158 research outputs found

    Evaluation des pratiques et des coûts de lutte antivectorielle à l'échelon familial en Afrique centrale : 2 Ville de Douala (Cameroun), juillet 1988

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    Une enquête Connaissances, Attitudes, Pratiques (CAP) a été réalisée en juillet 1988 dans la ville de Douala, par sondage en grappe et visites domiciliaires, 98 % des foyers déclarent être gênés par les moustiques (piqûre, maladie, bruit); 91 % des familles utilisent un moyen de lutte antivectorielle; les principaux moyens utilisés sont : les moustiquaires (48 %) les bombes insecticides (39,5 %) et les serpentines (36,7 %). Les coûts moyens cumulés par foyer de la lutte antivectorielle (116,6 ECU/an) et des besoins pour maladies imputées aux moustiques (147,4 ECU/an) ont été évalués à environ trois mois de . Plus de 90 % des personnes interrogées accepteraient d'acheter et d'utiliser une moustiquaire imprégnée d'insecticide à condition que le prix d'un tel produit soit inférieur aux prix courants actuellement pratiqués pour les moustiquaires ordinaires. La diffusion de la technique d'imprégnation doit se faire au niveau de centres d'imprégnation, en imprégnant d'abord les moustiquaires existantes et en s'appuyant sur l'information des populations. (Résumé d'auteur

    Le paludisme-maladie dans la ville de Yaoundé (Cameroun) : prise en charge et lutte antivectorielle au niveau familial

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    Pour évaluer - dans ses composantes de prise en charge et de lutte antivectorielle au niveau familial le problème du "paludisme-maladie" tel qu'il est perçu par les habitants de Yaoundé - une enquête transversale a été réalisée sur un échantillon représentatif de population obtenu par sondage aléatoire à plusieurs degrés. Le paludisme ainsi défini représente le problème médical dominant pour lequel l'effort financier annuellement consenti par chaque famille s'élève à 57.000 FCFA représentant le traitement médical et ses à-côtés ainsi que la lutte antivectorielle, pour l'essentiel chimique. Développer des comportements thérapeutiques plus pertinents et promouvoir une plus large utilisation des moustiquaires de lit imprégnées d'insecticides rémanents passe d'abord par la mise en place de programmes formatifs en direction tant des personnels de santé que des populations dont ils ont la responsabilité. (Résumé d'auteur

    Esophageal atresia: data from a national cohort

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    PURPOSE: A prospective national register was established in 2008 to record all new cases of live-birth newborns with esophageal atresia (EA). This epidemiological survey was recommended as part of a national rare diseases plan. METHODS: All 38 national centers treating EA participated by completing for each patient at first discharge a questionnaire validated by a national committee of experts. Data were centralized by the national reference center for esophageal anomalies. Quantitative and qualitative analyses were performed, with P-values of less than 0.05 considered statistically significant. Results of the 2008-2009 data collection are presented in this report. RESULTS: Three hundred seven new living cases of EA were recorded between January 1, 2008, and December 31, 2009. The male/female sex ratio was 1.3, and the live-birth prevalence of EA was 1.8 per 10,000 births. Major characteristics were comparable to those reported in the literature. Survival was 95%, and no correlation with caseload was noted. CONCLUSIONS: Epidemiologic surveys of congenital anomalies such as EA, which is a rare disease, provide valuable data for public health authorities and fulfill one important mission of reference centers. When compared with previous epidemiological data, this national population-based registry suggests that the incidence of EA remains stable

    Multilevel analysis of systolic blood pressure and ACE gene I/D polymorphism in 438 Swedish families – a public health perspective

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    BACKGROUND: Individuals belonging to the same family share a number of genetic as well as environmental circumstances that may condition a common SBP level. Among the genetic factors, the angiotensin converting enzyme (ACE) gene I/D polymorphism appears as a possible candidate as it might influence both SBP and the pharmacological effect of ACE inhibitors. We aimed to combine genetic epidemiology with public health ideas concerning life-course and multilevel epidemiology in order to understand the role of familial factors regarding individual SBP. METHODS: We applied multilevel regression analysis on 1926 individuals nested within 438 families from South Sweden. Modelling familial SBP variance as a function of age and use of ACE inhibitors we calculates a variance partition coefficient and the proportional change in familial SBP variance attributable to differences in ACE gene I/D polymorphism RESULTS: Our results suggest the existence of genetic or environmental circumstances that produce a considerable familial clustering of SBP, especially among individuals using ACE-inhibitors. However, ACE gene I/D polymorphism seems to play a minor role in this context. In addition, familial factors – genetic, environmental or their interaction – shape SBP among non-users of ACE inhibitors but their effect is expressed later in the life-course. CONCLUSION: Strategies directed to prevent hypertension should be launched in younger rather than in older ages and both prevention of hypertension and its treatment with ACE inhibitors should be focused on families rather than on individuals

    Le diagnostic anténatal modifie-t-il la prise en charge néonatale et le devenir à 1 an des enfants suivis pour atrésie de l’œsophage de type III ?

