This is an RSS newsfeed from BioMed CentralIt is intended to be used with an RSS reader. For more information about RSS newsfeeds from BioMed Central, visit http://www.biomedcentral.com/info/about/rss/Journal of Circadian Rhythms - Latest articles
http://www.jcircadianrhythms.com
The latest articles from Journal of Circadian Rhythms (ISSN 1740-3391) published by
BioMed Central
Efficacy and hypnotic effects of melatonin in shift-work nurses: double-blind, placebo-controlled crossover trialBackground:
Night work is associated with disturbed sleep and wakefulness, particularly in relation to the night shift. Circadian rhythm sleep disorders are characterized by complaints of insomnia and excessive daytime sleepiness that are primarily due to alterations in the internal circadian timing system or a misalignment between the timing of sleep and the 24-h social and physical environment.
Methods:
We evaluated the effect of oral intake of 5 mg melatonin taken 30 minutes before night time sleep on insomnia parameters as well as subjective sleep onset latency, number of awakenings, and duration of sleep. A double-blind, randomized, placebo-controlled crossover study with periods of 1 night and washouts of 4 days comparing melatonin with placebo tablets was conducted. We tried to improve night-time sleep during recovery from night work. Participants were 86 shift-worker nurses aged 24 to 46 years. Each participant completed a questionnaire immediately after awakening.
Results:
Sleep onset latency was significantly reduced while subjects were taking melatonin as compared with both placebo and baseline. There was no evidence that melatonin altered total sleep time (as compared with baseline total sleep time). No adverse effects of melatonin were noted during the treatment period.
Conclusion:
Melatonin may be an effective treatment for shift workers with difficulty falling asleep.
http://www.jcircadianrhythms.com/content/6/1/10
Khosro Sadeghniiat-Haghighi, Omid Aminian, Gholamreza Pouryaghoub and Zohreh YazdiJournal of Circadian Rhythms 2008, 6:102008-10-29doi:10.1186/1740-3391-6-10Journal of Circadian Rhythms1740-33916102008-10-29Ischemic stroke destabilizes circadian rhythmsBackground:
The central circadian pacemaker is a remarkably robust regulator of daily rhythmic variations of cardiovascular, endocrine, and neural physiology. Environmental lighting conditions are powerful modulators of circadian rhythms, but regulation of circadian rhythms by disease states is less clear. Here, we examine the effect of ischemic stroke on circadian rhythms in rats using high-resolution pineal microdialysis.
Methods:
Rats were housed in LD 12:12 h conditions and monitored by pineal microdialysis to determine baseline melatonin timing profiles. After demonstration that the circadian expression of melatonin was at steady state, rats were subjected to experimental stroke using two-hour intralumenal filament occlusion of the middle cerebral artery. The animals were returned to their cages, and melatonin monitoring was resumed. The timing of onset, offset, and duration of melatonin secretion were calculated before and after stroke to determine changes in circadian rhythms of melatonin secretion. At the end of the monitoring period, brains were analyzed to determine infarct volume.
Results:
Rats demonstrated immediate shifts in melatonin timing after stroke. We observed a broad range of perturbations in melatonin timing in subsequent days, with rats exhibiting onset/offset patterns which included: advance/advance, advance/delay, delay/advance, and delay/delay. Melatonin rhythms displayed prolonged instability several days after stroke, with a majority of rats showing a day-to-day alternation between advance and delay in melatonin onset and duration. Duration of melatonin secretion changed in response to stroke, and this change was strongly determined by the shift in melatonin onset time. There was no correlation between infarct size and the direction or amplitude of melatonin phase shifting.
