Orthogonal decomposition of left ventricular remodeling in myocardial infarction

Left ventricular size and shape are important for quantifying cardiac remodeling in response to cardiovascular disease. Geometric remodeling indices have been shown to have prognostic value in predicting adverse events in the clinical literature, but these often describe interrelated shape changes. We developed a novel method for deriving orthogonal remodeling components directly from any (moderately independent) set of clinical remodeling indices. Results: Six clinical remodeling indices (end-diastolic volume index, sphericity, relative wall thickness, ejection fraction, apical conicity, and longitudinal shortening) were evaluated using cardiac magnetic resonance images of 300 patients with myocardial infarction, and 1991 asymptomatic subjects, obtained from the Cardiac Atlas Project. Partial least squares (PLS) regression of left ventricular shape models resulted in remodeling components that were optimally associated with each remodeling index. A Gram–Schmidt orthogonalization process, by which remodeling components were successively removed from the shape space in the order of shape variance explained, resulted in a set of orthonormal remodeling components. Remodeling scores could then be calculated that quantify the amount of each remodeling component present in each case. A one-factor PLS regression led to more decoupling between scores from the different remodeling components across the entire cohort, and zero correlation between clinical indices and subsequent scores. Conclusions: The PLS orthogonal remodeling components had similar power to describe differences between myocardial infarction patients and asymptomatic subjects as principal component analysis, but were better associated with well-understood clinical indices of cardiac remodeling. The data and analyses are available from www.cardiacatlas.org

Large-scale collective action to avoid an Amazon tipping point - key actors and interventions

The destruction of the Amazon is a major global environmental issue, not only because of greenhouse gas emissions or direct impacts on biodiversity and livelihoods, but also due to the forest\u27s role as a tipping element in the Earth System. With nearly a fifth of the Amazon already lost, there are already signs of an imminent forest dieback process that risks transforming much of the rainforest into a drier ecosystem, with climatic implications across the globe. There is a large body of literature on the underlying drivers of Amazon deforestation. However, insufficient attention has been paid to the behavioral and institutional microfoundations of change. Fundamental issues concerning cooperation, as well as the mechanisms facilitating or hampering such actions, can play a much more central role in attempts to unravel and address Amazon deforestation. We thus present the issue of preventing the Amazon biome from crossing a biophysical tipping point as a large-scale collective action problem. Drawing from collective action theory, we apply a novel analytical framework on Amazon conservation, identifying six variables that synthesize relevant collective action stressors and facilitators: information, accountability, harmony of interests, horizontal trust, knowledge about consequences, and sense of responsibility. Drawing upon literature and data, we assess Amazon deforestation and conservation through our heuristic lens, showing that while growing transparency has made information availability a collective action facilitator, lack of accountability, distrust among actors, and little sense of responsibility for halting deforestation remain key stressors. We finalize by discussing interventions that can help break the gridlock

Direct and Indirect Induction of a Compensatory Phenotype that Alleviates the Costs of an Inducible Defense

Organisms often exhibit phenotypic plasticity in multiple traits in response to impending environmental change. Multiple traits phenotypic plasticity is complex syndrome brought on by causal relations in ecological and physiological context. Larvae of the salamander Hynobius retardatus exhibit inducible phenotypic plasticity of two traits, when at risk of predation by dragonfly larvae. One induced phenotype is an adaptive defense behaviour, i.e., stasis at the bottom of water column, directly triggered by the predation risk. Another one is a compensatory phenotype, i.e., enlarged external gills, for an unavoidable cost (hypoxia) associated with the induced defense. We identified two ways by which this compensatory phenotype could be induced. The compensatory phenotype is induced in response to not only the associated hypoxic conditions resulting from the induced defense but also the most primary but indirect cause, presence of the predator

Plague and Climate: Scales Matter

Plague is enzootic in wildlife populations of small mammals in central and eastern Asia, Africa, South and North America, and has been recognized recently as a reemerging threat to humans. Its causative agent Yersinia pestis relies on wild rodent hosts and flea vectors for its maintenance in nature. Climate influences all three components (i.e., bacteria, vectors, and hosts) of the plague system and is a likely factor to explain some of plague's variability from small and regional to large scales. Here, we review effects of climate variables on plague hosts and vectors from individual or population scales to studies on the whole plague system at a large scale. Upscaled versions of small-scale processes are often invoked to explain plague variability in time and space at larger scales, presumably because similar scale-independent mechanisms underlie these relationships. This linearity assumption is discussed in the light of recent research that suggests some of its limitations

Pharmaceuticals oxidation by chlorine and byproducts formation in aqueous matrices in bench scale.

