Role of IT and ICT in Smart Grid

The new era will be of Smart Grid in comparison with existing electricity grid.Smart grid is a combination of electricity grid and communication infrastructure. To give sustainable electricity supply, Smart grid connects with all the connected components to form a logical power network. To increase the effectiveness of power grid many sophisticated communication technologies have been recognized. These communication technologies increase the efficiency taken as a whole of electrical grid.This paper details the relevance and challenges of various communication technologies. Two major challenges have been found for implementing smart grid technology, first is standard inter operability and cognitive access to unlicensed radio spectrum. Paper also discusses the problems to implement smart grid communication on an evolutional path. Recent and future trends in Smart grid are elaborated. The paper provides the broad review of state of art research available on Smart grid communication

Withaferin A inhibits lysosomal activity to block autophagic flux and induces apoptosis via energetic impairment in breast cancer cells

Withaferin A (WFA), a steroidal lactone, negatively regulates breast cancer growth however, its mechanisms of action remain largely elusive. We found that WFA blocks autophagy flux and lysosomal proteolytic activity in breast cancer cells. WFA increases accumulation of autophagosomes, LC3B-II-conversion, expression of autophagy-related proteins and autophagosome/lysosome fusion. Autolysosomes display the characteristics of acidic compartments in WFA-treated cells; however, the protein degradation activity of lysosomes is inhibited. Blockade of autophagic flux reduces the recycling of cellular fuels leading to insufficient substrates for tricarboxylic acid (TCA) cycle and impaired oxidative phosphorylation. WFA decreases expression and phosphorylation of LDHA, the key enzyme that catalyzes pyruvate-to-lactate conversion, reduces ATP levels and increases AMPK activation. AMPK-inhibition abrogates while AMPK-activation potentiates WFA's effect. WFA and 2-deoxyglucose combination elicits synergistic inhibition of breast cancer cells. Genetic-knockout of BECN1 and ATG7 fails to rescue cells from WFA-treatment; in contrast, addition of methyl pyruvate to supplement TCA cycle protects WFA-treated cells. Together, these results implicate that WFA is a potent lysosomal inhibitor; energetic impairment is required for WFA-induced apoptosis and growth-inhibition and combining WFA and 2DG is a promising therapeutic strategy for breast cancer

A Comprehensive Review and Open Challenges on Visual Question Answering Models

Users are now able to actively interact with images and pose different questions based on images, thanks to recent developments in artificial intelligence. In turn, a response in a natural language answer is expected. The study discusses a variety of datasets that can be used to examine applications for visual question-answering (VQA), as well as their advantages and disadvantages. Four different forms of VQA models—simple joint embedding-based models, attention-based models, knowledge-incorporated models, and domain-specific VQA models—are in-depth examined in this article. We also critically assess the drawbacks and future possibilities of all current state-of-the-art (SoTa), end-to-end VQA models. Finally, we present the directions and guidelines for further development of the VQA models

TOXOCARIASIS IN PUPPY - MORPHOLOGICAL DESCRIPTION AND CLINICAL MANAGEMENT

A 34-day-old, male Bully pup was presented in veterinary clinics with an uncertain anamnestic history of anorexia, lethargy, abdominal pain, and discomfort. On clinical examination, the pup had pale conjunctiva with a pot-bellied appearance and expelled cream-colored roundworms in feces. Blood and fecal samples were collected and analyzed. Hemoglobin and PCV values were lower, depicting anemia. A qualitative and quantitative examination of the fecal sample was carried out and results showed infection with Toxocara canis with fecal egg count (FEC) of 3200/gram of feces. Gross and light microscopic examination revealed the presence of adults of Toxocara canis with distinctive morphological features. Apropos, the pup was treated with a combination of pyrantel pamoate and fenbendazole orally @10mg/kg body weight, repeated after 14 days. The pup recovered successfully, as evidenced by decreased FECs, increased weight gain, and a high hematocrit score

Comprehensive Evaluation of Anti-hyperglycemic Activity of Fractionated Momordica charantia