Conclusion:
This is the first demonstration that stroke induces immediate changes in the timing of pineal melatonin secretion, indicating that cortical and basal ganglia infarction impacts the timing of melatonin rhythms. The heterogeneous direction and amplitude of melatonin shifts suggests that the upstream regulation of hypothalamic timekeeping is likely anatomically diffuse and mechanistically complex. Finally, our study exemplifies the use of pineal microdialysis to evaluate the effect of neurological diseases on circadian function.
http://www.jcircadianrhythms.com/content/6/1/9
He Meng, Tiecheng Liu, Jimo Borjigin and Michael M WangJournal of Circadian Rhythms 2008, 6:92008-10-15doi:10.1186/1740-3391-6-9Journal of Circadian Rhythms1740-3391692008-10-15Variation in nocturnality and circadian activity rhythms between photoresponsive F344 and nonphotoresponsive Sprague Dawley ratsBackground:
Variation in circadian rhythms and nocturnality may, hypothetically, be related to or independent of genetic variation in photoperiodic mediation of seasonal changes in physiology and behavior. We hypothesized that strain variation in photoperiodism between photoperiodic F344 rats and nonphotoperiodic Harlan Sprague Dawley (HSD) rats might be caused by underlying variation in clock function. We predicted that HSD rats would have more activity during the day or subjective day, longer free-running rhythms, poor entrainment to short day length, and shorter duration of activity, traits that have been associated with nonphotoperiodism in other laboratory rodent species, relative to F344 rats. An alternative hypothesis, that differences are due to variation in melatonin secretion or responses to melatonin, predicts either no such differences or inconsistent combinations of differences.
Methods:
We tested these predictions by examining activity rhythms of young male F344 and HSD rats given access to running wheels in constant dark (DD), short day length (L8:D16; SD), and long day length (L16:D8; LD). We compared nocturnality (the proportion of activity during night or subjective night), duration of activity (alpha), activity onset and offset, phase angle of entrainment, and free running rhythms (tau) of F344 and HSD rats.
Results:
HSD rats had significantly greater activity during the day, were sometimes arrhythmic in DD, and had significantly longer tau than F344 rats, consistent with predictions. However, HSD rats had significantly longer alpha than F344 rats and both strains entrained to SD, inconsistent with predictions.
Conclusion:
The ability of HSD rats to entrain to SD, combined with longer alpha than F344 rats, suggests that the circadian system of HSD rats responds correctly to SD. These data offer best support for the alternative hypothesis, that differences in photoresponsiveness between F344 and HSD rats are caused by non-circadian differences in melatonin secretion or the response to melatonin.
http://www.jcircadianrhythms.com/content/6/1/8
Cheryl D Seroka, Cynthia E Johnson and Paul D HeidemanJournal of Circadian Rhythms 2008, 6:82008-09-09doi:10.1186/1740-3391-6-8Journal of Circadian Rhythms1740-3391682008-09-09A new approach to understanding the impact of circadian disruption on human healthBackground:
Light and dark patterns are the major synchronizer of circadian rhythms to the 24-hour solar day. Disruption of circadian rhythms has been associated with a variety of maladies. Ecological studies of human exposures to light are virtually nonexistent, however, making it difficult to determine if, in fact, light-induced circadian disruption directly affects human health.
Methods:
A newly developed field measurement device recorded circadian light exposures and activity from day-shift and rotating-shift nurses. Circadian disruption defined in terms of behavioral entrainment was quantified for these two groups using phasor analyses of the circular cross-correlations between light exposure and activity. Circadian disruption also was determined for rats subjected to a consistent 12-hour light/12-hour dark pattern (12L:12D) and ones subjected to a "jet-lagged" schedule.
Results:
Day-shift nurses and rats exposed to the consistent light-dark pattern exhibited pronounced similarities in their circular cross-correlation functions and 24-hour phasor representations except for an approximate 12-hour phase difference between species. The phase difference reflects the diurnal versus nocturnal behavior of humans versus rodents. Phase differences within species likely reflect chronotype differences among individuals. Rotating-shift nurses and rats subjected to the "jet-lagged" schedule exhibited significant reductions in phasor magnitudes compared to the day-shift nurses and the 12L:12D rats. The reductions in the 24-hour phasor magnitudes indicate a loss of behavioral entrainment compared to the nurses and the rats with regular light-dark exposure patterns.
