211 research outputs found

    Are women nursing academics represented in university leadership positions?

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    The nursing workforce constitutes the largest professional health workforce in Australia. Nursing is traditionally a female dominated profession. This study reviewed Australian universities that provide entry to practice nursing education. The study identified the distribution of females and males in leadership in nursing education, the positioning of the discipline in the university, and where nurses occupy leadership roles above the nursing discipline (faculty/college). Of the 37 universities that offered entry to practice nursing, more females were evident. However, more men were evident in academia than the proportion of men in nursing outside of the academic setting. Leadership nomenclature varied within each nursing discipline group reviewed. This study demonstrated that the number of nursing academics has decreased since the late 1990’s. The nursing workforce is still a significant contributor to the academic workforce and yet numbers of nurse academics working in roles senior to their discipline were few. This paper discusses how the nursing workforce as predominantly female, has implications to both females and males, and may impact opportunities for leadership and promotion to senior roles

    The Effects of 3-Weeks of Aerobic Exercise in Heat on Fitness and PGC1a in Females

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    The effects of exercise training in the heat are well documented in men. However, the effects of exercise training in the heat in women have not received as much attention. We have previously reported a blunted rise in PGC1α in men after acute aerobic exercise in the heat. Purpose: To determine the impact of three weeks of aerobic exercise training in the heat compared to training in room temperature on thermoregulation, PGC1α mRNA response, and aerobic capacity in women. Methods: Twenty-three untrained college aged females (24±4 yoa, 168±5 cm, and 67.3±11.2 kg) were randomly assigned to 3 weeks of aerobic exercise training in either 20°C (n=12) or 33°C (n=11). Results: VO2max in room temperature conditions increased with training (2.57±0.35 to 2.71±0.32 L·min-1, p=0.01), but independent of temperature condition (p=0.821). HR decreased with training (152±16 to 140±0.13 bpm, p\u3c0.001), but was independent of temperature condition (p=0.341). Sweat rate increased with training (0.655±0.192 to 0.775±0.212 L·hr-1, p=0.006) and was higher in 33°C (0.835±0.144 L·hr-1) than 20°C (0.605±0.132 L·hr-1, p\u3c0.001). PGC1α mRNA increased with an acute exercise bout before (1.01±0.10 to 4.96±2.08 fold, p\u3c0.001) and after training (1.07±0.10 to 3.21±1.39 fold, p\u3c0.001) and had a smaller response after training than before training (p=0.005), but there were no differences between temperature groups (p=0.661). Conclusions: Women can increase aerobic fitness and maintain their exercise induced PGC1α mRNA response in the heat equally to that of room temperature conditions. This response contrasts with the blunted PGC1α mRNA response and VO2 max alterations previously observed in men

    Skeletal Muscle Metabolic Gene Response to Carbohydrate Feeding During Exercise in the Heat

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    Background: Heat stress down-regulates mitochondrial function, while carbohydrate supplementation attenuates the exercise induced stimulation of mitochondrial biogenesis in humans. The effects of exogenous carbohydrate during exercise in the heat on metabolic mRNA have not been investigated in humans. The purpose of this study was to determine the impact of exercise with and without carbohydrate supplementation on skeletal muscle metabolic response in the heat. Methods: Eight recreationally active males (4.05 ± 0.2 L.min-1) completed 2 trials which included 1 hr of cycling at 70% workload max and 3 hr recovery in a hot environment. Both trials were conducted in a climate controlled environmental chamber (38°C and 40% RH). The trials differed by the consumption of either a 6% carbohydrate (CHO) containing beverage (8 ml.kg-1.hr-1) or placebo (P) during exercise in random order. Muscle biopsies were obtained from the vastus lateralis before exercise, immediately post-exercise and at the end of the 3 hr recovery period. Muscle was analyzed for muscle glycogen and mRNA related to metabolic and mitochondrial development (MFN2, PGC-1α, GLUT4, UCP3). Expired gases were measured to determine whole body substrate use during exercise. Results: Carbohydrate oxidation and muscle glycogen utilization did not differ between trials, whereas fat oxidation was elevated during exercise in P. Exercise caused an increase in PGC-1α, and GLUT4 (P \u3c 0.05) independent of exogenous carbohydrate provision. Carbohydrate consumption attenuated the mRNA response in UCP3 (P \u3c 0.05). Conclusions: This study indicates that the provision of exogenous carbohydrate attenuates the stimulation of mRNA expression of UCP3 following exercise in the heat

    Substrate Use and Biochemical Response to a 3,211-km Bicycle Tour in Trained Cyclists

