A highly sensitive, quick and simple quantification method for nicotianamine and 2'-deoxymugineic acid from minimum samples using LC/ESI-TOF-MS achieves functional analysis of these components in plants.
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We investigated the changes of matrix metalloproteinase (MMP) -9 in the peripheral blood samples of patients undergoing endovascular aneurysm repair (EVAR) for abdominal aortic aneurysms (AAAs), and the effect of azelnidipine on plasma MMP-9 levels in those patients. Levels of MMP-9 were measured in 22 patients who underwent EVAR for AAAs, and results were compared between a group receiving 16 mg azelnidipine daily (n=12) and a control group without azelnidipine (n=10). Measurements were taken preoperatively, and at 1 month and 3 months, postoperatively. Patients without endoleaks after EVAR showed a significant decrease in mean plasma MMP-9 levels (preoperative value: 39.5+/-14.3 ng/mL, after 1 month: 25.0+/-12.6, after 3 months: 28.2+/-10.2 ng/mL; P=0.004). In contrast, no significant decreases in mean plasma MMP-9 levels were observed in the patients with endoleaks after EVAR (preoperative value: 37.5+/-9.0 ng/mL, after 1 month: 26.8+/-8.4, after 3 months: 38.5+/-15.7 ng/mL; P=0.219). Moreover, among patients without endoleaks, those receiving azelnidipine showed a significantly greater decrease in the mean plasma MMP-9 levels for 3 months postoperatively (preoperative value: 47.7+/-13.2 ng/mL, after 1 month: 26.6+/-12.8, after 3 months: 26.1+/-11.4 ng/mL; P0.001) compared with the control group without endoleaks (preoperative value: 31.3+/-10.5 ng/mL, after 1 month: 33.4+/-12.1, after 3 months: 30.3+/-9.1 ng/mL; P=0.792). These results showed that azelnidipine treatment in patients without endoleak after EVAR was associated with a significant decrease in mean plasma MMP-9 levels for 3 months postoperatively. (+info)
Combination therapy with olmesartan and azelnidipine improves EDHF-mediated responses in diabetic apolipoprotein E-deficient mice.
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BACKGROUND: The endothelium modulates vascular tone by synthesizing and releasing several vasodilating factors, including vasodilator prostaglandins, nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). In the present study, we examined whether an angiotensin-receptor blocker, a calcium-channel blocker or their combination improved EDHF-mediated responses in diabetic apolipoprotein E-deficient (ApoE(-/-)) mice. METHODS AND RESULTS: We used male C57BL/6N (control) and streptozocin-induced diabetic ApoE(-/-) mice. The diabetic ApoE(-/-) mice were administered oral vehicle (untreated), olmesartan (OLM, 30 mgxkg(-1)xday(-1)), azelnidipine (AZL, 10 mgxkg(-1)xday(-1)), their combination (OLM + AZL), or hydralazine (HYD 5 mgxkg(-1)xday(-1)) for 5 weeks. In the untreated group, systolic blood pressure was significantly higher and both EDHF-mediated relaxation and endothelium-dependent hyperpolarization were markedly reduced as compared with the control group. Although EDHF-mediated relaxation was not significantly improved in the HYD, OLM and AZL groups, it was significantly improved in the OLM + AZL group, as was also the case with phosphorylation of Akt and endothelial NO synthase (eNOS). In contrast, the endothelium-independent relaxation response to sodium nitroprusside or NS-1619 (a direct opener of K(Ca) channels) was unaltered in any group. CONCLUSIONS: OLM + AZL may improve the severely impaired EDHF-mediated responses in diabetic ApoE(-/-) mice, in which activation of the endothelial Akt - eNOS pathway may be involved. (+info)
Plasma renin activity and aldosterone concentration are not altered by the novel calcium channel antagonist, azelnidipine, in hypertensive patients.
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OBJECTIVE: In hypertensive patients, primary aldosteronism (PA) is the most prevalent type of secondary hypertension, and screening for PA has become very important. Calcium channel blockers (CCB) are widely used to treat hypertension, but most CCBs stimulate plasma renin activity (PRA) and increase plasma aldosterone concentration (PAC), both of which are used in the screening for PA. The aim of this study was to determine whether the newly introduced CCB, azelnidipine, affects PRA and PAC. METHODS: 40 hypertensive patients were treated with 16 mg of azelnidipine for 4 weeks. RESULTS: Azelnidipine treatment in drug-naive (DN) cases significantly decreased systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR). PRA and PAC in the DN group on azelnidipine treatment were indistinguishable from those in the DN group before treatment. Compared with other CCB treatments such as amlodipine, manidipine and slow-release nifedipine, azelnidipine showed comparable or significant reductions in SBP, DBP and HR. In patients who were switched from other CCBs to azelnidipine, PRA and PAC were decreased, except for PAC on amlodipine treatment. Since the PRA reduction rate exceeded that of PAC, the aldosterone/renin ratio (ARR) was significantly increased in those on azelnidipine treatment who had been switched from manidipine or nifedipine treatment, suggesting the restoration of possibly underestimated ARR values. CONCLUSION: These data indicate that azelnidipine does not affect PRA or PAC, suggesting that azelnidipine could be a useful antihypertensive CCB while undergoing PA screening. (+info)
Nicotianamine, a novel enhancer of rice iron bioavailability to humans.
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The application of the yeast N-acetyltransferase MPR1 gene and the proline analogue L-azetidine-2-carboxylic acid as a selectable marker system for plant transformation.
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Cytokine reducing effect of azelnidipine in human peripheral blood mononuclear cells.
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Numerous clinical trials have shown that calcium channel blocker (CCB) therapy improves the clinical outcome in patients with cardiovascular diseases. Since the progression of several types of cardiovascular diseases is closely associated with inflammation, alleviation of inflammation may be one potential mechanism of those beneficial effects of CCB therapy. We examined whether a new CCB (azelnidipine) could influence the inflammatory response of human peripheral blood mononuclear cells (PBMCs), which are recruited to inflammatory lesions and modulate inflammation. We investigated whether azelnidipine affected intracellular signaling and cytokine production by phytohemagglutinin (PHA)-stimulated human PBMCs in vitro. PBMCs were obtained from 10 healthy volunteers and stimulated with PHA. Then relative intracellular calcium ion concentration ([Ca(2+)](i)) was assessed by fluorescence microscopy, and the production of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-alpha) were measured by enzyme-linked immunosorbent assay. Stimulation with PHA significantly raised [Ca(2+)](i) and enhanced the production of MCP-1 and TNF-alpha by human PBMCs. Azelnidipine significantly diminished the PHA-induced rise of [Ca(2+)](i), and the production of MCP-1 and TNF-alpha. These findings indicate that azelnidipine might have an anti-inflammatory influence on human PBMCs, although the mechanisms and the difference from other CCBs still remain unclear and further exploration should be required. (+info)