40 min + 3000 ppm for 20 min) and returned into room air. For histological evaluation, the animals were sacrificed 90 min, 1,7 and 14 days after CO exposure and the brain tissue was analyzed with hematoxylin-eosin (HE), Nissl and Gallyas myelin staining as well as immunohistochemistry for MBP and phosphorylated or nonphosphorylated neurofilament. No histological changes were observed on HE, Nissl or Gallyas staining.