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    OBJECTIVE: Evaluate neonatal management and outcome of neonates with either a prenatal or a post-natal diagnosis of EA type III. STUDY DESIGN: Population-based study using data from the French National Register for EA from 2008 to 2010. We compared children with prenatal versus post-natal diagnosis in regards to prenatal, maternal and neonatal characteristics. We define a composite variable of morbidity (anastomotic esophageal leaks, recurrent fistula, stenosis) and mortality at 1 year. RESULTS: Four hundred and eight live births with EA type III were recorded with a prenatal diagnosis rate of 18.1%. Transfer after birth was lower in prenatal subset (32.4% versus 81.5%, P<0.001). Delay between birth and first intervention was not significantly different. Defect size (2cm vs 1.4cm, P<0.001), gastrostomy (21.6% versus 8.7%, P<0.001) and length in neonatal unit care were higher in prenatal subset (47.9 days versus 33.6 days, P<0.001). The composite variables were higher in prenatal diagnosis subset (38.7% vs 26.1%, P=0.044). CONCLUSION: Despite the excellent survival rate of EA, cases with antenatal detection have a higher morbidity related to the EA type (longer gap). Even if it does not modify neonatal management and 1-year outcome, prenatal diagnosis allows antenatal parental counseling and avoids post-natal transfer

    Polymorphisms on PAI-1 and ACE genes in association with fibrinolytic bleeding after on-pump cardiac surgery

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    Publisher Copyright: © 2015 Ozolina et al.Background: Carriers of plasminogen activator inhibitor -1 (PAI-1) -675 genotype 5G/5G may be associated with lower preoperative PAI-1 plasma levels and higher blood loss after heart surgery using cardiopulmonary bypass (CPB). We speculate if polymorphisms of PAI-1 -844 A/G and angiotensin converting enzyme (ACE) intron 16 I/D also might promote fibrinolysis and increase postoperative bleeding. Methods: We assessed PAI-1 -844 A/G, and ACE intron 16 I/D polymorphisms by polymerase chain reaction technique and direct sequencing of genomic DNA from 83 open heart surgery patients that we have presented earlier. As primary outcome, accumulated chest tube drainage (CTD) at 4 and 24 h were analyzed for association with genetic polymorphisms. As secondary outcome, differences in plasma levels of PAI-1, t-PA/PAI-1 complex and D-dimer were determined for each polymorphism. SPSS® was used for statistical evaluation. Results: The lowest preoperative PAI-1 plasma levels were associated with PAI-1 -844 genotype G/G, and higher CTD, as compared with genotype A/A at 4 and 24 h after surgery. Correspondingly, 4 h after the surgery CTD was higher in carriers of ACE intron 16 genotype I/I, as compared with genotype D/D. PAI-1 plasma levels and t-PA/PAI-1 complex reached nadir in carriers of ACE intron 16 genotype I/I, in whom we also noticed the highest D-dimer levels immediately after surgery. Notably, carriers of PAI-1 -844 genotype G/G displayed higher D-dimer levels at 24 h after surgery as compared with those of genotype A/G. Conclusions: Increased postoperative blood loss secondary to enhanced fibrinolysis was associated with carriers of PAI-1 -844 G/G and ACE Intron 16 I/I, suggesting that these genotypes might predict increased postoperative blood loss after cardiac surgery using CPB.publishersversionPeer reviewe

    Human physiologically based pharmacokinetic model for ACE inhibitors: ramipril and ramiprilat

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    BACKGROUND: The angiotensin-converting enzyme (ACE) inhibitors have complicated and poorly characterized pharmacokinetics. There are two binding sites per ACE (high affinity "C", lower affinity "N") that have sub-nanomolar affinities and dissociation rates of hours. Most inhibitors are given orally in a prodrug form that is systemically converted to the active form. This paper describes the first human physiologically based pharmacokinetic (PBPK) model of this drug class. METHODS: The model was applied to the experimental data of van Griensven et. al for the pharmacokinetics of ramiprilat and its prodrug ramipril. It describes the time course of the inhibition of the N and C ACE sites in plasma and the different tissues. The model includes: 1) two independent ACE binding sites; 2) non-equilibrium time dependent binding; 3) liver and kidney ramipril intracellular uptake, conversion to ramiprilat and extrusion from the cell; 4) intestinal ramipril absorption. The experimental in vitro ramiprilat/ACE binding kinetics at 4°C and 300 mM NaCl were assumed for most of the PBPK calculations. The model was incorporated into the freely distributed PBPK program PKQuest. RESULTS: The PBPK model provides an accurate description of the individual variation of the plasma ramipril and ramiprilat and the ramiprilat renal clearance following IV ramiprilat and IV and oral ramipril. Summary of model features: Less than 2% of total body ACE is in plasma; 35% of the oral dose is absorbed; 75% of the ramipril metabolism is hepatic and 25% of this is converted to systemic ramiprilat; 100% of renal ramipril metabolism is converted to systemic ramiprilat. The inhibition was long lasting, with 80% of the C site and 33% of the N site inhibited 24 hours following a 2.5 mg oral ramipril dose. The plasma ACE inhibition determined by the standard assay is significantly less than the true in vivo inhibition because of assay dilution. CONCLUSION: If the in vitro plasma binding kinetics of the ACE inhibitor for the two binding sites are known, a unique PBPK model description of the Griensven et. al. experimental data can be obtained

    The measurement of stress and phase fraction distributions in pre and post-transition Zircaloy oxides using nano-beam synchrotron X-ray diffraction

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    Zircaloy-4 oxide stress profiles and tetragonal:monoclinic oxide phase fraction distributions were studied using nano-beam transmission X-ray diffraction. Continuous stress relief and phase transformation during the first cycle of oxide growth was observed. The in-plane monoclinic stress was shown to relax strongly up to each transition, whereas in-plane tetragonal stress-relief (near the metal-oxide interface) was only observed post transition. The research demonstrates that plasticity in the metal and the development of a band of in-plane cracking both relax the monoclinic in-plane stress.The observations are consistent with a model of transition in which in-plane cracking becomes interlinked prior to transition. These cracks, combined with the development of cracks with a through-thickness component (driven primarily by plasticity in the metal) and/or a porous network of fine cracks (associated with phase transformation), form a percolation path through the oxide layer. The oxidising species can then percolate from the oxide surface to the metal/oxide interface, at which stage transition then ensues
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