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Articles by A Miyamoto
Total Records ( 3 ) for A Miyamoto
  Y Miyashita , S Saito , A Miyamoto , O Iida and S. Nanto
 

Skin perfusion pressure (SPP) is a measure of peripheral circulation; low SPP (<40 mm Hg) indicates poor wound healing. Cilostazol is used to alleviate symptoms and improve walking distance in patients with peripheral artery disease (PAD), but its effect on SPP is unknown. We enrolled patients whose symptoms were Rutherford class 3 or 4 and whose SPP was <40 mm Hg. We analyzed patient symptoms, ankle-brachial index (ABI), and SPP before and 1 month after treatment with cilostazol. We analyzed 20 legs of 14 patients. Cilostazol improved symptoms in 12 legs. The average heart rate increased from 76 ± 16 to 84 ± 20 beats/min (P < .05). Cilostazol did not increase the ABI but caused a significant increase in the SPP from 24.5 ± 8.88 to 42.8 ± 21.0 mm Hg (P < .01). Cilostazol increases microvascular circulation in severely ischemic limbs and may be useful in critical limb ischemia.

  H Itoh , T Sakaguchi , W. G Ding , E Watanabe , I Watanabe , Y Nishio , T Makiyama , S Ohno , M Akao , Y Higashi , N Zenda , T Kubota , C Mori , K Okajima , T Haruna , A Miyamoto , M Kawamura , K Ishida , I Nagaoka , Y Oka , Y Nakazawa , T Yao , H Jo , Y Sugimoto , T Ashihara , H Hayashi , M Ito , K Imoto , H Matsuura and M. Horie
 

Background— Drugs with IKr-blocking action cause secondary long-QT syndrome. Several cases have been associated with mutations of genes coding cardiac ion channels, but their frequency among patients affected by drug-induced long-QT syndrome (dLQTS) and the resultant molecular effects remain unknown.

Methods and Results— Genetic testing was carried out for long-QT syndrome–related genes in 20 subjects with dLQTS and 176 subjects with congenital long-QT syndrome (cLQTS); electrophysiological characteristics of dLQTS-associated mutations were analyzed using a heterologous expression system with Chinese hamster ovary cells together with a computer simulation model. The positive mutation rate in dLQTS was similar to cLQTS (dLQTS versus cLQTS, 8 of 20 [40%] versus 91 of 176 [52%] subjects, P=0.32). The incidence of mutations was higher in patients with torsades de pointes induced by nonantiarrhythmic drugs than by antiarrhythmic drugs (antiarrhythmic versus others, 3 of 14 [21%] versus 5 of 6 [83%] subjects, P<0.05). When reconstituted in Chinese hamster ovary cells, KCNQ1 and KCNH2 mutant channels showed complex gating defects without dominant negative effects or a relatively mild decreased current density. Drug sensitivity for mutant channels was similar to that of the wild-type channel. With the Luo-Rudy simulation model of action potentials, action potential durations of most mutant channels were between those of wild-type and cLQTS.

Conclusions— dLQTS had a similar positive mutation rate compared with cLQTS, whereas the functional changes of these mutations identified in dLQTS were mild. When IKr-blocking agents produce excessive QT prolongation (dLQTS), the underlying genetic background of the dLQTS subject should also be taken into consideration, as would be the case with cLQTS; dLQTS can be regarded as a latent form of long-QT syndrome.

  E Arvisais , X Hou , T. A Wyatt , K Shirasuna , H Bollwein , A Miyamoto , T. R Hansen , B. R Rueda and J. S. Davis
 

Little is known about the early intracellular events that contribute to corpus luteum regression. Experiments were designed to determine the effects of prostaglandin F2 (PGF2) on phosphatidylinositol-3-kinase (PI3K)/Akt signaling in the corpus luteum in vivo and in vitro. Treatment of midluteal-phase cows with a luteolytic dose of PGF2 resulted in a rapid increase in ERK and mammalian target of rapamycin (mTOR)/p70 ribosomal protein S6 kinase (p70S6K1) signaling and a rapid suppression of Akt phosphorylation in luteal tissue. In vitro treatment of primary cultures of luteal cells with PGF2 also resulted in an increase in ERK and mTOR/p70S6K1 signaling and a diminished capacity of IGF-I to stimulate PI3K, Akt, and protein kinase C activation. Accounting for the reductions in PI3K and Akt activation observed in response to PGF2 treatment, we found that PGF2 promoted the phosphorylation of serine residues (307, 612, 636) in the insulin receptor substrate 1 (IRS1) peptide sequence in vivo and in vitro. Serine phosphorylation of IRS1 was associated with reduced formation of IGF-I-stimulated IRS1/PI3Kp85 complexes. Furthermore, treatment with inhibitors of the MAPK kinase 1/ERK or mTOR/p70S6K1 signaling pathways prevented PGF2-induced serine phosphorylation of IRS1 and abrogated the inhibitory actions of PGF2 on Akt activation. Taken together, these experiments provide compelling evidence that PGF2 treatment stimulates IRS1 serine phosphorylation, which may contribute to a diminished capacity to respond to IGF-I. It seems likely that the rapid changes in phosphorylation events are among the early events that mediate PGF2-induced corpus luteum regression.

 
 
 
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