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Articles by T Miura
Total Records ( 2 ) for T Miura
  K Noda , Y Sato , T Miura , K Katayama and R. Kojima
  Background

Chlorophosphonazo-III (2,7-bis[4-chloro-2-phosphonophenylazo]-1,8-dihydroxy-3,6-naphthalenedisulphonic acid, disodium salt; CPZ-III) reacts with calcium and magnesium in a sample under acidic to neutral conditions. However, the specific method of measuring calcium in serum using CPZ-III has not been established because of the difficulty of avoiding the interaction between CPZ-III and albumin.

Methods

In this study, we found that the non-specific reaction between CPZ-III and albumin could be controlled and calcium in serum could be specifically detected using CPZ-III combined with vanadate. On the basis of this finding, we evaluated a novel method of serum calcium determination using CPZ-III.

Results

This CPZ-III vanadate method gave linear results from 0 to 7.0 mmol/L. The coefficient of variation was 0.63–0.76%. There was no interference except with Omniscan. There was no change in control performance during 60 d under open-air conditions. The assay results correlated well with those of the Arsenazo-III (2,7-bis(2-arsonophenylazo)-1,8-dihydroxy-3,6-naphthalenedisulphonic acid) method (slope = 1.067; intercept = –0.120; r = 0.989; Sy/x = 0.036 mmol/L), o-cresolphthalein complexone method (slope = 0.911; intercept = 0.186; r = 0.988; Sy/x = 0.035 mmol/L), amylase enzymatic method (slope = 0.981; intercept = 0.072; r = 0.989; Sy/x = 0.036 mmol/L) and inductively coupled plasma emission spectroscopy method (slope = 0.955; intercept = –0.001; r = 0.979; Sy/x = 0.048 mmol/L).

Conclusions

These results suggested that the present method has great clinical potential for measuring calcium.

  H Hotta , T Miura , T Miki , N Togashi , T Maeda , S. J Kim , M Tanno , T Yano , A Kuno , T Itoh , T Satoh , Y Terashima , S Ishikawa and K. Shimamoto
 

Rationale: The diabetic heart is resistant to ischemic preconditioning because of diabetes-associated impairment of phosphatidylinositol 3-kinase (PI3K)-Akt signaling. The mechanism by which PI3K-Akt signaling is impaired by diabetes remains unclear.

Objective: Here, we examined the hypothesis that phosphorylation of Jak2 upstream of PI3K is impaired in diabetic hearts by an angiotensin II type 1 (AT1) receptor–mediated mechanism.

Methods and Results: Infarct size (as percentage of risk area) after 20-minute ischemia/2-hour reperfusion was larger in a rat model of type 2 diabetes (Otsuka–Long–Evans–Tokushima fatty [OLETF] rat) than in its control (Long–Evans–Tokushima–Otsuka [LETO] rat) (60.4±1.6% versus 48.4±1.3%). Activation of Jak2-mediated signaling by erythropoietin or DADLE ([d-Ala2, d-Leu5]-enkephalin acetate), a -opioid receptor agonist, limited infarct size in LETO rats (27.7±3.4% and 24.8±5.0%) but not in OLETF rats (53.9±5.3% and 55.0±2.2%). Blockade of the AT1 receptor by valsartan or losartan for 2 weeks restored the myocardial response of OLETF rats to erythropoietin-induced infarct size limitation (39.4±4.9% and 31.2±7.5). In OLETF rats, erythropoietin failed to phosphorylate both Jak2 and Akt, and calcineurin activity was significantly higher than in LETO rats. Two-week treatment with valsartan normalized calcineurin activity in OLETF rats and restored the response of Jak2 to erythropoietin. This effect of AT1 receptor blockade was mimicked by inhibition of calcineurin by FK506.

Conclusions: These results suggest that the diabetic heart is refractory to protection by Jak2-activating ligands because of AT1 receptor–mediated upregulation of calcineurin activity.

 
 
 
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