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  • 1
    Electronic Resource
    Electronic Resource
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 7 (2002), S. 0 
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 5 (2000), S. 0 
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: OBJECTIVE: To determine whether lipid-modifying therapy with atorvastatin improves impaired endothelial function in patients with nephrotic range proteinuria (NRP).METHODS: A sequential, open-label study of the effects of atorvastatin on dyslipidaemia and endothelial dysfunction in 9 patients with NRP. Endothelial function was assessed at baseline, after 12 weeks of atorvastatin treatment and after an 8 week wash-out period. Brachial artery endothelial function was studied by measuring post-ischaemic flow-mediated dilatation (FMD) using ultrasonography. Endothelium- independent, glyceryl trinitrate (GTN) mediated vasodilatation was also measured.RESULTS: At baseline, median serum albumin was 31g/L (range 20-40) and 24 hour protein excretion was 4.7g (1.0-16.23). There was no significant change in serum creatinine and 24 hour protein excretion during the study. Total cholesterol (TC) and triglycerides (TG) were significantly lower following treatment with atorvastatin 20mg (20-40): TC 8.1mmol/L (5.9-14.9) vs. 5.2 (4.0-8.6), TG 2.9mmol/L (1.3-15.0) vs. 1.6 (1.0-3.5), both p 〈 0.05. Brachial artery FMD improved significantly following atorvastatin treatment: 2.1% (-1.2- 5.2%) to 4.7% (0.8-16.3%), p 〈 0.05. At the end of the 8 week wash-out, FMD had significantly deteriorated to 3.2% (-2.8-8.2), p 〈 0.05 vs. week 12 FMD, and was similar to pre-treatment values. GTN mediated dilatation was unchanged through the study.CONCLUSION: Atorvastatin significantly reduced the hyperlipidaemia of NRP. This was associated with improved conduit artery endothelial function after 12 weeks of treatment. This is consistent with the hypothesis that dyslipoproteinaemia is the primary cause of endothelial dysfunction in NRP.
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  • 3
    Electronic Resource
    Electronic Resource
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 5 (2000), S. 0 
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: OBJECTIVE: To test the hypothesis that endothelial dysfunction occurs in nephrotic range proteinuria primarily as a consequence of dyslipidaemia.METHODS: Brachial artery and forearm microcirculatory endothelial function was compared among patients with nephrotic range proteinuria (NRP, n = 14 ), primary hyperlipidaemia (HL, n = 15) and normal controls (NC, n = 16). Endothelial function was studied by measuring post-ischaemic flow-mediated dilatation (FMD) of the brachial artery using high resolution ultrasonography. Endothelium-independent, glyceryl trinitrate (GTN) mediated brachial artery vasodilatation was also measured. Basal and post-ischaemic blood flow of the forearm microcirculation was measured using venous-occlusion strain gauge plethysmography.RESULTS: Serum creatinine was similar among groups. The proteinuric group had a mean albumin of 27.6g/L(1.8) and 24-hour urinary protein excretion of 6.3g(1.3). Plasma lipids and lipoproteins were not statistically different between the NRP and HL groups. Brachial artery FMD was significantly lower in the NRP and HL groups compared with the controls (NRP 4.7%(1.3)*, HL 4.9%(0.7)* and NC 8.3%(0.6), *p = 0.012 vs. NC); GTN mediated dilatation and basal and post-ischaemic forearm blood flow were not statistically different among the three groups.CONCLUSION: Patients with nephrotic range proteinuria have endothelial dysfunction of conduit arteries in the peripheral circulation, similar to that observed in patients with primary hyperlipidaemia. This suggests dyslipoproteinaemia is the principal cause of endothelial dysfunction of conduit arteries in nephrotic range proteinuria. Confirmation of this should be sought with an intervention trial of lipid-regulating therapy.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Pty
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The growth enzyme phosphatidylinositol 3-kinase (PI3K) was recently implicated in the mediation of arterial spontaneous tone, an event observed in arteries from hypertensive, but not normotensive, subjects that contributes to changes in total peripheral resistance in the hypertensive state. We have shown this occurrence in experimentally induced models of hypertension. However, because the majority of hypertension is genetically based, it is important to demonstrate a similar change in genetically hypertensive animals.2. Aorta from spontaneously hypertensive rats (SHR; systolic blood pressure = 183 ± 4 mmHg) and Wistar Kyoto (WKY) rats (115 ± 2 mmHg) were isolated for the measurement of isometric contractile force. Aorta from SHR displayed small increases (approximately 5% maximum