24 resultados para Approval of Calendar 2005-2006

em Deakin Research Online - Australia


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A study of the cholesterol content and fatty acid composition of fresh retail Australian pork was undertaken to determine whether new breeding, feeding and processing methods had resulted in any compositional changes in fresh pork in the market place since surveys undertaken in previous decades. Samples of 13 popular pork cuts were purchased from randomly selected supermarkets and butchers’ stores in urban areas across the socioeconomic scale in three States of Australia, and analysed, separable fat and separable lean, in late 2005 and early 2006. Variability was low across States for saturated and monounsaturated fatty acids, but more pronounced for polyunsaturated acids. The separable lean portions of all pork cuts contained levels of n-3 fatty acids and conjugated linoleic acid (C18:1c9t11) in measurable but not nutritionally claimable amounts, whilst total trans fatty acid levels were very low. There appeared to be some differences in fatty acid composition across States that may have resulted from feeding method. Cholesterol contents were similar to levels in the 80s and 90s for separable lean pork tissue, but presently are lower for separable fat tissue than for separable lean.

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Federal government changes to the funding of doctoral students have focussed the attention of university management on their completion rates. The aims are to inform the allocation of institutional resources in a manner that improves the likelihood of timely doctoral completions and to highlight a process that can also be used for analyses of other key indicators of progression and attrition. The analyses and model development used national data readily available to all universities, which is collected in a standard approach through the Graduate Destinations Survey (GDS). The findings show that the most important variable for timely completion was attendance (full‐ versus part‐time), where in terms of full‐time equivalent (FTE) years of study, part‐time students were far more likely to complete quickly than full‐time students. For the full‐time students the key predictors of timely completion were residency, field of study and English‐speaking background (ESB). The timeliness of part‐time students was predicted by field of study and ESB. This study confirms that there is considerable variation by discipline for timely doctoral completions. The pragmatic application and prospective test of the derived models present a variety of opportunities for research student administrators. For example, those full‐time students scoring highly represented a concentration of timely graduates more than 7.5 times higher than the lowest‐scoring group – almost an order of magnitude of difference. In short, university management could gain tremendous value from more widely using the data available.

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Objective: To determine the quality of abstracts reporting randomized clinical trials (RCT) at the 2005 Annual Scientific Meeting of the American College of Rheumatology.

Methods:
All 2005 abstracts including late-breaking abstracts were assessed. An abstract was deemed to be reporting an RCT if it indicated that participants were randomized in the title or body of the abstract. RCT were excluded if they included only pharmacokinetic data. The CONSORT checklist was applied and relevant data extracted. We defined manufacturer support as acknowledgment of industry support or industry employee as co-author.

Results: Of 2146 abstracts, 143 (6.7%) reported RCT. Of these, 78.3% were drug trials, and 63.6% indicated manufacturer support. Only 30.8% of abstracts used "randomized" in the title, 44.1% did not explicitly state whether blinding was undertaken, and only 7.0% clearly stated who was blinded. Thirty percent of studies did not give an explicit definition of eligibility criteria of participants. While 84.6% explicitly described the experimental intervention, only 37.1% explicitly described the comparator intervention. Only 21% explicitly stated that an intention to treat analysis was performed. Baseline demographic and clinical characteristics were reported in 48.3%. While most abstracts reported summary results for each treatment group, only 35.7% reported effect size with its precision.

Conclusion:
The quality of reporting is suboptimal in many RCT abstracts. Abstracts reporting RCT would benefit from a structured approach that ensures more detailed reporting of eligibility criteria, active and comparator interventions, flow of participants, and adequate summary and precision of results.

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2015 marks a decade since the release of the Victorian Law Reform Commission's Defences to Homicide: Final Report. The Commission's Final Report recommended major changes to the law of homicide in Victoria and in 2005, the Victorian government responded to the 56 recommendations by implementing the largest package of homicide law reforms since the abolition of the death penalty. This book brings together leading scholars, legal practitioners and the former Victorian Attorney-General to provide a comprehensive examination of the Victorian experience of reform, including its perceived successes and failures. This is a controversial area of the law that continues to present challenges in practice. Since the 2005 reforms further reform of the law has occurred in Victoria and a range of divergent approaches to homicide law reform have been introduced and animated debate across Australia and internationally. With such a high level of law reform activity nationally this book provides a timely analysis of the extent to which the Victorian reforms have improved legal responses to lethal violence and with what effect in practice. To enhance this analysis the book also looks internationally to consider the operation of homicide law in England and Wales, Canada and New Zealand and what lessons could be gained from an Australian perspective from differing approaches to reform.

