44 research outputs found

    Assessing the impact of a waiting time survey on reducing waiting times in urban primary care clinics in Cape Town, South Africa

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    A waiting time survey (WTS) conducted in several clinics in Cape Town, South Africa provided recommendations on how to shorten waiting times (WT). A follow-up study was conducted to assess whether WT had reduced. Using a stratified sample of 22 clinics, a before and after study design assessed changes in WT. The WT was measured and perceptions of clinic managers were elicited, about the previous survey’s recommendations. The overall median WT decreased by 21 minutes (95%CI: 11.77- 30.23), a 28% decrease from the previous WTS. Although no specific factor was associated with decreases in WT, implementation of recommendations to reduce WT was 2.67 times (95%CI: 1.33-5.40) more likely amongst those who received written recommendations and 2.3 times (95%CI: 1.28- 4.19) more likely amongst managers with 5 or more years’ experience. The decrease in WT found demonstrates the utility of a WTS in busy urban clinics in developing country contexts. Experienced facility managers who timeously receive customised reports of their clinic’s performance are more likely to implement changes that positively impact on reducing WT

    Assessing the impact of a waiting time survey on reducing waiting times in primary care clinics in Cape Town, South Africa

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    Includes bibliographical references.Objective: A waiting time survey (WTS), conducted in 2007 at 94% of clinics in Cape Town, measured length of patient waiting times (WT) for services and provided recommendations to shorten waiting times. Whether subsequent implementation of these recommendations occurred was unknown, hence a study was conducted to assess the impact of the previous waiting time survey recommendations on stimulating efforts to reduce waiting times and whether waiting times had reduced. Methods: A cross-sectional analytical study design assessed the perceptions of 92% of clinic managers in Cape Town, regarding the 2007 survey, while a before and after study design assessed changes in waiting time between 2007 and 2011, using a random sample of 22 clinics. Results: The overall median waiting time of all clinics in the sample decreased by 21 minutes in 2011 (95% CI 11.77-30.23), a 28% decrease from 2007. This reduction was manifest at individual clinic level as well, with 55% of clinics reducing their median waiting time by at least 15 minutes. No specific factors, including whether recommendations to reduce waiting times were implemented, were associated with decreases in waiting times. Implementation of recommendations to reduce waiting times was 2.67 times (95% CI 1.33-5.40) more likely amongst those who received written recommendations and 2.3 times ) 95% CI 1.28-4.19) more likely amongst managers with 5 or more years' experience. Conclusion: The decrease in waiting times in primary care urban clinics subsequent to a waiting time survey, demonstrates the utility of waiting times surveys, although no specific factors associated with the decrease in waiting time were identified

    The importance of identified cause-of-death information being available for public health surveillance, actions and research

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    An amendment to the South African Births and Deaths Registration Act has compromised efforts to strengthen local mortality surveillance to provide statistics for small areas and enable data linkage to provide information for public health actions. Internationally it has been recognised that a careful balance needs to be kept between protecting individual patient confidentiality and enabling effective public health intelligence to guide patient care and service delivery and prevent harmful exposures. This article describes the public health benefits of a local mortality surveillance system in the Western Cape Province, South Africa (SA), as well as its potential for improving the quality of vital statistics data with integration into the national civil registration and vital statistics system. It also identifies other important uses for identifiable cause-of-death data in SA that have been compromised by this legislation

    A new model for the pathophysiology of Alzheimer's disease: Aluminium toxicity is exacerbated by hydrogen peroxide and attenuated by an amyloid protein fragment and melatonin

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    Objectives. Although Alzheimer's disease (AD) is the leading cause of dementia in developed countries, there is an as yet unexplained lower prevalence of the disease in parts of Africa. AD is characterised by a catastrophic loss of neurons; free radicals (oxidative toxins) have been implicated in the destruction of the cells through the process of lipid peroxidative damage of cell membranes. Previously aluminium (Al) and a fragment of beta amyloid (Aβ 25 - 35) were shown to exacerbate tree-radical damage, while melatonin reduced this effect. The aim of the present study was: (i) to investigate the conditions detennining the toxicity of Al and Aβ 25 - 35; and (ii) to assess whether melatonin could attenuate the damage done by both aluminium and the amyloid fragment, thus suggesting a pathway for the aetiology of AD.Design. An in vitro model system was used in which free radicals were generated, causing lipid peroxidation of platelet membranes, thus simulating the disease process found in the brain.Results. 1. Al and Aβ 25 - 35 caused lipid peroxidation in the presence of the iron (II) ion (Fe2+, Al being more toxic than Aβ 25 - 35. 2. Aβ 25 - 35 attenuated the lipid peroxidation promoted by Al. 3. Hydrogen peroxide (H2O2 greatly exacerbated the toxicity of Al and Aβ 25 - 35. 4. Melatonin prevented lipid peroxidation by Al and Aβ 25 - 35 in the absence of H2O2, but only reduced the process when H2O2 was present.Conclusions. In the light of the results obtained from the present study, the following hypotheses are formulated. 1. In AD, excessive quantities of Al are taken up into the  brain, where the Al exacerbates iron-induced lipid peroxidatian in the Iysosomes. 2. In response, the normal synthetic pathway of amyloid protein is altered to produce Aβ fragments which attenuate the toxicity of Al. In the process of sequestering the Al and iron, immature plaques are formed in the brain. 3. Microglia are activated, in an attempt to destroy the plaques by secreting reactive oxygen species such as H2O2. At this point in the disease process, lipid peroxidation causes a catastrophic loss of brain cells. 4. Melatonin, together with other free radical scavengers in the brain, reduces the free-radical damage caused by Al and Aβ, except in the latter stages of the disease process. Since melatonin is produced by the pineal gland only in the dark, the excess of electric light in developed countries may help explain why AD is more prevalent in these countries than in rural Africa

