27 resultados para ELEVATED BLOOD LEAD

em Deakin Research Online - Australia


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Aims. To evaluate the effectiveness of a health promotion
programme targeting dietary behaviours and physical
activity among male hourly-paid workers and to explore
demographic and attitudinal influences on dietary patterns
at baseline.
Methods. A controlled field trial compared workers at one
intervention and one control worksite. The intervention
comprised nutrition displays in the cafeteria and monthly
30-minute workshops for six months. Key outcome
measures at six and twelve-months were self-reported
dietary and lifestyle behaviours, nutrition knowledge, body
mass index (BMI), waist circumference and blood pressure.
Results. 132 men at the intervention site and 121 men at the
control site participated in the study and a high retention rate
(94% at 6-months and 89% at 12-months) was achieved. At
baseline, 40% of the total sample (253) were obese, 30% had
elevated blood pressure, 59% indicated an excessive fat intake
and 92% did not meet the recommended vegetable and fruit
intake. The intervention reduced fat intake, increased
vegetable intake and physical activity, improved nutrition
knowledge and reduced systolic blood pressure when
compared to the control site. There was no difference in
change in mean BMI or waist circumference. Reduction in
BMI was associated with reduction in fat intake.
Discussion. Low intensity workplace intervention can
significantly improve reported health behaviours and
nutrition knowledge although the impact on more
objective measures of risk was variable. A longer duration
or more intensive intervention may be required to achieve
further reduction in risk factors.

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The client in this case report self referred for the use of hypnosis during childbirth. The current pregnancy had been uneventful except for intermittent problems with elevated blood pressure. The client was seen for four sessions prior to a successful delivery using hypnosis. This paper describes in detail the preparation for childbirth using hypnotic techniques, an abreaction that occurred during this time and the use of hypnosis to control blood pressure.

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This study was designed to test the effectiveness of a culturally appropriate diet and lifestyle intervention to treat metabolic syndrome in female Pakistani immigrants residing in Melbourne, Australia. Forty Pakistani women with metabolic syndrome (aged 20-50 years) completed a 12-week culturally appropriate diet and exercise program. Results indicate that, before intervention, participants were sedentary, taking 4000 ± 22.6 steps per day, and had an obese-classified body mass index (BMI) of 29.2 ± 0.46 kg/m2 (BMI was categorized in accordance with guidelines specifically designed for Asians) and high waist circumference of 132 ± 25.95 cm. Participants were hypertensive (systolic, 135 ± 1.3 mm Hg; diastolic, 86 ± 0.68 mm Hg), were dyslipidemic (total cholesterol, 6.8 ± 0.15 mmol/L; triglycerides, 2.9 ± 0.09 mmol/L), and had elevated blood glucose (6.4 ± 0.33 mmol/L) and fasting blood insulin (45 ± 6.3 μU/mL) levels. After the 12-week culturally appropriate intervention, activity increased (8600 ± 596.7 steps per day, P < .05); and BMI (27.8 ± 0.45 kg/m2), blood pressure (systolic, 125 ± 1.4 mm Hg; diastolic, 80 ± 0.6 mm Hg), cholesterol (5.5 ± 0.1 mmol/L), blood glucose (5.9 ± 0.33 mmol/L), and blood insulin (24.14 ± 1.8 μU/mL) levels were all significantly reduced (P < .05). This study revealed that the Pakistani female migrants who had metabolic syndrome and its components can successfully be treated via a culturally appropriate diet and lifestyle intervention. The success of the current program raises the possibility that other high-risk ethnic groups can also be treated with a culturally appropriate program.

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Background and objectives The digestion rate of proteins and subsequent absorption of amino acids can independently modulate protein metabolism. The objective of the present study was to examine the blood amino acid response to whey protein isolate (WPI), β-lactoglobulin-enriched WPI, hydrolysed WPI and a flavour-identical control.

Methods Eight healthy adults (four female, four male) were recruited (mean±standard error of the mean: age, 27.0±0.76 years; body mass index, 23.2±0.8 kg/cm2) and after an overnight fast consumed 500 ml of each drink, each containing 25g protein, in a cross-over design. Blood was taken at rest and then every 15 min for 2 h post ingestion.

Results Ingesting the β-lactoglobulin-enriched WPI drink resulted in significantly greater plasma leucine concentrations at 45-120 min and significantly greater branched-chain amino acid concentrations at 60-105 min post ingestion compared with hydrolysed WPI. No differences were observed between WPI and β-lactoglobulin-enriched WPI, and all protein drinks resulted in elevated blood amino acids compared with flavour-identical control.

