999 resultados para 7140-206


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O objetivo deste trabalho foi avaliar o efeito dos sistemas de manejo do solo e de coberturas de inverno sobre o número de propágulos de Fusarium spp. no solo, a incidência da podridão‑vermelha‑da‑raiz (PVR) e a produtividade das cultivares de soja CD 206 e FT Fênix. Foram realizados dois experimentos nos anos agrícolas de 2006/2007 e 2007/2008. Utilizou-se o delineamento experimental de blocos ao acaso, em parcelas subsubdivididas, com três repetições. Foram avaliados dois sistemas de preparo do solo: plantio direto e revolvimento do solo na profundidade de 25 cm. As coberturas de inverno utilizadas foram: aveia‑preta, com duas densidades de plantio; aveia‑preta + ervilhaca; azevém; e pousio. A incidência da doença, na safra de 2006/2007, na cultivar FT Fênix, foi menor que na CD 206. Na safra 2007/2008, não houve diferença significativa. Houve incremento na produtividade, de 125 kg ha‑1, com o solo revolvido, em comparação ao plantio direto. A cobertura com aveia‑preta + ervilhaca apresentou maior número de propágulos de Fusarium spp. no solo, na safra de 2006/2007. No entanto, no segundo ano, essa diferença não foi observada. Os sistemas de preparo do solo e as coberturas de inverno utilizadas não influenciam a incidência da PVR em cultivares de soja ou o número de propágulos de Fusarium spp. no solo. O sistema com solo revolvido proporciona aumento de produtividade da soja, no segundo ano de manejo.

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O objetivo deste trabalho foi avaliar o efeito isolado ou simultâneo dos estresses hídrico e térmico na expressão gênica em nódulos de feijão-caupi. A bactéria Bradyrhizobium japonicum (estirpe BR 3267) foi inoculada em sementes de feijão-caupi da cultivar IPA 206 e, 35 dias após a germinação, as plantas foram submetidas a diferentes regimes de disponibilidade hídrica e a estresse térmico, em casa de vegetação. Para a identificação dos genes diferencialmente expressos, foi utilizada a técnica de cDNA-AFLP, tendo-se isolado 67 fragmentos derivados de transcritos (FDTs) diferencialmente expressos. Após o sequenciamento dos FDTs e das análises de similaridade, com uso do programa Blastx, foram identificados 14 genes diferencialmente expressos envolvidos em diferentes processos metabólicos. O padrão de expressão de seis genes sob estresse abiótico foi confirmado por RT-qPCR, e observou-se indução de genes pertencentes a diferentes categorias funcionais, como biossíntese de ácido abscísico, sinalização celular, transportador de prolina e biossíntese de lipídeos de membranas. A expressão desses genes indica sua participação em processos relacionados à proteção dos nódulos ao estresse abiótico.

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F. IIv-2v Incipits des vêpres et des petites heures (addit. XVIe s.). F. 3 Temporal. F. 200 Calendrier de Paris, avec notes marginales concernant la famille de Fontenay (XVIe s.). F. 206-283 Psautier et litanies. F. 284 Ordo officii pour l'Avent. F. 296 Commun des saints. F. 320 Sanctoral. F. 566v Bénédictions pour les leçons de matines (XVIe s.). F. II Certificat de confirmation de Jérôme de Fontenay (1530).