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    The purpose of this study was to assess the physiological adaptations in physically fit individuals to a period of intensified training. Ten trained males cycled outdoors ~170 km day−1 on 19 out of 21 days. Expired gas was collected on days 1 and 21 during maximal graded exercise and used for the determination of gross efficiency and whole body substrate use. Muscle biopsies were obtained before and after exercise on days 2 and 22 for the determination of mtDNA/gDNA ratio, gene expression, metabolic enzyme activity and glycogen use. Muscle glycogen before and after exercise, fat oxidation, and gross efficiency increased, carbohydrate oxidation decreased (p \u3c 0.05), and VO2max did not change over the 21 days of training. Citrate synthase (CS), β-hydroxyacyl CoA dehydrogenase (β-HAD) and cytochrome c oxidase (COX) enzyme activity did not change with training. CS and β-HAD mRNA did not change with acute exercise or training. COX (subunit IV) mRNA increased with acute exercise (p \u3c 0.05) but did not change over the 21 days. PGC-1α mRNA increased with acute exercise, but did not increase to the same degree on day 22 as it did on day 2 (p \u3c 0.05). UCP3 mRNA decreased with training (p \u3c 0.05). Acute exercise caused an increase in mitofusin2 (MFN2) mRNA (p \u3c 0.05) and a trend for an increase in mtDNA/gDNA ratio (p = 0.057). However, training did not affect MFN2 mRNA or mtDNA/gDNA ratio. In response to 3,211 km of cycling, changes in substrate use and gross efficiency appear to be more profound than mitochondrial adaptations in trained individuals

    Metabolic Profile of the Ironman World Championships: A Case Study

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    Purpose: The purpose of this study was to determine the metabolic profile during the 2006 Ironman World Championship in Kailua-Kona, Hawaii. Methods: One recreational male triathlete completed the race in 10:40:16. Before the race, linear regression models were established from both laboratory and field measures to estimate energy expenditure and substrate utilization. The subject was provided with an oral dose of (2)H(2)(18)O approximately 64 h before the race to calculate total energy expenditure (TEE) and water turnover with the doubly labeled water (DLW) technique. Body weight, blood sodium and hematocrit, and muscle glycogen (via muscle biopsy) were analyzed pre- and postrace. Results: The TEE from DLW and indirect calorimetry was similar: 37.3 MJ (8,926 kcal) and 37.8 MJ (9,029 kcal), respectively. Total body water turnover was 16.6 L. and body weight decreased 5.9 kg. Hematocrit increased from 46 to 51% PCV. Muscle glycogen decreased from 152 to 48 mmoL/kg wet weight pre- to postrace. Conclusion: These data demonstrate the unique physiological demands of the Ironman World Championship and should be considered by athletes and coaches to prepare sufficient nutritional and hydration plans

    Global shortfalls in documented actions to conserve biodiversity

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    Threatened species are by definition species that are in need of assistance. In the absence of suitable conservation interventions, they are likely to disappear soon1. There is limited understanding of how and where conservation interventions are applied globally, or how well they work2, 3. Here, using information from the International Union for Conservation of Nature Red List and other global databases, we find that for species at risk from three of the biggest drivers of biodiversity loss—habitat loss, overexploitation for international trade and invasive species4—many appear to lack the appropriate types of conservation interventions. Indeed, although there has been substantial recent expansion of the protected area network, we still find that 91% of threatened species have insufficient representation of their habitats within protected areas. Conservation interventions are not implemented uniformly across different taxa and regions and, even when present, have infrequently led to substantial improvements in the status of species. For 58% of the world’s threatened terrestrial species, we find conservation interventions to be notably insufficient or absent. We cannot determine whether such species are truly neglected, or whether efforts to recover them are not included in major conservation databases. If they are indeed neglected, the outlook for many of the world’s threatened species is grim without more and better targeted action

    Effects on Oxygen Consumption and Metabolic Gene Expression when Determining Experimental Exercise Intensity Based on Exercise Capacity Tests Conducted in Hypoxic and Normoxic Environments

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    Abstract: Exercise intensity can be set relative to VO2 max measured during hypoxic or control conditions in studies investigating exercise in hypoxic environments. It currently is not clear which is the most appropriate method. Objective: The objective of this brief report is to determine the response to 1 hour of cycling at 60% of peak power when measured in either normoxic or hypoxic conditions. Methods: Eleven recreationally active male participants (24 ± 4 yrs, 173 ± 20 cm, 82 ± 12 kg, 15.2 ± 7.1% fat, 4.0 ± 0.6 L x min-1 VO2 max) completed two 1 hour cycling exercise trials at 60% of peak power followed by 4 hours of recovery in ambient environmental conditions (975 m) and at normobaric hypoxic conditions simulating 3000 m in a randomized counter balanced order. Results: VO2 max was not different between trials in relative (p=0.272) or absolute terms (p=0.105) but peak power at VO2 max was higher in the 975 m trial (288 ± 17 watts) than the 3000 m trial (262 ± 12 watts, p=0.003) corresponding to differences at 60% of VO2 max power. Gene expression of HIF-1α, COX, PGC-1α, HK, and PFK increased with exercise (p\u3c0.05) but did not differ between trials. There was a trend (p=0.072) toward increased muscle glycogen use in 975m. Conclusions: Although there were not statistical differences for muscle markers in the current study, these data should be considered when determining exercise intensity in hypoxia related research

    Phase I trial of iodine-131-chimeric B72. 3 (human IgG4) in metastatic colorectal cancer

