991 resultados para SUZUKI


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FUNDAMENTO: No âmbito da transição epidemiológica, estudos de tendência secular podem subsidiar a formulação de hipóteses para o gerenciamento em Saúde. OBJETIVO: Identificar o padrão de mortalidade por doenças do aparelho circulatório (DAC) no município de Ribeirão Preto, SP, no período de 1980 a 2004. MÉTODOS: Os óbitos por DAC foram obtidos do Sistema de Informações sobre Mortalidade (SIM). As estimativas populacionais para o município, segundo sexo, faixa etária e anos-calendário, foram obtidas do Instituto Brasileiro de Geografia e Estatística (IBGE). Os coeficientes específicos de mortalidade foram calculados, anualmente, segundo sexo e faixa etária classificada em intervalos de 10 anos, a partir dos 30 anos de idade. O estudo de tendência foi realizado por meio da construção de modelos de regressão polinomial para séries históricas, adotando-se nível de significância < 0,05. RESULTADOS: Os coeficientes específicos de mortalidade por DAC aumentaram com a idade, em ambos os sexos, sendo mais elevados no sexo masculino até a faixa etária de 40 a 49 anos, quando ocorreu aproximação em magnitude, sendo que, na faixa etária de 80 anos ou mais, esses indicadores, no sexo feminino e em alguns anos da série, ultrapassaram os do sexo masculino. Ao longo do período estudado, em ambos os sexos e em todas as faixas etárias, ocorreu declínio significante das taxas de mortalidade por esse grupo de causas (p<0,001). CONCLUSÕES: O padrão de mortalidade por DAC no município de Ribeirão Preto foi similar ao encontrado em regiões desenvolvidas, permitindo a formulação de hipóteses sobre possíveis fatores de proteção que podem explicar o declínio observado.

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A Tomografia de Coerência Ótica (TCO) é uma nova tecnologia de imagem baseada em interferometria de baixa coerência que utiliza a dispersão de luz quase-infravermelha como uma fonte de sinal para fornecer imagens transversais vasculares com definição muito superior à de qualquer outra modalidade disponível. Com uma resolução espacial de até 10μm, a TCO fornece uma resolução 20 vezes maior do que o ultrassom intravascular (USIV), a modalidade atualmente mais utilizada para obter imagens intra-coronárias. A TCO tem uma capacidade de fornecer um entendimento das várias fases da doença aterosclerótica e a resposta vascular ao tratamento. Estudos tem mostrado a capacidade da TCO em detectar estruturas arteriais e ajudar na determinação de diferentes constituintes histológicos. Sua capacidade de distinguir diferentes graus de alterações ateroscleróticas e os vários tipos de placas, quando comparada à histologia, tem sido recentemente demonstrada com correlações inter e intra-observador aceitáveis para esses achados. A TCO fornece uma resolução endovascular excepcional em tempo real in vivo, que tem sido explorada para avaliar as estruturas vasculares e a resposta ao uso do equipamento. Embora a profundidade permaneça uma limitação para a caracterização de placa além de 2 mm através da TCO, uma resolução próxima à histológica pode ser obtida dentro do primeiro milímetro da parede do vaso, permitindo uma avaliação extraordinária das características e espessura da capa fibrosa. Além disso, a avaliação da cobertura de neoíntima, padrões de tecido para-haste e aposição de stent podem agora ser escrutinizados para hastes individuais na escala de mícrons, a assim chamada análise em nível de haste. A TCO levou a imagem intravascular ao nível de mícron na análise vascular in vivo e espera-se que breve se torne uma ferramenta valiosa e indispensável para cardiologistas em aplicações clínicas e de pesquisa.

