Given the enormous implications in regulation of cellular function by the modulation of gene expression that regulate gene expression. Transcription regulatory machinenary in Folinic acid calcium salt pentahydrate eukaryotes involves specific transcription factors and transcription inhibitors; proteins that are required to turn on and turn off the expression of particular genes. These considerations point to a possible mechanism of how oxalate differentially regulates the gene expression of such a large number of genes. Given that oxalate is a metabolic end product in humans that cannot be further metabolized, such large scale changes in gene expression in renal epithelial cells in response to high oxalate levels points to an indirect mechanism of action, which may involve the interaction of oxalate with the cell membrane or in intracellular components. The primary site of oxalate action in cell remains unknown. Irrespective of primary site of action, one of the most common means by which cells sense changes is by activating the signal transduction pathways, especially the stress signal pathways. The stress associated signals are transduced through a series of proteins that are activated by phosphorylation/dephosphorylation steps and are finally turned into transcription factors, causing changes in gene expression. Though the present study design does not allow for the identification of activity changes due to phosphorylation, we identified changes in the gene expressions of upstream activators of several signaling pathways. Proteins like Ras, Fas and MKK are highly up-regulated as a result of oxalate exposure. These proteins are known to play important roles in JNK/SAPK signaling and p38 MAPK signaling. These results are in agreement with previous studies, by us and others, that identified an active role for Stress Activated Protein Kinases in oxalate renal cell interactions. We also identified changes in the expression of genes associated with retinoic Acid Receptor Signaling Pathway. Clearly additional studies are required to evaluate the functional consequence of these gene expression changes. In summary, our study is the first attempt at profiling the Genome-wide expression changes in human renal epithelial cells as a result of exposure to oxalate. Results from our study point to complex and intricate mechanisms, including differential gene expression, in renal epithelial cells in response to oxalate exposure. Clearly further studies are required to completely understand the implications of the plethora of changes in gene expression occurring as a result of oxalate exposure in renal epithelial cells. We must separate and characterize the genes that are derived from the by-stander effect and identify the genes whose altered expression is responsible for oxalate nephrotoxicity. Malaria due to Plasmodium falciparum remains a major global health burden and a leading cause of death worldwide among children under five. Benzethonium Chloride Increasing drug resistance, including emerging resistance to the artemisinin drugs, and the declining efficacy of vector control interventions in some populations make the development of effective malaria vaccines an urgent priority. During blood-stage infection, P. falciparum merozoites invade erythrocytes, mediated by the release of invasion ligands from apical organelles that interact with receptors on the erythrocyte surface. The repertoire of invasion ligands includes two major families, the P. falciparum reticulocyte-binding homologues, and erythrocyte binding antigens. The ability of P. falciparum to vary the expression and/or use of EBA and PfRh proteins enables the use of alternate invasion pathways, facilitating immune evasion that enables P. falciparum to cause repeated and chronic infections. Invasion pathways can be broadly classified into two main pathways, sialic acid dependent invasion and SA-independent invasion.