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Articles by T Tamaki
Total Records ( 2 ) for T Tamaki
  K Yomiya , N Matsuo , S Tomiyasu , T Yoshimoto , T Tamaki , T Suzuki and M. Matoba

Purpose: Baclofen is a g-aminobutyric acid receptor agonist commonly used for managing many types of neuropathic pain. The effect of baclofen on cancer pain has not previously been studied. This retrospective study evaluated the efficacy of baclofen in patients with cancer pain.

Methods: We reviewed the medical records of all patients given baclofen orally as an analgesic for cancer at 5 institutions.

Result: Twenty-five patients received 10 to 40 mg of baclofen for cancer pain relief. Twenty patients have undergone neuropathic pain such as paroxysmal or lancing, sharp, or like an electric shock. Baclofen was effective in 21 of 25 patients and significantly reduced Numeric Rating Scale (pain score, 0-10; P < .0001). Nine patients reported mild adverse events: none of these 9 patients had to discontinue baclofen due to adverse events.

Conclusion: Our findings suggest that baclofen may be a useful adjuvant analgesic in the treatment of cancer pain.

  Y Ikeda , K. i Aihara , M Akaike , T Sato , K Ishikawa , T Ise , S Yagi , T Iwase , Y Ueda , S Yoshida , H Azuma , K Walsh , T Tamaki , S Kato and T. Matsumoto

Doxorubicin (Dox) has been used as a potent anticancer agent, but serious cardiotoxicity precludes its use in a wide range of patients. We have reported that the androgen-androgen receptor (AR) system plays important roles in cardiac growth and protection from angiotensin II-induced cardiac remodeling. The present study was undertaken to clarify whether the androgen-AR system exerts a cardioprotective effect against Dox-induced cardiotoxicity. Male AR knockout (ARKO) and age-matched littermate male wild-type (WT) mice at 25 wk of age were given ip injections of Dox (20 mg/kg) or a vehicle. The survival rate and left ventricular function in Dox-treated male ARKO mice were reduced compared with those in Dox-treated male WT mice. Electron microscopic study showed prominent vacuole formation of myocardial mitochondria in Dox-treated male ARKO mice. Cardiac oxidative stress and apoptosis of cardiomyocytes were increased more prominently by Dox treatment in male ARKO mice than in male WT mice. In addition, Dox-induced reduction in the expression of cardiac mitochondria transcription factor A (Tfam) and phosphorylation of serine-threonine kinase (Akt) was more pronounced in male ARKO mice than in male WT mice. In cardiac myoblast cells, testosterone up-regulated Akt phosphorylation and Tfam expression and exerted an antiapoptotic effect against Dox-induced cardiotoxicity. Collectively, the results demonstrate that Dox-induced cardiotoxicity is aggravated in male ARKO mice via exacerbation of mitochondrial damage and superoxide generation, leading to enhanced apoptosis of cardiomyocytes. Thus, the androgen-AR system is thought to counteract Dox-induced cardiotoxicity partly through activation of the Akt pathway and up-regulation of Tfam to protect cardiomyocytes from mitochondrial damage and apoptosis.

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