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FUNDAMENTO: Síndromes coronarianas agudas são a maior causa de mortalidade no mundo. Estímulos externos, também conhecidos como gatilhos, como estado emocional ou atividade física, podem produzir mudanças fisiopatológicas desencadeantes. Dentre os gatilhos estudados, eventos estressantes, como campeonatos de futebol, são controversos na literatura e não há dados efetivos para a população brasileira. OBJETIVO: Avaliar os efeitos agudos do estresse ambiental induzido pelos jogos da Copa do Mundo de Futebol no aumento da incidência de doenças cardiovasculares no Brasil. MÉTODOS: Foram obtidos dados publicamente disponíveis do Sistema Único de Saúde referentes às internações hospitalares com código internacional de doenças, referentes às síndromes isquêmicas agudas, no período de maio a agosto de 1998 a 2010 (155.992 internações). Restringiu-se a análise aos pacientes maiores que 35 anos e internados por especialidades clínicas. Comparou-se a incidência de infarto e óbito entre os dias sem copa (Grupo I: 144.166; 61,7 ± 12,3 anos; 59,4%masculino), dias de copa sem jogos do Brasil (Grupo II: 9.768; 61,8 ± 12,3 anos; 60,0% masculino) e dias de jogos do Brasil (Grupo III: 2.058; 61,6 ± 12,6 anos; 57,8% masculino). Utilizou-se regressão logística e de Poisson para ajustar por idade, gênero, densidade populacional e número de postos de atendimento. RESULTADOS: Houve aumento da incidência de infarto para jogos de copa do mundo (1,09; IC95% = 1,05-1,15) e do Brasil (1,16; IC95% = 1,06-1,27). Não houve impacto sobre mortalidade - copa (1,00; IC95% = 0,93-1,08) e Brasil (1,04; IC95% = 0,93-1,22). CONCLUSÃO: A copa do mundo e, especialmente, os jogos da seleção brasileira implicam maior incidência de infarto agudo do miocárdio, mas não de mortalidade intra-hospitalar.

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Estudi elaborat a partir d’una estada a l’ Ecole Nationale Supérieure de Chimie de Montpellier, França, durant 2006. S’han sintetitzat materials híbrids orgànico-inorgànics mitjançant el procés sol-gel i altres estratègies sintètiques. En alguns casos, s’ha intentat estructurar aquests materials, ja sigui per autoestructuració o per mitjà de tensioactius. Com a catalitzadors de les reaccions d'hidròlisi i policondensació s’han utilitzat àcids, bases i fluorurs. Els materials obtinguts s’han caracteritzat mitjançant diferents tècniques: BET (Brunauer-Emmett-Teller), TEM (microscopia electrònica de transmissió), SEM (microscòpia electrònica de rastreig), raigs X en pols , IR i RMN (ressonància magnètica nuclear) en estat sòlid. Amb aquests materials es pretén preparar catalitzadors heterogenis de Pd per reaccions d’acoblament creuat, i de Ru per reaccions de metàtesi. També s’han sintetitzat sals d'imidazoli amb cadenes hidrocarbonades llargues amb l'objectiu de preparar gels de sílice amb aquestes molècules atrapades dins la matriu inorgànica. Aquests materials s’utilitzaran com a organocatalitzadors i també es prepararan els corresponents catalitzadors de Pd per reaccions de Heck, Suzuki i Sonogashira. Les sals d’imidazoli s’han utilitzat com a tensioactius en la preparació de gels de sílice estructurats. Aquestes molècules han resultat ser cristalls líquids i s’han caracteritzar mitjançant DSC (differential scanning calorimetry), microscopia òptica i raigs X.

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In mammalian circadian clockwork, the CLOCK-BMAL1 complex binds to DNA enhancers of target genes and drives circadian oscillation of transcription. Here we identified 7,978 CLOCK-binding sites in mouse liver by chromatin immunoprecipitation-sequencing (ChIP-Seq), and a newly developed bioinformatics method, motif centrality analysis of ChIP-Seq (MOCCS), revealed a genome-wide distribution of previously unappreciated noncanonical E-boxes targeted by CLOCK. In vitro promoter assays showed that CACGNG, CACGTT, and CATG(T/C)G are functional CLOCK-binding motifs. Furthermore, we extensively revealed rhythmically expressed genes by poly(A)-tailed RNA-Seq and identified 1,629 CLOCK target genes within 11,926 genes expressed in the liver. Our analysis also revealed rhythmically expressed genes that have no apparent CLOCK-binding site, indicating the importance of indirect transcriptional and posttranscriptional regulations. Indirect transcriptional regulation is represented by rhythmic expression of CLOCK-regulated transcription factors, such as Krüppel-like factors (KLFs). Indirect posttranscriptional regulation involves rhythmic microRNAs that were identified by small-RNA-Seq. Collectively, CLOCK-dependent direct transactivation through multiple E-boxes and indirect regulations polyphonically orchestrate dynamic circadian outputs.

