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Ocean acidification: One potential driver of phosphorus eutrophication.
© 2015 The Molecular Biology Society of Japan and Wiley Publishing Asia Pty Ltd. Our study shows that miR- 29-mediated suppression of elastin expression in VSMCs plays a pivotal role in osteoblastic differentiation leading to vascular calcification. RT-qPCR analysis showed knockdown of elastin expression in VSMCs induced expression of osteoblast-related genes, similar to Pi stimulation, and recovery of elastin expression by miR- 29 inhibition reduced their expression. Furthermore, over-expression of miR- 29b promoted Pi-induced VSMC calcification. Inhibition of miR- 29 recovered elastin expression and suppressed calcification in Pi-treated VSMCs. Conversely, Pi stimulation increased miR- 29a and miR- 29b expression. Elastin pre-mRNA measurements indicated that Pi stimulation suppressed elastin expression without changing transcriptional activity. Knockdown of elastin expression by shRNA also promoted Pi-induced VSMC calcification. Pi stimulation promoted Ca deposition and suppressed elastin expression in VSMCs. Calcification of human VSMCs was induced by Pi and evaluated measuring calcium deposition. Therefore, we aimed to determine the effect of miR- 29 on elastin expression and Pi-induced vascular calcification. MicroRNA- 29 family members (miR- 29a, b and c) are reported to mediate elastin mRNA expression. However, the regulatory mechanisms of elastin mRNA expression during vascular calcification remain unclear. We previously reported that expression of elastin decreases with progression of inorganic phosphorus (Pi)-induced vascular smooth muscle cell (VSMC) calcification. Vascular calcification increases the risk of cardiovascular mortality. Sudo, Ryo Sato, Fumiaki Azechi, Takuya Wachi, Hiroshi MiR- 29-mediated elastin down-regulation contributes to inorganic phosphorus-induced osteoblastic differentiation in vascular smooth muscle cells. We report the first case of yellow phosphorus-related Brugada phenocopy, without hemodynamic compromise or malignant arrhythmia. Toxins such as aluminum and zinc phosphide have been reported to induce Brugada ECG patterns due to the generation of phosphine. He had both type 1 (day1) and type 2 (day2) Brugada patterns in the electrocardiogram, which resolved spontaneously by the third day without hemodynamic compromise. Brugada phenocopy and hepatic dysfunction were observed in a 29-year-old male following yellow phosphorus consumption. Cardiotoxicity with associated Brugada ECG pattern has been reported only in poisoning with metallic phosphides.
Toxicity of yellow phosphorus mostly pertains to the liver, kidney, heart, pancreas and the brain. Metallic phosphides (of aluminum and phosphide) and yellow phosphorus are commonly used rodenticide compounds in developing countries. Yellow phosphorus-induced Brugada phenocopy.ĭharanipradab, Mayakrishnan Viswanathan, Stalin Kumar, Gokula Raman Krishnamurthy, Vijayalatchumy Stanley, Daphene Divya
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