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Renewable energy-based decentralized supply of electricity in rural areas is becoming the basic needs of the society. This study proposes an optimal grid connected microgrid to generate electricity from renewable energy resources to satisfy the electrical needs of Nirjuli II village, PapumPare district, Arunachal Pradesh, India. This study contains estimation of the residential demand and electrical usage of the existing grid connectivity. First a, microgrid system models having existing grid connection with an ideal and an unreliable grid is designed according to the survey conducted in the village. Secondly, performance and cost analysis is done on the given systems to highlight the merits and demerits of the microgrid systems in order to propose an optimum and efficient hybrid grid renewable system for Nirjuli II village.

This study is based on a secondary frequency control of micro-grids along with voltage control by the use of synergetic control in compliance with multi agent system. In the projected control, a voltage source control is being performed to found the micro-grid automated power supply from a renewable energy source. The plant output is being converged to a stable response in the presence of this MAS system.

Obesity and aging are associated with periodontitis, which represents a chronic inflammatory disease of the tooth-supporting tissues, i.e. the periodontium. However, if both risk factors also have a negative impact on crestal alveolar bone in a clinically healthy periodontium, has yet to be elucidated and was analyzed in this in-vivo study. Eight C57BL/6 mice were fed a normal diet during the entire study. Half of these mice were sacrificed at week 19 (group 1: younger lean mice), whereas the other half of the animals were sacrificed at week 25 (group 2: older lean mice). In addition, four mice were fed a high-fat diet until their sacrifice at week 19 (group 3: younger obese mice). Mandibles and maxillae were scanned by micro-computed tomography and, subsequently, the distance between the cementoenamel junction and alveolar bone crest (CEJ-ABC) at all molars was determined. Levels of interleukin-6, cyclooxygenase-2, visfatin and adiponectin in gingival samples were quantified by real-time PCR. For statistical analyses, the Mann-Whitney-U test was applied (p

Cold-induced activation of brown adipose tissue (BAT) is mediated by norepinephrine and adenosine that are released during sympathetic nerve activation. Both signaling molecules induce an increase in intracellular levels of 3',5'-cyclic adenosine monophosphate (cAMP) in murine and human BAT. In brown adipocytes, cAMP plays a central role, because it activates lipolysis, glucose uptake, and thermogenesis. Another well-studied intracellular second messenger is 3',5'-cyclic guanosine monophosphate (cGMP), which closely resembles cAMP. Several studies have shown that intact cGMP signaling is essential for normal adipogenic differentiation and BAT-mediated thermogenesis in mice. This chapter highlights recent observations, demonstrating the physiological significance of cyclic nucleotide signaling in BAT as well as their potential to induce browning of white adipose tissue (WAT) in mice and humans.

Cold-induced activation of brown adipose tissue (BAT) is mediated by norepinephrine and adenosine that are released during sympathetic nerve activation. Both signaling molecules induce an increase in intracellular levels of 3′,5′-cyclic adenosine monophosphate (cAMP) in murine and human BAT. In brown adipocytes, cAMP plays a central role, because it activates lipolysis, glucose uptake, and thermogenesis. Another well-studied intracellular second messenger is 3′,5′-cyclic guanosine monophosphate (cGMP), which closely resembles cAMP. Several studies have shown that intact cGMP signaling is essential for normal adipogenic differentiation and BAT-mediated thermogenesis in mice. This chapter highlights recent observations, demonstrating the physiological significance of cyclic nucleotide signaling in BAT as well as their potential to induce browning of white adipose tissue (WAT) in mice and humans.

Current worldwide figures suggest that obesity is pandemic. Understanding the underlying molecular mechanisms would help develop viable anti-obesity therapies. Here, we assess the influence of obesity-induced inflammation on white adipocyte cyclic guanosine monophosphate (cGMP) signaling, which is beneficial for adipocyte differentiation and thermogenesis. We find that murine gonadal and not inguinal fat is prone to obesity-induced inflammation. Correspondingly, the cGMP cascade is dysregulated in gonadal but not in inguinal fat of obese mice. Analysis of two independent human cohorts reveals a defective cGMP pathway only in visceral fat of obese subjects. Congruently, cGMP signaling is dysregulated in tumor necrosis factor α (TNF-α)-treated primary white adipocytes. TNF-α-mediated suppression of sGCβ1 is mediated via NF-κB, whereas PKG is repressed by JNK signaling. Additionally, TNF-α-activated JNK signaling suppresses PPARγ and aP2. Taken together, the intensity of obesity-induced inflammation dictates the amplitude of cGMP signaling dysregulation in white adipocytes through distinct pathways.

