A pesca artesanal na bacia do Rio Branco: dos antecedentes históricos ao abandono das estatísticas pesqueiras em Roraima.

Este trabalho apresenta um panorama do conhecimento disponível sobre a pesca comercial na bacia do rio Branco, concentrando-se principalmente no seu trecho inferior, o baixo rio Branco, a mais importante área de pesca do estado de Roraima. Destacamos os aspectos mais relevantes da exploração dos recursos pesqueiros nesta bacia ao longo de mais de duzentos anos, incluindo o estabelecimento pela coroa Portuguesa dos ?pesqueiros reais?, os relatos dos naturalistas que contribuíram com o conhecimento sobre a ictiofauna local, uma caracterização da pesca comercial atualmente praticada na região, e uma análise histórica sobre a influência que a criação de dois parques nacionais e duas estações ecológicas, unidades de conservação de proteção integral, impuseram à prática da atividade pesqueira no baixo rio Branco

The Genome of a Pathogenic Rhodococcus: Cooptive Virulence Underpinned by Key Gene Acquisitions

We report the genome of the facultative intracellular parasite Rhodococcus equi, the only animal pathogen within the biotechnologically important actinobacterial genus Rhodococcus. The 5.0-Mb R. equi 103S genome is significantly smaller than those of environmental rhodococci. This is due to genome expansion in nonpathogenic species, via a linear gain of paralogous genes and an accelerated genetic flux, rather than reductive evolution in R. equi. The 103S genome lacks the extensive catabolic and secondary metabolic complement of environmental rhodococci, and it displays unique adaptations for host colonization and competition in the short-chain fatty acid–rich intestine and manure of herbivores—two main R. equi reservoirs. Except for a few horizontally acquired (HGT) pathogenicity loci, including a cytoadhesive pilus determinant (rpl) and the virulence plasmid vap pathogenicity island (PAI) required for intramacrophage survival, most of the potential virulence-associated genes identified in R. equi are conserved in environmental rhodococci or have homologs in nonpathogenic Actinobacteria. This suggests a mechanism of virulence evolution based on the cooption of existing core actinobacterial traits, triggered by key host niche–adaptive HGT events. We tested this hypothesis by investigating R. equi virulence plasmid-chromosome crosstalk, by global transcription profiling and expression network analysis. Two chromosomal genes conserved in environmental rhodococci, encoding putative chorismate mutase and anthranilate synthase enzymes involved in aromatic amino acid biosynthesis, were strongly coregulated with vap PAI virulence genes and required for optimal proliferation in macrophages. The regulatory integration of chromosomal metabolic genes under the control of the HGT–acquired plasmid PAI is thus an important element in the cooptive virulence of R. equi

Sotalol, propafenone, and flecainide: compared multiparametric analysis of ventricular repolarization in subjects without organic cardiopathy

Antiarrhythmic drugs are known to affect depolarization and repolarization time in a different fashion. The aim of the present study was to compare the effects of sotalol, flecainide and propafenone on some common (mean QT and QTc, mean JT and JTc), or uncommon (QTc dispersion, T-peak to T-end interval-Tp-Te) electrocardiographic parameters in order to evaluate the effects of these antiarrhythmic drugs on repolarization time. QTc dispersion, defined as the difference between maximum and minimum QTc calculated from the standard 12 ECG leads, and the average Tp-Te interval, reflect regional variation in ventricular repolarization. We have analyzed retrospectively the standard 12-lead electrocardiograms of 28 patients (15 females and 13 males, age 36.11 +/- 16 years, range 11-67 years), recorded in the free-drug state and at the steady state after oral treatment with sotalol (160 mg/ die), flecainide (200 mg/die) and propafenone (450 mg/die). These drugs were prescribed, separately, for the treatment of patients with supraventricular tachycardia without underlying structural heart disease. Sotalol treatment prolongs ventricular repolarization times (QT, p = 0.0001; JT, p = 0.0001 and JTc, p = 0.0001) in an homogeneous fashion, as showed by the significant decrease in QTc dispersion (p = 0.026) and Tp-Te interval (p = 0.011). On the contrary, flecainide treatment is associated with an increase in QTc dispersion (p = 0.039) and Tp-Te interval (p = 0.0001), mean QT (p = 0.0001), QTc (p = 0.0001) and QRS (p = 0.0001), with no significant changes in JT and JTc (NS). Propafenone treatment does not affect repolarization time indexes, affecting only depolarization time as expressed by an increase in QRS (p = 0.046)