980 resultados para Wright, Janet M


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This article represents a critique of the 'spiritual literacy' approach to spiritual education developed by Andrew Wright (e.g. 2000a), with particular reference to the inclusion of Michael Polanyi's theory of 'tacit knowledge'. Wright's assessment of the current state of religious education is summarised and his proposed method is outlined. Polanyi's ideas are then described and assessed for their compatibility with the 'spiritual literacy' approach.

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Background and purpose: Molecular mechanisms underlying the links between dietary intake of flavonoids and reduced cardiovascular disease risk are only partially understood. Key events in the pathogenesis of cardiovascular disease, particularly thrombosis, are inhibited by these polyphenolic compounds via mechanisms such as inhibition of platelet activation and associated signal transduction, attenuation of generation of reactive oxygen species, enhancement of nitric oxide production and binding to thromboxane A2 receptors. In vivo, effects of flavonoids are mediated by their metabolites, but the effects and modes of action of these compounds are not well-characterized. A good understanding of flavonoid structure–activity relationships with regard to platelet function is also lacking. Experimental approach: Inhibitory potencies of structurally distinct flavonoids (quercetin, apigenin and catechin) and plasma metabolites (tamarixetin, quercetin-3′-sulphate and quercetin-3-glucuronide) for collagen-stimulated platelet aggregation and 5-hydroxytryptamine secretion were measured in human platelets. Tyrosine phosphorylation of total protein, Syk and PLCγ2 (immunoprecipitation and Western blot analyses), and Fyn kinase activity were also measured in platelets. Internalization of flavonoids and metabolites in a megakaryocytic cell line (MEG-01 cells) was studied by fluorescence confocal microscopy. Key results: The inhibitory mechanisms of these compounds included blocking Fyn kinase activity and the tyrosine phosphorylation of Syk and PLCγ2 following internalization. Principal functional groups attributed to potent inhibition were a planar, C-4 carbonyl substituted and C-3 hydroxylated C ring in addition to a B ring catechol moiety. Conclusions and implications: The structure–activity relationship for flavonoids on platelet function presented here may be exploited to design selective inhibitors of cell signalling.

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The health effects of milk and dairy food consumption would best be determined in randomised controlled trials. No adequately powered trial has been reported and none is likely because of the numbers required. The best evidence comes, therefore, from prospective cohort studies with disease events and death as outcomes. Medline was searched for prospective studies of dairy food consumption and incident vascular disease and Type 2 diabetes, based on representative population samples. Reports in which evaluation was in incident disease or death were selected. Meta-analyses of the adjusted estimates of relative risk for disease outcomes in these reports were conducted. Relevant case–control retrospective studies were also identified and the results are summarised in this article. Meta-analyses suggest a reduction in risk in the subjects with the highest dairy consumption relative to those with the lowest intake: 0.87 (0.77, 0.98) for all-cause deaths, 0.92 (0.80, 0.99) for ischaemic heart disease, 0.79 (0.68, 0.91) for stroke and 0.85 (0.75, 0.96) for incident diabetes. The number of cohort studies which give evidence on individual dairy food items is very small, but, again, there is no convincing evidence of harm from consumption of the separate food items. In conclusion, there appears to be an enormous mis-match between the evidence from long-term prospective studies and perceptions of harm from the consumption of dairy food items.

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An improved stratospheric representation has been included in simulations with the Hadley Centre HadGEM1 coupled ocean atmosphere model with natural and anthropogenic forcings for the period 1979–2003. An improved stratospheric ozone dataset is employed that includes natural variations in ozone as well as the usual anthropogenic trends. In addition, in a second set of simulations the quasi biennial oscillation (QBO) of stratospheric equatorial zonal wind is also imposed using a relaxation towards ERA-40 zonal wind values. The resulting impact on tropospheric variability and trends is described. We show that the modelled cooling rate at the tropopause is enhanced by the improved ozone dataset and this improvement is even more marked when the QBO is also included. The same applies to warming trends in the upper tropical troposphere which are slightly reduced. Our stratospheric improvements produce a significant increase of internal variability but no change in the positive trend of annual mean global mean near-surface temperature. Warming rates are increased significantly over a large portion of the Arctic Ocean. The improved stratospheric representation, especially the QBO relaxation, causes a substantial reduction in near-surface temperature and precipitation response to the El Chichón eruption, especially in the tropical region. The winter increase in the phase of the northern annular mode observed in the aftermath of the two major recent volcanic eruptions is partly captured, especially after the El Chichón eruption. The positive trend in the southern annular mode (SAM) is increased and becomes statistically significant which demonstrates that the observed increase in the SAM is largely subject to internal variability in the stratosphere. The possible inclusion in simulations for future assessments of full ozone chemistry and a gravity wave scheme to internally generate a QBO is discussed.