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BACKGROUND: Mortality among HIV-infected persons is decreasing, and causes of death are changing. Classification of deaths is hampered because of low autopsy rates, frequent deaths outside of hospitals, and shortcomings of International Statistical Classification of Diseases and Related Health Problems (ICD-10) coding. METHODS: We studied mortality among Swiss HIV Cohort Study (SHCS) participants (1988-2010) and causes of death using the Coding Causes of Death in HIV (CoDe) protocol (2005-2009). Furthermore, we linked the SHCS data to the Swiss National Cohort (SNC) cause of death registry. RESULTS: AIDS-related mortality peaked in 1992 [11.0/100 person-years (PY)] and decreased to 0.144/100 PY (2006); non-AIDS-related mortality ranged between 1.74 (1993) and 0.776/100 PY (2006); mortality of unknown cause ranged between 2.33 and 0.206/100 PY. From 2005 to 2009, 459 of 9053 participants (5.1%) died. Underlying causes of deaths were: non-AIDS malignancies [total, 85 (19%) of 446 deceased persons with known hepatitis C virus (HCV) status; HCV-negative persons, 59 (24%); HCV-coinfected persons, 26 (13%)]; AIDS [73 (16%); 50 (21%); 23 (11%)]; liver failure [67 (15%); 12 (5%); 55 (27%)]; non-AIDS infections [42 (9%); 13 (5%); 29 (14%)]; substance use [31 (7%); 9 (4%); 22 (11%)]; suicide [28 (6%); 17 (7%), 11 (6%)]; myocardial infarction [28 (6%); 24 (10%), 4 (2%)]. Characteristics of deceased persons differed in 2005 vs. 2009: median age (45 vs. 49 years, respectively); median CD4 count (257 vs. 321 cells/μL, respectively); the percentage of individuals who were antiretroviral therapy-naïve (13 vs. 5%, respectively); the percentage of deaths that were AIDS-related (23 vs. 9%, respectively); and the percentage of deaths from non-AIDS-related malignancies (13 vs. 24%, respectively). Concordance in the classification of deaths was 72% between CoDe and ICD-10 coding in the SHCS; and 60% between the SHCS and the SNC registry. CONCLUSIONS: Mortality in HIV-positive persons decreased to 1.33/100 PY in 2010. Hepatitis B or C virus coinfections increased the risk of death. Between 2005 and 2009, 84% of deaths were non-AIDS-related. Causes of deaths varied according to data source and coding system.

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There is a sustained controversy in the literature about the role and utility of self-monitoring of blood glucose (SMBG) in type 2 diabetes. The study results in this field do not provide really useful clues for the integration of SMBG in the follow-up of the individual patient, because they are based on a misconception of SMBG. It is studied as if it was a medical treatment whose effect on glycemic control is to be isolated. However, SMBG has no such intrinsic effect. It gains its purpose only as an inseparable component of a comprehensive and structured educational strategy. To be appropriate this strategy cannot be based on the health care professionals' view on diabetes only. It rather has to be tailored to the individual patient's needs through an ongoing process of shared reflection with him.

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A nationwide investigation was conducted in Switzerland to establish the exposure of the population by medical x rays and update the results of the 1998 survey. Both the frequency and the dose variations were studied in order to determine the change in the collective dose. The frequency study addressed 206 general practitioners (GPs), 30 hospitals, and 10 private radiology institutes. Except for the latter, the response rate was very satisfactory. The dose study relied on the assessment of the speed class of the screen-film combinations used by the GPs as well as the results of two separate studies dedicated to fluoroscopy and CT. The investigation showed that the total number of all medical x-ray examinations performed by GPs registered a 1% decrease between 1998 and 2003, and that the sensitivities of the film-screen combinations registered a shift towards higher values, leading to a reduction of the dose delivered by a GP of the order of 20%. The study indicated also that the total number of all x-ray examinations performed in hospitals increased by 4%, with a slight increase of radiographies by 1% but significant decrease of examinations involving fluoroscopy (39%), and a 70% increase for CT examinations. Concerning the doses, the investigation of a selection of examinations involving fluoroscopy showed a significant increase of the kerma-area product (KAP) per procedure. For CT the study showed an increase of the dose-length product (DLP) per procedure for skull and abdomen examinations, and a decrease for chest examination. Both changes in the frequency and the effective dose per examination led to a 20% increase in the total collective dose.

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Obesity is heritable and predisposes to many diseases. To understand the genetic basis of obesity better, here we conduct a genome-wide association study and Metabochip meta-analysis of body mass index (BMI), a measure commonly used to define obesity and assess adiposity, in up to 339,224 individuals. This analysis identifies 97 BMI-associated loci (P < 5 × 10(-8)), 56 of which are novel. Five loci demonstrate clear evidence of several independent association signals, and many loci have significant effects on other metabolic phenotypes. The 97 loci account for ∼2.7% of BMI variation, and genome-wide estimates suggest that common variation accounts for >20% of BMI variation. Pathway analyses provide strong support for a role of the central nervous system in obesity susceptibility and implicate new genes and pathways, including those related to synaptic function, glutamate signalling, insulin secretion/action, energy metabolism, lipid biology and adipogenesis.

