Data Mining aims at discovering knowledge out of data and presenting it in a form that is easily compressible to humans. Data Mining represents a process developed to examine large amounts of data routinely collected. The term also refers to a collection of tools used to perform the process. One of the useful applications in the field of medicine is the incurable chronic disease diabetes. Data Mining algorithm is used for testing the accuracy in predicting diabetic status. Fuzzy Systems are been used for solving a wide range of problems in different application domain and Genetic Algorithm for designing. Fuzzy systems allows in introducing the learning and adaptation capabilities. Neural Networks are efficiently used for learning membership functions. Diabetes occurs throughout the world, but Type 2 is more common in the most developed countries. The greater increase in prevalence is however expected in Asia and Africa where most patients will likely be found by 2030. This paper is proposed on the Levenberg -Marquardt algorithm which is specifically designed to minimize sum-of-square error functions. Levernberg-Marquardt algorithm gives the best performance in the prediction of diabetes compared to any other backpropogation algorithm.
Cardiac fibroblasts contribute to multiple aspects of myocardial function and pathophysiology. The pathogenetic relevance of cytokine production by these cells under hypoxia, however, remains unexplored. With the use of an in vitro cell culture model, this study evaluated cytokine production by hypoxic cardiac fibroblasts and examined two distinct effects of hypoxic fibroblast-conditioned medium (HFCM) on cardiac myocytes and fibroblasts. Hypoxia caused a marked increase in the production of tumor necrosis factor (TNF)-alpha by cardiac fibroblasts. HFCM significantly enhanced the susceptibility of cardiac myocytes to reactive oxygen species (ROS)-induced mitochondrial permeability transition (MPT), determined by high-precision confocal line-scan imaging following controlled, photoexcitation-induced ROS production within individual mitochondria. Furthermore, exposure of cardiac myocytes to HFCM for 5 h led to loss of viability, as evidenced by change in morphology and annexin staining. HFCM also decreased DNA synthesis in cardiac fibroblasts. Normoxic fibroblast-conditioned medium spiked with TNF-alpha at 200 pg/ml, a concentration comparable to that in HFCM, promoted loss of myocyte viability and decreased DNA synthesis in cardiac fibroblasts. These effects of HFCM are similar to the reported effects of hypoxia per se on these cell types, showing that hypoxic fibroblast-derived factors may amplify the distinct effects of hypoxia on cardiac cells. Importantly, because both hypoxia and oxidant stress prevail in a setting of ischemia and reperfusion, the effects of soluble factors from hypoxic fibroblasts on the MPT-ROS threshold and viability of myocytes may represent a novel paracrine mechanism that could exacerbate ischemia-reperfusion injury to cardiomyocytes.
Sapna, S., S. K. Ranjith, and K. Shivakumar. Cardiac fibrogenesis in magnesium deficiency: a role for circulating angiotensin II and aldosterone. Am J Physiol Heart Circ Physiol 291: H436 -H440, 2006. First published February 10, 2006 doi:10.1152/ajpheart.01185.2005.-Mechanisms underlying cardiac fibrogenesis in magnesium deficiency are unclear. It was reported earlier from this laboratory that serum from magnesium-deficient rats has a more pronounced stimulatory effect on cell proliferation, net collagen production, and superoxide generation in adult rat cardiac fibroblasts than serum from rats on the control diet. The profibrotic serum factors were, however, not identified. This study tested the hypothesis that circulating angiotensin II may modulate cardiac fibroblast activity in hypomagnesemic rats. Male Sprague-Dawley rats were pair-fed a magnesium-deficient (0.0008% Mg) or -sufficient (0.05%) diet for 6 days, and the effects of serum from these rats on [3 H]thymidine and [ 3 H]proline incorporation into cardiac fibroblasts from young adult rats were evaluated in the presence of losartan, an angiotensin II type 1 (AT 1) receptor antagonist, and spironolactone, an aldosterone antagonist. Losartan and spironolactone markedly attenuated the stimulatory effects in vitro of serum from the magnesium-deficient and control groups, but the inhibitory effects were considerably higher in cells exposed to serum from magnesium-deficient animals. Circulating and cardiac tissue levels of angiotensin II were significantly elevated in magnesium-deficient animals (67.6% and 93.1%, respectively, vs. control). Plasma renin activity was 61.9% higher in magnesium-deficient rats, but serum angiotensin-converting enzyme activity was comparable in the two groups. Furthermore, preliminary experiments in vivo using enalapril supported a role for angiotensin II in magnesium deficiency. There was no significant difference between the groups in serum aldosterone levels. The findings suggest that circulating angiotensin II and aldosterone may stimulate fibroblast activity and contribute to a fibrogenic response in the heart in magnesium deficiency. cardiac fibroblasts; renin-angiotensin-aldosterone system; magnesium-deficient rats MAGNESIUM PLAYS an important role in maintaining the structural and functional integrity of the cardiovascular system (1, 2, 19). It has been known for a long time that magnesium deficiency produces a cardiomyopathy characterized by focal myocardial necrosis and fibrosis (3, 9). Many theories have been advanced to explain the molecular basis of myocardial damage associated with magnesium deficiency (22). A large body of experimental evidence suggests that increased oxidative stress in the setting of an immunoinflammatory reaction may produce cardiovascular injury in magnesium deficiency (30). Furthermore, alterations in collagen metabolism and fibroblast proliferation rates, reported earlier from this laboratory (12), point to the activation of cardiac fibroblasts in a rodent model of acute magnesium deficienc...
Substance P, a pro-inflammatory neuropeptide, is released from cardiac peptidergic nerves under conditions like ischemia but whether it modulates inflammatory processes in the heart remains unexplored. This study demonstrates for the first time that substance P augments the production of the soluble form of intercellular adhesion molecule-1, sICAM-1, by adult rat cardiac fibroblasts. However, RT-PCR showed no concomitant increase in ICAM-1 transcript levels, suggesting that the increase in sICAM-1 may involve post-transcriptional/translational mechanisms. Use of pharmacological inhibitors revealed that the stimulatory effect of substance P on sICAM-1 production is mediated by p42/44 MAPK and protein kinase C. Preliminary experiments also showed that the neuropeptide stimulates the production of prostaglandin E(2) by cardiac fibroblasts. The findings support the postulation that substance P may modulate multiple inflammatory responses within the myocardium through release of pro-inflammatory mediators from resident fibroblasts.
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