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The mean state, variability and extreme variability of the stratospheric polar vortices, with an emphasis on the Northern Hemisphere vortex, are examined using 2-dimensional moment analysis and Extreme Value Theory (EVT). The use of moments as an analysis to ol gives rise to information about the vortex area, centroid latitude, aspect ratio and kurtosis. The application of EVT to these moment derived quantaties allows the extreme variability of the vortex to be assessed. The data used for this study is ECMWF ERA-40 potential vorticity fields on interpolated isentropic surfaces that range from 450K-1450K. Analyses show that the most extreme vortex variability occurs most commonly in late January and early February, consistent with when most planetary wave driving from the troposphere is observed. Composites around sudden stratospheric warming (SSW) events reveal that the moment diagnostics evolve in statistically different ways between vortex splitting events and vortex displacement events, in contrast to the traditional diagnostics. Histograms of the vortex diagnostics on the 850K (∼10hPa) surface over the 1958-2001 period are fitted with parametric distributions, and show that SSW events comprise the majority of data in the tails of the distributions. The distribution of each diagnostic is computed on various surfaces throughout the depth of the stratosphere, and shows that in general the vortex becomes more circular with higher filamentation at the upper levels. The Northern Hemisphere (NH) and Southern Hemisphere (SH) vortices are also compared through the analysis of their respective vortex diagnostics, and confirm that the SH vortex is less variable and lacks extreme events compared to the NH vortex. Finally extreme value theory is used to statistically mo del the vortex diagnostics and make inferences about the underlying dynamics of the polar vortices.

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There is emerging evidence to show that high levels of NEFA contribute to endothelial dysfunction and impaired insulin sensitivity. However, the impact of NEFA composition remains unclear. A total of ten healthy men consumed test drinks containing 50 g of palm stearin (rich in SFA) or high-oleic sunflower oil (rich in MUFA) on separate occasions; a third day included no fat as a control. The fats were emulsified into chocolate drinks and given as a bolus (approximately 10 g fat) at baseline followed by smaller amounts (approximately 3 g fat) every 30 min throughout the 6 h study day. An intravenous heparin infusion was initiated 2 h after the bolus, which resulted in a three- to fourfold increase in circulating NEFA level from baseline. Mean arterial stiffness as measured by digital volume pulse was higher during the consumption of SFA (P,0·001) but not MUFA (P¼0·089) compared with the control. Overall insulin and gastric inhibitory peptide response was greater during the consumption of both fats compared with the control (P,0·001); there was a second insulin peak in response to MUFA unlike SFA. Consumption of SFA resulted in higher levels of soluble intercellular adhesion molecule-1 (sI-CAM) at 330 min than that of MUFA or control (P#0·048). There was no effect of the test drinks on glucose, total nitrite, plasminogen activator inhibitor-1 or endothelin-1 concentrations. The present study indicates a potential negative impact of elevated NEFA derived from the consumption of SFA on arterial stiffness and sI-CAM levels. More studies are needed to fully investigate the impact of NEFA composition on risk factors for CVD.

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There have been relatively few tracer experiments carried out that have looked at vertical plume spread in urban areas. In this paper we present results from two tracer (cyclic perfluorocarbon) experiments carried out in 2006 and 2007 in central London centred on the BT Tower as part of the REPARTEE (Regent’s Park and Tower Environmental Experiment) campaign. The height of the tower gives a unique opportunity to study vertical dispersion profiles and transport times in central London. Vertical gradients are contrasted with the relevant Pasquill stability classes. Estimation of lateral advection and vertical mixing times are made and compared with previous measurements. Data are then compared with a simple operational dispersion model and contrasted with data taken in central London as part of the DAPPLE campaign. This correlates dosage with non-dimensionalised distance from source. Such analyses illustrate the feasibility of the use of these empirical correlations over these prescribed distances in central London.

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Previous analyses of Australian samples have suggested that populations of the same broad racial group (Caucasian, Asian, Aboriginal) tend to be genetically similar across states. This suggests that a single national Australian database for each such group may be feasible, which would greatly facilitate casework. We have investigated samples drawn from each of these groups in different Australian states, and have quantified the genetic homogeneity across states within each racial group in terms of the "coancestry coefficient" F(ST). In accord with earlier results, we find that F(ST) values, as estimated from these data, are very small for Caucasians and Asians, usually <0.5%. We find that "declared" Aborigines (which includes many with partly Aboriginal genetic heritage) are also genetically similar across states, although they display some differentiation from a "pure" Aboriginal population (almost entirely of Aboriginal genetic heritage).

