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Articles by Y Tsuji
Total Records ( 2 ) for Y Tsuji
  X Qi , Y. H Yeh , D Chartier , L Xiao , Y Tsuji , B. J.J.M Brundel , I Kodama and S. Nattel

Background— Sustained bradycardia is associated with long-QT syndrome in human beings and causes spontaneous torsades de pointes in rabbits with chronic atrioventricular block (CAVB), at least partly by downregulating delayed-rectifier K+-current to cause action potential (AP) prolongation. We addressed the importance of altered Ca2+ handling, studying underlying mechanisms and consequences.

Methods and Results— We measured ventricular cardiomyocyte [Ca2+]i (Indo1-AM), L-type Ca2+-current (ICaL) and APs (whole-cell perforated-patch), and Ca2+-handling protein expression (immunoblot). CAVB increased AP duration, cell shortening, systolic [Ca2+]i transients, and caffeine-induced [Ca2+]i release, and CAVB cells showed spontaneous early afterdepolarizations (EADs). ICaL density was unaffected by CAVB, but inactivation was shifted to more positive voltages, increasing the activation-inactivation overlap zone for ICaL window current. Ca2+-calmodulin–dependent protein kinase-II (CaMKII) autophosphorylation was enhanced in CAVB, indicating CaMKII activation. CAVB also enhanced CaMKII-dependent phospholamban-phosphorylation and accelerated [Ca2+]i-transient decay, consistent with phosphorylation-induced reductions in phospholamban inhibition of sarcoplasmic reticulum (SR) Ca2+-ATPase as a contributor to enhanced SR Ca2+ loading. The CaMKII-inhibitor KN93 reversed CAVB-induced changes in caffeine-releasable [Ca2+]i and ICaL inactivation voltage and suppressed CAVB-induced EADs. Similarly, the calmodulin inhibitor W7 suppressed CAVB-induced ICaL inactivation voltage shifts and EADs, and a specific CaMKII inhibitory peptide prevented ICaL inactivation voltage shifts. The SR Ca2+-uptake inhibitor thapsigargin and the SR Ca2+ release inhibitor ryanodine also suppressed CAVB-induced EADs, consistent with an important role for SR Ca2+ loading and release in arrhythmogenesis. AP-duration changes reached a maximum after 1 week of bradypacing, but peak alterations in CaMKII and [Ca2+]i required 2 weeks, paralleling the EAD time course.

Conclusions— CAVB-induced remodeling enhances [Ca2+]i load and activates the Ca2+-calmodulin-CaMKII system, producing [Ca2+]i-handling abnormalities that contribute importantly to CAVB-induced arrhythmogenic afterdepolarizations.

  S Abe , Y Tsuji , T Tsushima , T Kogawa , M Abe , Y Onodera , T Mizushima , T Kukitsu , T Sumiyoshi , N Yoshizaki , T Ishii and H. Kondo

Although combination chemotherapy with 3 weeks of S-1 and cisplatin is effective for advanced gastric cancer, the toxicities of S-1 which mostly occur during the third week of administration are a major problem. To achieve fewer adverse effects with S-1 and higher dose intensity of cisplatin, we performed combination chemotherapy with 2 weeks of S-1 and cisplatin as first line. The aim of this retrospective study was to analyse the efficacy and feasibility of this regimen.


S-1 (40–60 mg depending on patient's body surface area) was given orally twice daily for 2 consecutive weeks, and 70 mg/m2 cisplatin was given intravenously on day 8, followed by a 2-week rest period.


Forty-eight patients received a total of 184 courses of chemotherapy. Overall response rate was 40.6% and median survival time was 411 days. Dose intensities were 257.6 mg/m2/week for S-1 and 16.4 mg/m2/week for cisplatin. The incidences of grade 3/4 haematological toxicities were leucopenia (19%), neutropenia (29%) and anaemia (17%), and those of grade 3 non-haematological toxicities were anorexia (31%) and nausea (21%). The rate of treatment discontinuation owing to toxicity was 10%.


This regimen may be effective as an alternative therapy to 3 weeks of S-1 and cisplatin to reduce the toxicity of chemotherapy for advanced gastric cancer.

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