968 resultados para haemophilus influenzae type b
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La fracture périprothétique du fémur (FPF) représente une complication sérieuse des arthroplasties de hanche. Différents matériels d'ostéosynthèse ont été utilisés pour l'ostéosynthèse des FPFs. Toutefois, aucune étude n'a rapporté les résultats obtenus avec une plaque anatomique non-verrouillée avec des trous excentrés. Les buts de ce travail étaient de présenter 1) le taux de consolidation des FPF traitées par cet implant, 2) les caractéristiques péri-opératoires 3) le taux de complications, et 4) les résultats en terme d'autonomie obtenus après le traitement des FPF du groupe B selon Vancouver avec une plaque anatomique à trous excentrés. Hypothèse L'utilisation de cette plaque permet d'obtenir un taux élevé de consolidation avec un minimum de complications mécaniques. Matériels et Méthodes Quarante-trois patients, d'âge moyen 79 ans ± 13 (41 - 98), qui ont été traités pour une ostéosynthèse d'une FPF de type B selon Vancouver avec cette plaque entre 2002 et 2007 ont été inclus. Les patients ont été classifiées selon les scores ASA et de Charnley. Le temps opératoire, les pertes sanguines chirurgicales, le nombre de transfusion, la durée d'hospitalisation, le délai de consolidation, le lieu de vie ainsi que l'autonomie (score de Parker) ont été évalués. Le taux de survie sans révision a été calculé par la méthode de Kaplan-Meier. Le recul moyen est de 42 mois ± 20 (min - max : 16 - 90). Résultats La consolidation a été obtenue chez tous les patients avec un délai moyen de 2,4 mois ± 0,6 (2-4). 1 patient avec un cal vicieux en varus était à déplorer. Le score de Parker a diminué de 5,93 ± 1,94 (2-9) à 4,93 ± 1,8 (1- 9) (p = 0.01). 2 révisions chirurgicales ont été nécessaires sur la série. Le taux de survie à 5 ans des prothèses après ostéosynthèse de la FPF était de 83,3 % ± 12,6 %. Conclusion Cette plaque anatomique avec trous excentrés permet le traitement des FPF du type B et garantit une consolidation de la fracture avec un faible taux de complications liés à l'ostéosynthèse. Toutefois, les FPF représentent une complication sérieuse des arthroplasties de hanche assortie d'un fort taux de morbidités et de mortalité.
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Non-typable Haemophilus influenzae (NTHi) is a Gram negative pathogen that causes acute respiratory infections and is associated with the progression of chronic respiratory diseases. Previous studies have established the existence of a remarkable genetic variability among NTHi strains. In this study we show that, in spite of a high level of genetic heterogeneity, NTHi clinical isolates display a prevalent molecular feature, which could confer fitness during infectious processes. A total of 111 non-isogenic NTHi strains from an identical number of patients, isolated in two distinct geographical locations in the same period of time, were used to analyse nine genes encoding bacterial surface molecules, and revealed the existence of one highly prevalent molecular pattern (lgtF+, lic2A+, lic1D+, lic3A+, lic3B+, siaA−, lic2C+, ompP5+, oapA+) displayed by 94.6% of isolates. Such a genetic profile was associated with a higher bacterial resistance to serum mediated killing and enhanced adherence to human respiratory epithelial cells.
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Nontypable Haemophilus influenzae (NTHi) has emerged as an important opportunistic pathogen causing infection in adults suffering obstructive lung diseases. Existing evidence associates chronic infection by NTHi to the progression of the chronic respiratory disease, but specific features of NTHi associated with persistence have not been comprehensively addressed. To provide clues about adaptive strategies adopted by NTHi during persistent infection, we compared sequential persistent isolates with newly acquired isolates in sputa from six patients with chronic obstructive lung disease. Pulse field gel electrophoresis (PFGE) identified three patients with consecutive persistent strains and three with new strains. Phenotypic characterisation included infection of respiratory epithelial cells, bacterial self-aggregation, biofilm formation and resistance to antimicrobial peptides (AMP). Persistent isolates differed from new strains in showing low epithelial adhesion and inability to form biofilms when grown under continuous-flow culture conditions in microfermenters. Self-aggregation clustered the strains by patient, not by persistence. Increasing resistance to AMPs was observed for each series of persistent isolates; this was not associated with lipooligosaccharide decoration with phosphorylcholine or with lipid A acylation. Variation was further analyzed for the series of three persistent isolates recovered from patient 1. These isolates displayed comparable growth rate, natural transformation frequency and murine pulmonary infection. Genome sequencing of these three isolates revealed sequential acquisition of single-nucleotide variants in the AMP permease sapC, the heme acquisition systems hgpB, hgpC, hup and hxuC, the 3-deoxy-D-manno-octulosonic acid kinase kdkA, the long-chain fatty acid transporter ompP1, and the phosphoribosylamine glycine ligase purD. Collectively, we frame a range of pathogenic traits and a repertoire of genetic variants in the context of persistent infection by NTHi.
