68 resultados para enforced disappearance

em Deakin Research Online - Australia


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To evaluate the putative advantages of student self pacing in automated instruction,the studies in this thesis compare the effects of self-paced, and externally-paced, programmed instruction on student accuracy, retention, efficiency, and satisfaction. The results of the experiments show that self-pacing reduced accuracy, retention, and workrates compared to external pacing and indicated that learners often make poor choices about optimum learning conditions. They also show that small changes in the learning environment can result in consistent and substantial changes in learner performance, and that behaviour analysts have an important role to play in the design and implementation of instructional material.

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This paper investigates the nullification of homo juridicus and the vanishing of the jurist in relation to the liberal global-order project and the emergence and spread of soft-networked channels of post-national governance. By inquiring into the shift from the individual’s active will to the sterile behavioural schemes prompted by the universalisation of liberalism and economic analysis of social interactions, it will be argued that the jurist and the (rule of) law are no longer needed in a post-national system of rational and mechanic causations. Through an analysis of Susan Sontag’s and Josef Esser’s accounts for and against the interpretative task, it will be contended that the re-discovery of the anthropological and onto-sociopolitical function of the jurist depends upon the re-affirmation of: (1) the will’s oscillation between velle and nolle as constitutive of human uniqueness; (2) the need to interpret homo juridicus’s will power normativistically, and what this power leads to.

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Several studies have demonstrated that oral glucose tolerance is impaired in the immediate postexercise period. A double-tracer technique was used to examine glucose kinetics during a 2-h oral glucose (75 g) tolerance test (OGTT) 30 min after exercise (Ex, 55 min at 71 ± 2% of peak O2 uptake) and 24 h after exercise (Rest) in endurance-trained men. The area under the plasma glucose curve was 71% greater in Ex than in Rest (P = 0.01). The higher glucose response occurred even though whole body rate of glucose disappearance was 24% higher after exercise (P = 0.04, main effect). Whole body rate of glucose appearance was 25% higher after exercise (P = 0.03, main effect). There were no differences in total (2 h) endogenous glucose appearance (RaE) or the magnitude of suppression of RaE, although RaE was higher from 15 to 30 min during the OGTT in Ex. However, the cumulative appearance of oral glucose was 30% higher in Ex (P = 0.03, main effect). There were no differences in glucose clearance rate or plasma insulin responses between the two conditions. These results suggest that adaptations in splanchnic tissues by prior exercise facilitate greater glucose output from the splanchnic region after glucose ingestion, resulting in a greater glycemic response and, consequently, a greater rate of whole body glucose uptake.

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The evolutionary relationships of the freshwater prawn genus Macrobrachium are obscure. Members of this genus are widely distributed across tropical and subtropical regions. The phylogenetic relationships among the seven endemic and six non-endemic Australian Macrobrachium, along with five non-Australian species, were inferred from the mitochondrial 16S rRNA gene sequences. Methods of analysis yielded phylogenetic trees of differing topologies; however, none supported a monophyletic origin for endemic Australian Macrobrachium. Enforced monophyly of a single origin of endemic Macrobrachium was statistically tested and rejected. These results support the view that the endemic Australian Macrobrachium arose from multiple origins. Previous biogeographical hypotheses related to the radiation of Macrobrachium into Australia are re-examined in the context of these results.

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This paper discusses Michel de Certeau’s theories of spatialised power and of resistance, especially his characterisation of what he describes as ‘tactics’ by which marginalised groups resist the strategies by which those in power gain and maintain control, in relation to a group of settler society picture books: Edna Tantjingu Williams, Eileen Wani Wingfield and Kunyi June-Anne McInerney’s Down the hole (2000); the Papunya School Book of Country and History (2001); Chiori Santiago and Judith Lowry’s Home to Medicine Mountain (1998); George Littlechild’s This Land Is My Land (1993); and Allen Say’s Home of the Brave (2002). These texts thematise colonial and assimilationist policies in Australia, Canada and the United States which required that racialised groups of children should be removed from their homes and families and placed in institutions. I argue that the first four of these texts position child readers both to understand the dislocation and pain caused by government policies such as those which enforced the removal of the Stolen Generation in Australia, and to appreciate the tactics of resistance by which children evaded or subverted institutional power. Home of the Brave deploys the symbolism of an adult’s journey into the past to show how strategies of repression serve to protect individuals and nations from shame and guilt, and demonstrates the transformative effects which result when the past is scrutinized.

