Critique of Auguste Comte’s ideology on the death of religion

Secularism dealt with the known, whereas religion dealt with the unknown. The rise of secularism threatened the survival of religion. This was the thesis of Auguste Comte. He said there would be a time when the irrelevant nature and death of religion would be recorded. At this point, man would have been able to unravel most of the unknown around him, hence no need for religion. The article has as its aim to examine the flaws in Auguste Comte’s ideology on the existence of religion and secularism together. Using the descriptive phenomenological method of research, which allows for an objective analysis of the problem, it was discovered that, notwithstanding Comte’s theory, religion and secularism have continued to exist side by side since the 20th century to the contemporary 21st century because they are complementary. It was also discovered that religion exerts a force that cannot be silenced by an industrial revolution of the world. Religion provides the solution to man’s innermost needs which cannot be threatened with the rise of secularism

DDR1 contributes to kidney inflammation and fibrosis by promoting the phosphorylation of BCR and STAT3

Discoidin domain receptor 1 (DDR1), a receptor tyrosine kinase activated by collagen, contributes to chronic kidney disease. However, its role in acute kidney injury and subsequent development of kidney fibrosis is not clear. Thus, we performed a model of severe ischemia/reperfusion-induced acute kidney injury that progressed to kidney fibrosis in WT and Ddr1-null mice. We showed that Ddr1-null mice had reduced acute tubular injury, inflammation, and tubulointerstitial fibrosis with overall decreased renal monocyte chemoattractant protein (MCP-1) levels and STAT3 activation. We identified breakpoint cluster region (BCR) protein as a phosphorylated target of DDR1 that controls MCP-1 production in renal proximal tubule epithelial cells. DDR1-induced BCR phosphorylation or BCR downregulation increased MCP-1 secretion, suggesting that BCR negatively regulates the levels of MCP-1. Mechanistically, phosphorylation or downregulation of BCR increased β-catenin activity and in turn MCP-1 production. Finally, we showed that DDR1-mediated STAT3 activation was required to stimulate the secretion of TGF-β. Thus, DDR1 contributes to acute and chronic kidney injury by regulating BCR and STAT3 phosphorylation and in turn the production of MCP-1 and TGF-β. These findings identify DDR1 an attractive therapeutic target for ameliorating both proinflammatory and profibrotic signaling in kidney disease