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A total of 1712 strains of Haemophilus influenzae isolated from patients with invasive diseases were obtained from ten Brazilian states from 1996 to 2000. ß-Lactamase production was assessed and the minimum inhibitory concentrations (MIC) of ampicillin, chloramphenicol, ceftriaxone and rifampin were determined using a method for broth microdilution of Haemophilus test medium. The prevalence of strains producing ß-lactamase ranged from 6.6 to 57.7%, with an overall prevalence of 18.4%. High frequency of ß-lactamase-mediated ampicillin resistance was observed in Distrito Federal (25%), São Paulo (21.7%) and Paraná (18.5%). Of the 1712 strains analyzed, none was ß-lactamase negative, ampicillin resistant. A total of 16.8% of the strains were resistant to chloramphenicol, and 13.8% of these also presented resistance to ampicillin, and only 3.0% were resistant to chloramphenicol alone. All strains were susceptible to ceftriaxone and rifampin and the MIC90 were 0.015 µg/ml and 0.25 µg/ml, respectively. Ceftriaxone is the drug of choice for empirical treatment of bacterial meningitis in pediatric patients who have not been screened for drug susceptibility. The emergence of drug resistance is a serious challenge for the management of invasive H. influenzae disease, which emphasizes the fundamental role of laboratory-based surveillance for antimicrobial resistance.
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The efficacy of endothelin receptor antagonists in protecting against myocardial ischemia/reperfusion (I/R) injury is controversial, and the mechanisms remain unclear. The aim of this study was to investigate the effects of CPU0123, a novel endothelin type A and type B receptor antagonist, on myocardial I/R injury and to explore the mechanisms involved. Male Sprague-Dawley rats weighing 200-250 g were randomized to three groups (6-7 per group): group 1, Sham; group 2, I/R + vehicle. Rats were subjected to in vivo myocardial I/R injury by ligation of the left anterior descending coronary artery and 0.5% sodium carboxymethyl cellulose (1 mL/kg) was injected intraperitoneally immediately prior to coronary occlusion. Group 3, I/R + CPU0213. Rats were subjected to identical surgical procedures and CPU0213 (30 mg/kg) was injected intraperitoneally immediately prior to coronary occlusion. Infarct size, cardiac function and biochemical changes were measured. CPU0213 pretreatment reduced infarct size as a percentage of the ischemic area by 44.5% (I/R + vehicle: 61.3 ± 3.2 vs I/R + CPU0213: 34.0 ± 5.5%, P < 0.05) and improved ejection fraction by 17.2% (I/R + vehicle: 58.4 ± 2.8 vs I/R + CPU0213: 68.5 ± 2.2%, P < 0.05) compared to vehicle-treated animals. This protection was associated with inhibition of myocardial inflammation and oxidative stress. Moreover, reduction in Akt (protein kinase B) and endothelial nitric oxide synthase (eNOS) phosphorylation induced by myocardial I/R injury was limited by CPU0213 (P < 0.05). These data suggest that CPU0123, a non-selective antagonist, has protective effects against myocardial I/R injury in rats, which may be related to the Akt/eNOS pathway.