This book explores a number of issues concerning the operation of the law of homicide, sentencing practices, the role of the media, evidence reforms, legal culture, political influences and future reform challenges for Victoria and other Australian jurisdictions. In examining all aspects of the 2005 homicide law reforms, the book draws on the views of those who were involved in reviewing the law of homicide in Victoria, those who recommended and implemented reform, and those who have played a key role in the monitoring and evaluation of the law post-reform in Victoria but also more widely in Australia and internationally. The resulting analysis will be of great interest to law, criminology and socio-legal scholars as well as legal practitioners and law reformers in Australia and comparative international jurisdictions.

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This Report concerns capacity development in the economic and public sectors of PNG. In particular, it focuses on the use of advisers to develop the capacity of PNG counterparts in economic and public sector agencies. Such advisers were funded by the Government of Australia and completed or commenced their placements during the period 2006–2013. The research was commissioned by (then) AusAID and commenced in mid-2012. It was completed in mid-2014 under the auspices of Australian Aid, Department of Foreign Affairs & Trade. The project was overseen by the Economic and Public Sector Program administered by Coffey International. The research addressed several research questions about adviser-counterpart placements: What are the advisers’ and counterparts’ views of the success or otherwise of their partnerships in achieving their placements’ stated aims? What approaches were adopted to enable counterparts to learn what was required to fulfil their placements’ aims? What were the main things learned by counterparts? What can be understood from these experiences and how might capacity development be improved? What were the main enablers of and impediments to the success of the placements? What have been the outcomes of the introduction of other modalities of capacity development including short-term consultants, twinning arrangements, targeted training, grants and research? Do these modalities provide increased efficiencies and effectiveness compared to adviser-counterpart placements? What are the main improvements that can be made to ensure the success of future adviser-counterpart placements? What do major stakeholders in PNG conclude from the evidence produced by this study about the impact and success of adviser-counterpart placements? What may be asserted from the evidence of the worth or otherwise of adviser-counterpart placements and other capacity development modalities undertaken since 2006? What suggestions or recommendations may be made for the future?

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The subcellular localization of insulin signaling proteins is altered by various stimuli such as insulin, insulin-like growth factor I, and oxidative stress and is thought to be an important mechanism that can influence intracellular signal transduction and cellular function. This study examined the possibility that exercise may also alter the subcellular localization of insulin signaling proteins in human skeletal muscle. Nine untrained males performed 60 min of cycling exercise (~67% peak pulmonary O2 uptake). Muscle biopsies were sampled at rest, immediately after exercise, and 3 h postexercise. Muscle was fractionated by centrifugation into the following crude fractions: cytosolic, nuclear, and a high-speed pellet containing membrane and cytoskeletal components. Fractions were analyzed for protein content of insulin receptor, insulin receptor substrate (IRS)-1 and -2, p85 subunit of phosphatidylinositol 3-kinase, Akt, and glycogen synthase kinase-3 (GSK-3). There was no significant change in the protein content of the insulin signaling proteins in any of the crude fractions after exercise or 3 h postexercise. Exercise had no significant effect on the phosphorylation of IRS-1 Tyr612 in any of the fractions. In contrast, exercise increased (P < 0.05) the phosphorylation of Akt Ser473 and GSK-3α/ß Ser9/21 in the cytosolic fraction only. In conclusion, exercise can increase phosphorylation of downstream insulin signaling proteins specifically in the cytosolic fraction but does not result in changes in the subcellular localization of insulin signaling proteins in human skeletal muscle. Change in the subcellular protein localization is therefore an unlikely mechanism to influence signal transduction pathways and cellular function in skeletal muscle after exercise.