    The importance of identified cause-of-death information being available for public health surveillance, actions and research

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    An amendment to the South African Births and Deaths Registration Act has compromised efforts to strengthen local mortality surveillance to provide statistics for small areas and enable data linkage to provide information for public health actions. Internationally it has been recognised that a careful balance needs to be kept between protecting individual patient confidentiality and enabling effective public health intelligence to guide patient care and service delivery and prevent harmful exposures. This article describes the public health benefits of a local mortality surveillance system in the Western Cape Province, South Africa (SA), as well as its potential for improving the quality of vital statistics data with integration into the national civil registration and vital statistics system. It also identifies other important uses for identifiable cause-of-death data in SA that have been compromised by this legislation.

    In search of the authentic nation: landscape and national identity in Canada and Switzerland

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    While the study of nationalism and national identity has flourished in the last decade, little attention has been devoted to the conditions under which natural environments acquire significance in definitions of nationhood. This article examines the identity-forming role of landscape depictions in two polyethnic nation-states: Canada and Switzerland. Two types of geographical national identity are identified. The first – what we call the ‘nationalisation of nature’– portrays zarticular landscapes as expressions of national authenticity. The second pattern – what we refer to as the ‘naturalisation of the nation’– rests upon a notion of geographical determinism that depicts specific landscapes as forces capable of determining national identity. The authors offer two reasons why the second pattern came to prevail in the cases under consideration: (1) the affinity between wild landscape and the Romantic ideal of pure, rugged nature, and (2) a divergence between the nationalist ideal of ethnic homogeneity and the polyethnic composition of the two societies under consideration

    Natriuretic peptides and integrated risk assessment for cardiovascular disease: an individual-participant-data meta-analysis

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    BACKGROUND: Guidelines for primary prevention of cardiovascular diseases focus on prediction of coronary heart disease and stroke. We assessed whether or not measurement of N-terminal-pro-B-type natriuretic peptide (NT-proBNP) concentration could enable a more integrated approach than at present by predicting heart failure and enhancing coronary heart disease and stroke risk assessment. METHODS: In this individual-participant-data meta-analysis, we generated and harmonised individual-participant data from relevant prospective studies via both de-novo NT-proBNP concentration measurement of stored samples and collection of data from studies identified through a systematic search of the literature (PubMed, Scientific Citation Index Expanded, and Embase) for articles published up to Sept 4, 2014, using search terms related to natriuretic peptide family members and the primary outcomes, with no language restrictions. We calculated risk ratios and measures of risk discrimination and reclassification across predicted 10 year risk categories (ie, <5%, 5% to <7·5%, and ≥7·5%), adding assessment of NT-proBNP concentration to that of conventional risk factors (ie, age, sex, smoking status, systolic blood pressure, history of diabetes, and total and HDL cholesterol concentrations). Primary outcomes were the combination of coronary heart disease and stroke, and the combination of coronary heart disease, stroke, and heart failure. FINDINGS: We recorded 5500 coronary heart disease, 4002 stroke, and 2212 heart failure outcomes among 95 617 participants without a history of cardiovascular disease in 40 prospective studies. Risk ratios (for a comparison of the top third vs bottom third of NT-proBNP concentrations, adjusted for conventional risk factors) were 1·76 (95% CI 1·56-1·98) for the combination of coronary heart disease and stroke and 2·00 (1·77-2·26) for the combination of coronary heart disease, stroke, and heart failure. Addition of information about NT-proBNP concentration to a model containing conventional risk factors was associated with a C-index increase of 0·012 (0·010-0·014) and a net reclassification improvement of 0·027 (0·019-0·036) for the combination of coronary heart disease and stroke and a C-index increase of 0·019 (0·016-0·022) and a net reclassification improvement of 0·028 (0·019-0·038) for the combination of coronary heart disease, stroke, and heart failure. INTERPRETATION: In people without baseline cardiovascular disease, NT-proBNP concentration assessment strongly predicted first-onset heart failure and augmented coronary heart disease and stroke prediction, suggesting that NT-proBNP concentration assessment could be used to integrate heart failure into cardiovascular disease primary prevention. FUNDING: British Heart Foundation, Austrian Science Fund, UK Medical Research Council, National Institute for Health Research, European Research Council, and European Commission Framework Programme 7

    Sequencing of prostate cancers identifies new cancer genes, routes of progression and drug targets

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    Prostate cancer represents a substantial clinical challenge because it is difficult to predict outcome and advanced disease is often fatal. We sequenced the whole genomes of 112 primary and metastatic prostate cancer samples. From joint analysis of these cancers with those from previous studies (930 cancers in total), we found evidence for 22 previously unidentified putative driver genes harboring coding mutations, as well as evidence for NEAT1 and FOXA1 acting as drivers through noncoding mutations. Through the temporal dissection of aberrations, we identified driver mutations specifically associated with steps in the progression of prostate cancer, establishing, for example, loss of CHD1 and BRCA2 as early events in cancer development of ETS fusion-negative cancers. Computational chemogenomic (canSAR) analysis of prostate cancer mutations identified 11 targets of approved drugs, 7 targets of investigational drugs, and 62 targets of compounds that may be active and should be considered candidates for future clinical trials
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