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Rationale: Peroxisome proliferator activated receptor (PPAR)-beta/delta is a transcription factor that belongs to the PPAR nuclear hormone receptor family, but the role of PPAR-beta/delta in sepsis is unknown. Objectives: We investigated the role of PPAR-beta/delta in murine models of LPS-induced organ injury and dysfunction and cecal ligation and puncture (CLP)-induced polymicrobial sepsis. Methods: Wild-type (WT) and PPAR-beta/delta knockout (1(0) mice and C57BL/6 mice were subjected to LPS for 16 hours. C57BL/6 mice received the PPAR-beta/delta agonist GW0742 (0.03 mg/kg intravenously, 1 h after LPS) or GW0742 plus the PPAR-beta/delta antagonist GSK0660 (0.1 mg/kg intravenously, 30 min before LPS). CD-1 mice subjected to CLP received GW0742 or GW0742 plus GSK0660. Measurements and Main Results: In PPAR-beta/delta KO mice, endotoxemia exacerbated organ injury and dysfunction (cardiac, renal, and hepatic) and inflammation (lung) compared with WT mice. In C57BL/6 mice subjected to endotoxemia, GW0742 significantly (1) attenuated organ (cardiac and renal) dysfunction and inflammation (lung); (2) increased the phosphorylation of Akt and glycogen synthase kinase (GSK)-3 beta; (3) attenuated the increase in extracellular signal-regulated kinase (ERK)1/2 and signal transducer and activator of transcription (STAT)-3 phosphorylation; and (4) attenuated the activation of nuclear factor (NF)-kappa B and the expression of inducible nitric oxide synthase (iNOS). In CD-1 mice subjected to CLP, GW0742 improved 10-day survival. All the observed beneficial effects of GW0742 were attenuated by the PPAR-beta/delta antagonist GSK0660. Conclusions: PPAR-beta/delta protects against multiple organ injury and dysfunction, and inflammation caused by endotoxic shock and improves survival in polymicrobial sepsis by a mechanism that may involve activation of Akt and inhibition of GSK-3 beta and NF-kappa B.

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Aeromonas hydrophila is a Gram-negative pathogen that causes serious infectious disease in humans. A. hydrophila induces apoptosis in infected macrophages, but the host proinflammatory responses triggered by macrophage death are largely unknown. Here, we demonstrate that the infection of mouse macrophages with A. hydrophila triggers the activation of caspase-1 and release of IL-1β. Caspase-1 activation was abrogated in macrophages deficient in Nod-like receptor family, pyrin domain containing 3 (NLRP3) and apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), but not NLR family, CARD domain containing 4 (NLRC4). The activation of the NLRP3 inflammasome was mediated by three cytotoxins (aerolysin, hemolysin and multifunctional repeat-in-toxin) produced by A. hydrophila. Our results indicated that the NLRP3 inflammasome senses A. hydrophila infection through the action of bacterial cytotoxins.

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Mechanical load-induced intracellular signaling events are important for subsequent skeletal muscle hypertrophy. We previously showed that load-induced activation of the cation channel TRPV1 caused an increase in intracellular calcium concentrations ([Ca ( 2+) ]i) and that this activated mammalian target of rapamycin (mTOR) and promoted muscle hypertrophy. However, the link between mechanical load-induced intracellular signaling events, and the TRPV1-mediated increases in [Ca ( 2+) ]i are not fully understood. Here we show that administration of the TRPV1 agonist, capsaicin, induces phosphorylation of mTOR, p70S6K, S6, Erk1/2 and p38 MAPK, but not Akt, AMPK or GSK3β. Furthermore, the TRPV1-induced phosphorylation patterns resembled those induced by mechanical load. Our results continue to highlight the importance of TRPV1-mediated calcium signaling in load-induced intracellular signaling pathways.