phenylephrine (PE)-induced contraction) in spontaneous tone, whereas aorta from WKY rats displayed none. The non-selective PI3K inhibitor LY294002 (20 µmol/L) and the selective inhibitor of the p110δ catalytic subunit of PI3K IC87114 (20 µmol/L) caused a fall of basal tone in SHR aorta (20 ± 7 and 24 ± 6% of the initial PE contraction, respectively), but did not alter tone in arteries from WKY rats. LY294002, but not IC87114, normalized the increased potency of noradrenaline (NA) observed in aorta from SHR (–log EC50 values for NA in the presence of vehicle in WKY rats and SHR 7.5 ± 0.1 and 7.8 ± 0.1, respectively (P 〈 0.05); –log EC50 values for NA in the presence of LY294002 in WKY rats and SHR 7.0 ± 0.1 and 7.0 ± 0.1, respectively).3. Biochemical expression of the p110 catalytic and p85 regulator subunits of PI3K in western analyses revealed no difference in expression of the regulatory p85α or p110α protein subunits between WKY rats and SHR; p110γ was not detected. In contrast, p110δ expression was increased greater than 30% in aorta from SHR compared with WKY rats (827.6 ± 88.5 vs 576.8 ± 53.4 arbitrary densitometry units, respectively). Immunohistochemical analyses revealed expression of the p110δ isoform in the smooth muscle of arteries.4. These data underscore the relevance of an enzyme historically classified as one committed to growth/anti-apoptosis in modifying contractility and supports involvement of PI3K in genetically based hypertension.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Melbourne, Australia : Blackwell Science Pty
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Decline in β-adrenoceptor (β-AR)-mediated function occurs with increasing age, as well as in multiple disease conditions. The mechanisms responsible for this decline include alterations in β-AR itself, β-AR coupling proteins, such as G-proteins, or other β-AR-linked proteins, such as G-protein receptor kinases and/or phosphatases.2. The present study examines the physiological effects of in vitro transfer of constitutively activated Gαs (Gαs-Q227L) to both cultured vascular smooth muscle cells (VSMC) and whole aortic tissue of 6-month-old (adult) animals via a replication-deficient Herpes simplex virus (HSV) vector. These studies were conducted to provide a model for future examination of the role of Gαs in the age-related decline in β-AR-mediated vasorelaxation.3. Gene transfer was confirmed by western blotting for specific proteins. Aortic tissue infected with HSV–Gαs-Q227L had reduced phenylephrine-induced contraction and enhanced isoproterenol-stimulated vasorelaxation. Infection of cultured VSMC with HSV–Gαs-Q227L increased both basal- and isoproterenol-stimulated cAMP accumulation, whereas forskolin-stimulated cAMP production was unchanged.4. These results implicate Gαs as a target for further investigation in age-related changes in vascular reactivity and support the use of viral-mediated gene transfer as an effective tool to study adrenergic signal transduction and physiology in vascular tissue.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 5 (2000), S. 0 
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: OBJECTIVE: To determine whether lipid-modifying therapy with atorvastatin improves impaired endothelial function in patients with nephrotic range proteinuria (NRP).METHODS: A sequential, open-label study of the effects of atorvastatin on dyslipidaemia and endothelial dysfunction in 9 patients with NRP. Endothelial function was assessed at baseline, after 12 weeks of atorvastatin treatment and after an 8 week wash-out period. Brachial artery endothelial function was studied by measuring post-ischaemic flow-mediated dilatation (FMD) using ultrasonography. Endothelium- independent, glyceryl trinitrate (GTN) mediated vasodilatation was also measured.RESULTS: At baseline, median serum albumin was 31g/L (range 20-40) and 24 hour protein excretion was 4.7g (1.0-16.23). There was no significant change in serum creatinine and 24 hour protein excretion during the study. Total cholesterol (TC) and triglycerides (TG) were significantly lower following treatment with atorvastatin 20mg (20-40): TC 8.1mmol/L (5.9-14.9) vs. 5.2 (4.0-8.6), TG 2.9mmol/L (1.3-15.0) vs. 1.6 (1.0-3.5), both p 〈 0.05. Brachial artery FMD improved significantly following atorvastatin treatment: 2.1% (-1.2- 5.2%) to 4.7% (0.8-16.3%), p 〈 0.05. At the end of the 8 week wash-out, FMD had significantly deteriorated to 3.2% (-2.8-8.2), p 〈 0.05 vs. week 12 FMD, and was similar to pre-treatment values. GTN mediated dilatation was unchanged through the study.CONCLUSION: Atorvastatin significantly reduced the hyperlipidaemia of NRP. This was associated with improved conduit artery endothelial function after 12 weeks of treatment. This is consistent with the hypothesis that dyslipoproteinaemia is the primary cause of endothelial dysfunction in NRP.
