27 research outputs found
Anticipating Spring: Wild Populations of Great Tits (Parus major) Differ in Expression of Key Genes for Photoperiodic Time Measurement
Measuring day length is critical for timing annual changes in physiology and behavior in many species. Recently, rapid changes in several photoperiodically-controlled genes following exposure to a single long day have been described. Components of this ‘first day release’ model have so far only been tested in highly domesticated species: quail, sheep, goats and rodents. Because artificial selection accompanying domestication acts on genes related to photoperiodicity, we must also study this phenomenon in wild organisms for it to be accepted as universal. In a songbird, the great tit (Parus major), we tested whether a) these genes are involved in photoperiodic time measurement (PTM) in a wild species, and b) whether predictable species and population differences in expression patterns exist. Using quantitative RT-PCR, we compared gene expression after a single long day in male great tits from Sweden (57°42′N) with that from a German (47°43′N) population. Hypothalamic gene expression key for PTM changed only in the northern population, and occurred earlier after dawn during the single long day than demonstrated in quail; however, gonadotropins (secretion and synthesis) were stimulated in both populations, albeit with different timing. Our data are the first to show acute changes in gene expression in response to photostimulation in any wild species not selected for study of photoperiodism. The pronounced differences in gene expression in response to a single long day between two populations raise exciting new questions about potential environmental selection on photoperiodic cue sensitivity
Brake response time before and after total knee arthroplasty: a prospective cohort study
<p>Abstract</p> <p>Background</p> <p>Although the numbers of total knee arthroplasty (TKA) are increasing, there is only a small number of studies investigating driving safety after TKA. The parameter 'Brake Response Time (BRT)' is one of the most important criteria for driving safety and was therefore chosen for investigation.</p> <p>The present study was conducted to test the hypotheses that patients with right- or left-sided TKA show a significant increase in BRT from pre-operative (pre-op, 1 day before surgery) to post-operative (post-op, 2 weeks post surgery), and a significant decrease in BRT from post-op to the follow-up investigation (FU, 8 weeks post surgery). Additionally, it was hypothesized that the BRT of patients after TKA is significantly higher than that of healthy controls.</p> <p>Methods</p> <p>31 of 70 consecutive patients (mean age 65.7 +/- 10.2 years) receiving TKA were tested for their BRT pre-op, post-op and at FU. BRT was assessed using a custom-made driving simulator. We used normative BRT data from 31 healthy controls for comparison.</p> <p>Results</p> <p>There were no significant increases between pre-op and post-op BRT values for patients who had undergone left- or right-sided TKA. Even the proportion of patients above a BRT threshold of 700 ms was not significantly increased postop. Controls had a BRT which was significantly better than the BRT of patients with right- or left-sided TKA at all three time points.</p> <p>Conclusion</p> <p>The present study showed a small and insignificant postoperative increase in the BRT of patients who had undergone right- or left-sided TKA. Therefore, we believe it is not justified to impair the patient's quality of social and occupational life post-surgery by imposing restrictions on driving motor vehicles beyond an interval of two weeks after surgery.</p
Natural Selection Against a circadian clock gene mutation in mice
Circadian rhythms with an endogenous period close or equal to the natural light-dark cycle are considered evolutionarily adaptive (‘circadian resonance hypothesis’). Despite remarkable insight into the molecular mechanisms driving circadian cycles, this hypothesis has not been tested under natural conditions for any eukaryotic organism. We tested this in mice bearing a short-period mutation in the enzyme casein kinase 1 (tau mutation) which accelerates free-running circadian cycles. We compared daily activity (feeding) rhythms, survivorship and reproduction in six replicate populations in outdoor experimental enclosures, established with wild-type, hetero- or homozygous mice in a Mendelian ratio. In the release cohort, survival was reduced in the homozygote mutant mice revealing strong selection against short-period genotypes. Over the course of 14 months, the relative frequency of the tau allele dropped from initial parity to 20%. Adult survival and recruitment of juveniles into the population contributed about equally to the selection for wild type alleles. The expression of activity during daytime varied throughout the experiment and was significantly increased by the tau mutation. The strong selection against the short-period tau allele observed here contrasts with earlier studies showing absence of selection against a Per2 mutation, which disrupts internal clock function, but does not change period length. These findings are consistent with, and predicted by the theory that resonance of the circadian system plays an important role in individual fitness
Effect of polar day on plasma profiles of melatonin, testosterone, and estradiol in high-arctic Lapland longspurs
Food as a Circadian Zeitgeber for House Sparrows: The Effect of Different Food Access Durations
Simvastatin-induced endothelial cell detachment and microparticle release are prenylation dependent
Statins reduce cardiovascular disease risk and affect endothelial function by cholesterol-dependent and independent mechanisms. Recently, circulating (detached) endothelial cells and endothelial microparticles (EMP) have been associated with endothelial functioning in vitro and in vivo. We investigated whether simvastatin affects endothelial detachment and release of EMP. Human umbilical vein endothelial cells (HUVECs) were incubated with clinically relevant concentrations of simvastatin (1.0 and 5.0 microM), with or without mevalonic acid (100 microM) or geranylgeranylpyrophosphate (GGPP; 20 microM) for 24 hours, and analyzed by flowcytometry and Western blot. Simvastatin at 1.0 and 5.0 microM increased cell detachment from 12.5+/-4.1% to 26.0+/-7.6% (p=0.013) and 28.9 +/- 2.2% (p=0.002) as well as EMP release (p=0.098 and p=0.041, respectively). The majority of detached cells was apoptotic, although the fraction of detached cells that showed signs of apoptosis (>70%) was unaffected by simvastatin. Detached cells and EMP contained caspase 3 and caspase 8, but not caspase 9. Restoring either cholesterol biosynthesis and prenylation (mevalonate) or prenylation alone (GGPP) reversed all simvastatin-induced effects on cell detachment and EMP release. Adherent cells showed no signs of simvastatin-induced apoptosis. Simvastatin promotes detachment and EMP release by inhibiting prenylation, presumably via a caspase 8-dependent mechanism. We hypothesize that by facilitating detachment and EMP release, statins improve the overall condition of the remaining vascular endotheliu
Mid-line sagittal drawing (adapted from [42]) of a passerine brain.
<p>Dashed vertical lines represent approximate starting and ending points of tissue punches through the 3 mm of hypothalamus. Tissue punches were collected on alternating right and left sides of each section beginning at approximately A3.5 and ending at approximately A0.5.</p
Schematic demonstrating the potential modes of action of T3 to elicit GnRH release at the median eminence
<p>(<b>at 11 hrs</b>) <b>and later</b> (<b>at 18 hrs</b>) <b>on GnRH cell bodies in the preoptic area</b> (<b>POA</b>). T3 could act directly on the pituitary (1) or on GnRH terminals in the ME (2), causing release of GnRH there, or on glial cells causing retraction and then allowing localized release of GnRH in the fiber terminals (3). Several hours later, photostimulation causes up-regulation of GnRH expression potentially from action of T3 on tanycytes surrounding the third ventricle that send a signal to GnRH neurons (4), or from diffusion of locally produced T3 to the POA (5) or via a totally separate mechanism (6).</p