F?rmacos e desreguladores end?crinos s?o encontrados em ?guas naturais brasileiras, incluindo alguns mananciais de abastecimento, tamb?m em fun??o da baixa cobertura de coleta e tratamento de esgotos no Brasil. Nesse cen?rio, o presente trabalho intentou avaliar a remo??o de tr?s f?rmacos - sulfametoxazol (SMX), diclofenaco (DCF) e 17?-estradiol (E2) - em ?gua destilada por meio da oxida??o com cloro (hipoclorito de s?dio), variando-se a dose de cloro e o tempo de contato em ensaios de batelada. As solu??es cloradas foram analisadas, ainda, por cromatografia acoplada ? espectrometria de massas para identifica??o de eventuais subprodutos de oxida??o. Para tempo de contato de 10 min e dose de cloro de 1,5 mg.L-1, foi observada remo??o m?dia de 61% para DCF, 36% para E2 e 33% para SMX. Apenas para o DCF verificou-se diferen?a estatisticamente significativa (?=0,05) para dose de cloro de 3,0 mg.L-1. A oxida??o seguiu modelo cin?tico de pseudossegunda ordem, com valores de k2 de 0,0168 L.?g.min-1 para SMX (para ambas doses testadas), de 0,0133 e 0,0798 L.?g.min-1 para DCF, e de 0,0326 e 0,0289 L.?g.min-1 para E2, para doses de cloro de 1,5 e 3,0 mg.L-1, respectivamente. Por fim, verificou-se que o aumento do tempo de contato favoreceu a oxida??o dos f?rmacos, ainda que com a perspectiva de forma??o de subprodutos para SMX e E2.Pharmaceuticals and endocrine disrupting compounds are found in Brazilian natural waters, including some water sources for public supply, also due to the low coverage of sewage collection and treatment in Brazil. This study investigated the removal of three pharmaceutical compounds - sulfamethoxazole (SMX), diclofenac (DCF) and 17?-estradiol (E2) - from aqueous solutions by means of chlorine oxidation (sodium hypochlorite) by varying the dose of chlorine and contact time in batch tests. The chlorine solutions were examined by chromatography attached to the mass spectrometry in order to identify the oxidation by-products. For 10 min contact time, mean removal values of 61% were observed for DCF; 36% for E2; and 33% for SMX, when the chlorine dose was 1.5 mg L-1. Just for DCF there was a statistically significant difference (?=0.05) in the removal efficiency when increasing the chlorine dose to 3.0 mg.L-1. The oxidation followed the kinetic model of pseudo-second order, with k2 values of 0.0168 L.?g.min-1 for SMX (at both chlorine doses tested); 0.0133 and 0.0798 L.?g.min-1 to DCF; and 0.0326 and 0.0289 L.?g.min-1 to the E2 at chlorine doses of 1.5 and 3.0 mg L-1, respectively. Finally, it was verified that an increase of the contact time favored the oxidation of all pharmaceuticals tested, although with the perspective of by-products formation for SMX and E2

Multi-site and multi-depth near-infrared spectroscopy in a model of simulated (central) hypovolemia: lower body negative pressure

Purpose: To test the hypothesis that the sensitivity of near-infrared spectroscopy (NIRS) in reflecting the degree of (compensated) hypovolemia would be affected by the application site and probing depth. We simultaneously applied multi-site (thenar and forearm) and multi-depth (15-2.5 and 25-2.5 mm probe distance) NIRS in a model of simulated hypovolemia: lower body negative pressure (LBNP). Methods: The study group comprised 24 healthy male volunteers who were subjected to an LBNP protocol in which a baseline period of 30 min was followed by a step-wise manipulation of negative pressure in the following steps: 0, -20, -40, -60, -80 and -100 mmHg. Stroke volume and heart rate were measured using volume-clamp finger plethysmography. Two multi-depth NIRS devices were used to measure tissue oxygen saturation (StO2) and tissue hemoglobin index (THI) continuously in the thenar and the forearm. To monitor the shift of blood volume towards the lower extremities, calf THI was measured by single-depth NIRS. Results: The main findings were that the application of LBNP resulted in a significant reduction in stroke volume which was accompanied by a reduction in forearm StO2 and THI. Conclusions: NIRS can be used to detect changes in StO2 and THI consequent upon central hypovolemia. Forearm NIRS measurements reflect hypovolemia more sensitively than thenar NIRS measurements. The sensitivity of these NIRS measurements does not depend on NIRS probing depth. The LBNP-induced shift in blood volume is reflected by a decreased THI in the forearm and an increased THI in the calf