Conclusion:
This paper provides a quantitative foundation for systematically studying the impact of light-induced circadian disruption in humans and in animal models. Ecological light and activity data are needed to develop the essential insights into circadian entrainment/disruption actually experienced by modern people. These data can now be obtained and analyzed to reveal the interrelationship between actual light exposures and markers of circadian rhythm such as rest-activity patterns, core body temperature, and melatonin synthesis. Moreover, it should now be possible to bridge ecological studies of circadian disruption in humans to parametric studies of the relationships between circadian disruption and health outcomes using animal models.
http://www.jcircadianrhythms.com/content/6/1/7
Mark S Rea, Andrew Bierman, Mariana G Figueiro and John D BulloughJournal of Circadian Rhythms 2008, 6:72008-05-29doi:10.1186/1740-3391-6-7Journal of Circadian Rhythms1740-3391672008-05-29Delayed sleep phase cases and controlsBackground:
Delayed sleep phase disorder (DSPD) is a condition in which patients have difficulty falling asleep before the early morning hours and commonly have trouble awakening before late morning or even early afternoon. Several studies have suggested that variations in habitual bedtime are 40–50% heritable.
Methods:
We recruited a case series of 205 participants, along with 221 controls (DSPD-C) with normal sleep, roughly matched for age, gender, and ancestry. A representative sample of San Diego adults recruited some years before was already available to confirm the control group. Both DSPD and DSPD-C provided blood or saliva samples for DNA and completed extensive questionnaires about sleep habits, sleep history, family history, sleep quality, morningness-eveningness traits, depression, mania, and seasonality of symptoms. The DSPD group wore wrist actigraphs for a median of 13.2 days. The representative sample collected previously had undergone actigraphic recordings, from which 48 hours of data were generally available.
Results:
The DSPD and DSPD-C samples showed almost no overlap on morningness-eveningness scores. DSPD cases went to bed and arose about 3 hours later than the DSPD-C and the representative sample. DSPD cases reported more difficulties with sleep, poorer sleep quality, and more depression, but there was no significant difference in a history of mania. DSPD cases reported more family history of late bedtimes, but female DSPD reported that their fathers' bedtimes were later than the fathers of male DSPD.
Conclusion:
These results indicate a DSPD phenotype is familial and associated with unipolar depression.
http://www.jcircadianrhythms.com/content/6/1/6
Daniel F Kripke, Katharine M Rex, Sonia Ancoli-Israel, Caroline M Nievergelt, Walt Klimecki and John R KelsoeJournal of Circadian Rhythms 2008, 6:62008-04-29doi:10.1186/1740-3391-6-6Journal of Circadian Rhythms1740-3391662008-04-29SCN-AVP release of mPer1/mPer2 double-mutant mice in vitroBackground:
Circadian organisation of behavioural and physiological rhythms in mammals is largely driven by the clock in the suprachiasmatic nuclei (SCN) of the hypothalamus. In this clock, a molecular transcriptional repression and activation mechanism generates near 24 hour rhythms. One of the outputs of the molecular clock in specific SCN neurons is arginine-vasopressin (AVP), which is responsive to transcriptional activation by clock gene products. As negative regulators, the protein products of the period genes are thought to repress transcriptional activity of the positive limb after heterodimerisation with CRYPTOCHROME. When both the Per1 and Per2 genes are dysfunctional by targeted deletion of the PAS heterodimer binding domain, mice lose circadian organization of behaviour upon release into constant environmental conditions. To which degree the period genes are involved in the control of AVP output is unknown.
Methods:
Using an in vitro slice culture setup, SCN-AVP release of cultures made of 10 wildtype and 9 Per1/2 double-mutant mice was assayed. Mice were sacrificed in either the early light phase of the light-dark cycle, or in the early subjective day on the first day of constant dark.