    Type of Medium: Electronic Resource
    Location Call Number Limitation Availability
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  • 7
    Electronic Resource
    Electronic Resource
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 5 (2000), S. 0 
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: OBJECTIVE: To test the hypothesis that endothelial dysfunction occurs in nephrotic range proteinuria primarily as a consequence of dyslipidaemia.METHODS: Brachial artery and forearm microcirculatory endothelial function was compared among patients with nephrotic range proteinuria (NRP, n = 14 ), primary hyperlipidaemia (HL, n = 15) and normal controls (NC, n = 16). Endothelial function was studied by measuring post-ischaemic flow-mediated dilatation (FMD) of the brachial artery using high resolution ultrasonography. Endothelium-independent, glyceryl trinitrate (GTN) mediated brachial artery vasodilatation was also measured. Basal and post-ischaemic blood flow of the forearm microcirculation was measured using venous-occlusion strain gauge plethysmography.RESULTS: Serum creatinine was similar among groups. The proteinuric group had a mean albumin of 27.6g/L(1.8) and 24-hour urinary protein excretion of 6.3g(1.3). Plasma lipids and lipoproteins were not statistically different between the NRP and HL groups. Brachial artery FMD was significantly lower in the NRP and HL groups compared with the controls (NRP 4.7%(1.3)*, HL 4.9%(0.7)* and NC 8.3%(0.6), *p = 0.012 vs. NC); GTN mediated dilatation and basal and post-ischaemic forearm blood flow were not statistically different among the three groups.CONCLUSION: Patients with nephrotic range proteinuria have endothelial dysfunction of conduit arteries in the peripheral circulation, similar to that observed in patients with primary hyperlipidaemia. This suggests dyslipoproteinaemia is the principal cause of endothelial dysfunction of conduit arteries in nephrotic range proteinuria. Confirmation of this should be sought with an intervention trial of lipid-regulating therapy.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Melbourne, Australia : Blackwell Science Pty
    ISSN: 1440-172X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Objectives:  The aim of the present review was to determine whether the best available evidence supports the types and timing of the various nursing interventions that are commonly used to reduce fever in non-critically-ill children, and to what extent the outcomes are influenced by these nursing actions.Methods:  Studies included were randomised or quasi-randomised controlled trials that involved non-critically-ill children with a fever aged between 3 months and 16 years.〈list style="custom"〉• The search strategy sought to identify both published and unpublished research reports in the English language and covered all major databases up to 1998.• The methodological quality of each study was assessed by two independent reviewers using a piloted critical appraisal checklist.• Despite all studies being randomised, heterogeneity precluded conduction of a meta-analysis; therefore, evidence was synthesised using narrative summaries.Results: Ten studies were assessed as being of sufficient quality to be included in the review. These studies addressed two of the intervention categories identified in the protocol: (i) administration of antipyretics (paracetamol); and (ii) direct cooling measures on the outcome measure (reduction of or prevention of increase in fever).The review found little benefit from sponging in temperate climates and usually at the expense of the child's comfort. There may be situations in high environmental temperatures and high humidity, or where there is a need for immediate temperature reduction, in which sponging may be warranted. Risks were identified when paracetamol was administered on a sustained basis over even a short period of time and above a relatively low total daily dosage. There was a lack of evidence to support the administration of antipyretics to reduce the incidence of febrile convulsions.There is a need for parental education that focuses on knowledge of the body's protective physiological responses and how to support these responses.Conclusion: The primary purpose for intervening when a child has a fever is to increase the child's comfort. This consideration should be weighed against any harm that might result from intervening. There was a lack of evidence to support the routine use of sponging. The administration of paracetamol should be used selectively and with caution. In summary, care needs to be individualised, based on current knowledge of the effectiveness and risks of interventions.
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