Genetic Diversity in Zoysiagrass Ecotypes Based on Morphological Characteristics and SSR Markers

Zoysiagrass consists of a number of interfertile species, some of which are important grasses for turfgrass and grazing pasture in Japan. Recently, we developed simple sequence repeats (SSRs) markers from Zoysia japonica “Asagake” genomic DNA by enriched genomic library method (Yamamoto et al., 2002). Here we identify genetic diversity in 38 ecotypes of zoysiagrass (Z. matrella and Z. tenuifolia) from a group of southwest islands of Japan based on morphological characteristics and SSR markers

Módulo de suporte à decisão para licenciamento e regularização ambiental.

RESUMO: Este artigo descreve a modelagem e implementação de um sistema de suporte à decisão para licenciamento e regularização ambiental baseado em lógica fuzzy, desenvolvido como um módulo componente do Sistema Interativo de Suporte ao Licenciamento Ambiental (SISLA). O SISLA é um produto do projeto GeoMS, uma parceria entre a Embrapa Informática Agropecuária e o Instituto de Meio Ambiente de Mato Grosso do Sul (Imasul). Por meio desse módulo, o usuário poderá obter um suporte à tomada de decisão para processos de licenciamento ambiental. Esse suporte é fornecido a partir de variáveis de entrada, como distância e intersecção da área do empreendimento solicitante de licenciamento ambiental com áreas protegidas pelo governo estadual. Como saída, o sistema fornece o grau de ?Aptidão? do processo, que pode ser "Deferido", "Indeferido" ou "Pendência". Ao longo desse trabalho, serão descritos os métodos utilizados para a criação desse módulo, bem como alguns resultados obtidos com dados reais.SBIAgro 2011

Endothelial Dysfunction In Cardiovascular And Endocrine-metabolic Diseases: An Update.

The endothelium plays a vital role in maintaining circulatory homeostasis by the release of relaxing and contracting factors. Any change in this balance may result in a process known as endothelial dysfunction that leads to impaired control of vascular tone and contributes to the pathogenesis of some cardiovascular and endocrine/metabolic diseases. Reduced endothelium-derived nitric oxide (NO) bioavailability and increased production of thromboxane A2, prostaglandin H2 and superoxide anion in conductance and resistance arteries are commonly associated with endothelial dysfunction in hypertensive, diabetic and obese animals, resulting in reduced endothelium-dependent vasodilatation and in increased vasoconstrictor responses. In addition, recent studies have demonstrated the role of enhanced overactivation of β-adrenergic receptors inducing vascular cytokine production and endothelial NO synthase (eNOS) uncoupling that seem to be the mechanisms underlying endothelial dysfunction in hypertension, heart failure and in endocrine-metabolic disorders. However, some adaptive mechanisms can occur in the initial stages of hypertension, such as increased NO production by eNOS. The present review focuses on the role of NO bioavailability, eNOS uncoupling, cyclooxygenase-derived products and pro-inflammatory factors on the endothelial dysfunction that occurs in hypertension, sympathetic hyperactivity, diabetes mellitus, and obesity. These are cardiovascular and endocrine-metabolic diseases of high incidence and mortality around the world, especially in developing countries and endothelial dysfunction contributes to triggering, maintenance and worsening of these pathological situations.44920-3

Endothelial dysfunction in cardiovascular and endocrine-metabolic diseases: an update