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The Menkes protein (ATP7A) is defective in the Cu deficiency disorder Menkes disease and is an important contributor to the maintenance of physiological Cu homeostasis. To investigate more fully the role of ATP7A, transgenic mice expressing the human Menkes gene ATP7A from chicken beta-actin composite promoter (CAG) were produced. The transgenic mice expressed ATP7A in lung, heart, liver, kidney, small intestine, and brain but displayed no overt phenotype resulting from expression of the human protein. Immunohistochemical analysis revealed that ATP7A was found primarily in the cardiac muscle, smooth muscle of the lung, distal tubules of the kidney, intestinal enterocytes, and patches of hepatocytes, as well as in the hippocampus, cerebellum, and choroid plexus of the brain. In 60-day- and 300-day-old mice, Cu concentrations were reduced in most tissues, consistent with ATP7A playing a role in Cu efflux. The reduction in Cu was most pronounced in the hearts of older T22#2 females (24%), T22#2 males (18%), and T25#5 females (23%), as well as in the brains of 60-day-old T22#2 females and males (23% and 30%, respectively).

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To examine the influence of exercise intensity on the increases in vastus lateralis GLUT4 mRNA and protein after exercise, six untrained men exercised for 60 min at 39 ± 3% peak oxygen consumption (VO2 peak) (Lo) or 27 ± 2 min at 83 ± 2% VO2 peak (Hi) in counterbalanced order. Preexercise muscle glycogen levels were not different between trials (Lo: 408 ± 35 mmol/kg dry mass; Hi: 420 ± 43 mmol/kg dry mass); however, postexercise levels were lower (P < 0.05) in Hi (169 ± 18 mmol/kg dry mass) compared with Lo (262 ± 35 mmol/kg dry mass). Thus calculated muscle glycogen utilization was greater (P < 0.05) in Hi (251 ± 24 mmol/kg) than in Lo (146 ± 34). Exercise resulted in similar increases in GLUT4 gene expression in both trials. GLUT4 mRNA was increased immediately at the end of exercise (~2-fold; P < 0.05) and remained elevated after 3 h of postexercise recovery. When measured 3 h after exercise, total crude membrane GLUT4 protein levels were 106% higher in Lo (3.3 ± 0.7 vs. 1.6 ± 0.3 arbitrary units) and 61% higher in Hi (2.9 ± 0.5 vs. 1.8 ± 0.5 arbitrary units) relative to preexercise levels. A main effect for exercise was observed, with no significant differences between trials. In conclusion, exercise at ~40 and ~80% VO2 peak, with total work equal, increased GLUT4 mRNA and GLUT4 protein in human skeletal muscle to a similar extent, despite differences in exercise intensity and duration.

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Hormone-sensitive lipase (HSL) is important for the degradation of triacylglycerol in adipose and muscle tissue, but the tissue-specific regulation of this enzyme is not fully understood. We investigated the effects of adrenergic stimulation and AMPK activation in vitro and in circumstances where AMPK activity and catecholamines are physiologically elevated in humans in vivo (during physical exercise) on HSL activity and phosphorylation at Ser563 and Ser660, the PKA regulatory sites, and Ser565, the AMPK regulatory site. In human experiments, skeletal muscle, subcutaneous adipose and venous blood samples were obtained before, at 15 and 90 min during, and 120 min after exercise. Skeletal muscle HSL activity was increased by ~80% at 15 min compared with rest and returned to resting rates at the cessation of and 120 min after exercise. Consistent with changes in plasma epinephrine, skeletal muscle HSL Ser563 and Ser660 phosphorylation were increased by 27% at 15 min (P < 0.05), remained elevated at 90 min, and returned to preexercise values postexercise. Skeletal muscle HSL Ser565 phosphorylation and AMPK signaling were increased at 90 min during, and after, exercise. Phosphorylation of adipose tissue HSL paralleled changes in skeletal muscle in vivo, except HSL Ser660 was elevated 80% in adipose compared with 35% in skeletal muscle during exercise. Studies in L6 myotubes and 3T3-L1 adipocytes revealed important tissue differences in the regulation of HSL. AMPK inhibited epinephrine-induced HSL activity in L6 myotubes and was associated with reduced HSL Ser660 but not Ser563 phosphorylation. HSL activity was reduced in L6 myotubes expressing constitutively active AMPK, confirming the inhibitory effects of AMPK on HSL activity. Conversely, in 3T3-L1 adipocytes, AMPK activation after epinephrine stimulation did not prevent HSL activity or glycerol release, which coincided with maintenance of HSL Ser660 phosphorylation. Taken together, these data indicate that HSL activity is maintained in the face of AMPK activation as a result of elevated HSL Ser660 phosphorylation in adipose tissue but not skeletal muscle.