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The aim of this study was to identify medico-legal situations characterized by increased vitreous glucose concentrations, potentially lethal blood 3-hydroxybutyrate levels and conditions that could either incapacitate or lead to death on their own. The above was investigated in order to verify whether prolonged states of unconsciousness may play a role in precipitating diabetic ketoacidosis. Six groups of medico-legal situations (corresponding to 206 autopsy cases) were identified. Among these, three cases were characterized by pathologically increased vitreous glucose and blood 3-hydroxybutyrate levels. In one case diabetic ketoacidosis coexisted with underlying features that might have potentially incapacitated or lead to death on their own, whereas in two cases it corresponded with potentially lethal or lethal drug concentrations. The results of this study highlight the usefulness of systematically performing biochemistry in order to identify diabetic ketoacidosis-related deaths, even when autopsy and toxicology results provide apparently conclusive findings.

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Työn tavoitteena oli kehittää automaattinen optimointijärjestelmä energiayhtiön omistamaan pieneen sähkön- ja lämmöntuotantolaitokseen (CHP-laitos). Optimointitarve perustuu energiayhtiön sähkön hankintaan sähköpörssistä, kaasun hankintahintaan, kohteen paikallisiin sähkö- ja lämpökuormituksiin ja muihin laitoksen talouteen vaikuttaviin tekijöihin. Kehitettävällä optimointijärjestelmällä ontarkoitus tulevaisuudessa hallita useita hajautetun energiantuotannon yksiköitäkeskitetysti. Työssä kehitettiin algoritmi, joka optimoi voimalaitoksen taloutta sähkötehoa säätävillä ajomalleilla ja suoralla sähköteho-ohjeella. Työssä kehitetyn algoritmin tuottamia hyötyjä selvitettiin Harjun oppimiskeskuksen CHP-laitoksen mittaushistoriatiedoilla. CHP-laitosten käytön optimointiin luotiin keskitettyyn laskentaan ja hajautettuun ohjaukseen perustuva järjestelmä. Se ohjaa CHP-laitoksia reaaliaikaisesti ja ennustaa historiatietoihin perustuvalla aikasarjamallilla laitoksen tulevaa käyttöä. Optimointijärjestelmän toimivuus ja saatu hyöty selvitettiin Harjun oppimiskeskuksen CHP-laitoksella vertaamalla mittauksista laskettua toteutunutta hyötyä optimointijärjestelmän laskemaan ennustettuun hyötyyn.

