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Moreover, utilization of overlapping promoters depends on particular state of a cell and, at least in some groups of genes, is not merely coincidental.Predicting the risk of cardiovascular disease is the key to primary prevention. Machine learning has attracted attention in analyzing increasingly large, complex healthcare data. We assessed discrimination and calibration of pre-existing cardiovascular risk prediction models and developed machine learning-based prediction algorithms. This study included 222,998 Korean adults aged 40-79 years, naïve to lipid-lowering therapy, had no history of cardiovascular disease. Pre-existing models showed moderate to good discrimination in predicting future cardiovascular events (C-statistics 0.70-0.80). Pooled cohort equation (PCE) specifically showed C-statistics of 0.738. Among other machine learning models such as logistic regression, treebag, random forest, and adaboost, the neural network model showed the greatest C-statistic (0.751), which was significantly higher than that for PCE. It also showed improved agreement between the predicted risk and observed outcomes (Hosmer-Lemeshow χ2 = 86.1, P less then 0.001) than PCE for whites did (Hosmer-Lemeshow χ2 = 171.1, P less then 0.001). Similar improvements were observed for Framingham risk score, systematic coronary risk evaluation, and QRISK3. This study demonstrated that machine learning-based algorithms could improve performance in cardiovascular risk prediction over contemporary cardiovascular risk models in statin-naïve healthy Korean adults without cardiovascular disease. The model can be easily adopted for risk assessment and clinical decision making.The practice of estimating the transfer coefficient ([Formula see text]) and the exchange current ([Formula see text]) by arbitrarily placing a straight line on Tafel plots has led to high variance in these parameters between different research groups. Generating Tafel plots by finding kinetic current, [Formula see text] from the conventional mass transfer correction method does not guarantee an accurate estimation of the [Formula see text] and [Formula see text]. This is because a substantial difference in values of [Formula see text] and [Formula see text] can arise from only minor deviations in the calculated values of [Formula see text]. These minor deviations are often not easy to recognise in polarisation curves and Tafel plots. find more Recalling the IUPAC definition of [Formula see text] , the Tafel plots can be alternatively represented as differential Tafel plots (DTPs) by taking the first order differential of Tafel plots with respect to overpotential. Without further complex processing of the existing raw data, many crucial observations can be made from DTP which is otherwise very difficult to observe from Tafel plots. These for example include a) many perfectly looking experimental linear Tafel plots (R2 > 0.999) can give rise to incorrect kinetic parameters b) substantial differences in values of [Formula see text] and [Formula see text] can arise when the limiting current ([Formula see text]) is just off by 5% while performing the mass transfer correction c) irrespective of the magnitude of the double layer charging current ([Formula see text]), the Tafel plots can still get significantly skewed when the ratio of [Formula see text] is small. Hence, in order to determine accurate values of [Formula see text] and [Formula see text], we show how the DTP approach can be applied to experimental polarisation curves having well defined [Formula see text], poorly defined [Formula see text] and no [Formula see text] at all.The elevated CO2 (eCO2) has positive response on plant growth and negative response on insect pests. As a contemplation, the feeding pattern of the brown plant hopper, Nilaparvata lugens Stål on susceptible and resistant rice cultivars and their growth rates exposed to eCO2 conditions were analyzed. The eCO2 treatment showed significant differences in percentage of emergence and rice biomass that were consistent across the rice cultivars, when compared to the ambient conditions. Similarly, increase in carbon and decrese in nitrogen ratio of leaves and alterations in defensive peroxidase enzyme levels were observed, but was non-linear among the cultivars tested. Lower survivorship and nutritional indices of N. lugens were observed in conditions of eCO2 levels over ambient conditions. Results were nonlinear in manner. We conclude that the plant carbon accumulation increased due to eCO2, causing physiological changes that decreased nitrogen content. Similarly, eCO2 increased insect feeding, and did alter other variables such as their biology or reproduction.Variants identified in earlier genome-wide association studies (GWAS) on differentiated thyroid carcinoma (DTC) explain about 10% of the overall estimated genetic contribution and could not provide complete insights into biological mechanisms involved in DTC susceptibility. Integrating systems biology information from model organisms, genome-wide expression data from tumor and matched normal tissue and GWAS data could help identifying DTC-associated genes, and pathways or functional networks in which they are involved. We performed data mining of GWAS data of the EPITHYR consortium (1551 cases and 1957 controls) using various pathways and protein-protein interaction (PPI) annotation databases and gene expression data from The Cancer Genome Atlas. We identified eight DTC-associated genes at known loci 2q35 (DIRC3), 8p12 (NRG1), 9q22 (FOXE1, TRMO, HEMGN, ANP32B, NANS) and 14q13 (MBIP). Using the EW_dmGWAS approach we found that gene networks related to glycogenolysis, glycogen metabolism, insulin metabolism and signal transduction pathways associated with muscle contraction were overrepresented with association signals (false discovery rate adjusted p-value less then 0.05). Additionally, suggestive association of 21 KEGG and 75 REACTOME pathways with DTC indicate a link between DTC susceptibility and functions related to metabolism of cholesterol, amino sugar and nucleotide sugar metabolism, steroid biosynthesis, and downregulation of ERBB2 signaling pathways. Together, our results provide novel insights into biological mechanisms contributing to DTC risk.
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