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BACKGROUND Challenges exist in the clinical diagnosis of drug-induced liver injury (DILI) and in obtaining information on hepatotoxicity in humans. OBJECTIVE (i) To develop a unified list that combines drugs incriminated in well vetted or adjudicated DILI cases from many recognized sources and drugs that have been subjected to serious regulatory actions due to hepatotoxicity; and (ii) to supplement the drug list with data on reporting frequencies of liver events in the WHO individual case safety report database (VigiBase). DATA SOURCES AND EXTRACTION (i) Drugs identified as causes of DILI at three major DILI registries; (ii) drugs identified as causes of drug-induced acute liver failure (ALF) in six different data sources, including major ALF registries and previously published ALF studies; and (iii) drugs identified as being subjected to serious governmental regulatory actions due to their hepatotoxicity in Europe or the US were collected. The reporting frequency of adverse events was determined using VigiBase, computed as Empirical Bayes Geometric Mean (EBGM) with 90% confidence interval for two customized terms, 'overall liver injury' and 'ALF'. EBGM of >or=2 was considered a disproportional increase in reporting frequency. The identified drugs were then characterized in terms of regional divergence, published case reports, serious regulatory actions, and reporting frequency of 'overall liver injury' and 'ALF' calculated from VigiBase. DATA SYNTHESIS After excluding herbs, supplements and alternative medicines, a total of 385 individual drugs were identified; 319 drugs were identified in the three DILI registries, 107 from the six ALF registries (or studies) and 47 drugs that were subjected to suspension or withdrawal in the US or Europe due to their hepatotoxicity. The identified drugs varied significantly between Spain, the US and Sweden. Of the 319 drugs identified in the DILI registries of adjudicated cases, 93.4% were found in published case reports, 1.9% were suspended or withdrawn due to hepatotoxicity and 25.7% were also identified in the ALF registries/studies. In VigiBase, 30.4% of the 319 drugs were associated with disproportionally higher reporting frequency of 'overall liver injury' and 83.1% were associated with at least one reported case of ALF. CONCLUSIONS This newly developed list of drugs associated with hepatotoxicity and the multifaceted analysis on hepatotoxicity will aid in causality assessment and clinical diagnosis of DILI and will provide a basis for further characterization of hepatotoxicity.

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The international Functional Annotation Of the Mammalian Genomes 4 (FANTOM4) research collaboration set out to better understand the transcriptional network that regulates macrophage differentiation and to uncover novel components of the transcriptome employing a series of high-throughput experiments. The primary and unique technique is cap analysis of gene expression (CAGE), sequencing mRNA 5'-ends with a second-generation sequencer to quantify promoter activities even in the absence of gene annotation. Additional genome-wide experiments complement the setup including short RNA sequencing, microarray gene expression profiling on large-scale perturbation experiments and ChIP-chip for epigenetic marks and transcription factors. All the experiments are performed in a differentiation time course of the THP-1 human leukemic cell line. Furthermore, we performed a large-scale mammalian two-hybrid (M2H) assay between transcription factors and monitored their expression profile across human and mouse tissues with qRT-PCR to address combinatorial effects of regulation by transcription factors. These interdependent data have been analyzed individually and in combination with each other and are published in related but distinct papers. We provide all data together with systematic annotation in an integrated view as resource for the scientific community (http://fantom.gsc.riken.jp/4/). Additionally, we assembled a rich set of derived analysis results including published predicted and validated regulatory interactions. Here we introduce the resource and its update after the initial release.

