876 resultados para sleep laboratory


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This work describes the phenology of Spalangia endius Walker in pupae of Musca domestica Linnaeus under laboratory conditions. In order to understand the developmental cycle of Spalangia endius under laboratory conditions, 360 Musca domestica pupae aged from 24 to 48 hours were exposed to 15 S. endius pairs for a period of 24 hours at 26 ± 2ºC. These pupae were kept in a BOD incubator at the same temperature, with a relative humidity of <70%, and 12 hours photophase. Fifteen hymenopteran specimens were dissected daily to evaluate their stage and development time. The phenology concluded that S. endius had a development cycle of 19 days with an incubation period of 24 hours. The development of the larvae of S. endius occurred in the subsequent eight days, during which a series of morphological alterations were observed. The pre-pupal stage occurred on the tenth day, where the movement ceased and elimination of the meconium started. The pupal stage occurred from the 11th to the 19th day, with emergence of males first, followed by female emergence approximately 24 hours later. These results allowed the evaluation of aspects of the detailed bionomics of the development of S. endius in order to record and program production of this parasitoid, thus optimizing its utilization as a biological control agent.

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Patent foramen ovale and obstructive sleep apnoea are frequently encountered in the general population. Owing to their prevalence, they may coexist fortuitously; however, the prevalence of patent foramen ovale seems to be higher in patients with obstructive sleep apnoea. We have reviewed the epidemiological data, pathophysiology, and the diagnostic and therapeutic options for both patent foramen ovale and obstructive sleep apnoea. We focus on the interesting pathophysiological links that could explain a potential association between both pathologies and their implications, especially on the risk of stroke.

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Biotic potential and reprodutcive parameters of Spodoptera eridania (Stoll) (Lepidoptera, Noctuidae) in the laboratory: This study aimed to evaluate the biotic potential and reproductive parameters of Spodoptera eridania (Stoll, 1782) under controlled conditions (25 ± 1ºC, 70 ± 10% RH and 14 hour photophase). The longevity, pre-, post- and oviposition periods, fecundity and fertility of 15 couples was evaluated. The longevity of females (10.80 days) was not significantly higher than those of males (9.27 days). The mean durations of the pre, post and oviposition periods were 2.067, 0.600 and 8.133 days, respectively. The mean fecundity per female was 1,398 eggs and the mean fertility was 1,367.50 larvae. On average, females copulated 1.133 times. A strong positive correlation was observed between the number of mating and fecundity (r = 0.881, P <0.001). However a strong negative correlation was observed between the number of copulations and the duration of the pre-oviposition period (r = -0.826, P = 0.002) and longevity (r = -0.823, P = 0.001). The biotic potential of S. eridania was estimated at 1.894 x 10(25) individuals/female/year. The net reproductive rate (Ro) was 560.531 times per generation and the mean generation time (T) was 35.807 days. The intrinsic rate of increase (rm) was 0.177, with a finite rate of increase (l) of 1.193, per week

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New method for rearing Spodoptera frugiperda in laboratory shows that larval cannibalism is not obligatory. Here we show, for the first time, that larvae of the fall armyworm (FAW), Spodoptera frugiperda (Lepidoptera, Noctuidae), can be successfully reared in a cohort-based manner with virtually no cannibalism. FAW larvae were reared since the second instar to pupation in rectangular plastic containers containing 40 individuals with a surprisingly ca. 90% larval survivorship. Adult females from the cohort-based method showed fecundity similar to that already reported on literature for larvae reared individually, and fertility higher than 99%, with the advantage of combining economy of time, space and material resources. These findings suggest that the factors affecting cannibalism of FAW larvae in laboratory rearings need to be reevaluated, whilst the new technique also show potential to increase the efficiency of both small and mass FAW rearings.

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Bioactivity of the latex from Parahancornia amapa (Apocynaceae) on the development of Rhodnius nasutus (Hemiptera, Reduviidae, Triatominae) under laboratory conditions. The aim of this study was to verify the effects of the methanolic fraction of the latex from Parahancornia amapa (Apocynaceae) (PALAM) on individuals of the species Rhodnius nasutus Stål (Hemiptera, Triatominae). Many of the insects treated with the substance presented deformities and these may interfere in the feeding and possibly hinder the reproductive capacity. They also presented significant mortality during the molt when compared to the control group, noting a gradual increase in mortality. The treated insects also presented delayed nymphal development (5th instar) and higher adult longevity.

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Nyssomyia whitmani (Antunes and Coutinho, 1939) has been considered as a complex of cryptic species, and some of the populations of this complex plays an important role in the transmission of Leishmania spp. in Brazil. The present study reports the biological aspects concerning the productivity out of eggs and the development time of the descendants of females obtained in Dourados municipality, Mato Grosso do Sul state. The females were captured with modified electric aspirators, fed in hamsters and further individualized in containers for breeding. At the insectary, temperature and relative humidity were maintained on average of 24.5 °C and 67.3%, respectively. From 944 females 3737 eggs were obtained, 748 (20.0%) evolved to the stage of larvae, and 93 (12.4%) of these reached adult stage. The life cycle lasted 80.6 days and the last larval instar was the longest. The use of a higher protein diet revealed a significant improvement in larval development.