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    Twelve patients with metastatic colorectal cancer participated in a Phase I trial of 1311-labeled chimeric B72.3 (human IgG4). Consecutive groups of patients received 18 mCi/m 2, 27 mCi/ m 2 and 36 mCi/m a. No acute side effects related to antibody administration were noted. Bone marrow suppression was the only side effect; it was dose-dependent and correlated with whole-body radiation dose estimates. The lowest dose level produced no marrow suppression, whereas 27 mCi/m 2 resulted in Grade 1 and 2 marrow suppression in two of three patients. The maximum tolerated close was 36 mCi/m 2 with all six patients at this dose level having at least Grade 1 and two patients with Grade 3 and 4 marrow suppression. Eight of 12 patients had radioimmune imaging of tumor sites at 5- 22 days. Seven patients had an antibody response to initial infusion. On retreatment, whole-body kinetics and imaging were altered for patients with a high anti-ch-B72.3 response. Thus, chimeric B72.3 (IgG4) has limited utility as a means of delivering multiple therapeutic doses of 1311 in the majority of patients; alternative strategies including second generation anti-TAG-72 monoclonal antibodies, other radioisotopes and other chimeric human isotypes will need to be pursued

    Pharmacokinetics, immune response, and biodistribution of iodine-131-labeled chimeric mouse/human IgG1, k 17-1A monoclonal antibody

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    Pharmacokinetics,immunogenicity,and biodistributionof a 131I-Iabeledmouse/human chimenc monoclonal antibody (C17-1A) was studiedin six metastaticcoloncancerpatients. Pharmacokinetics obtalned from serum radioactivity or chi mera concentration were identical after 5 mCi of 131I(\u3e17-1A withmeanalphahalf-livesof 17.6±2.3 and19.7±2.9 and meanbeta half-livesof 100.9±16.1 and 106.4±14.1 hr, respectively. HPLC analysis documented the monomeric chi rneiic17-lA withoutevidenceof immunecomplexesorfree 1311 None of the patients developed antibody after ‘31I-chi merle17-1A exposure.Radiolocalizationoccurredin known areas of disease \u3e4 cm in all patients. The half-life of total body radioactivity was 58 ±7 hr by whole-body counts and 64 ±13 hr by urine measurements. Whole-body and bone marrow dose estimates ranged from 0.75-1 .03 and 0.76- 1.05rad/mCi,respectively.Thesestudiesconfirmthe pro longedcirculationand reducedimmunogenicityof chimeric 171Aversusmunne17-1A.Marrowradiationexposureusing antibodies with prolonged circulation is a critical factor in planningforradioimmunotherapeutic application

    Maternal and child health nurse screening and care for mothers experiencing domestic violence (MOVE): A cluster randomised trial

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    BACKGROUND: Mothers are at risk of domestic violence (DV) and its harmful consequences postpartum. There is no evidence to date for sustainability of DV screening in primary care settings. We aimed to test whether a theory-informed, maternal and child health (MCH) nurse-designed model increased and sustained DV screening, disclosure, safety planning and referrals compared with usual care. METHODS: Cluster randomised controlled trial of 12 month MCH DV screening and care intervention with 24 month follow-up. The study was set in community-based MCH nurse teams (91 centres, 163 nurses) in north-west Melbourne, Australia. Eight eligible teams were recruited. Team randomisation occurred at a public meeting using opaque envelopes. Teams were unable to be blinded. The intervention was informed by Normalisation Process Theory, the nurse-designed good practice model incorporated nurse mentors, strengthened relationships with DV services, nurse safety, a self-completion maternal health screening checklist at three or four month consultations and DV clinical guidelines. Usual care involved government mandated face-to-face DV screening at four weeks postpartum and follow-up as required. Primary outcomes were MCH team screening, disclosure, safety planning and referral rates from routine government data and a postal survey sent to 10,472 women with babies ≤ 12 months in study areas. Secondary outcomes included DV prevalence (Composite Abuse Scale, CAS) and harm measures (postal survey). RESULTS: No significant differences were found in routine screening at four months (IG 2,330/6,381 consultations (36.5 %) versus CG 1,792/7,638 consultations (23.5 %), RR = 1.56 CI 0.96-2.52) but data from maternal health checklists (n = 2,771) at three month IG consultations showed average screening rates of 63.1 %. Two years post-intervention, IG safety planning rates had increased from three (RR 2.95, CI 1.11-7.82) to four times those of CG (RR 4.22 CI 1.64-10.9). Referrals remained low in both intervention groups (IGs) and comparison groups (CGs) (<1 %). 2,621/10,472 mothers (25 %) returned surveys. No difference was found between arms in preference or comfort with being asked about DV or feelings about self. CONCLUSION: A nurse-designed screening and care model did not increase routine screening or referrals, but achieved significantly increased safety planning over 36 months among postpartum women. Self-completion DV screening was welcomed by nurses and women and contributed to sustainability. TRIAL REGISTRATION: Australian New Zealand Clinical Trials Registry, ACTRN12609000424202, 10/03/2009
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