Increased Oxidative Stress in Injured and Ill Elite International Olympic Rowers.

BACKGROUND: Identifying strategies that reduce the risk of illness and injury is an objective of sports science and medicine teams. No studies have examined the relationship between oxidative stress (OS) and illness or injury in international athletes undergoing periods of intensified training and competition. PURPOSE: The authors aimed to identify relationships between illness, injury, and OS. METHODS: A longitudinal, observational study of elite male rowers (n = 10) was conducted over 18 weeks, leading into World Championships. Following a recovery day and a 12-hour fast, hydroperoxides (free oxygen radicals test) and total antioxidant capacity (free oxygen radicals defense) were measured in venous blood, with the ratio calculated as the oxidative stress index (OSI). At all study time points, athletes were independently dichotomized as ill or not ill, injured or not injured. OS data were compared between groups using independent t tests. A Cox proportional hazard model was used to assess the association of OS with injury and illness while adjusting for age and body mass index. RESULTS: Free oxygen radicals defense was lower (P < .02) and OSI was higher (P < .001) with illness than without illness. Free oxygen radicals test and OSI were higher with injury than without injury (P < .001). A 0.5 mmol·L-1 increase in free oxygen radicals defense was associated with a 30.6% illness risk reduction (95% confidence interval, 7%-48%, P = .014), whereas 0.5 unit increase in OSI was related to a 11.3% increased illness risk (95% confidence interval, 1%-23%, P = .036). CONCLUSIONS: OS is increased in injured and ill athletes. Monitoring OS may be advantageous in assessing recovery from and in reducing injury and illness risk given the association.

Effects of two nights partial sleep deprivation on an evening submaximal weightlifting performance; are 1 h powernaps useful on the day of competition?

We have investigated the effects that sleep restriction (3-h sleep during two consecutive nights) have on an evening (17:00 h) submaximal weightlifting session; and whether this performance improves following a 1-h post-lunch powernap. Fifteen resistance-trained males participated in this study. Before the experimental protocol commenced, 1RM bench press and inclined leg press and normative habitual sleep were recorded. Participants were familiarised with the testing protocol, then completed three experimental conditions with two nights of prescribed sleep: (i) Normal (N): retire at 23:00 h and wake at 06:30 h, (ii) partial sleep-deprivation (SD): retire at 03:30 h and wake at 06:30 h and (iii) partial sleep-deprivation with nap (SDN): retire at 03:30 h and wake at 06:30 h with a 1-h nap at 13:00 h. Each condition was separated by at least 7 days and the order of administration was randomised and counterbalanced. Rectal (Trec) and mean skin (Ts) temperatures, Profile of Mood Scores, subjective tiredness, alertness and sleepiness values were measured at 08:00, 11:00, 14:00 and 17:00 h on the day of the weightlifting session. Following the final temperature measurements at 17:00 h, participants completed a 5-min active warm-up before a 'strength' protocol. Participants performed three repetitions of right-hand grip strength, then three repetitions at each incremental load (40%, 60% and 80% of 1RM) for bench press and inclined leg press, with a 5-min recovery in between each repetition. A linear encoder was attached perpendicular to the movement, to the bar used for the exercises. Average power (AP), average force (AF), peak velocity (PV), distance (D) and time-to-peak velocity (tPV) were measured (MuscleLab software) during the concentric phase of the movements for each lift. Data were analysed using general linear models with repeated measures. The main findings were that SD reduced maximal grip (2.7%), bench press (11.2% AP, 3.3% AF and 9.4% PV) and leg press submaximal values (5.7% AP) with a trend for a reduction in AF (3.3% P = 0.06). Furthermore, RPE increased for measures of grip strength, leg and bench press during SD. Following a 1-h powernap (SDN), values of grip and bench press improved to values similar in N, as did tiredness, alertness and sleepiness. There was a main effect for "load" on the bar for both bench and leg press where AP, AF, tPV values increased with load (P < 0.05) and PV decreased from the lightest to the heaviest load for both bench and leg press. An interaction of "load and condition" was present in leg press only, where the rate of change of AP is greater in the N than SD and SDN conditions. In addition, for PV and tPV the rate of change was greater for SDN than N or SD condition values. In summary, SD had a negative effect on grip strength and some components of bench and inclined leg press. The use of a 1-h power nap that ended 3 h before the "strength" assessment had a positive effect on weightlifting performance, subjective mood and ratings of tiredness.