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L'athérosclérose est un processus inflammatoire chronique à l'origine des accidents cardiovasculaires qui constitue l'une des premières causes de mortalité en France. L'inflammation est le facteur essentiel dans l'initiation, la progression et l'instabilité des lésions athéromateuses à l'origine des accidents aigus. Les données récentes suggèrent que l'activation des récepteurs nucléaires PPAR (Peroxysome-Proliferator Activated Receptor) par des ligands pharmacologiques prévient le développement et la progression de l'athérosclérose et diminue de manière importante la mortalité cardiovasculaire. À côté de ces traitements pharmacologiques, l'exercice physique prévient aussi la mortalité cardiovasculaire de manière significative. L'objectif de notre premier travail a été d'explorer les effets de l'exercice physique de natation, sur le déve¬loppement des lésions athéromateuses d'une part et d'autre part, sur l'expression des récepteurs nucléaires PPAR. Nos résultats montrent que l'exercice physique de natation diminue la progression de l'athérosclérose et stimule l'expression des PPAR-γ vasculaires. De manière intéressante, lorsque le PPAR-γ est inhibé avec l'antagoniste BADGE, les effets antiathérogènes de l'exercice physique sont abolis. L'hypertension est à l'origine des complications graves telles que la rupture de plaque d'athérosclérose. L'objectif de notre deuxième travail a été d'explorer l'implication des PPAR dans la progression et la stabilité des lésions athéromateuses chez des souris ApoE-/- hypercholestérolemiques et hypertendues (2K1C), soumises à des exercices physiques (volontaire ou imposé) ou traités avec le telmisartan, un antihypertenseur. Nos résultats montrent que l'exercice physique possède différents mécanismes protecteurs. De manière similaire, l'exercice physique favorise la stabilité de lésions athéromateuses de manière comparable au traitement pharmacologique. De plus, nos résultats montrent que les souris traitées avec l'exercice imposé ou le telmisartan présentent un mécanisme comparable qui permet de réduire significativement l'expression des cytokines pro-inflammatoire et d'activer les PPAR-γ vasculaires. L'exercice volontaire favorise l'expression des marqueurs des macrophages alternatifs M2 et des cytokines anti-inflammatoires (CD 206, IL-1 Ra). L'exercice volontaire diminue significativement l'extension des lésions athéromateuses de manière comparable au telmisartan. Ces résultats montrent que l'exercice physique volontaire et l'exercice physique imposé ont deux mécanismes d'actions distincts. De plus, la surexpression des M2 en réponse à l'exercice volontaire modifie la balance inflammatoire en faveur des M2. Ce renversement de la balance au profit des macrophages alternatifs M2 est significativement corrélé à la diminution de la progression des lésions athéromateuses. Les exercices imposé et volontaire possèdent des mécanismes d'action distincts. L'exercice soumis diminue l'expression des cytokines pro-inflammatoires tandis que l'exercice volontaire augmente l'expression des cytokines anti-inflammatoires et favorise un phénotype anti-inflammatoire des macrophages M2 qui s'accompagne d'une réduction des lésions athéromateuses. - Atherosclerosis is a complex inflammatory process, leading cause of morbidity and mortality in France. Inflammation is essential in initiation, progression and atherosclerosis plaque destabilization leading to acute cardiovascular events. Recent studies suggest that pharmacological PPAR activation prevents ΑΤΗ développement and progression and decreased cardiovascular mortality. Compared to pharmacological treatment, physical exercise also significantly prevents cardiovascular mortality. The aim of the first study was to investigate the influence of physical exercise on ATS development and PPAR expression in arterial wall. Our results had shown that physical exercise decrease ΑΤΗ progression and increase PPAR-γ expression in arterial wall. Interestingly, PPAR-γ inhibition with BADGE, a PPAR-γ antagonist abolishes these antiatherogenic effects. Hypertension increase ΑΤΗ complication such as plaque rupture. The aim of the second study were to inves¬tigate PPAR-γ implication in progression and stabilization of ΑΤΗ lesions in hypercholesterolemic and hypertensive ApoE-/- mice (2K1C) submitted to different exercises (voluntary wheel running and submitted treadmill running) or treated with telmisartan an anti-hypertensive drug. Our results shown that, physical exercise prevents ATS cardiovascular events by several mechanisms. Similarly to telmisartan, physical exercises stabilize ΑΤΗ lesion. Moreover results shown that, submitted exercise and telmisartan have an comparable mechanism. In fact, they significantly decrease pro-inflammatory cytokines expression and in the same time activated PPAR-γ expression in arterial wall. Contrary to submitted exercise, voluntary exercises increases expression of anti-inflammatory cytokines IL-1ra and increase M2 marker CD206. These results suggest that voluntary and submitted exercise have two different mechanism of action. Moreover, M2 surexpression in response to voluntary exercise shift the inflammatory balance in favor to M2. Further, this change of balance in favor to M2, is significantly correlated to decrease of ΑΤΗ progression. Voluntary exercises significantly decreases ΑΤΗ progression in the same levels like telmisartan treatment. Voluntary and submitted exercise has two different mechanisms, submitted exercise decrease proinflammatory cytokines expression whereas voluntary exercise increase anti-inflammatory cytokines expression and promote an anti-inflammatory phenotype of macrophages M2. The shift of M1/M2 balance towards M2 decreases atherosclerosis progression.