Conclusions In conclusion, whole proteins resulted in a more rapid absorption of leucine and branched-chain amino acid into the blood compared with the hydrolysed molecular form of whey protein.

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Aims/hypothesis We assessed whether the relationships between insulin sensitivity and all-cause mortality as well as fatal or non-fatal cardiovascular disease (CVD) events are independent of elevated blood glucose, high blood pressure, dyslipidaemia and body composition in individuals without diagnosed diabetes.
Methods
Between 1999 and 2000, baseline fasting insulin, glucose and lipids, 2 h plasma glucose, HbA1c, anthropometrics, blood pressure, medication use, smoking and history of CVD were collected from 8,533 adults aged >35 years from the population-based Australian Diabetes, Obesity and Lifestyle study. Insulin sensitivity was estimated by HOMA of insulin sensitivity (HOMA-%S). Deaths and fatal or non-fatal CVD events were ascertained through linkage to the National Death Index and medical records adjudication.
Results
After a median of 5.0 years there were 277 deaths and 225 CVD events. HOMA-%S was not associated with all-cause mortality. Compared with the most insulin-sensitive quintile, the combined fatal or non-fatal CVD HR (95% CI) for quintiles of decreasing HOMA-%S were 1.1 (0.6–1.9), 1.4 (0.9–2.3), 1.6 (1.0–2.5) and 2.0 (1.3–3.1), adjusting for age and sex. Smoking, CVD history, hypertension, lipid-lowering medication, total cholesterol and waist-to-hip ratio moderately attenuated this relationship. However, the association was rendered non-significant by adding HDL. Fasting plasma glucose, but not HOMA-%S significantly improved the prediction of CVD, beyond that seen with other risk factors.
Conclusions/interpretation In this cohort, HOMA-%S showed no association with all-cause mortality and only a modest association with CVD events, largely explained by its association with HDL. Fasting plasma glucose was a better predictor of CVD than HOMA-%S.

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Metabolic syndrome (MetS), also previously known by a variety of other names, including insulin resistance syndrome and the deadly quartet, is characterized by clustering of abdominal (visceral and retroperitoneal) obesity and other cardiovascular risk factors, including impaired glucose regulation, raised triglycerides, decreased high-density lipoprotein cholesterol (HDL-C), elevated blood pressure (BP).

Associated with increased risk of both type 2 diabetes and cardiovascular disease (CVD), MetS is believed to be a contributor to the modern-day epidemics of diabetes and CVD and has become a major public health challenge around the world [I]. Currently, there are five different sets of criteria which have been developed to characterize the syndrome. These definitions differ in the components included and the cut-points used for each component. The prevalence of MetS in the westernized world is significant (10-50%) and believed to be increasing over time. The pathophysiology of the syndrome is unclear, but it is thought that obesity and/or insulin resistance are key underlying components. Genetics, lifestyle and environment factors are also important causes of MetS.

This chapter provides:

• a historical overview of the evolution of MetS;
• a summary of the value of the different definitions used to characterize the syndrome;
• a summary of the underlying pathophysiology, the causes and other important risk factors of MetS;
• a summary of the evidence describing the association of MetS with CVD and diabetes;
• a summary of the prevalence of MetS using the various definitions in different countries.

