The Luminosity Function of Galaxies in Compact Groups

From R-band images of 39 Hickson compact groups (HCGs), we use galaxy counts to determine a luminosity function extending to M_R=-14.0, approximately two magnitudes deeper than previous compact group luminosity functions. We find that a single Schechter function is a poor fit to the data, so we fit a composite function consisting of separate Schechter functions for the bright and faint galaxies. The bright end is best fit with M^*=-21.6 and alpha=-0.52 and the faint end with M^*=-16.1 and alpha=-1.17. The decreasing bright end slope implies a deficit of intermediate luminosity galaxies in our sample of HCGs and the faint end slope is slightly steeper than that reported for earlier HCG luminosity functions. Furthermore, luminosity functions of subsets of our sample reveal more substantial dwarf populations for groups with x-ray halos, groups with tidal dwarf candidates, and groups with a dominant elliptical or lenticular galaxy. Collectively, these results support the hypothesis that within compact groups, the initial dwarf galaxy population is replenished by "subsequent generations" formed in the tidal debris of giant galaxy interactions.Comment: 26 pages, to be published in The Astrophysical Journal, 8 greyscale plates (figures 1 and 2) can be retrieved at http://www.astro.psu.edu/users/sdh/pubs.htm

Design of a valid simulation for researching physical, physiological and cognitive performance in volunteer firefighters during bushfire deployment.

Every year, Australian firefighters protect our nation from the devastation of bushfire. Understanding the impact of consecutive long shifts in hot, smoky conditions is essential for making decisions during campaign fires. At present, the evidence-base for such decisions is limited to laboratory studies with little relevance to bushfire suppression or field research where the impact of environmental and workload stressors cannot be measured. To counter these limitations, we have developed a three-day simulation that mimics the work and environment of campaign bushfire suppression. Construction of the simulation involved three stages; 1) data collection and analysis; 2) design and development; and 3) trial and refinement. The frequency, intensity, duration and type of physical work performed on the fireground is well documented and a modified applied cognitive task analysis, using experienced firefighters was used as a framework to describe in detail the non-physical aspects of the work. The design and development of the simulation incorporated the physical and non-physical aspects of the work into simulated tasks. Finally, experienced firefighters participated in trials of the simulation and reviewed digital recordings to ensure that the simulation accurately represented campaign bushfire suppression work. The outcome of this project is a valid, realistic, and reliable simulation of the physiological, physical and cognitive aspects of a volunteer firefighter on a three-day bushfire deployment.<br /

Exercising Caution Upon Waking–Can Exercise Reduce Sleep Inertia?

Sleep inertia, the transitional state of reduced alertness and impaired cognitive performance upon waking, is a safety risk for on-call personnel who can be required to perform critical tasks soon after waking. Sleep inertia countermeasures have previously been investigated; however, none have successfully dissipated sleep inertia within the first 15 min following waking. During this time, on-call personnel could already be driving, providing advice, or performing other safety-critical tasks. Exercise has not yet been investigated as a sleep inertia countermeasure but has the potential to stimulate the key physiological mechanisms that occur upon waking, including changes in cerebral blood flow, the cortisol awakening response, and increases in core body temperature. Here, we examine these physiological processes and hypothesize how exercise can stimulate them, positioning exercise as an effective sleep inertia countermeasure. We then propose key considerations for research investigating the efficacy of exercise as a sleep inertia countermeasure, including the need to determine the intensity and duration of exercise required to reduce sleep inertia, as well as testing the effectiveness of exercise across a range of conditions in which the severity of sleep inertia may vary. Finally, practical considerations are identified, including the recommendation that qualitative field-based research be conducted with on-call personnel to determine the potential constraints in utilizing exercise as a sleep inertia countermeasure in real-world scenarios

Exercising Caution Upon Waking–Can Exercise Reduce Sleep Inertia?