Today, everything has gone distributed for so many types of server applications. We have Web servers, application servers, database servers, file servers, and mail servers that maintain worker queues and thread pools to handle large numbers of short tasks that arrive from remote sources. In this paper we have done analysis for multithreaded programs, focusing on ways to improve the efficiency of analyzing interactions between threads. A multithreaded program always contains two or more parts that can run concurrently without lagging and each part can handle different tasks at the same time making optimal use of the available resources. Each task is independent of the other. Multithreading is based on the idea of multitasking in applications where specific operations within a single application are further divided into individual threads. This application of multithreading is developed using Eclipse IDE. Eclipse consists of a base workspace and an extensible plug-in system for customizing the environment.

Obesity is characterized by a positive energy balance and expansion of white adipose tissue (WAT). In contrast, brown adipose tissue (BAT) combusts energy to produce heat. Here we show that a small molecule stimulator (BAY 41-8543) of soluble guanylyl cyclase (sGC), which produces the second messenger cyclic GMP (cGMP), protects against diet-induced weight gain, induces weight loss in established obesity, and also improves the diabetic phenotype. Mechanistically, the haeme-dependent sGC stimulator BAY 41–8543 enhances lipid uptake into BAT and increases whole-body energy expenditure, whereas ablation of the haeme-containing β1-subunit of sGC severely impairs BAT function. Notably, the sGC stimulator enhances differentiation of human brown adipocytes as well as induces ‘browning' of primary white adipocytes. Taken together, our data suggest that sGC is a potential pharmacological target for the treatment of obesity and its comorbidities., The enzyme soluble guanylyl cyclase (sGC) regulates differentiation of brown fat. Here, Hoffman et al. show that a small molecule sGC stimulator increases brown fat activity and browning of white fat, thereby inducing energy expenditure, weight loss and partial protection from diet-induced obesity in mice.

Background Extracellular Amyloid-b (Ab) plaques and intracellular neuro-fibrillary tangles (NFTs) of hyperphosphorylated Tau (τ) protein are considered to be the hallmarks of Alzheimer’s disease (AD) [1]. Ab is secreted due to the sequential cleavage of the amyloidb precursor protein (APP) by band gsecretases (b cleavage) [1], whereas the intracellular signalling protein glycogen synthase kinase 3 (GSK3) has been implicated to cause τhyperphosphorylation leading to the formation of NFTs [2]. It has been shown earlier that the cleavage of APP by aand gsecretases (acleavage) is enhanced by insulin through the PI3KAkt pathway [3]. GSK3 is a further downstream component of this pathway which has been shown to induce τ phosphorylation. Inhibition of GSK3 has also been shown to increase lysosomal biogenesis leading to autophagic degradation of APP [4].

Background Obesity has reached pandemic proportions with 1.9 billion overweight adults; 600 million of whom are obese [1]. It has been shown that stimulating cyclic 3’-5’ guanosine monophosphate (cGMP) signaling is able to promote adipose tissue homeostasis in obese mice [2]. Conversely, genetic depletion of cGMP dependent protein kinase 1 (PKG1), causes hepatic inflammation and fasting hyperglycemia in mice [3]. Furthermore, cGMP signaling is essential for differentiation of preadipocytes to mature adipocytes in vitro [4,5]. PKG1 activation blocks RhoA mediated inhibition of insulin receptor substrate 1 in adipocytes in vitro [4,5], thus maintaining insulin sensitivity. The status of cGMP signaling cascade in adipose tissue under obese conditions is not yet fully understood. Here, we examine the functional status of cGMP signaling in white adipose tissue (WAT) of lean and obese mice.