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--- home:starting:physician:reluctant [06.01.2019] – [Specific research] sallieq
+++ home:starting:physician:reluctant [07.19.2019] – [Specific research] sallieq
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-Benefits of RAS blockade with olmesartan treatment are sustained after study discontinued. (({{pubmed>long:24772521}})) PMID 24772521
+Benefits of RAS blockade with olmesartan treatment sustained after study discontinued. PMID 24772521.(({{pubmed>long:24772521}}))  //  Implies that immunopathology may occur unpredictably after discontinuing Olmesartan until microbial infection gets the upper hand again.//
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 mg/kg olmesartan reduces the inflammatory process and bone loss [in rats] (({{pubmed>long:23775504}} )) PMID 23775504
-Olmesartan at a dose of 10 mg/kg prevented the mucosal damage and inflammation associated with 5-FU-induced OM, increasing granulation and tissue repair. [in hamsters] (({{pubmed>long:    30125396}}))
+Olmesartan at a dose of 10 mg/kg prevented the mucosal damage and inflammation associated with 5-FU-induced OM, increasing granulation and tissue repair. [in hamsters] (({{pubmed>long:30125396}})) PMID 30125396
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 OLM substantially delayed the development of left ventricular remodeling in type 2 diabetes (({{pubmed>long:25275251}}))  PMID 25275251
+we investigated the effects of RNH-6270, an active metabolite of olmesartan, on TNF-α-induced human glomerular EC (HGEC) damage to clarify the renoprotective mechanisms of ARBs. Our findings suggested that olmesartan might have protective effects against TNF-α-induced glomerular EC dysfunction.(({{pubmed>long:    23052181}})) PMID 23052181
+We orally administered olmesartan 1, 3, and 10 mg/kg/day to rats with EAM for 3 weeks. The cardioprotection of olmesartan may be due to suppression of inflammatory cytokines dependent of the hemodynamic modifications.  (({{pubmed>long:15124927}}))  PMID 15124927
+AlphaTau1 receptor blockers, olmesartan and valsartan (10(-9)-10(-6) mol/L) showed a significant reduction on TNF-alpha-induced LDH and NAG release in human renal proximal tubular epithelial cells (({{pubmed>long:    18331441}})) PMID 18331441
+The administration of olmesartan improved blood pressure, insulin, HOMA, visfatin and lipid profile in hypertensive obese women. (({{pubmed>long:21061834}})) PMID 21061834
+These data added to our previous results further provide a mechanistic rationale for olmesartan's antioxidant/anti-inflammatory potential translation, in the long term, toward anti-atherosclerotic/anti-remodeling effects reported by clinical trials. (({{pubmed>long:26240115}})) PMID 26240115
+Olmesartan attenuated CTGF induction, reduced perivascular fibrosis and ameliorated cardiac dysfunction in a PO heart. Our results provide insight into the beneficial effects of olmesartan on PO hearts, independent of blood-pressure lowering. [in rat] (({{pubmed>long:20944640}}))  PMID 20944640
+ Wistar-Kyoto rats were treated with high-dose olmesartan (3 mg.kg(-1).day(-1)), low-dose olmesartan (0.3 mg.kg(-1).day(-1)) Low-dose ARB had no anti-inflammatory effects in anti-GBM GN. However, high-dose ARB reduced glomerular infiltration of CD8+ cells and ED1+ macrophages and suppressed necrotizing and crescentic lesions by days 5 to 7 (P < 0.05). In addition, high-dose ARB reduced the numbers of ED3+-activated macrophages, suppressed glomerular TNF-α and IFN-γ production, and downregulated M1-related chemokine and cytokines (monocyte chemoattractant protein type 1, IL-6, and IL-12). High-dose ARB also enhanced ED2+ M2 macrophages by day 7 with upregulation of glomerular IL-4 and IL-13 and augmented CCL17, IL-1 receptor antagonist, and IL-10. We concluded that high-dose ARB inhibits glomerular inflammation by increasing the numbers of M2 macrophages and upregulation of anti-inflammatory cytokines and by suppressing M1 macrophage development with downregulation of M1-related proinflammatory cytokines. (({{pubmed>long:20071465}})) PMID 20071465
+Olmesartan treatment reversed virtually all neuroendocrine and histopathological cardiac changes induced by EAM (We used experimental autoimmune myocarditis in rats) (({{pubmed>long:18408131}})) PMID 18408131
+Treatment with ARB prevents the progression of peritoneal fibrosis and suppresses expression of adhesion molecules in the peritoneum. (({{pubmed>long:14763058}})) PMID 14763058
+( in cultured human renal proximal tubular cells) Olmesartan inhibited the effect of costimulation with ANG II and IL-6 on AGT expression, indicating that AT1R is critical for AGT enhancement by ANG II. Moreover, IL-6R antibody also neutralized the effect, suggesting that these agents exert a synergistic effect, even though they do not independently induce human AGT expression. These findings suggest that AT1R blockers may attenuate the secondary pathophysiological effects of ANG II even though ANG II alone does not exert any direct effects, and this may partially account for the powerful renoprotective effects of AT1R blocker beyond its depressor effect. (({{pubmed>long:18463317}}))  PMID 18463317
+Olmesartan treatment had already significantly reduced serum levels of high-sensitivity C-reactive protein (-15.1%; P<0.05), high-sensitivity tumor necrosis factor-alpha (-8.9%; P<0.02), interleukin-6 (-14.0%; P<0.05), and monocyte chemotactic protein-1 (-6.5%; P<0.01) after 6 weeks of therapy, whereas placebo treatment (ie, blood pressure reduction) had no major effect on inflammation markers. (({{pubmed>long:15313950}}))  PMID 15313950
 Long term treatment Data suggest 40 & 80 mg olmesartan are able to significantly remodel & destiffen the arterial wall material during long-term treatment, partly independently of blood pressure, compared with 20 mg. hyper.ahajournals.org/content/early/2014/07/07/HYPERTENSIONAHA.114.03282.reprint (({{pubmed>long:25001274}}))   PMID 25001274

home/starting/physician/reluctant.txt · Last modified: 09.14.2022 by 127.0.0.1