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• Optimal Bayesian life tests plans are presented under Progressive Type-I Interval Censoring Scheme. • Bayesian C -optimal design criterion is used. • An algorithm is presented for log-location-scale family of distributions. • A comparative study is provided for Weibull and log-normal lifetime distributions. • Sampling variations are visualized through MCMC methods. This work considers optimal planning of progressive type-I interval censoring schemes for log-location-scale family of distributions. Optimum schemes are obtained by using a Bayesian C -optimality design criterion. The C -optimality criterion is formed to attain precision in estimating a particular lifetime quantile. An algorithm is proposed to obtain the optimal censoring schemes. Optimal schemes are obtained under two different scenarios for the Weibull and log-normal models, which are two popular special cases of log-location-scale family of distributions. A sensitivity analysis is conducted to study the effect of various prior inputs on the optimal censoring schemes. Furthermore, a simulation study is undertaken to illustrate the sampling variations resulting from the optimal censoring schemes. [ABSTRACT FROM AUTHOR]

This article presents optimal Bayesian accelerated life test plans for series systems under Type-I censoring scheme. First, the component lifetimes are assumed to follow independent Weibull distributions. The scale parameters of Weibull lifetime distributions are related to the external stress variable through a general stress translation function. For a fixed number of design points, optimal Bayesian ALT plans are first obtained by solving constrained optimization problems under two different Bayesian design criteria. The global optimality of the resulting fixed-point optimal designs is then verified via the General Equivalence Theorem. This article also provides the optimized compromise ALT plans which are extremely useful in real-life applications. A detailed sensitivity analysis is then performed to find out the effect of various planning inputs on the resulting optimal Bayesian ALT plans. A simulation study is then conducted to visualize the resulting sampling variations from the optimal Bayesian ALT plans. Finally, this article considers a series system with dependent component lifetimes. Optimal ALT plans are obtained assuming a Gamma frailty model. [ABSTRACT FROM AUTHOR]

Irrigation happens to be the backbone of the civilized society since time immemorial. With population increasing at an exponential rate and land areas being curved short accommodating this enormous population, several new and innovative practices are coming up. The subject of talk in this paper therefore relates to the different techniques of using natural resources. Although many innovative techniques have been employed towards Automated Irrigation, they mostly indulge simple On - Off based controller. Artificial Neural Network can give us a good amount of remedy from the existing problems as it can operate upon the valves and actuators connected to the system as and when required. Taking into consideration of the parameters which play deciding role in irrigation of a particular kind of crop or plantation, we look forward to designing an ANN based MATLAB simulated model which does give much better results than the conventional ON/OFF ones. The system starts from taking signals from various sensors and ends up at giving much better required output from the Final Control Elements. [ABSTRACT FROM AUTHOR]

Abstract: Local Ca2+ transfer between adjoining domains of the sarcoendoplasmic reticulum (ER/SR) and mitochondria allows ER/SR Ca2+ release to activate mitochondrial Ca2+ uptake and to evoke a matrix [Ca2+] ([Ca2+]m) rise. [Ca2+]m exerts control on several steps of energy metabolism to synchronize ATP generation with cell function. However, calcium signal propagation to the mitochondria may also ignite a cell death program through opening of the permeability transition pore (PTP). This occurs when the Ca2+ release from the ER/SR is enhanced or is coincident with sensitization of the PTP. Recent studies have shown that several pro-apoptotic factors, including members of the Bcl-2 family proteins and reactive oxygen species (ROS) regulate the Ca2+ sensitivity of both the Ca2+ release channels in the ER and the PTP in the mitochondria. To test the relevance of the mitochondrial Ca2+ accumulation in various apoptotic paradigms, methods are available for buffering of [Ca2+], for dissipation of the driving force of the mitochondrial Ca2+ uptake and for inhibition of the mitochondrial Ca2+ transport mechanisms. However, in intact cells, the efficacy and the specificity of these approaches have to be established. Here we discuss mechanisms that recruit the mitochondrial calcium signal to a pro-apoptotic cascade and the approaches available for assessment of the relevance of the mitochondrial Ca2+ handling in apoptosis. We also present a systematic evaluation of the effect of ruthenium red and Ru360, two inhibitors of mitochondrial Ca2+ uptake on cytosolic [Ca2+] and [Ca2+]m in intact cultured cells. [Copyright &y& Elsevier]

Calcium (Ca2+) signalling is well known to dictate cellular functioning and fate. In recent years, the accumulation of Ca2+ in the mitochondria has emerged as an important factor in Chronic Respiratory Diseases (CRD) such as Asthma and Chronic Obstructive Pulmonary Disease (COPD). Various reports underline an aberrant increase in the intracellular Ca2+, leading to mitochondrial ROS generation, and further activation of the apoptotic pathway in these diseases. Mitochondria contribute to Ca2+ buffering which in turn regulates mitochondrial metabolism and ATP production. Disruption of this Ca2+ balance leads to impaired cellular processes like apoptosis or necrosis and thus contributes to the pathophysiology of airway diseases. This review highlights the key role of cytoplasmic and mitochondrial Ca2+ signalling in regulating CRD, such as asthma and COPD. A better understanding of the dysregulation of mitochondrial Ca2+ homeostasis in these diseases could provide cues for the development of advanced therapeutic interventions in these diseases. [ABSTRACT FROM AUTHOR]

Non-alcoholic fatty liver disease (NAFLD) is a metabolic syndrome characterized by excessive accumulation of hepatic lipid droplets. The disease progresses with steatosis as the premise for hepatocytic damage and tissue scarring, often culminating in hepatocellular carcinoma (HCC). Perturbations in mitochondrial metabolism and energetics were found to be associated with, and often instrumental in various stages of this progression. Functional impairment of the mitochondria affects all aspects of cellular functioning and a particularly important one is calcium signalling. Changes in mitochondrial calcium specifically in hepatocytes of a fatty liver, is reflected by alterations in calcium signalling as well as calcium transporter activities. This deranged Ca2+ homeostasis aids in even more uptake of lipids into the mitochondria and a shift in equilibrium, both metabolically as well as in terms of energy production, leading to completely altered cellular states. These alterations have been reviewed as a perspective to understand the disease progression through NAFLD leading to HCC. [ABSTRACT FROM AUTHOR]