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Distinguishing drug-induced liver injury (DILI) from idiopathic autoimmune hepatitis (AIH) can be challenging. We performed a standardized histologic evaluation to explore potential hallmarks to differentiate AIH versus DILI. Biopsies from patients with clinically well-characterized DILI [n = 35, including 19 hepatocellular injury (HC) and 16 cholestatic/mixed injury (CS)] and AIH (n = 28) were evaluated for Ishak scores, prominent inflammatory cell types in portal and intra-acinar areas, the presence or absence of emperipolesis, rosette formation, and cholestasis in a blinded fashion by four experienced hepatopathologists. Histologic diagnosis was concordant with clinical diagnosis in 65% of cases; but agreement on final diagnosis among the four pathologists was complete in only 46% of cases. Interface hepatitis, focal necrosis, and portal inflammation were present in all evaluated cases, but were more severe in AIH (P < 0.05) than DILI (HC). Portal and intra-acinar plasma cells, rosette formation, and emperiopolesis were features that favored AIH (P < 0.02). A model combining portal inflammation, portal plasma cells, intra-acinar lymphocytes and eosinophils, rosette formation, and canalicular cholestasis yielded an area under the receiver operating characteristic curve (AUROC) of 0.90 in predicting DILI (HC) versus AIH. All Ishak inflammation scores were more severe in AIH than DILI (CS) (P ≤ 0.05). The four AIH-favoring features listed above were consistently more prevalent in AIH, whereas portal neutrophils and intracellular (hepatocellular) cholestasis were more prevalent in DILI (CS) (P < 0.02). The combination of portal inflammation, fibrosis, portal neutrophils and plasma cells, and intracellular (hepatocellular) cholestasis yielded an AUC of 0.91 in predicting DILI (CS) versus AIH. Conclusion: Although an overlap of histologic findings exists for AIH and DILI, sufficient differences exist so that pathologists can use the pattern of injury to suggest the correct diagnosis.

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The rate-limiting step of dietary calcium absorption in the intestine requires the brush border calcium entry channel TRPV6. The TRPV6 gene was completely sequenced in 170 renal calcium stone patients. The frequency of an ancestral TRPV6 haplotype consisting of three non-synonymous polymorphisms (C157R, M378V, M681T) was significantly higher (P = 0.039) in calcium stone formers (8.4%; derived = 502, ancestral = 46) compared to non-stone-forming individuals (5.4%; derived = 645, ancestral = 37). Mineral metabolism was investigated on four different calcium regimens: (i) free-choice diet, (ii) low calcium diet, (iii) fasting and (iv) after a 1 g oral calcium load. When patients homozygous for the derived haplotype were compared with heterozygous patients, no differences were found with respect to the plasma concentrations of 1,25-vitamin D, PTH and calcium, and the urinary excretion of calcium. In one stone-forming patient, the ancestral haplotype was found to be homozygous. This patient had absorptive hypercalciuria. We therefore expressed the ancestral protein (157R+378V+681T) in Xenopus oocytes and found a significantly enhanced calcium permeability when tested by a (45)Ca(2+) uptake assay (7.11 +/- 1.93 versus 3.61 +/- 1.01 pmol/min/oocyte for ancestral versus derived haplotype, P < 0.01). These results suggest that the ancestral gain-of-function haplotype in TRPV6 plays a role in calcium stone formation in certain forms of absorptive hypercalciuria.

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In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.

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As complicações agudas e crônicas enfrentadas pelo paciente diabético e sua família após a alta hospitalar podem ser consequência de deficiências no processo educativo ao longo da hospitalização e do preparo formal para alta. O objetivo deste estudo é apresentar uma proposta de planejamento da alta hospitalar do paciente diabético adulto. Foi realizada revisão de literatura sobre alta hospitalar da clientela em questão, selecionando-se artigos publicados de 2004 a fevereiro de 2009. Considerando a literatura, foi desenvolvido um impresso para nortear o planejamento da alta. Este abrange informações a serem colhidas e trabalhadas junto ao cliente, ao longo dos primeiros quatro dias de internação, considerando as necessidades individuais e o Autocontrole ineficaz da saúde. A alta precisa estar inserida no Processo de Enfermagem, uma vez que o enfermeiro tem papel fundamental na identificação das necessidades do paciente e família. O impresso auxilia a identificação das necessidades do cliente e das ações realizadas pela equipe.

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This chpter is dedicated the comparative Syntatic analysis of two portuguese-based creoles.