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Hypertension is one of many side effects of oral contraceptive use in a small percentage of women. Although the underlying pathology has yet to be fully resolved, alterations in the renin-angiotensin-aldosterone axis, sympathetic nervous system/ renal and cardiac function have been implicated. In the thesis to be presented, the possible involvement of alterations in renal and myocardial adrenoceptor characteristics in the pathogenesis of steroid contraceptive-induced hypertension in rats was examined by radioligand binding techniques. In Chapter 2, a rat model of OC hypertension is described. Chronic low-dose administration of ethynyloestradiol (EE2), levonorgestrel (NG) or a combination of both steroids (EE2/NG) to female Sprague-Dawley rats was shown to significantly increase systolic blood pressure (SBP). Renal and cardiac hypertrophy developed in association with EE2-, EE2/NG- but not NG-induced hypertension. Moreover, whereas administration of NG alone attenuated body weight gain, combined EE2/NG administration increased body weight gain from the second week of treatment onwards. Based on the above observations, it is proposed that EE2 and NG induce hypertension in rats via different mechanisms. Although SBP was elevated to a similar maximum in all steroid-treated groups (+ 20 mmHg compared to controls), only with EE2 administration did SBP remain elevated for the duration of the 17 week treatment regimen. NG may therefore have a protective effect on blood pressure with long-term combined steroid contraceptive treatment. In Chapter 4, renal adrenoceptors were characterized using radioactively labelled adrenocephor antagonists. Under appropriate conditions, binding of [3H]-prazosin and [3H]-rauwolscine to membrane preparations of whole rat kidney displayed the kinetics, saturability and specificity of α1- and α2 -adrenoceptors respectively, which were present in a ratio 3:1. In contrast, [3H]-dihydroergocryptine ([3H]-DHE) apparently bound to both α1 and α2-adrenoceptors. Binding sites identified by [125I] –iodocyanopindolol (ICYP) had the recognition characteristics of β-adrenoceptors. In drug competition studies using the subtype-selective antagonists practolol (β1) and ICI 118,551 (β2)/ the ratio of β1- to β2 -adrenoceptors was found to be approximately 2:1. Subsequently, renal adrenoceptors were investigated at various stages during the development of hypertension with the different steroid contraceptive treatments (Chapters 5 and 6). Preliminary binding studies with [3H]-DHE and [3H]-prazosin suggested that the number of renal α2 - but not α1-adrenoceptors was reduced in rats with established EE2-induced hypertension (17 weeks treatment). This was subsequently confirmed using [3H]-rauwolscine, which in addition showed that the reduction in renal α2 -adrenoceptor number occurred during the developmental stage of EE2/NG~induced hypertension (6 weeks treatment) and established EE2-induced hypertension (12 weeks treatment). NG induced hypertension was unassociated with changes in renal α1- and α2-adrenoceptor characteristics. Renal β-adrenoceptor affinity was reduced in established EE2-, but not NG- or EE2/NG- induced hypertension. Moreover, the β-adrenoceptor agonist (-)-isoprenaline bound to renal β-adrenoceptors with reduced affinity following EE2 administration. Several endogenous and synthetic steroids were found to be ineffective inhibitors of [3H] –prazosin, [3H] –rauwolscine and ICYP binding excluding a direct interaction of these steroids with renal α1-, α2- and β -adrenoceptors. In Chapter 7, myocardial adrenoceptors were characterized and investigated in steroid-treated rats. In membrane preparations of whole myocardium, [3H]-prazosin binding was characteristically to α1- adrenoceptors, whereas there was a notable absence of [3H]-rauwolscine binding. Using ICYP, β-adrenoceptors were also detected, the ratio of β1- to β2~adrenoceptors being 3:1. Steroid contraceptive-induced hypertension was not associated with myocardial α1-adrenoceptor changes. Similarly, myocardial β-adrenoceptors were unchanged in established EE2-, NG- and EE2/NG-induced hypertension (12 weeks treatment). The affinity of (-)-isoprenaline for myocardial β-adrenoceptors was unaffected by EE2 aditiinistration. These studies suggest that established EE2- but not NG-induced hypertension in rats is associated with selective alterations in renal α2- and (β-adrenoceptors. These adrenoceptor changes may help to maintain elevated blood pressure by affecting the control of renal function by the sympathetic nervous system, catecholamines and several hormones which affect renin release and the transport of fluid and electrolytes in the nephron.

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Infiltration of macrophages into the artery wall plays detrimental roles during hypertension by promoting vascular inflammation and endothelial dysfunction, and it occurs via a chemo-attractant action of chemokines on macrophage cytokine receptors. We sought to identify the key chemokine receptors associated with macrophage infiltration into the vascular wall during deoxycorticosterone acetate (DOCA)/salt-induced hypertension in mice and to evaluate the impact of pharmacological inhibition of these receptors on blood pressure and leukocyte accumulation. Mice treated with DOCA/salt for 21 days displayed markedly elevated systolic blood pressure (158±2 versus 114±5 mm Hg in sham group; P<0.0001). Polymerase chain reaction screening via a gene array of 20 chemokine receptors indicated an increased expression of CCR2 in aortas of DOCA/salt-treated mice. Real-time polymerase chain reaction confirmed mRNA upregulation of CCR2 in aortas from DOCA/salt-treated animals and of the CCR2 ligands CCL2, CCL7, CCL8, and CCL12 (all >2-fold versus sham; P<0.05). Flow cytometry revealed 2.9-fold higher macrophage numbers (ie, CD45+ CD11b+ F4/80+ cells) in the aortic wall of DOCA/salt versus sham-treated mice. Intervention with a CCR2 antagonist, INCB3344 (30 mg/kg per day, IP), 10 days after the induction of hypertension with DOCA/salt treatment, reduced the aortic expression of CCR2 mRNA and completely reversed the DOCA/salt-induced influx of macrophages. Importantly, INCB3344 substantially reduced the elevated blood pressure in DOCA/salt-treated mice. Hence, our findings highlight CCR2 as a promising therapeutic target to reduce both macrophage accumulation in the vascular wall and blood pressure in hypertension.