Sleep inertia, the transitional state of reduced alertness and impaired cognitive performance upon waking, is a safety risk for on-call personnel who can be required to perform critical tasks soon after waking. Sleep inertia countermeasures have previously been investigated; however, none have successfully dissipated sleep inertia within the first 15 min following waking. During this time, on-call personnel could already be driving, providing advice, or performing other safety-critical tasks. Exercise has not yet been investigated as a sleep inertia countermeasure but has the potential to stimulate the key physiological mechanisms that occur upon waking, including changes in cerebral blood flow, the cortisol awakening response, and increases in core body temperature. Here, we examine these physiological processes and hypothesize how exercise can stimulate them, positioning exercise as an effective sleep inertia countermeasure. We then propose key considerations for research investigating the efficacy of exercise as a sleep inertia countermeasure, including the need to determine the intensity and duration of exercise required to reduce sleep inertia, as well as testing the effectiveness of exercise across a range of conditions in which the severity of sleep inertia may vary. Finally, practical considerations are identified, including the recommendation that qualitative field-based research be conducted with on-call personnel to determine the potential constraints in utilizing exercise as a sleep inertia countermeasure in real-world scenarios

Dynamic and Regulated Association of Caveolin with Lipid Bodies: Modulation of Lipid Body Motility and Function by a Dominant Negative Mutant

Caveolins are a crucial component of caveolae but have also been localized to the Golgi complex, and, under some experimental conditions, to lipid bodies (LBs). The physiological relevance and dynamics of LB association remain unclear. We now show that endogenous caveolin-1 and caveolin-2 redistribute to LBs in lipid loaded A431 and FRT cells. Association with LBs is regulated and reversible; removal of fatty acids causes caveolin to rapidly leave the lipid body. We also show by subcellular fractionation, light and electron microscopy that during the first hours of liver regeneration, caveolins show a dramatic redistribution from the cell surface to the newly formed LBs. At later stages of the regeneration process (when LBs are still abundant), the levels of caveolins in LBs decrease dramatically. As a model system to study association of caveolins with LBs we have used brefeldin A (BFA). BFA causes rapid redistribution of endogenous caveolins to LBs and this association was reversed upon BFA washout. Finally, we have used a dominant negative LB-associated caveolin mutant (cavDGV) to study LB formation and to examine its effect on LB function. We now show that the cavDGV mutant inhibits microtubule-dependent LB motility and blocks the reversal of lipid accumulation in LBs

TRPV4 mediates cell damage induced by hyperphysiological compression and regulates COX2/PGE2 in intervertebral discs

Background Aberrant mechanical loading of the spine causes intervertebral disc (IVD) degeneration and low back pain. Current therapies do not target the mediators of the underlying mechanosensing and mechanotransduction pathways, as these are poorly understood. This study investigated the role of the mechanosensitive transient receptor potential vanilloid 4 (TRPV4) ion channel in dynamic compression of bovine nucleus pulposus (NP) cells in vitro and mouse IVDs in vivo. Methods Degenerative changes and the expression of the inflammatory mediator cyclooxygenase 2 (COX2) were examined histologically in the IVDs of mouse tails that were dynamically compressed at a short repetitive hyperphysiological regime (vs sham). Bovine NP cells embedded in an agarose-collagen hydrogel were dynamically compressed at a hyperphysiological regime in the presence or absence of the selective TRPV4 antagonist GSK2193874. Lactate dehydrogenase (LDH) and prostaglandin E2 (PGE2) release, as well as phosphorylation of mitogen-activated protein kinases (MAPKs), were analyzed. Degenerative changes and COX2 expression were further evaluated in the IVDs of trpv4-deficient mice (vs wild-type; WT). Results Dynamic compression caused IVD degeneration in vivo as previously shown but did not affect COX2 expression. Dynamic compression significantly augmented LDH and PGE2 releases in vitro, which were significantly reduced by TRPV4 inhibition. Moreover, TRPV4 inhibition during dynamic compression increased the activation of the extracellular signal-regulated kinases 1/2 (ERK) MAPK pathway by 3.13-fold compared to non-compressed samples. Trpv4-deficient mice displayed mild IVD degeneration and decreased COX2 expression compared to WT mice. Conclusions TRPV4 therefore regulates COX2/PGE2 and mediates cell damage induced by hyperphysiological dynamic compression, possibly via ERK. Targeted TRPV4 inhibition or knockdown might thus constitute promising therapeutic approaches to treat patients suffering from IVD pathologies caused by aberrant mechanical stress

The impact of sleep restriction and simulated physical firefighting work on acute inflammatory stress responses

