Of the targets predicted here, NFAT5, a member of the nuclear factors of activated T cells family of transcription factors and a component of the mitogen-activated protein kinase pathway, is of particular interest as it has previously been linked with TB; the innate immune response to M.tb infection strongly induces NFAT5 gene and protein expression. In addition, other proteins belonging to the NFAT family are known to play a central role in inducible gene transcription during the immune response. NFAT5 expression has been shown to depend on p38 mitogen-activated protein kinase ; addition of a p38 MAPK inhibitor was found to correlate with decreased NFAT5 expression, even in the presence of osmotic stress signals. NFAT5 has also been found to play a crucial role in M.tb regulation of HIV-1 replication on co-infection via a direct interaction with the viral promoter. These findings suggest a general role for NFAT5 in M.tb-mediated control of gene expression. In conclusion, this is the first comprehensive RNA-seq study of global microRNA expression levels in different individuals according to their TB disease and inoculation status. We have been able to accurately identify microRNAs that are significantly up- or down-regulated in different groups according to their TB disease and inoculation status. These results provide an excellent starting point for further studies regarding the potential of these microRNAs as biomarkers for diagnosis and prognosis. Cerebral ischemia as a consequence of restricted blood flow, implicating insufficient glucose and oxygen supply, leads to increased production of free radical species. Enormous production of reactive oxygen and nitrogen species has deleterious effects during pathogenesis of ischemic insult. Brain is highly susceptible to the presence of free INCB28060 c-Met inhibitor radicals due to high content of lipids and relatively low level of endogenous antioxidants. Massive production of ROS might has overall effects on all physiological functions important for surviving. During cerebral ischemia, production of free radicals overwhelm possibility of detoxification and capacity for its removal by enzymes of antioxidative protection like superoxide dismutase, catalase, glutathione peroxidase and nonenzymatic antioxidants resulting in fast and severe damage of cellular proteins, lipids and DNA. Although production of ROS in mitochondria from molecular oxygen presents normal physiological reaction, enormous activation of N-methyl-D-aspartate receptors during cerebral ischemia results in higher production of ROS and nitric oxide. Oxidation of xanthine to hypoxanthine is accompanied by production of superoxide anion and hydrogen peroxide, which further compromises neuronal damage during reperfusion. Peroxidation of lipid membranes produces toxic aldehydes like 4-hydroxynonenal which damage ion channels, transporters and cytoskeletal proteins.