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The reactions of group 14 tetrachlorides MCl4 (M=Si, Ge, Sn) with oleum (65 % SO3) at elevated temperatures lead to the unique complex ions [M(S2O7)3]2−, which show the central M atoms in coordination with three chelating S2O72− groups. The mean distances M[BOND]O within the anions increase from 175.6(2)–177.5(2) pm (M=Si) to 186.4(4)–187.7(4) pm (M=Ge) to 201.9(2)–203.5(2) pm (M=Sn). These distances are reproduced well by DFT calculations. The same calculations show an increasing positive charge for the central M atom in the row Si, Ge, Sn, which can be interpreted as the decreasing covalency of the M[BOND]O bonds. For the silicon compound (NH4)2[Si(S2O7)3], 29Si solid-state NMR measurements have been performed, with the results showing a signal at −215.5 ppm for (NH4)2[Si(S2O7)3], which is in very good agreement with theoretical estimations. In addition, the vibrational modes within the [MO6] skeleton have been monitored by Raman spectroscopy for selected examples, and are well reproduced by theory. The charge balance for the [M(S2O7)3]2− ions is achieved by monovalent A+ counter ions (A=NH4, Ag), which are implemented in the syntheses in the form of their sulfates. The sizes of the A+ ions, that is, their coordination requirements, cause the crystallographic differences in the crystal structures, although the complex [M(S2O7)3]2− ions remain essentially unaffected with the different A+ ions. Furthermore, the nature of the A+ ions influences the thermal behavior of the compounds, which has been monitored for selected examples by thermogravimetric differential thermal analysis (DTA/TG) and XRD measurements.

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AIMS: The metabolic syndrome (MetS) is a risk factor for cancer. However, it is not known if the MetS confers a greater cancer risk than the sum of its individual components, which components drive the association, or if the MetS predicts future cancer risk. MATERIALS AND METHODS: We linked 20,648 participants from the Australian and New Zealand Diabetes and Cancer Collaboration with complete data on the MetS to national cancer registries and used Cox proportional hazards models to estimate associations of the MetS, the number of positive MetS components, and each of the five MetS components separately with the risk for overall, colorectal, prostate and breast cancer. Hazard ratios (HR) and 95% confidence intervals (95%CI) are reported. We assessed predictive ability of the MetS using Harrell's c-statistic. RESULTS: The MetS was inversely associated with prostate cancer (HR 0.85; 95% CI 0.72-0.99). We found no evidence of an association between the MetS overall, colorectal and breast cancers. For those with five positive MetS components the HR was 1.12 (1.02-1.48) and 2.07 (1.26-3.39) for overall, and colorectal cancer, respectively, compared with those with zero positive MetS components. Greater waist circumference (WC) (1.38; 1.13-1.70) and elevated blood pressure (1.29; 1.01-1.64) were associated with colorectal cancer. Elevated WC and triglycerides were (inversely) associated with prostate cancer. MetS models were only poor to moderate discriminators for all cancer outcomes. CONCLUSIONS: We show that the MetS is (inversely) associated with prostate cancer, but is not associated with overall, colorectal or breast cancer. Although, persons with five positive components of the MetS are at a 1.2 and 2.1 increased risk for overall and colorectal cancer, respectively, and these associations appear to be driven, largely, by elevated WC and BP. We also demonstrate that the MetS is only a moderate discriminator of cancer risk.

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Background : Dietary ω-3 fatty acid deficiency can lead to hypertension in later life; however, hypertension is affected by numerous other dietary factors. We examined the effect of altering the dietary protein level on blood pressure in animals deficient or sufficient in ω-3 fatty acids.

Methods : Female rats were placed on one of four experimental diets 1 week prior to mating. Diets were either deficient (10% safflower oil; DEF) or sufficient (7% safflower oil, 3% flaxseed oil; SUF) in ω-3 fatty acids and contained 20 or 30% casein (DEF20, SUF20, DEF30, SUF30). Offspring were maintained on the maternal diet for the duration of the experiment. At 12, 18, 24, and 30 weeks, blood pressure was assessed by tail cuff plethysmography.

