Influência da dispersao da refratariedade atrial e do distúrbio da conduçao atrial na induçao de fibrilaçao ou flutter atrial em indivíduos com síndrome de Wolff-Parkinson-White*,**

Para avaliar a influência da dispersao da refratariedade atrial e distúrbio da conduçao atrial na induçao de fibrilaçao ou flutter atrial na síndrome de Wolff-Parkinson-White (WPW) , revimos os resultados de estudo eletrofisiológico de36 indivíduos, portadores desta síndrome, sem cardiopatia orgânica, consecutivamente avaliados em nossa instituiçao. A populaçao foi dividida em dois grupos: grupo A, 13 indivíduos (36%) com fibrilaçao ou flutter atrial induzido e, grupo B, 23 indivíduos (64%) sem estas arritmias induzidos artificialmente. Nao houve diferença estatisticamente significativa, comparando-se grupo A versus grupo B, com relaçao aos seguintes parâmetros: idade (34±14 vs., 33±14a, p = 0,85); intervalo PA (34±6 vs., 33±6 ms, p = 0,75); intervalo AD-AE (69±12 vs., 70±6 ms, p = 0,83); período refratário efetivo atrial direito (207±41 vs., 212±45, P = 0,74) e esquerdo (226±36 vs., 226±35 ms, p = 1,00); período refratário efetivo anterógrado da via acessória (319±1 06 vs., 301 ±63 ms, p = 0,52); tempo de conduçao sino-atrial (164±36 VS., 157±38 ms, p = 0,59) etempo de recuperaçao sinusal corrigido (249±71 vs., 212±61 ms, p = 0,10). A dispersao da refratariedade atrial isolada ou associada a distúrbio da conduçao atrial foi observada em 22 indivíduos (61 %) e, destes, 9 (41 %) tinham fibrilaçao ou flutter atrial induzido artificialmente; em 14 indivíduos (39%) controles, 4 (29%) tinham tais arritmias induzidas (x2 = 0,58, P = 0,74). Concluindo, a dispersao da refratariedade atrial e/ou distúrbio da conduçao atrial nao identificou indivíduos com WPW com maior propensao à induçao de fibrilaçao ou flutter atrial durante estudo eletrofisiológico

Identification of lignocellulose-degrading enzymes using metagenomic approaches

Composting units which handle lignocellulosic residues are suitable sources of novel and promising lignocellulose-degrading enzymes such as cellulases, xylanases and amylases. These enzymes have practical application in many industries where lignocellulose is converted into several added-value bioproducts. However, the effective conversion of lignocellulose by a sustainable process is currently incomplete. Therefore, there is a need to find novel and robust catalysts to overcome this fact. Function- and sequence-based metagenomic approaches were used to identify novel lignocellulose-degrading enzymes with interesting industrial applications.info:eu-repo/semantics/publishedVersio

Genetic Variants of Diabetes Risk and Incident Cardiovascular Events in Chronic Coronary Artery Disease

Objective: To determine whether information from genetic risk variants for diabetes is associated with cardiovascular events incidence. Methods: From the about 30 known genes associated with diabetes, we genotyped single-nucleotide polymorphisms at the 10 loci most associated with type-2 diabetes in 425 subjects from the MASS-II Study, a randomized study in patients with multi-vessel coronary artery disease. The combined genetic information was evaluated by number of risk alleles for diabetes. Performance of genetic models relative to major cardiovascular events incidence was analyzed through Kaplan-Meier curve comparison and Cox Hazard Models and the discriminatory ability of models was assessed for cardiovascular events by calculating the area under the ROC curve. Results: Genetic information was able to predict 5-year incidence of major cardiovascular events and overall-mortality in non-diabetic individuals, even after adjustment for potential confounders including fasting glycemia. Non-diabetic individuals with high genetic risk had a similar incidence of events then diabetic individuals (cumulative hazard of 33.0 versus 35.1% of diabetic subjects). The addition of combined genetic information to clinical predictors significantly improved the AUC for cardiovascular events incidence (AUC = 0.641 versus 0.610). Conclusions: Combined information of genetic variants for diabetes risk is associated to major cardiovascular events incidence, including overall mortality, in non-diabetic individuals with coronary artery disease.FAPESP[2007/54138-2

Rarity of monodominance in hyperdiverse Amazonian forests.

