455 research outputs found

    Light-Dependent Behavioral Phenotypes in PER3-Deficient Mice

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    Complete mitochondrial DNA sequence of the tropical hornet Vespa affinis (Insecta, Hymenoptera)

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    We analyzed the complete mitochondrial genome of the Asian tropical hornet Vespa affinis from Ishigaki Island, Japan. It consisted of a circular molecule with 19,109 bp, which is larger to other hornet species e.g. V. velutina. We predicted the genome contained 13 protein-coding, 22 tRNA, and two rRNA genes, along with one A+T-rich control region. The repetitive sequences were confirmed at multiple positions in the non-coding genes. The initiation codons ATA was found in one, ATG in seven, ATT in five genes, while the termination codons TAA and TAG were observed 11 and two genes, respectively. The average AT content of the genome was 78.4%

    Daily and Seasonal Variation in the Spectral Composition of Light Exposure in Humans

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    Light is considered the most potent synchronizer of the human circadian system and exerts many other non-image-forming effects, including those that affect brain function. These effects are mediated in part by intrinsically photosensitive retinal ganglion cells that express the photopigment melanopsin. The spectral sensitivity of melanopsin is greatest for blue light at approximately 480 nm. At present, there is little information on how the spectral composition of light to which people are exposed varies over the 24 h period and across seasons. Twenty-two subjects, aged 22±4 yrs (mean±SD) participated during the winter months (November–February), and 12 subjects aged 25±3 yrs participated during the summer months (April–August). Subjects wore Actiwatch-RGB monitors, as well as Actiwatch-L monitors, for seven consecutive days while living in England. These monitors measured activity and light exposure in the red, green, and blue spectral regions, in addition to broad-spectrum white light, with a 2 min resolution. Light exposure during the day was analyzed for the interval between 09:00 and 21:00 h. The time course of white-light exposure differed significantly between seasons (p = 0.0022), with light exposure increasing in the morning hours and declining in the afternoon hours, and with a more prominent decline in the winter. Overall light exposure was significantly higher in summer than winter (p = 0.0002). Seasonal differences in the relative contribution of blue-light exposure to overall light exposure were also observed (p = 0.0006), in particular during the evening hours. During the summer evenings (17:00–21:00 h), the relative contribution of blue light was significantly higher (p < 0.0001) (40.2±1.1%) than during winter evenings (26.6±0.9%). The present data show that in addition to overall light exposure, the spectral composition of light exposure varies over the day and with season

    The Effect of Different Photoperiods in Circadian Rhythms of Per3

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    The aim of this study was to analyse the circadian behavioural responses of mice carrying a functional knockout of the Per3 gene (Per3(-/-)) to different light : dark (L : D) cycles. Male adult wild- type (WT) and Per3(-/-) mice were kept under 12- hour light : 12hour dark conditions (12L : 12D) and then transferred to either a short or long photoperiod and subsequently released into total darkness. All micewere exposed to both conditions, and behavioural activity datawere acquired through runningwheel activity and analysed for circadian characteristics during these conditions. We observed that, during the transition from 12L : 12D to 16L : 8D, Per3(-/-)mice take approximately one additional day to synchronise to the new L : D cycle compared toWT mice. Under these long photoperiod conditions, Per3(-/-) mice were more active in the light phase. Our results suggest that Per3(-/-) mice are less sensitive to light. the data presented here provides further evidence that Per3 is involved in the suppression of behavioural activity in direct response to light.Biotechnology and Biological Sciences Research Council (BBSRC)Royal Society (Malcolm von Schantz)Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Universidade Federal de São Paulo UNIFESP, Dept Psicobiol, BR-04024002 São Paulo, BrazilUniv Surrey, Fac Hlth & Med Sci, Guildford GU2 5XH, Surrey, EnglandUniv Fed Rio Grande do Norte, UFRN, Dept Fisiol, BR-59072970 Natal, RN, BrazilInst Fed Sudeste Minas Gerais, Barbacena, MG, BrazilUniv São Paulo, Escola Artes Ciencias & Humanidades, São Paulo, BrazilUniversidade Federal de São Paulo UNIFESP, Dept Psicobiol, BR-04024002 São Paulo, BrazilBiotechnology and Biological Sciences Research Council (BBSRC): BB/E003672/1FAPESP: 2007/05037-9FAPESP: CEPID 98/14303-3Web of Scienc

    Circadian period and the timing of melatonin onset in men and women: Predictors of sleep during the weekend and in the laboratory