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There is an increasing use of herbal medicines worldwide, and the extracts from the root of Salvia miltiorrhiza are widely used in the treatment of angina and stroke. In this study, we investigated the mechanism for the intestinal absorption of tanshinone IIB (TSB), a major constituent of S. miltiorrhiza. The oral bioavailability of TSB was about 3% in rats with less proportional increase in its maximum plasma concentration (Cmax) and area under the plasma concentration-time curve (AUC) with increasing dosage. The time to Cmax (Tmax) was prolonged at higher oral dosage. In a single pass rat intestinal perfusion model, the permeability coefficients (Papp) based on TSB disappearance from the lumen (Plumen) were 6.2- to 7.2-fold higher (p < 0.01) than those based on drug appearance in mesenteric venous blood (Pblood). The uptake and efflux of TSB in Caco-2 cells were also significantly altered in the presence of an inhibitor for P-glycoprotein (PgP) or for multi-drug resistance associated protein (MRP1/2). TSB transport from the apical (AP) to basolateral (BL) side in Caco-2 monolayers was 3.3- to 5.7-fold lower than that from BL to AP side, but this polarized transport was attenuated by co-incubation of PgP or MRP1/2 inhibitors. The Papp values of TSB in the BL-AP direction were significantly higher in MDCKII cells over-expressing MDR1 or MRP1, but not in cells over-expressing MRP2-5, as compared with the wild-type cells. The plasma AUC0-24hr in mdr1a and mrp1 gene-deficient mice was 10.2- to 1.7-fold higher than that in the wild-type mice. Furthermore, TSB significantly inhibited the uptake of digoxin and vinblastine in membrane vesicles containing PgP or MRP1. TSB also moderately stimulated PgP ATPase activity. Taken collectively, our findings indicate that TSB is a substrate for PgP and MRP1 and that drug resistance to TSB therapy and drug interactions may occur through PgP and MRP1 modulation.

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Six endurance-trained men [peak oxygen uptake (VO2) = 4.58 ± 0.50 (SE) l/min] completed 60 min of exercise at a workload requiring 68 ± 2% peak VO2 in an environmental chamber maintained at 35°C (<50% relative humidity) on two occasions, separated by at least 1 wk. Subjects ingested either a 6% glucose solution containing 1 µCi [3-3H]glucose/g glucose (CHO trial) or a sweet placebo (Con trial) during the trials. Rates of hepatic glucose production [HGP = glucose rate of appearance (Ra) in Con trial] and glucose disappearance (Rd), were measured using a primed, continuous infusion of [6,6-2H]glucose, corrected for gut-derived glucose (gut Ra) in the CHO trial. No differences in heart rate, VO2, respiratory exchange ratio, or rectal temperature were observed between trials. Plasma glucose concentrations were similar at rest but increased (P < 0.05) to a greater extent in the CHO trial compared with the Con trial. This was due to the absorption of ingested glucose in the CHO trial, because gut Ra after 30 and 50 min (16 ± 5 µmol · kg-1 · min-1) was higher (P < 0.05) compared with rest, whereas HGP during exercise was not different between trials. Glucose Rd was higher (P < 0.05) in the CHO trial after 30 and 50 min (48.0 ± 6.3 vs 34.6 ± 3.8 µmol · kg-1 · min-1, CHO vs. Con, respectively). These results indicate that ingestion of carbohydrate, at a rate of ~1.0 g/min, increases glucose Rd but does not blunt the rise in HGP during exercise in the heat.

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Aims/hypothesis: To study the secondary consequences of impaired suppression of endogenous glucose production (EGP) we have created a transgenic rat overexpressing the gluconeogenic enzyme phosphoenolpyruvate carboxykinase (PEPCK) in the kidney. The aim of this study was to determine whether peripheral insulin resistance develops in these transgenic rats.
Methods: Whole body rate of glucose disappearance (Rd) and endogenous glucose production were measured basally and during a euglycaemic/hyperinsulinaemic clamp in phosphoenolpyruvate carboxykinase transgenic and control rats using [6-3H]-glucose. Glucose uptake into individual tissues was measured in vivo using 2-[1-14C]-deoxyglucose.
Results: Phosphoenolpyruvate carboxykinase transgenic rats were heavier and had increased gonadal and infrarenal fat pad weights. Under basal conditions, endogenous glucose production was similar in phosphoenolpyruvate carboxykinase transgenic and control rats (37.4±1.1 vs 34.6±2.6 µmol/kg/min). Moderate hyperinsulinaemia (810 pmol/l) completely suppressed EGP in control rats (–0.6±5.5 µmol/kg/min, p<0.05) while there was no suppression in phosphoenolpyruvate carboxykinase rats (45.2±7.9 µmol/kg/min). Basal Rd was comparable between PEPCK transgenic and control rats (37.4±1.1 vs 34.6±2.6 µmol/kg/min) but under insulin-stimulated conditions the increase in Rd was greater in control compared to phosphoenolpyruvate carboxykinase transgenic rats indicative of insulin resistance (73.4±11.2 vs 112.0±8.0 µmol/kg/min, p<0.05). Basal glucose uptake was reduced in white and brown adipose tissue, heart and soleus while insulin-stimulated transport was reduced in white and brown adipose tissue, white quadriceps, white gastrocnemius and soleus in phosphoenolpyruvate carboxykinase transgenic compared to control rats. The impairment in both white and brown adipose tissue glucose uptake in phosphoenolpyruvate carboxykinase transgenic rats was associated with a decrease in GLUT4 protein content. In contrast, muscle GLUT4 protein, triglyceride and long-chain acylCoA levels were comparable between PEPCK transgenic and control rats.
Conclusions/interpretation: A primary defect in suppression of EGP caused adipose tissue and muscle insulin resistance.