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Background To determine the diagnostic and prognostic capability of urinary and tumoral syndecan-1 (SDC-1) levels in patients with cancer of the urinary bladder. Methods SDC-1 levels were quantitated by enzyme-linked immunosorbent assay (ELISA) in 308 subjects (102 cancer subjects and 206 non-cancer subjects) to assess its diagnostic capabilities in voided urine. The performance of SDC-1 was evaluated using the area under the curve of a receiver operating characteristic curve. In addition, immunohistochemical (IHC) staining assessed SDC-1 protein expression in 193 bladder specimens (185 cancer subjects and 8 non-cancer subjects). Outcomes were correlated to SDC-1 levels. Results Mean urinary levels of SDC-1 did not differ between the cancer subjects and the non-cancer subjects, however, the mean urinary levels of SDC-1 were reduced in high-grade compared to low-grade disease (p < 0.0001), and in muscle invasive bladder cancer (MIBC) compared to non-muscle invasive bladder cancer (NMIBC) (p = 0.005). Correspondingly, preliminary data note a shift from a membranous cellular localization of SDC-1 in normal tissue, low-grade tumors and NMIBC, to a distinctly cytoplasmic localization in high-grade tumors and MIBC was observed in tissue specimens. Conclusion Alone urinary SDC-1 may not be a diagnostic biomarker for bladder cancer, but its urinary levels and cellular localization were associated with the differentiation status of patients with bladder tumors. Further studies are warranted to define the potential role for SDC-1 in bladder cancer progression.

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Background To determine the diagnostic and prognostic capability of urinary and tumoral syndecan-1 (SDC-1) levels in patients with cancer of the urinary bladder. Methods SDC-1 levels were quantitated by enzyme-linked immunosorbent assay (ELISA) in 308 subjects (102 cancer subjects and 206 non-cancer subjects) to assess its diagnostic capabilities in voided urine. The performance of SDC-1 was evaluated using the area under the curve of a receiver operating characteristic curve. In addition, immunohistochemical (IHC) staining assessed SDC-1 protein expression in 193 bladder specimens (185 cancer subjects and 8 non-cancer subjects). Outcomes were correlated to SDC-1 levels. Results Mean urinary levels of SDC-1 did not differ between the cancer subjects and the non-cancer subjects, however, the mean urinary levels of SDC-1 were reduced in high-grade compared to low-grade disease (p < 0.0001), and in muscle invasive bladder cancer (MIBC) compared to non-muscle invasive bladder cancer (NMIBC) (p = 0.005). Correspondingly, preliminary data note a shift from a membranous cellular localization of SDC-1 in normal tissue, low-grade tumors and NMIBC, to a distinctly cytoplasmic localization in high-grade tumors and MIBC was observed in tissue specimens. Conclusion Alone urinary SDC-1 may not be a diagnostic biomarker for bladder cancer, but its urinary levels and cellular localization were associated with the differentiation status of patients with bladder tumors. Further studies are warranted to define the potential role for SDC-1 in bladder cancer progression.

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Background: Intravenous thrombolysis with alteplase for ischemic stroke is fixed at a maximal dose of 90 mg for safety reasons. Little is known about the clinical outcomes of stroke patients weighing >100 kg, who may benefit less from thrombolysis due to this dose limitation. Methods: Prospective data on 1,479 consecutive stroke patients treated with intravenous alteplase in six Swiss stroke units were analyzed. Presenting characteristics and the frequency of favorable outcomes, defined as a modified Rankin scale (mRS) score of 0 or 1, a good outcome (mRS score 0-2), mortality and symptomatic intracranial hemorrhage (SICH) were compared between patients weighing >100 kg and those weighing ≤100 kg. Results: Compared to their counterparts (n = 1,384, mean body weight 73 kg), patients weighing >100 kg (n = 95, mean body weight 108 kg) were younger (61 vs. 67 years, p < 0.001), were more frequently males (83 vs. 60%, p < 0.001) and more frequently suffered from diabetes mellitus (30 vs. 13%, p < 0.001). As compared with patients weighing ≤100 kg, patients weighing >100 kg had similar rates of favorable outcomes (45 vs. 48%, p = 0.656), good outcomes (58 vs. 64%, p = 0.270) and mortality (17 vs. 12%, p = 0.196), and SICH risk (1 vs. 5%, p = 0.182). After multivariable adjustment, body weight >100 kg was strongly associated with mortality (p = 0.007) and poor outcome (p = 0.007). Conclusion: Our data do not suggest a reduced likehood of favorable outcomes in patients weighing >100 kg treated with the current dose regimen. The association of body weight >100 kg with mortality and poor outcome, however, demands further large-scale studies to replicate our findings and to explore the underlying mechanisms.