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Tesis (Doctorado en Ciencias con Especialidad en Química Biomédica) UANL
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Ce mémoire présente l’application de la méthode de décomposition en termes de diagrammes aux désintégrations de mésons B vers trois mésons de type pseudos- calaire ne comportant pas de quarks charmés. La décomposition diagrammatique des désintégrations de types B → Kππ, B → KKK ̄, B → KK ̄π et B → πππ est effectuée de façon systématique. Il est démontré que lorsque l’on néglige les dia- grammes d’échanges et d’annihilations, dont les contributions sont estimées être petites, de nouvelles relations apparaissent entre les amplitudes. Ces relations sont de nouveaux tests du modèle standard qui ne peuvent être obtenus que par la méthode diagrammatique. Lorsque les données nécessaires sont disponibles, nous vérifions ces relations et obtenons un bon accord avec les données expérimentales. Nous démontrons également qu’il est possible d’utiliser le secteur B → Kππ pour mesurer la phase faible γ avec une incertitude théorique que nous estimons être de l’ordre de 5%. Les autres secteurs de désintégrations ne permettent d’extraire des phases faibles que si l’on invoque des approximations de précisions inconnues.
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The phylogenetic interrelationships of members of the Clostridium botulinum complex of species was investigated by direct sequencing of their 16S rRNA genes. Comparative analysis of the 16S rRNA sequences demonstrated the presence of four phylogenetically distinct lineages corresponding to: i) proteolytic C. botulinum types Al B, and F, and C. sporogenes, ii) saccharolytic types B, E and F, iii) types C and D and C. novyi type A, and iv) type G and C. subterminale. The phylogenetic groupings obtained from the 16S rRNA were in complete agreement with the four divisions recognised within the 'species complex' on the basis of phenotypic criteria.
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Conservative management of acute type B aortic dissection is currently being challenged by primary thoracic endovascular aortic repair. Aim was to assess outcome and quality of life after these different approaches using an adjusted standard population as benchmark.
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Endovascular stent grafting represents a novel concept for type B aortic dissection both in the acute and subacute/chronic setting, with an unknown effect on outcomes.
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The purpose of this study was to assess the efficacy and midterm results of endovascular treatment of acute, complicated type B aortic dissection.
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Midterm results of TEVAR (thoracic endovascular aortic repair) in patients with aneurysms involving the descending aorta originating from chronic type B dissections are not known.
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Many dissections seem to also have a retrograde component. The aim of the study was to evaluate different sites of primary entry tears and the propagation of the dissecting membrane, antegrade and retrograde, in an experimental model of acute type B aortic dissection.
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It is not well known if the size of the ascending thoracic aorta at presentation predicts features of presentation, management, and outcomes in patients with acute type B aortic dissection. The International Registry of Acute Aortic Dissection (IRAD) database was queried for all patients with acute type B dissection who had documentation of ascending thoracic aortic size at time of presentation. Patients were categorized according to ascending thoracic aortic diameters ≤4.0, 4.1 to 4.5, and ≥4.6 cm. Four hundred eighteen patients met inclusion criteria; 291 patients (69.6%) were men with a mean age of 63.2 ± 13.5 years. Ascending thoracic aortic diameter ≤4.0 cm was noted in 250 patients (59.8%), 4.1 to 4.5 cm in 105 patients (25.1%), and ≥4.6 cm in 63 patients (15.1%). Patients with an ascending thoracic aortic diameter ≥4.6 cm were more likely to be men (p = 0.01) and have Marfan syndrome (p <0.001) and known bicuspid aortic valve disease (p = 0.003). In patients with an ascending thoracic aorta ≥4.1 cm, there was an increased incidence of surgical intervention (p = 0.013). In those with an ascending thoracic aorta ≥4.6 cm, the root, ascending aorta, arch, and aortic valve were more often involved in surgical repair. Patients with an ascending thoracic aorta ≤4.0 were more likely to have endovascular therapy than those with larger ascending thoracic aortas (p = 0.009). There was no difference in overall mortality or cause of death. In conclusion, ascending thoracic aortic enlargement in patients with acute type B aortic dissection is common. Although its presence does not appear to predict an increased risk of mortality, it is associated with more frequent open surgical intervention that often involves replacement of the proximal aorta. Those with smaller proximal aortas are more likely to receive endovascular therapy.
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To analyse the outcome and need for intervention [surgery or thoracic endovascular aortic repair (TEVAR)] in patients after surgery for remaining type B dissection after type A repair and primary type B aortic dissection.