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Kakinada, India

The college it is situated at JNTU Kakinada Campus, Pithapuram Road in Kakinada, of the East Godavari district district, Andhra Pradesh, in the large area of 110 acres in Kakinada, north of the Indian state of Andhra Pradesh . Established in 1946, as the 'The College of Engineering, Vizagpatnam' at the then Composite Madras Presidency, apart from imparting training to engineering, management, science, humanities and languages languages in Andhra Pradesh and those from friendly states, the college also plays an advisory role to the ' Department of Technical Education Government of Andhra Pradesh ' ,'andhra Pradesh State Council of Higher Education', State Board of Technical Education and Training and also conducts ECET For admission for Diploma Holders and for B.Sc. Degree Holders in accordance with G.O.Ms.No:24, G.O.Ms.No:25, dated:28.06.2006 and G.O.Ms.No:19 or Diploma Holders and G.O.Ms.No.57 & G.O.Ms.No58 dated:12.05.2008 ., and college is involved in research projects and experimentation. Wikipedia.


Das U.N.,Jawaharlal Nehru Technological University Kakinada
Medical Hypotheses | Year: 2011

An increase in pro-inflammatory cytokines, decrease in endothelial nitric oxide (eNO) and adiponectin levels and an alteration in hypothalamic peptides and gastrointestinal hormones such as incretins and cholecystokinin that regulate satiety, hunger, and food intake occur in metabolic syndrome. Thus, metabolic syndrome is a low-grade systemic inflammatory condition and could be due to inappropriate cross-talk between the peripheral tissues and the hypothalamic centers implying that methods designed to restore these two abnormalities to normal could be of significant benefit in metabolic syndrome. Vagus nerve stimulation has been shown to suppress inflammation and acetylcholine, the principal vagal neurotransmitter, modulates the actions of several hypothalamic peptides and incretins and cholecystokinin. Based on these evidences, it is proposed that vagus nerve stimulation could be of significant benefit in the management of the metabolic syndrome. © 2010 Elsevier Ltd. Source


Rao N.M.,Jawaharlal Nehru Technological University Kakinada
International Journal of Advanced Manufacturing Technology | Year: 2011

This paper presents dimensional synthesis of a 3-RPS parallel manipulator according to the limitations on the actuating link lengths and on the range of motion of the spherical joints. The synthesis of the manipulator consists of determining the dimensions of a moving platform and a fixed base along with the directions of revolute joint axes such that a point on the moving platform passes through a set of prescribed positions in space. The dimensions of the moving platform are determined using a hybrid optimization method called GA-simplex method. While determining the dimensions of the fixed base, the limitations on the motion of the joints are considered to design a practical manipulator. The synthesis procedure presented confines to that class of problems where the number of prescribed positions required to complete a task is more than the number of positions a parallel manipulator can offer. The practical applications include automated assembly, contour machining, etc. A numerical example for the synthesis with ten positions is presented. This paper also presents direct kinematic equations for the manipulators with non-equilateral triangular platforms in order to validate the results of the numerical example. © 2010 Springer-Verlag London Limited. Source


Das U.N.,Jawaharlal Nehru Technological University Kakinada
Medical Hypotheses | Year: 2011

Cardiac arrhythmias cause significant morbidity and mortality in patients with coronary heart disease, hypertension, and congestive cardiac failure and in the elderly. Inflammation, oxidative injury, altered myocyte metabolism, extracellular matrix remodeling and fibrosis initiate and perpetuate cardiac arrhythmias, especially atrial fibrillation. Enhanced myeloperoxidase (MPO) activity by infiltrating activated leukocytes could bind to myocardial cells and cause fibrosis resulting in the initiation and progression of arrhythmias. Supplementation of eicosapentaenoic and docosahexaenoic acids (EPA and DHA, respectively) suppresses arrhythmias. EPA and DHA form precursors to anti-inflammatory lipid molecules: lipoxins, resolvins, protectins and maresins that are known to suppress inflammation, have anti-fibrotic actions and inhibit MPO activity. Hence, it is likely that leukocyte and/or myocardial deficiency of EPA and DHA and consequent reduced formation of lipoxins, resolvins, protectins and maresins enhance inflammation and MPO activity that leads to myocardial damage and fibrosis and initiation and progression of cardiac arrhythmias. Based on these evidences, I propose that lipoxins, resolvins and protectins function as endogenous anti-arrhythmic molecules and their stable synthetic analogs could be useful in the management of cardiac arrhythmias. © 2010 Elsevier Ltd. Source


Das U.N.,Jawaharlal Nehru Technological University Kakinada | Das U.N.,Bio Science Research Center
Nutrition | Year: 2013

Diabetic macular edema and retinopathy are low-grade inflammatory conditions. Infusions of antitumor necrosis factor-α (anti-TNF-α) antibody and antivascular endothelial growth factor (anti-VEGF) antibody have been shown to be at least partly effective in the treatment of diabetic macular edema and proliferative diabetic retinopathy. Intravitreal therapy of diabetic macular edema by the anti-TNF-α antibody has been found to produce significant side effects and anti-VEGF therapy to be ineffective. Nevertheless, these studies have indicated that the suppression of TNF-α and other proinflammatory cytokines and VEGF could be of benefit in diabetic macular edema and retinopathy. The retina is rich in polyunsaturated fatty acids, especially in ω-3, and several studies have shown that polyunsaturated fatty acids prevent diabetic retinopathy. Lipoxins, resolvins, and protectins derived from various polyunsaturated fatty acids possess anti-inflammatory actions and suppress the production of interleukin-6, and TNF-α and VEGF have antiangiogenic actions. In view of these evidences, I propose that lipoxins, resolvins, and protectins could be of significant benefit in the prevention and management of diabetic macular edema and retinopathy. © 2013 Elsevier Inc. Source


Das U.N.,UND Life science | Das U.N.,Jawaharlal Nehru Technological University Kakinada | Das U.N.,Bioscience Research Center
Nutrition | Year: 2013

Autism has a strong genetic and environmental basis in which inflammatory markers and factors concerned with synapse formation, nerve transmission, and information processing such as brain-derived neurotrophic factor (BDNF), polyunsaturated fatty acids (PUFAs): arachidonic (AA), eicosapentaenoic (EPA), and docosahexaenoic acids (DHA) and their products and neurotransmitters: dopamine, serotonin, acetylcholine, γ-aminobutyric acid, and catecholamines and cytokines are altered. Antioxidants, vitamins, minerals, and trace elements are needed for the normal metabolism of neurotrophic factors, eicosanoids, and neurotransmitters, supporting reports of their alterations in autism. But, the exact relationship among these factors and their interaction with genes and proteins concerned with brain development and growth is not clear. It is suggested that maternal infections and inflammation and adverse events during intrauterine growth of the fetus could lead to alterations in the gene expression profile and proteomics that results in dysfunction of the neuronal function and neurotransmitters, alteration(s) in the metabolism of PUFAs and their metabolites resulting in excess production of proinflammatory eicosanoids and cytokines and a deficiency of anti-inflammatory cytokines and bioactive lipids that ultimately results in the development of autism. Based on these evidences, it is proposed that selective delivery of BDNF and methods designed to augment the production of anti-inflammatory cytokines and eicosanoids and PUFAs may prevent, arrest, or reverse the autism disease process. © 2013 Elsevier Inc. Source

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