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Report on a special investigation of the UNI Malcolm Price Laboratory School for the period July 1, 2006 through March 31, 2009

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There are many case reports of serious complications and death among obstructive sleep apnea patients (OSA) during general anesthesia or postoperative analgesia. Sedatives and anesthetic agents, pharyngeal anatomy of these patients, opiates given for analgesia, and post operative REM sleep rebound represent potential hazards for general anesthesia in OSA patients. Ideally these patients should be treated with continuous positive airway pressure (CPAP) during premedication, directly after extubation and during postoperative analgesia. Unfortunately, only about 20% of these patients are diagnosed before surgery. A special attention should be given to the symptoms and signs suggestive of OSA during preoperative visits. Screening tests should be performed in patients with suspected OSA and, if positive, a treatment should be initiated.

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The life history of the fruit fly (Drosophila melanogaster) is well understood, but fitness components are rarely measured by following single individuals over their lifetime, thereby limiting insights into lifetime reproductive success, reproductive senescence and post-reproductive lifespan. Moreover, most studies have examined long-established laboratory strains rather than freshly caught individuals and may thus be confounded by adaptation to laboratory culture, inbreeding or mutation accumulation. Here, we have followed the life histories of individual females from three recently caught, non-laboratory-adapted wild populations of D. melanogaster. Populations varied in a number of life-history traits, including ovariole number, fecundity, hatchability and lifespan. To describe individual patterns of age-specific fecundity, we developed a new model that allowed us to distinguish four phases during a female's life: a phase of reproductive maturation, followed by a period of linear and then exponential decline in fecundity and, finally, a post-ovipository period. Individual females exhibited clear-cut fecundity peaks, which contrasts with previous analyses, and post-peak levels of fecundity declined independently of how long females lived. Notably, females had a pronounced post-reproductive lifespan, which on average made up 40% of total lifespan. Post-reproductive lifespan did not differ among populations and was not correlated with reproductive fitness components, supporting the hypothesis that this period is a highly variable, random 'add-on' at the end of reproductive life rather than a correlate of selection on reproductive fitness. Most life-history traits were positively correlated, a pattern that might be due to genotype by environment interactions when wild flies are brought into a novel laboratory environment but that is unlikely explained by inbreeding or positive mutational covariance caused by mutation accumulation.

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We hypothesized that a function of sleep is to replenish brain glycogen stores that become depleted while awake. We have previously tested this hypothesis in three inbred strains of mice by measuring brain glycogen after a 6h sleep deprivation (SD). Unexpectedly, glycogen content in the cerebral cortex did not decrease with SD in two of the strains and was even found to increase in mice of the C57BL/6J (B6) strain. Manipulations that initially induce glycogenolysis can also induce subsequent glycogen synthesis thereby elevating glycogen content beyond baseline. It is thus possible that in B6 mice, cortical glycogen content decreased early during SD and became elevated later in SD. In the present study, we therefore measured changes in brain glycogen over the course of a 6 h SD and during recovery sleep in B6 mice. We found no evidence of a decrease at any time during the SD, instead, cortical glycogen content monotonically increased with time-spent-awake and, when sleep was allowed, started to revert to control levels. Such a time-course is opposite to the one predicted by our initial hypothesis. These results demonstrate that glycogen synthesis can be achieved during prolonged wakefulness to the extent that it outweighs glycogenolysis. Maintaining this energy store seems thus not to be functionally related to sleep in this strain.

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The contribution of genes, environment and gene-environment interactions to sleep disorders is increasingly recognized. Well-documented familial and twin sleep disorder studies suggest an important influence of genetic factors. However, only few sleep disorders have an established genetic basis including four rare diseases that may result from a single gene mutation: fatal familial insomnia, familial advanced sleep-phase syndrome, chronic primary insomnia, and narcolepsy with cataplexy. However, most sleep disorders are complex in terms of their genetic susceptibility together with the variable expressivity of the phenotype even within a same family. Recent linkage, genome-wide and candidate gene association studies resulted in the identification of gene mutations, gene localizations, or evidence for susceptibility genes and/or loci in several sleep disorders. Molecular techniques including mainly genome-wide linkage and association studies are further required to identify the contribution of new genes. These identified susceptibility genetic determinants will provide clues to better understand pathogenesis of sleep disorders, to assess the risk for diseases and also to find new drug targets to treat and to prevent the underlying conditions. We reviewed here the role of genetic basis in most of key sleep disorders.