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AMPK plays a central role in influencing fuel usage and selection. The aim of this study was to analyze the impact of low-dose AMP analog 5-aminoimidazole-4-carboxamide-1-ß-D-ribosyl monophosphate (ZMP) on whole body glucose turnover and skeletal muscle (SkM) glucose metabolism. Dogs were restudied after prior 48-h fatty acid oxidation (FAOX) blockade by methylpalmoxirate (MP; 5 x 12 hourly 10 mg/kg doses). During the basal equilibrium period (0–150 min), fasting dogs (n = 8) were infused with [3-3H]glucose followed by either 2-h saline or AICAR (1.5–2.0 mg·kg–1·min–1) infusions. SkM was biopsied at completion of each study. On a separate day, the same protocol was undertaken after 48-h in vivo FAOX blockade. The AICAR and AICAR + MP studies were repeated in three chronic alloxan-diabetic dogs. AICAR produced a transient fall in plasma glucose and increase in insulin and a small decline in free fatty acid (FFA). Parallel increases in hepatic glucose production (HGP), glucose disappearance (Rd tissue), and glycolytic flux (GF) occurred, whereas metabolic clearance rate of glucose (MCRg) did not change significantly. Intracellular SkM glucose, glucose 6-phosphate, and glycogen were unchanged. Acetyl-CoA carboxylase (ACC~pSer221) increased by 50%. In the AICAR + MP studies, the metabolic responses were modified: the glucose was lower over 120 min, only minor changes occurred with insulin and FFA, and HGP and Rd tissue responses were markedly attenuated, but MCRg and GF increased significantly. SkM substrates were unchanged, but ACC~pSer221 rose by 80%. Thus low-dose AICAR leads to increases in HGP and SkM glucose uptake, which are modified by prior FAox blockade.

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Skeletal muscle displays enormous plasticity to respond to contractile activity with muscle from strength- (ST) and endurance-trained (ET) athletes representing diverse states of the adaptation continuum. Training adaptation can be viewed as the accumulation of specific proteins. Hence, the altered gene expression that allows for changes in protein concentration is of major importance for any training adaptation. Accordingly, the aim of the present study was to quantify acute subcellular responses in muscle to habitual and unfamiliar exercise. After 24-h diet/exercise control, 13 male subjects (7 ST and 6 ET) performed a random order of either resistance (8 x 5 maximal leg extensions) or endurance exercise (1 h of cycling at 70% peak O2 uptake). Muscle biopsies were taken from vastus lateralis at rest and 3 h after exercise. Gene expression was analyzed using real-time PCR with changes normalized relative to preexercise values. After cycling exercise, peroxisome proliferator-activated receptor- coactivator-1 (ET 8.5-fold, ST 10-fold, P < 0.001), pyruvate dehydrogenase kinase-4 (PDK-4; ET 26-fold, ST 39-fold), vascular endothelial growth factor (VEGF; ET 4.5-fold, ST 4-fold), and muscle atrophy F-box protein (MAFbx) (ET 2-fold, ST 0.4-fold) mRNA increased in both groups, whereas MyoD (3-fold), myogenin (0.9-fold), and myostatin (2-fold) mRNA increased in ET but not in ST (P < 0.05). After resistance exercise PDK-4 (7-fold, P < 0.01) and MyoD (0.7-fold) increased, whereas MAFbx (0.7-fold) and myostatin (0.6-fold) decreased in ET but not in ST. We conclude that prior training history can modify the acute gene responses in skeletal muscle to subsequent exercise.