Negative regulation of Caenorhabditis elegans epidermal damage responses by death-associated protein kinase.

Wounding of epidermal layers triggers multiple coordinated responses to damage. We show here that the Caenorhabditis elegans ortholog of the tumor suppressor death-associated protein kinase, dapk-1, acts as a previously undescribed negative regulator of barrier repair and innate immune responses to wounding. Loss of DAPK-1 function results in constitutive formation of scar-like structures in the cuticle, and up-regulation of innate immune responses to damage. Overexpression of DAPK-1 represses innate immune responses to needle wounding. Up-regulation of innate immune responses in dapk-1 requires the TIR-1/p38 signal transduction pathway; loss of function in this pathway synergizes with dapk-1 to drastically reduce adult lifespan. Our results reveal a previously undescribed function for the DAPK tumor suppressor family in regulation of epithelial damage responses.

Limited use of the human patient simulator by nurse faculty: an intervention program designed to increase use.

Underutilization of human patient simulators (HPS) is not only a curricular issue but also a resource allocation problem. The study explored factors contributing to the limited HPS by faculty in a large ADN program. There is limited empirical evidence published to address this phenomenon. The researchers surveyed the faculty to identify their beliefs and challenges with implementing simulation based upon the constructs (attitudes, subjective norms, perceived behavioral control and intent to use) of the Theory of Planned Behavior (TPB). An educational intervention to address these specific challenges was implemented. The intervention had a positive influence on all TPB construct means (attitudes, p < .01; subjective norms, p < .01; perceived behavioral control, p < .01; intent, p < .05). Attitude (beta = .896) was the strongest predictor in explaining intent to use the HPS. This evidenced-based study offers an approach to increasing the use of the HPS by faculty.

Genetic screens for enhancers of brahma reveal functional interactions between the BRM chromatin-remodeling complex and the delta-notch signal transduction pathway in Drosophila.

The Drosophila trithorax group gene brahma (brm) encodes the ATPase subunit of a 2-MDa chromatin-remodeling complex. brm was identified in a screen for transcriptional activators of homeotic genes and subsequently shown to play a global role in transcription by RNA polymerase II. To gain insight into the targeting, function, and regulation of the BRM complex, we screened for mutations that genetically interact with a dominant-negative allele of brm (brm(K804R)). We first screened for dominant mutations that are lethal in combination with a brm(K804R) transgene under control of the brm promoter. In a distinct but related screen, we identified dominant mutations that modify eye defects resulting from expression of brm(K804R) in the eye-antennal imaginal disc. Mutations in three classes of genes were identified in our screens: genes encoding subunits of the BRM complex (brm, moira, and osa), other proteins directly involved in transcription (zerknullt and RpII140), and signaling molecules (Delta and vein). Expression of brm(K804R) in the adult sense organ precursor lineage causes phenotypes similar to those resulting from impaired Delta-Notch signaling. Our results suggest that signaling pathways may regulate the transcription of target genes by regulating the activity of the BRM complex.

The divergent C. elegans ephrin EFN-4 functions inembryonic morphogenesis in a pathway independent of the VAB-1 Eph receptor.

The C. elegans genome encodes a single Eph receptor tyrosine kinase, VAB-1, which functions in neurons to control epidermal morphogenesis. Four members of the ephrin family of ligands for Eph receptors have been identified in C. elegans. Three ephrins (EFN-1/VAB-2, EFN-2 and EFN-3) have been previously shown to function in VAB-1 signaling. We show that mutations in the gene mab-26 affect the fourth C. elegans ephrin, EFN-4. We show that efn-4 also functions in embryonic morphogenesis, and that it is expressed in the developing nervous system. Interestingly, efn-4 mutations display synergistic interactions with mutations in the VAB-1 receptor and in the EFN-1 ephrin, indicating that EFN-4 may function independently of the VAB-1 Eph receptor in morphogenesis. Mutations in the LAR-like receptor tyrosine phosphatase PTP-3 and in the Semaphorin-2A homolog MAB-20 disrupt embryonic neural morphogenesis. efn-4 mutations synergize with ptp-3 mutations, but not with mab-20 mutations, suggesting that EFN-4 and Semaphorin signaling could function in a common pathway or in opposing pathways in C. elegans embryogenesis.