Results : At both 12 and 18 weeks of age, no differences in blood pressure were observed based on diet, however, by 24 weeks hypertension was evident in DEF30 animals; there were no blood pressure differences between the other groups. This hypertension in DEF30 group was increased at 30 weeks, with systolic, diastolic, and mean arterial pressure all elevated.

Conclusions : These results indicate that the hypertension previously attributed to ω-3 fatty acid deficiency is dependent on additional dietary factors, including protein content. Furthermore, this study is the first to plot the establishment of ω-3 fatty acid deficiency hypertension over time.

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Introduction
Angiotensin II (Ang II) is known to induce cardiac growth and modulate myocardial contractility. It has been reported that elevated levels of endogenous Ang II contribute to the development of cardiac hypertrophy in hypertensives. However, the long-term functional effects of cardiac exposure to Ang II in normotensives is unclear.

A recently developed transgenic mouse (TG1306/1R), in which cardiac-specific overproduction of Ang II produces primary hypertrophy, provides a new experimental model for investigation of this phenotype. The aim of the present study was to use this model to investigate whether there is a functional deficit in primary hypertrophy that may predispose to cardiac failure and sudden death. We hypothesised that primary cardiac hypertrophy is associated with mechanical dysfunction in the basal state.

Methods
Normotensive heterozygous TG1306/1R mice harbouring multiple copies of a cardiac-specific rat angiotensinogen gene were studied at age 30—40 weeks and compared with age-matched wild-type littermates. Left ventricular function was measured ex vivo in bicarbonate buffer-perfused, Langendorffmounted hearts ( at a perfusion pressure of 80 mmHg, 37°C) using a fluid-filled PVC balloon interfaced to a pressure transducer and digital data acquisition system.

Results
There was no difference in the mean (±SEM) intrinsic heart rate of TG1306/1R and wild-type control mice (357.4±11.8 vs. 367.5±20.9 bpm, n=9 & 7). Under standardised end-diastolic pressure conditions, TG1306/1R hearts exhibited a significant reduction in peak developed pressure (132.2±9.4 vs. 161.5±3.1 mmHg, n=9 & 7, p<0.05) and maximum rate of pressure development (3566.7±323.7 vs. 4486.3±109.4 mmHg, n=9 & 7, p<0.05). TG1306/1R mice show a significant correlation between incidence of arrhythmia and increasing heart size (Spearman's correlation coefficient 0.61).

Conclusion
These data demonstrate that chronic in vivo exposure to elevated levels of intra-cardiac Ang II is associated with significant contractile abnormalities evident in the ex vivo intact heart. Our findings suggest that endogenous overproduction of cardiac Ang II, independent of changes in blood pressure, is sufficient to induce ventricular remodelling that culminates in impaired cardiac function which may precede failure.

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Obesity, strongly associated with the risk for coronary heart disease (CHD), is becoming increasingly prevalent. This study was designed to establish first whether systemic arterial compliance (SAC), an index of arterial function, is improved with weight loss and second, whether cardiovascular risk factors that improve with weight loss are reduced equally with lean meat or with an equivalent amount of plant protein in the diet. Thirty-six women, mostly overweight or obess, aged 40 ± 9 years, were allocated nonrandomly to a 16-week parallel-design trial of two equienergetic diets designed to lead to weight loss, with one arm of the study emphasizing red meat and the other soybeans as the major protein source. Body weight, waist and hip circumference, and plasma lipids, glucose, insulin, and leptin levels were measured, and SAC was calculated from ultrasound measurement of aortic flow velocity and aortic root driving pressure. Subjects lost weight (9% of body weight in 16 weeks) and showed decreased plasma total and low-density lipoprotein (LDL) cholesterol (12% and 14%, P < .0001, respectively), triacylglycerol (17%, P < .05), and leptin (24%, P < .01) concentrations. However, lipoprotein(a) [Lp(a)] levels did not change significantly. Mean arterial pressure (MAP) decreased 7% and SAC increased 28% (P < .001 for both). However, only the decrease in arterial pressure correlated significantly with the reduction in the waist to hip ratio (WHR), and the improvement in SAC correlated inversely with the blood pressure reduction (P < .001 for both). Further, weight loss and the metabolic benefits of weight loss occurred equally with the meat-based and plant-based diets. We conclude that moderate weight loss in women leads to a substantial reduction in the cardiovascular risk, including SAC.