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ABSTRACT: BACKGROUND: One central concept in evolutionary ecology is that current and residual reproductive values are negatively linked by the so-called cost of reproduction. Previous studies examining the nature of this cost suggested a possible involvement of oxidative stress resulting from the imbalance between pro- and anti-oxidant processes. Still, data remain conflictory probably because, although oxidative damage increases during reproduction, high systemic levels of oxidative stress might also constrain parental investment in reproduction. Here, we investigated variation in oxidative balance (i.e. oxidative damage and antioxidant defences) over the course of reproduction by comparing female laboratory mice rearing or not pups. RESULTS: A significant increase in oxidative damage over time was only observed in females caring for offspring, whereas antioxidant defences increased over time regardless of reproductive status. Interestingly, oxidative damage measured prior to reproduction was negatively associated with litter size at birth (constraint), whereas damage measured after reproduction was positively related to litter size at weaning (cost). CONCLUSIONS: Globally, our correlative results and the review of literature describing the links between reproduction and oxidative stress underline the importance of timing/dynamics when studying and interpreting oxidative balance in relation to reproduction. Our study highlights the duality (constraint and cost) of oxidative stress in life-history trade-offs, thus supporting the theory that oxidative stress plays a key role in life-history evolution.

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Humans spend one third of their life sleeping, then we could raise the basic question: Why do we sleep? Despite the fact that we still don't fully understand its function, we made much progress in understanding at different levels how sleep is regulated. One model suggests that sleep is regulated by two processes: a homeostatic process that tracks the need for sleep and by a circadian rhythm that determines the preferred time-of-day sleep occurs. At the molecular level circadian rhythms are a property of interlocking transcriptional regula-tors referred to as clock genes. The heterodimeric transcription factors BMAL1::CLOCK/NPAS2 drive the transcription of many target genes including the clock genes Cryptochome1 (Cry1), Cry2, Period1 (Per1), and Per2. The encoded CRY/PER proteins are transcriptional inhibitors of BMAL1::CLOCK/NPAS2 thereby providing negative feedback to their own transcription. These genes seem, however, also involved in sleep homeostasis because the brain expression of clock genes, es-pecially that of Per2, increase as a function of time-spent-awake and because mice lacking clock genes display altered sleep homeostasis. The aim of first part of my doctoral work has been to advance our understanding the link that exists between sleep homeostasis and circadian rhythms investigating a possible mechanism by which sleep deprivation could alter clock gene expression by quantifying DNA-binding of the core-clock genes BMAL1, CLOCK and NPAS2 to their target chromatin loci including the E-box enhancers of the Per2 promoter. We made use of chromatin immunoprecipitation (ChIP) and quantitative poly-merase chain reaction (qPCR) to show that DNA-binding of CLOCK and BMAL1 to their target genes changes as a function of time-of-day in both liver and cerebral cortex. We then performed a 6h sleep deprivation (SD) and observed a significant decrease in DNA-binding of CLOCK and BMAL1 to Dbp. This is consistent with a decrease in Dbp mRNA levels after SD. The DNA-binding of NPAS2 and BMAL1 to Per2 was similarly decreased following SD. However, SD has been previously shown to in-crease Per2 expression in the cortex which seems paradoxical. Our results demonstrate that sleep-wake history can affect the molecular clock machinery directly at the level of the chromatin thereby altering the cortical expression of Dbp and Per2, and likely other targets. However, the precise dy-namic relationship between DNA-binding and mRNA expression, especially for Per2, remains elusive. The second aim of my doctoral work has been to perform an in depth characterization of cir-cadian rhythmicity, sleep architecture, analyze the response to SD in full null-Per2 knock-out (Per2-/-) mice, and Per1-/- mice, as well as their double knock-out offspring (Per1,2-/-) and littermate wildtype (Wt) mice. The techniques used include locomotor activity recording by passive infrared (PIR) sen-sors, EEG/EMG surgery, recording, and analysis, and cerebral cortex extraction and quantification of mRNA levels by qPCR. Under standard LD12:12 conditions, we found that wakefulness onset, as well as the time courses of clock gene expression in the brain and corticosterone plasma levels were ad-vanced by about 2h in Per2-/- mice compared to Wt mice. When released under constant dark condi-tions almost all Per2-/- mice (97%) became arrhythmic immediately. From these observations, we conclude that while Per2-/- mice seem to be able to anticipate dark onset, this does not result from a self-sustained circadian clock. Our results suggest instead that the earlier onset of activity results from a labile, not-self sustained 22h rhythm linked to light onset suggesting the existence of a light-driven rhythm. Analyses of sleep under LD12:12 conditions revealed that in both Per2-/- and Per1,2-/- mice the same sleep phenotypes are observed compared to Wt mice: increased NREM sleep frag-mentation and inability to adequately compensate the loss of NREM sleep. That suggests a possible role of PER2 in sleep consolidation and recovery.