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Fish-oil supplementation can reduce circulating triacylglycerol (TG) levels and cardiovascular risk. This study aimed to assess independent associations between changes in platelet eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and fasting and postprandial (PP) lipoprotein concentrations and LDL oxidation status, following fish-oil intervention. Fiftyfive mildly hypertriacylglycerolaemic (TG 1·5–4·0 mmol/l) men completed a double-blind placebo controlled cross over study, where individuals consumed 6 g fish oil (3 g EPA � DHA) or 6 g olive oil (placebo)/d for two 6-week intervention periods, with a 12-week wash-out period in between. Fish-oil intervention resulted in a significant increase in the platelet phospholipid EPA (+491 %, P,0·001) and DHA (+44 %, P,0·001) content and a significant decrease in the arachidonic acid (210 %, P,0·001) and g-linolenic acid (224 %, P,0·001) levels. A 30% increase in ex vivo LDL oxidation (P,0·001) was observed. In addition, fish oil resulted in a significant decrease in fasting and PP TG levels (P,0·001), PP non-esterified fatty acid (NEFA) levels, and in the percentage LDL as LDL-3 (P�0·040), and an increase in LDLcholesterol (P�0·027). In multivariate analysis, changes in platelet phospholipid DHA emerged as being independently associated with the rise in LDL-cholesterol, accounting for 16% of the variability in this outcome measure (P�0·030). In contrast, increases in platelet EPA were independently associated with the reductions in fasting (P�0·046) and PP TG (P�0·023), and PP NEFA (P�0·015), explaining 15–20% and 25% of the variability in response respectively. Increases in platelet EPA � DHA were independently and positively associated with the increase in LDL oxidation (P�0·011). EPA and DHA may have differential effects on plasma lipids in mildly hypertriacylglycerolaemic men.

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We sought to test the hypothesis that dietary long-chain n-3 PUFA (LC n-3 PUFA) in fish oil stimulate the gene expression of lipoprotein lipase (LPL) in human adipose tissue (AT). In a randomized, double blind, placebo-controlled, cross-over study, 51 male subjects expressing an atherogenic lipoprotein phenotype (ALP) had their diets supplemented with fish oil for 6 weeks. As we previously reported for this group, supplementation with LC n-3 PUFA produced a decrease in fasting plasma triglyceride (TG) (−35%, P < 0.05), attenuation of the postprandial TG response (area and incremental area under the curve; AUC and IAUC, P < 0.05), and a decrease in small, dense LDL. The present study extended these observations by showing that these changes were accompanied by a marked increase in the concentration of LPL mRNA in adipose tissue (AT-LPL mRNA, +55%, P = 0.003) and post-heparin LPL activity (PH-LPL, +31%, P = 0.036). There was also evidence of an association between LPL gene expression and polymorphism in the apolipoprotein E gene. We conclude that the favorable influence of dietary n-3 PUFA on the ALP may be mediated, in part, through an increase in the plasma activity and gene expression of lipoprotein lipase in human adipose tissue.

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OBJECTIVE: To investigate relationships between body fat and its distribution and carbohydrate and lipid tolerance using statistical comparisons in post-menopausal women. DESIGN: Sequential meal, postprandial study (600 min) which included a mixed standard breakfast (30 g fat) and lunch (44 g fat) given at 0 and 270 min, respectively, after an overnight fast. SUBJECTS: Twenty-eight post-menopausal women with a diverse range of body weight (body mass index (BMI), mean 27.2, range 20.5-38.8 kg/m2) and abdominal fat deposition (waist, mean 86.4, range 63.5-124.0 cm). Women with BMI <18 or >37 kg/m2, age>80 y and taking hormone replacement therapy (HRT) were excluded. MEASUREMENTS: Anthropometric measurements were performed to assess total and regional fat deposits. The concentrations of plasma total cholesterol, high density lipoprotein (HDL) cholesterol, triacylglycerol (TAG), glucose, insulin (ins), non-esterified fatty acids (NEFA) and apolipoprotein (apo) B-48 were analysed in plasma collected at baseline (fasted state) and at 13 postprandial time points for a 600 min period. RESULTS: Insulin concentrations in the fasted and fed state were significantly correlated with all measures of adiposity (BMI, waist, waist-hip ratio (W/H), waist-height ratio (W/Ht) and sum of skinfold thickness (SSk)). After controlling for BMI, waist remained significantly and positively associated with fasted insulin (r=0.559) with waist contributing 53% to the variability after multiple regression analysis. After controlling for waist, BMI remained significantly correlated with postprandial (IAUC) insulin (r=0.535) contributing 66% of the variability of this measurement. No association was found between any measures of adiposity and glucose concentrations, although insulin concentration in relation to glucose concentration (glucose-insulin ratio) was significantly negatively correlated with all measures of adiposity. A significant positive correlation was found between fasted TAG and BMI (r=0.416), waist (r=0.393) and Ssk (r=0.457) and postprandial (AUC) TAG with BMI (r=0.385) and Ssk (r=0.406). A significantly higher postprandial apolipoprotein (apo) B-48 response was observed in those women with high BMI (>27 kg/m2). Fasting levels of NEFA were significantly and positively correlated with all measures of adiposity (except W/H). No association was found between cholesterol containing particles and any measure of adiposity. CONCLUSION: Hyperinsulinaemia associated with increasing body fat and central fat distribution is associated with normal glucose but not TAG or NEFA concentrations in postmenopausal women.

