2,927 research outputs found
A New Screening Method for Algal Photosynthetic Mutants (CO2-Insensitive Mutants of the Green Alga Chlorella ellipsoidea)
InfluĆŖncia de sistemas de integraĆ§Ć£o lavoura-pecuĆ”ria-floresta sobre a biomassa microbiana do solo.
JIPE 2013
Monitoramento de parĆ¢metros microbiolĆ³gicos em sistemas de produĆ§Ć£o agropecuĆ”ria.
JIPE 2013
Indicadores microbiolĆ³gicos para avaliaĆ§Ć£o da qualidade do solo em diferentes sistemas de integraĆ§Ć£o lavoura-pecuĆ”ria-floresta.
PCN39 TREATMENT PATTERNS AMONG PATIENTS WITH ADVANCED MELANOMA:A RETROSPECTIVE LONGITUDINAL STUDY
Pericas, Enri
Biomassa microbiana de um latossolo da regiĆ£o sudoeste dos cerrados com diferentes sistemas de manejo.
JIPE 2013
In silico assessment of genetic variation in KCNA5 reveals multiple mechanisms of human atrial arrhythmogenesis
A recent experimental study investigating patients with lone atrial fibrillation identified six novel mutations in the KCNA5 gene. The mutants exhibited both gain- and loss-of-function of the atrial specific ultra-rapid delayed rectifier K+ current, IKur. The aim of this study is to elucidate and quantify the functional impact of these KCNA5 mutations on atrial electrical activity. A multi-scale model of the human atria was updated to incorporate detailed experimental data on IKur from both wild-type and mutants. The effects of the mutations on human atrial action potential and rate dependence were investigated at the cellular level. In tissue, we assessed the effects of the mutations on the vulnerability to unidirectional conduction patterns and dynamics of re-entrant excitation waves. Gain-of-function mutations shortened the action potential duration in single cells, and stabilised and accelerated re-entrant excitation in tissue. Loss-of-function mutations had heterogeneous effects on action potential duration and promoted early-after-depolarisations following beta-adrenergic stimulation. In the tissue model, loss-of-function mutations facilitated breakdown of excitation waves at more physiological excitation rates than the wild-type, and the generation of early-after-depolarisations promoted unidirectional patterns of excitation. Gain- and loss-of-function IKur mutations produced multiple mechanisms of atrial arrhythmogenesis, with significant differences between the two groups of mutations. This study provides new insights into understanding the mechanisms by which mutant IKur contributes to atrial arrhythmias. In addition, as IKur is an atrial-specific channel and a number of IKur-selective blockers have been developed as anti-AF agents, this study also helps to understand some contradictory results on both pro- and anti-arrhythmic effects of blocking IKur
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