OBJECTIVES: This study investigated the effect restricted sleep has on wildland firefighters\u27 acute cytokine levels during 3 days and 2 nights of simulated physical wildfire suppression work. METHODS: Firefighters completed multiple days of physical firefighting work separated by either an 8-h (Control condition; n = 18) or 4-h (Sleep restriction condition; n = 17) sleep opportunity each night. Blood samples were collected 4 times a day (i.e., 06:15, 11:30, 18:15, 21:30) from which plasma cytokine levels (IL-6, IL-8, IL-1&beta;, TNF-&alpha;, IL-4, IL-10) were measured. RESULTS: The primary findings for cytokine levels revealed a fixed effect for condition that showed higher IL-8 levels among firefighters who received an 8-h sleep each night. An interaction effect demonstrated differing increases in IL-6 over successive days of work for the SR and CON conditions. Fixed effects for time indicated that IL-6 and IL-4 levels increased, while IL-1&beta;, TNF-&alpha; and IL-8 levels decreased. There were no significant effects for IL-10 observed. CONCLUSION: Findings demonstrate increased IL-8 levels among firefighters who received an 8-h sleep when compared to those who had a restricted 4-h sleep. Firefighters\u27 IL-6 levels increased in both conditions which may indicate that a 4-h sleep restriction duration and/or period (i.e., 2 nights) was not a significant enough stressor to affect this cytokine. Considering the immunomodulatory properties of IL-6 and IL-4 that inhibit pro-inflammatory cytokines, the rise in IL-6 and IL-4, independent of increases in IL-1&beta; and TNF-&alpha;, could indicate a non-damaging response to the stress of simulated physical firefighting work. However, given the link between chronically elevated cytokine levels and several diseases, further research is needed to determine if firefighters\u27 IL-8 and IL-6 levels are elevated following repeated firefighting deployments across a fire season and over multiple fire seasons

Sleep in wildland firefighters: what do we know and why does it matter?

Wildland firefighters perform physical work while being subjected to multiple stressors and adverse, volatile working environments for extended periods. Recent research has highlighted sleep as a significant and potentially modifiable factor impacting operational performance. The aim of this review was to (1) examine the existing literature on firefighters&rsquo; sleep quantity and quality during wildland firefighting operations; (2) synthesise the operational and environmental factors that impact on sleep during wildland firefighting; and (3) assess how sleep impacts aspects of firefighters&rsquo; health and safety, including mental and physical health, physical task performance, physical activity and cognitive performance. Firefighters&rsquo; sleep is restricted during wildfire deployments, particularly when shifts have early start times, are of long duration and when sleeping in temporary accommodation. Shortened sleep impairs cognitive but not physical performance under simulated wildfire conditions. The longer-term impacts of sleep restriction on physiological and mental health require further research. Work shifts should be structured, wherever possible, to provide regular and sufficient recovery opportunities (rest during and sleep between shifts), especially in dangerous working environments where fatigue-related errors have severe consequences. Fire agencies should implement strategies to improve and manage firefighters&rsquo; sleep and reduce any adverse impacts on firefighters&rsquo; work

Improving cardiometabolic health with diet, physical activity, and breaking up sitting: what about sleep?

Cardiometabolic disease poses a serious health and economic burden worldwide and its prevalence is predicted to increase. Prolonged sitting, lack of physical activity, poor diet, and short sleep duration are ubiquitous behaviors in modern society, and all are independent risk factors in the development of cardiometabolic disease. Existing evidence demonstrates that breaking up prolonged periods of sitting is beneficial for cardiometabolic health, however, studies have not controlled for prior sleep duration. This article examines how prolonged sitting and short sleep duration independently contribute to cardiometabolic risk, and how breaking up sitting and obtaining adequate sleep may reduce this risk. We suggest that as prolonged sitting and short sleep duration influence the same cardiometabolic parameters, there is potential for short sleep to attenuate the positive impact of breaking up prolonged sitting with physical activity. Likewise, breaking up prolonged sitting and obtaining adequate sleep together could improve predictors of cardiometabolic disease, i.e., the combined effect may be stronger than either alone. To explore these perspectives, we propose a research agenda to investigate the relationship between breaking up prolonged sitting with physical activity and short sleep duration. This will provide an evidence-base for informing the design of interventions to reduce the burden of cardiometabolic disease on communities worldwide