Results:
Here we report that in arrhythmic homozygous Per1/2 double-mutant mice there is still a diurnal peak in in vitro AVP release from the SCN similar to that of wildtypes but distinctively different from the release pattern from the paraventricular nucleus. Such a modulation of AVP release is unexpected in mice where the circadian clockwork is thought to be disrupted.
Conclusion:
Our results suggest that the circadian clock in these animals, although deficient in (most) behavioural and molecular rhythms, may still be (partially) functional, possibly as an hourglass mechanism. The level of perturbation of the clock in Per1/2 double mutants may therefore be less than was originally thought.
http://www.jcircadianrhythms.com/content/6/1/5
Daan R van der Veen, Ellis GA Mulder, Henrik Oster, Menno P Gerkema and Roelof A HutJournal of Circadian Rhythms 2008, 6:52008-03-20doi:10.1186/1740-3391-6-5Journal of Circadian Rhythms1740-3391652008-03-20Period-2: a tumor suppressor gene in breast cancerPrevious reports have suggested that the ablation of the Period 2 gene (Per 2) leads to enhanced development of lymphoma and leukemia in mice. Employing immunoblot analyses, we have demonstrated that PER 2 is endogenously expressed in human breast epithelial cell lines but is not expressed or is expressed at significantly reduced level in human breast cancer cell lines. Expression of PER 2 in MCF-7 breast cancer cells significantly inhibited the growth of MCF-7 human breast cancer cells, and, when PER 2 was co-expressed with the Crytochrome 2 (Cry 2) gene, an even greater growth-inhibitory effect was observed. The inhibitory effect of PER 2 on breast cancer cells was also demonstrated by its suppression of the anchorage-independent growth of MCF-7 cells as evidenced by the reduced number and size of colonies. A corresponding blockade of MCF-7 cells in the G1 phase of the cell cycle was also observed in response to the expression of PER 2 alone or in combination with CRY 2. Expression of PER 2 also induced apoptosis of MCF-7 breast cancer cells as demonstrated by an increase in PARP [poly (ADP-ribose) polymerase] cleavage. Finally, our studies demonstrate that PER 2 expression in MCF-7 breast cancer cells is associated with a significant decrease in the expression of cyclin D1 and an up-regulation of p53 levels.
http://www.jcircadianrhythms.com/content/6/1/4
Shulin Xiang, Seth B Coffelt, Lulu Mao, Lin Yuan, Qi Cheng and Steven M HillJournal of Circadian Rhythms 2008, 6:42008-03-11doi:10.1186/1740-3391-6-4Journal of Circadian Rhythms1740-3391642008-03-11Structural insights into the function of the core-circadian factor TIMING OF CAB2 EXPRESSION 1 (TOC1)Background:
The plant circadian clock has at its core a feedback loop that includes TIMING OF CAB2 EXPRESSION 1 (TOC1). This protein has an as of yet unknown biochemical activity. It has been noted that the extreme amino-terminus of this protein is distantly related in sequence to response regulators (RR), and thus TOC1 is a member of the so-called pseudo response regulator (PRR) family. As well, the extreme carboxy-terminus has a small sequence stretch related to the other PRRs and CONSTANS (CO)-like proteins, and this peptide stretch has been termed the CCT (for CONSTANS, CONSTANS-LIKE, TOC1) domain.
Methods:
To extend further our understanding of the TOC1 protein, we performed a ROSETTA structural prediction on TOC1 orthologues from four plant species. Phylogenetic interpretations assisted in model construction.
Results:
From our models, we suggest that TOC1 is a three-domain protein: TOC1 has an amino-terminal signaling-domain related to response receivers, a carboxy-terminal domain that could participate both in metal binding and in transcriptional regulation, and a linker domain that connects the two.