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The aim was to determine in 32 healthy young men from northern and southern Europe whether differences in the secretion of insulin and glucose-dependent insulinotropic polypeptide (GIP) might explain these findings through the actions of these hormones on lipoprotein lipase. In a randomized, single-blind, crossover study the effects of 2 test meals of identical macronutrient composition but different saturated fatty acid (SFA) and monounsaturated fatty acid (MUFA) contents were investigated on postprandial GIP, insulin, the ratio of incremental triacylglycerol to apolipoprotein B-48 (a marker of chylomicron size), and the activity of postheparin lipases. Fasting and postprandial GIP concentrations and postheparin hepatic lipase (HL) activities were higher in the southern Europeans (P<0.001 and P<0.02, respectively). Lipoprotein lipase activity after the SFA-rich meal was higher in the northern Europeans (P<0.01). HL activity 9 h after the SFA-rich meal and the area under the curve (AUC) for the postprandial insulin response correlated with the AUC for the postprandial GIP response (r=0.44 (P<0.04) and r=0.46 (P<0.05), respectively). There were no significant differences in chylomicron size between the 2 groups for either meal, but when the groups were combined there was a difference in chylomicron size between the SFA- and MUFA-rich meals (P<0.05), which could be due to the formation of larger chylomicrons after the MUFA-rich meal. The significantly higher GIP and insulin responses and HL activities in southern Europeans may provide an explanation for a previous report of attenuated postprandial triacylglycerol and apolipoprotein B-48 responses in them.

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OBJECTIVE: To investigate the associations between indices of adiposity and cardiovascular risk factors in individuals with an atherogenic lipoprotein phenotype (ALP). SUBJECTS: Fifty-five men, aged 34-69 y, body mass index (BMI) 22-35 kg/m2, with an ALP lipid profile (triglycerides (TG) 1.5-4.0 mmol/l, HDL<1.1 mmol/l; %LDL-3>40% total LDL). DESIGN: Each participant provided a fasting blood sample and underwent an 8 h postprandial assessment and had anthropometric measurements taken. OUTCOME MEASURES: BMI, waist circumference (W), waist-to-hip ratio (W/H), sum of skinfolds (SSK), fasting and postprandial concentrations of glucose, insulin and plasma lipids, post-heparin lipase activity, and apoE genotype. RESULTS: The expected positive associations between BMI, W and SSK and fasting and postprandial insulin were observed (r=0.42-0.65). Little association between glucose responses and any measures of adiposity was evident. Unexpectedly, there were no positive associations between measures of central adiposity (W and W/H) and fasting and postprandial TG responses, with a trend towards negative associations in this study group (TG AUC vs W, r=-0.23, P=0.097; TG IAUC vs W/H, r=-0.26, P=0.068). Subgroup analysis indicated that lack of a positive association between central adiposity and postprandial TG values was more evident in those with one E4 allele (r=-0.42, P=0.077) relative to non-E4 carriers (r=-0.16, P=0.430). The expected positive associations between insulin and TG responses were not observed (r=-0.03 to -0.36). CONCLUSION: In this ALP group the expected positive association between TG responses and a centralized distribution of body fat was not observed, particularly in individuals with an apoE4 genotype. Our findings are not in line with the view that there is a clear causal relationship between insulin resistance and the lipid abnormalities associated with ALP.