The endothelium plays a vital role in maintaining circulatory homeostasis by the release of relaxing and contracting factors. Any change in this balance may result in a process known as endothelial dysfunction that leads to impaired control of vascular tone and contributes to the pathogenesis of some cardiovascular and endocrine/metabolic diseases. Reduced endothelium-derived nitric oxide (NO) bioavailability and increased production of thromboxane A2, prostaglandin H2 and superoxide anion in conductance and resistance arteries are commonly associated with endothelial dysfunction in hypertensive, diabetic and obese animals, resulting in reduced endothelium-dependent vasodilatation and in increased vasoconstrictor responses. In addition, recent studies have demonstrated the role of enhanced overactivation of β-adrenergic receptors inducing vascular cytokine production and endothelial NO synthase (eNOS) uncoupling that seem to be the mechanisms underlying endothelial dysfunction in hypertension, heart failure and in endocrine-metabolic disorders. However, some adaptive mechanisms can occur in the initial stages of hypertension, such as increased NO production by eNOS. The present review focuses on the role of NO bioavailability, eNOS uncoupling, cyclooxygenase-derived products and pro-inflammatory factors on the endothelial dysfunction that occurs in hypertension, sympathetic hyperactivity, diabetes mellitus, and obesity. These are cardiovascular and endocrine-metabolic diseases of high incidence and mortality around the world, especially in developing countries and endothelial dysfunction contributes to triggering, maintenance and worsening of these pathological situations449920932CONSELHO NACIONAL DE DESENVOLVIMENTO CIENTÍFICO E TECNOLÓGICO - CNPQFUNDAÇÃO DE AMPARO À PESQUISA DO ESTADO DE SÃO PAULO - FAPESPsem informaçã

Uncertainty-principle noise in vacuum-tunneling transducers

The fundamental sources of noise in a vacuum-tunneling probe used as an electromechanical transducer to monitor the location of a test mass are examined using a first-quantization formalism. We show that a tunneling transducer enforces the Heisenberg uncertainty principle for the position and momentum of a test mass monitored by the transducer through the presence of two sources of noise: the shot noise of the tunneling current and the momentum fluctuations transferred by the tunneling electrons to the test mass. We analyze a number of cases including symmetric and asymmetric rectangular potential barriers and a barrier in which there is a constant electric field. Practical configurations for reaching the quantum limit in measurements of the position of macroscopic bodies with such a class of transducers are studied

Upregulation of ERK1/2-eNOS via AT2 Receptors Decreases the Contractile Response to Angiotensin II in Resistance Mesenteric Arteries from Obese Rats

It has been clearly established that mitogen-activated protein kinases (MAPKS) are important mediators of angiotensin II (Ang II) signaling via AT1 receptors in the vasculature. However, evidence for a role of these kinases in changes of Ang II-induced vasoconstriction in obesity is still lacking. Here we sought to determine whether vascular MAPKs are differentially activated by Ang II in obese animals. the role of AT2 receptors was also evaluated. Male monosodium glutamate-induced obese (obese) and non-obese Wistar rats (control) were used. the circulating concentrations of Ang I and Ang II, determined by HPLC, were increased in obese rats. Ang II-induced isometric contraction was decreased in endothelium-intact resistance mesenteric arteries from obese compared with control rats and exhibited a retarded AT1 receptor antagonist response. Blocking of AT2 receptors and inhibition of either endothelial nitric oxide synthase (eNOS) or extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) restored Ang II-induced contraction in obese rats. Western blot analysis revealed increased protein expression of AT2 receptors in arteries from obese rats. Basal and Ang II-induced ERK1/2 phosphorylation was also increased in obese rats. Blockade of either AT1 or AT2 receptors corrected the increased ERK1/2 phosphorylation in arteries from obese rats to levels observed in control preparations. Phosphorylation of eNOS was increased in obese rats. Incubation with the ERK1/2 inhibitor before Ang II stimulation did not affect eNOS phosphorylation in control rats; however, it corrected the increased phosphorylation of eNOS in obese rats. These results clearly demonstrate that enhanced AT2 receptor and ERK1/2-induced, NO-mediated vasodilation reduces Ang II-induced contraction in an endothelium-dependent manner in obese rats.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Univ São Paulo, Inst Biomed Sci, Dept Pharmacol, São Paulo, BrazilUniv Fed Goias, Div Cardiovasc Physiol, Dept Biol Sci, Jatai, BrazilUniversidade Federal de São Paulo, Div Nephrol, Dept Med, Escola Paulista Med, São Paulo, BrazilUniversidade Federal de São Paulo, Div Nephrol, Dept Med, Escola Paulista Med, São Paulo, BrazilFAPESP: 2007/58311-0FAPESP: 2008/51622-3FAPESP: 2010/03642-5Web of Scienc