Tropical forests are known for their high diversity. Yet, forest patches do occur in the tropics where a single tree species is dominant. Such "monodominant" forests are known from all of the main tropical regions. For Amazonia, we sampled the occurrence of monodominance in a massive, basin-wide database of forest-inventory plots from the Amazon Tree Diversity Network (ATDN). Utilizing a simple defining metric of at least half of the trees ≥ 10 cm diameter belonging to one species, we found only a few occurrences of monodominance in Amazonia, and the phenomenon was not significantly linked to previously hypothesized life history traits such wood density, seed mass, ectomycorrhizal associations, or Rhizobium nodulation. In our analysis, coppicing (the formation of sprouts at the base of the tree or on roots) was the only trait significantly linked to monodominance. While at specific locales coppicing or ectomycorrhizal associations may confer a considerable advantage to a tree species and lead to its monodominance, very few species have these traits. Mining of the ATDN dataset suggests that monodominance is quite rare in Amazonia, and may be linked primarily to edaphic factors

Clinical phenotypes and prognosis of dilated cardiomyopathy caused by truncating variants in the TTN Gene.

Background: Truncating variants in the TTN gene (TTNtv) are the commonest cause of heritable dilated cardiomyopathy. This study aimed to study the phenotypes and outcomes of TTNtv carriers. Methods: Five hundred thirty-seven individuals (61% men; 317 probands) with TTNtv were recruited in 14 centers (372 [69%] with baseline left ventricular systolic dysfunction [LVSD]). Baseline and longitudinal clinical data were obtained. The primary end point was a composite of malignant ventricular arrhythmia and end-stage heart failure. The secondary end point was left ventricular reverse remodeling (left ventricular ejection fraction increase by ≥10% or normalization to ≥50%). Results: Median follow-up was 49 (18–105) months. Men developed LVSD more frequently and earlier than women (45±14 versus 49±16 years, respectively; P=0.04). By final evaluation, 31%, 45%, and 56% had atrial fibrillation, frequent ventricular ectopy, and nonsustained ventricular tachycardia, respectively. Seventy-six (14.2%) individuals reached the primary end point (52 [68%] end-stage heart failure events, 24 [32%] malignant ventricular arrhythmia events). Malignant ventricular arrhythmia end points most commonly occurred in patients with severe LVSD. Male sex (hazard ratio, 1.89 [95% CI, 1.04–3.44]; P=0.04) and left ventricular ejection fraction (per 10% decrement from left ventricular ejection fraction, 50%; hazard ratio, 1.63 [95% CI, 1.30–2.04]; P<0.001) were independent predictors of the primary end point. Two hundred seven of 300 (69%) patients with LVSD had evidence of left ventricular reverse remodeling. In a subgroup of 29 of 74 (39%) patients with initial left ventricular reverse remodeling, there was a subsequent left ventricular ejection fraction decrement. TTNtv location was not associated with statistically significant differences in baseline clinical characteristics, left ventricular reverse remodeling, or outcomes on multivariable analysis (P=0.07). Conclusions: TTNtv is characterized by frequent arrhythmia, but malignant ventricular arrhythmias are most commonly associated with severe LVSD. Male sex and LVSD are independent predictors of outcomes. Mutation location does not impact clinical phenotype or outcomes.pre-print1,66 M

Genetic polymorphisms located in genes related to immune and inflammatory processes are associated with end-stage renal disease: a preliminary study

Background Chronic kidney disease progression has been linked to pro-inflammatory cytokines and markers of inflammation. These markers are also elevated in end-stage renal disease (ESRD), which constitutes a serious public health problem. Objective To investigate whether single nucleotide polymorphisms (SNPs) located in genes related to immune and inflammatory processes, could be associated with ESRD development. Design and methods A retrospective case-control study was carried out on 276 patients with ESRD and 288 control subjects. Forty-eight SNPs were genotyped via SNPlex platform. Logistic regression was used to assess the relationship between each sigle polymorphism and the development of ESRD. Results Four polymorphisms showed association with ESRD: rs1801275 in the interleukin 4 receptor (IL4R) gene (OR: 0.66 (95%CI=0.46-0.95); p=0.025; overdominant model), rs4586 in chemokine (C-C motif) ligand 2 (CCL2) gene (OR: 0.70 (95%CI=0.54-0.90); p=0.005; additive model), rs301640 located in an intergenic binding site for signal transducer and activator of transcription 4 (STAT4) (OR: 1.82 (95%CI=1.17-2.83); p=0.006; additive model) and rs7830 in the nitric oxide synthase 3 (NOS3) gene (OR: 1.31 (95%CI=1.01-1.71); p=0.043; additive model). After adjusting for multiple testing, results lost significance. Conclusion Our preliminary data suggest that four genetic polymorphisms located in genes related to inflammation and immune processes could help to predict the risk of developing ESRD.This work was supported by grants from Instituto de Salud Carlos III (Ref: PI08/0738 and PI11/00245) to SR and Junta de Castilla y Leon (Ref: GRS 234/A/08) to ET. 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