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The effect of exercise intensity on skeletal muscle AMP-activated protein kinase (AMPK) signaling and substrate metabolism was examined in eight men cycling for 20 min at each of three sequential intensities: low (40 ± 2% Vo2 peak), medium (59 ± 1% Vo2 peak), and high (79 ± 1% Vo2 peak). Muscle free AMP/ATP ratio only increased at the two higher exercise intensities (P < 0.05). AMPK a1 (1.5-fold) and AMPK a2 (5-fold) activities increased from low to medium intensity, with AMPK a2 activity increasing further from medium to high intensity. The upstream AMPK kinase activity was substantial at rest and only increased 50% with exercise, indicating that, initially, signaling through AMPK did not require AMPK kinase posttranslational modification. Acetyl-CoA carboxylase (ACC)-ßphosphorylation was sensitive to exercise, increasing threefold from rest to low intensity, whereas neuronal NO synthase (nNOS)µphosphorylation was only observed at the higher exercise intensities. Glucose disappearance (tracer) did not increase from rest to low intensity, but increased sequentially from low to medium to high intensity. Calculated fat oxidation increased from rest to low intensity in parallel with ACCß phosphorylation, then declined during high intensity. These results indicate that ACCß phosphorylation is especially sensitive to exercise and tightly coupled to AMPK signaling and that AMPK activation does not depend on AMPK kinase activation during exercise.

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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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The nature of intestinal absorption of most herbal medicine is unknown. Cryptotanshinone (CTS) is the principal active constituent of the widely used cardiovascular herb Salvia miltiorrhiza (Danshen). We investigated the oral bioavailability of CTS in rats and the mechanism for its intestinal absorption using several in vitro and in vivo models:1) Caco-2 cell monolayers; 2) monolayers of MDCKII cells overexpressing P-glycoprotein
(PgP); and 3) single-pass rat intestinal perfusion with mesenteric vein cannulation. The systemic bioavailabilities of CTS after oral and intraperitoneal administration at 100 mg/kg were 2.05 and 10.60%, respectively. In the perfused rat intestinal model, permeability coefficients based on CTS disappearance from the luminal perfusate (Plumen) were 6.7- to 10.3-fold higher than permeability coefficients based on drug appearance in venous blood (Pblood). Pblood significantly increased in the presence of the P-gP inhibitor, verapamil. CTS transport across Caco-2 monolayers was pH-, temperature- and ATP-dependent. The transport from the apical (AP) to the basolateral (BL) side was 3- to 9-fold lower than that from the BL to the AP side. Inclusion of verapamil (50 µM) in both AP and BL sides abolished the polarized CTS transport across Caco-2 cells. Moreover, CTS was significantly more permeable in the BL to AP than in the AP to BL direction in MDCKII and MDR1-MDCKII cells. The permeability coefficients in the BL to AP direction were significantly higher in MDCKII cells overexpressing PgP. These findings indicate that CTS is a substrate for PgP that can pump CTS into the luminal side.

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Youth substance use is an important social and health problem in the United States, Australia and other Western nations. Schools are recognized as important sites for prevention efforts and school substance use policies are a key component of health promotion in schools. The first part of this paper reviews the known status of school policies on tobacco, alcohol and other illicit drugs in a number of Western countries and the existing evidence for the effectiveness of school drug policy in preventing drug use. The review shows that most schools in developed countries have substance use policies but that there is substantial variation in the comprehensiveness of these policies (i.e. the breadth of people, places and times of day that are explicitly subject to policy prohibitions), and the orientation of their enforcement (e.g. punitive versus remedial), both across and within schools. The few studies of policy impact focus solely on tobacco policy and provide preliminary evidence that more comprehensive and strictly enforced school policies are associated with less smoking. The second part of the paper introduces the International Youth Development Study, a new longitudinal research project aimed at comparing school policies and the developmental course of youth drug use in the United States, where drug policies are abstinence-based, with Australia, which has adopted a harm minimization approach to drug policy

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Using mail survey data collected from primary and secondary school administrators in Washington State, United States, and in Victoria, Australia, this study compared aspects of the school drug policy environment in the 2 states. Documented substance-use policies were prevalent in Washington and Victoria but less prevalent in primary schools, especially in Victoria. Victorian school policy-setting processes were significantly more likely to involve teachers, parents, and students than processes in Washington schools. Consistent with expectations based on their respective national drug policy frameworks, school drug policies in Washington schools were more oriented toward total abstinence and more frequently enforced with harsh punishment (such as expulsion or calling law enforcement), whereas policies in Victorian schools were more reflective of harm-minimization principles. Within both states, however, schools more regularly used harsh punishment and remediation consequences for alcohol and illicit-drug violations compared to tobacco policy violations, which were treated more leniently. (J Sch Health. 2005;75(4):134-140)