Conclusion:
The models we present should prove useful in future hypothesis-driven biochemical analyses to test the predictions that TOC1 is a multi-domain signaling component of the plant circadian clock.
http://www.jcircadianrhythms.com/content/6/1/3
Elsebeth Kolmos, Heiko Schoof, Michael Plümer and Seth J DavisJournal of Circadian Rhythms 2008, 6:32008-02-25doi:10.1186/1740-3391-6-3Journal of Circadian Rhythms1740-3391632008-02-25Ovipositional periodicity of caged Anopheles gambiae individualsBackground:
Anopheles gambiae s.s. Giles is a major malaria vector in Sub-Saharan Africa. Studies of the basic biology of this mosquito, including oviposition, provide a background for assessing which attributes might be exploited for suppressing A. gambiae populations. Here, we report on when during the diel cycle A. gambiae individuals deposit eggs as compared to the ovipositional patterns of groups.
Methods:
Battery-powered wall clocks were modified so as to present a unique section of dark and wet ovipositional substrate at hourly intervals over two consecutive 12 h periods. Ovipositional periodicity of mosquito groups (Kisumu laboratory strain or feral females) and individuals was determined by counting the number of eggs present on each section of the ovipositional substrate. Capacity for mid-afternoon oviposition by groups of Kisumu laboratory strain A. gambiae was determined by presenting hypergravid females with an ovipositional substrate exclusively between 1200 and 1600 h.
Results:
On equatorial time, caged laboratory strain A. gambiae groups deposited 65% of their total eggs between 1800 and 0 h, and the remaining 35% were spread between 0 and 1000 h. Caged house-collected A. gambiae groups deposited 74% of their total eggs between 1800 and 200 h, ceased oviposition for 3 h, and then spread the remaining 26% of their eggs near or after dawn. Ninety-six percent of individual A. gambiae females spread their eggs over a continuous 2–4 h period without interruption. In tests of capacity for mid-afternoon oviposition, females given evening access to an ovipositional resource deposited 2% of their total eggs between 1200 and 1700 h. A. gambiae females given only access to an ovipositional resource between 1200 and 1700 h deposited 3 times more eggs during that time period than did females previously given evening access.
Conclusion:
Confined individual A. gambiae oviposit in a single ca. 2–4 h continuous bout per 24 h. Oviposition is most probable in early scotophase, mid scotophase, or early photophase. However, some oviposition can occur at any hour during 24 h, especially if females were previously deprived of ovipositional substrate.
http://www.jcircadianrhythms.com/content/6/1/2
Megan L Fritz, Juan Huang, Edward D Walker, M Nabie Bayoh, John Vulule and James R MillerJournal of Circadian Rhythms 2008, 6:22008-01-25doi:10.1186/1740-3391-6-2Journal of Circadian Rhythms1740-3391622008-01-25Circadian rhythm dysfunction in glaucoma: A hypothesisThe absence of circadian zeitgebers in the social environment causes circadian misalignment, which is often associated with sleep disturbances. Circadian misalignment, defined as a mismatch between the sleep-wake cycle and the timing of the circadian system, can occur either because of inadequate exposure to the light-dark cycle, the most important synchronizer of the circadian system, or reduction in light transmission resulting from ophthalmic diseases (e.g., senile miosis, cataract, diabetic retinopathy, macular degeneration, retinitis pigmentosa, and glaucoma). We propose that glaucoma may be the primary ocular disease that directly compromises photic input to the circadian time-keeping system because of inherent ganglion cell death. Glaucomatous damage to the ganglion cell layer might be particularly harmful to melanopsin. According to histologic and circadian data, a subset of intrinsically photoresponsive retinal ganglion cells, expressing melanopsin and cryptochromes, entrain the endogenous circadian system via transduction of photic input to the thalamus, projecting either to the suprachiasmatic nucleus or the lateral geniculate nucleus. Glaucoma provides a unique opportunity to explore whether in fact light transmission to the circadian system is compromised as a result of ganglion cell loss.
http://www.jcircadianrhythms.com/content/6/1/1
Girardin Jean-Louis, Ferdinand Zizi, Douglas R Lazzaro and Arthur H WolintzJournal of Circadian Rhythms 2008, 6:12008-01-10doi:10.1186/1740-3391-6-1Journal of Circadian Rhythms1740-3391612008-01-10