The present study evaluates anti-hyperglycemic activity of fractionated Momordica charantia (bitter gourd) seed extracts. Fasting blood glucose levels were evaluated before and after administration of different fractions of the seed extract. Among the three fractions tested, fraction Mc-3 (15 mg/kg b.wt.) showed the maximum anti-hyperglycemic activity and reduced blood glucose levels in experimental diabetic rats significantly. The activities of the key regulatory enzymes of glucose metabolism (hexokinase, pyruvate kinase, lactate dehydrogenase, and glucose-6-phosphate dehydrogenase) were determined in Mc-3-treated diabetic animals. Once-daily administration of the fraction Mc-3 for prolonged period of 18 days to the experimental diabetic animals did not result in any nephrotoxicity or hepatotoxicity as evident from insignificant changes in biochemical parameters indicative of liver and kidney functions. Further fractionation of the fraction Mc-3 by size exclusion chromatography resulted in a fraction, designated Mc-3.2, possessing anti-hyperglycemic activity. The fraction Mc-3.2 showed the presence of a predominant protein band of ~11 kDa on SDS-PAGE. Loss in anti-hyperglycemic activity of the Mc-3.2 upon protease treatment indicates the proteinaceous nature of the anti-hyperglycemic principles. Overall, the results suggest that Momordica charantia seeds contain an effective anti-hyperglycemic protein(s) which may find application in treatment of diabetes without evident toxic effects

Sustained proliferation in cancer: mechanisms and novel therapeutic targets

Proliferation is an important part of cancer development and progression. This is manifest by altered expression and/or activity of cell cycle related proteins. Constitutive activation of many signal transduction pathways also stimulates cell growth. Early steps in tumor development are associated with a fibrogenic response and the development of a hypoxic environment which favors the survival and proliferation of cancer stem cells. Part of the survival strategy of cancer stem cells may manifested by alterations in cell metabolism. Once tumors appear, growth and metastasis may be supported by overproduction of appropriate hormones (in hormonally dependent cancers), by promoting angiogenesis, by undergoing epithelial to mesenchymal transition, by triggering autophagy, and by taking cues from surrounding stromal cells. A number of natural compounds (e.g., curcumin, resveratrol, indole-3-carbinol, brassinin, sulforaphane, epigallocatechin-3-gallate, genistein, ellagitannins, lycopene and quercetin) have been found to inhibit one or more pathways that contribute to proliferation (e.g., hypoxia inducible factor 1, nuclear factor kappa B, phosphoinositide 3 kinase/Akt, insulin-like growth factor receptor 1, Wnt, cell cycle associated proteins, as well as androgen and estrogen receptor signaling). These data, in combination with bioinformatics analyses, will be very important for identifying signaling pathways and molecular targets that may provide early diagnostic markers and/or critical targets for the development of new drugs or drug combinations that block tumor formation and progression

The Microbiome–Estrogen Connection and Breast Cancer Risk

The microbiome is undoubtedly the second genome of the human body and has diverse roles in health and disease. However, translational progress is limited due to the vastness of the microbiome, which accounts for over 3.3 million genes, whose functions are still unclear. Numerous studies in the past decade have demonstrated how microbiome impacts various organ-specific cancers by altering the energy balance of the body, increasing adiposity, synthesizing genotoxins and small signaling molecules, and priming and regulating immune response and metabolism of indigestible dietary components, xenobiotics, and pharmaceuticals. In relation to breast cancer, one of the most prominent roles of the human microbiome is the regulation of steroid hormone metabolism since endogenous estrogens are the most important risk factor in breast cancer development especially in postmenopausal women. Intestinal microbes encode enzymes capable of deconjugating conjugated estrogen metabolites marked for excretion, pushing them back into the enterohepatic circulation in a biologically active form. In addition, the intestinal microbes also break down otherwise indigestible dietary polyphenols to synthesize estrogen-like compounds or estrogen mimics that exhibit varied estrogenic potency. The present account discusses the potential role of gastrointestinal microbiome in breast cancer development by mediating metabolism of steroid hormones and synthesis of biologically active estrogen mimics

The gut microbiota in breast cancer development and treatment: The good, the bad, and the useful!

ABSTRACTRegardless of the global progress in early diagnosis and novel therapeutic regimens, breast carcinoma poses a devastating threat, and the advances are somewhat marred by high mortality rates. Breast cancer risk prediction models based on the known risk factors are extremely useful, but a large number of breast cancers develop in women with no/low known risk. The gut microbiome exerts a profound impact on the host health and physiology and has emerged as a pivotal frontier in breast cancer pathogenesis. Progress in metagenomic analysis has enabled the identification of specific changes in the host microbial signature. In this review, we discuss the microbial and metabolomic changes associated with breast cancer initiation and metastatic progression. We summarize the bidirectional impact of various breast cancer-related therapies on gut microbiota and vice-versa. Finally, we discuss the strategies to modulate the gut microbiota toward a more favorable state that confers anticancer effects