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    Sleep complaints and irregular sleep patterns, such as curtailed sleep during workdays and longer and later sleep during weekends, are common. It is often implied that differences in circadian period and in entrained phase contribute to these patterns, but few data are available. We assessed parameters of the circadian rhythm of melatonin at baseline and in a forced desynchrony protocol in 35 participants (18 women) with no sleep disorders. Circadian period varied between 23 h 50 min and 24 h 31 min, and correlated positively (n = 31, rs = 0.43, P = 0.017) with the timing of the melatonin rhythm relative to habitual bedtime. The phase of the melatonin rhythm correlated with the Insomnia Severity Index (n = 35, rs = 0.47, P = 0.004). Self-reported time in bed during free days also correlated with the timing of the melatonin rhythm (n = 35, rs = 0.43, P = 0.01) as well as with the circadian period (n = 31, rs = 0.47, P = 0.007), such that individuals with a more delayed melatonin rhythm or a longer circadian period reported longer sleep during the weekend. The increase in time in bed during the free days correlated positively with circadian period (n = 31, rs = 0.54, P = 0.002). Polysomnographically assessed latency to persistent sleep (n = 34, rs = 0.48, P = 0.004) correlated with the timing of the melatonin rhythm when participants were sleeping at their habitual bedtimes in the laboratory. This correlation was significantly stronger in women than in men (Z = 2.38, P = 0.017). The findings show that individual differences in circadian period and phase of the melatonin rhythm associate with differences in sleep, and suggest that individuals with a long circadian period may be at risk of developing sleep problems

    Analysis of circadian pattern reveals tissue-specific alternative transcription in leptin signaling pathway

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    *Background*&#xd;&#xa;It has been previously reported that most mammalian genes display a circadian oscillation in their baseline expression. Consequently, the phase and amplitude of each component of a signal transduction cascade has downstream consequences. &#xd;&#xa;&#xd;&#xa;*Results*&#xd;&#xa;We report our analysis of alternative transcripts in the leptin signaling pathway which is responsible for the systemic regulation of macronutrient storage and energy balance. We focused on the circadian expression pattern of a critical component of the leptin signaling system, suppressor of cytokine signaling 3 (SOCS3). On an Affymetrix GeneChip 430A2 microarray, this gene is represented by three probe sets targeting different regions within the 3&#x2019; end of the last exon. We demonstrate that in murine brown adipose tissue two downstream 3&#x2019; probe sets experience circadian baseline oscillation in counter-phase to the upstream probe set. Such differences in expression patterns are a telltale sign of alternative splicing within the last exon of SOCS3. In contrast, all three probe sets oscillated in a common phase in murine liver and white adipose tissue. This suggests that the regulation of SOCS3 expression in brown fat is tissue specific. Another component of the signaling pathway, Janus kinase (JAK), is directly regulated by SOCS and has alternative transcript probe sets oscillating in counter-phase in a white adipose tissue specific manner.&#xd;&#xa; &#xd;&#xa;*Conclusion*&#xd;&#xa;We hypothesize that differential oscillation of alternative transcripts may provide a mechanism to maintain steady levels of expression in spite of circadian baseline variation

    Is testosterone linked to human aggression? A meta-analytic examination of the relationship between baseline, dynamic, and manipulated testosterone on human aggression

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    Testosterone is often considered a critical regulator of aggressive behaviour. There is castration/replacement evidence that testosterone indeed drives aggression in some species, but causal evidence in humans is generally lacking and/or—for the few studies that have pharmacologically manipulated testosterone concentrations—inconsistent. More often researchers have examined differences in baseline testosterone concentrations between groups known to differ in aggressiveness (e.g., violent vs non-violent criminals) or within a given sample using a correlational approach. Nevertheless, testosterone is not static but instead fluctuates in response to cues of challenge in the environment, and these challenge-induced fluctuations may more strongly regulate situation-specific aggressive behaviour. Here, we quantitatively summarize literature from all three approaches (baseline, change, and manipulation), providing the most comprehensive meta-analysis of these testosterone-aggression associations/effects in humans to date. Baseline testosterone shared a weak but significant association with aggression (r = 0.054, 95% CIs [0.028, 0.080]), an effect that was stronger and significant in men (r = 0.071, 95% CIs [0.041, 0.101]), but not women (r = 0.002, 95% CIs [−0.041, 0.044]). Changes in T were positively correlated with aggression (r = 0.108, 95% CIs [0.041, 0.174]), an effect that was also stronger and significant in men (r = 0.162, 95% CIs [0.076, 0.246]), but not women (r = 0.010, 95% CIs [−0.090, 0.109]). The causal effects of testosterone on human aggression were weaker yet, and not statistically significant (r = 0.046, 95% CIs [−0.015, 0.108]). We discuss the multiple moderators identified here (e.g., offender status of samples, sex) and elsewhere that may explain these generally weak effects. We also offer suggestions regarding methodology and sample sizes to best capture these associations in future work

    Interactions of polymorphisms in different clock genes associated with circadian phenotypes in humans

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    Several studies have shown that mutations and polymorphisms in clock genes are associated with abnormal circadian parameters in humans and also with more subtle non-pathological phenotypes like chronotypes. However, there have been conflicting results, and none of these studies analyzed the combined effects of more than one clock gene. Up to date, association studies in humans have focused on the analysis of only one clock gene per study. Since these genes encode proteins that physically interact with each other, combinations of polymorphisms in different clock genes could have a synergistic or an inhibitory effect upon circadian phenotypes. In the present study, we analyzed the combined effects of four polymorphisms in four clock genes (Per2, Per3, Clock and Bmal1) in people with extreme diurnal preferences (morning or evening). We found that a specific combination of polymorphisms in these genes is more frequent in people who have a morning preference for activity and there is a different combination in individuals with an evening preference for activity. Taken together, these results show that it is possible to detect clock gene interactions associated with human circadian phenotypes and bring an innovative idea of building a clock gene variation map that may be applied to human circadian biology
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