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Masaya Tamano

Publications and source records attributed to Masaya Tamano.

6 recordsLinked to original sources
PubMed2005

Central thyrotropin-releasing hormone increases hepatic cyclic AMP through vagal-cholinergic and prostaglandin-dependent pathways in rats.

Central neuropeptides play roles in many physiologic regulations through the autonomic nervous system. We have demonstrated that central thyrotropin-releasing hormone (TRH), one of neuropeptides, induces a stimulation of hepatic proliferation through vagal-cholinergic pathways. Since cAMP is known to play an important role in the hepatic proliferation, effect of central TRH on hepatic cAMP was investigated. Rats were intracisternally injected with either a TRH analog, RX-77368 (1-100 ng), or saline. The liver was removed 2-72 h after the TRH analog and hepatic cAMP content was determined by radioimmunoassay. In some experiments, pretreatment with hepatic vagotomy, atropine methyl nitrate, or 6-hydroxydopamine (6-OHDA) was performed. Hepatic cAMP was dose-dependently increased by intracisternal TRH analog (5-100 ng) with a peak response occurring 12 h postinjection. The central TRH-induced increase in hepatic cAMP was abolished by vagotomy, atropine and indomethacin, but not by 6-OHDA. Intravenous injection of the TRH analog (10 ng) did not affect hepatic cAMP. These results demonstrate that TRH acts in the brain to increase hepatic cAMP through vagal-cholinergic and prostaglandin-dependent pathways, suggesting that central TRH modulates hepatic functions through cAMP-mediated signaling pathways.

Animals↗
PubMed2004

Evaluation of esophageal varices using contrast-enhanced coded harmonic ultrasonography.

AIM: To investigate if esophageal varices can be evaluated using external contrast-enhanced ultrasonography with Levovist and coded harmonic angio (CHA). METHODS: Subjects were six healthy adult volunteers and 23 patients with liver cirrhosis. After identification of the lower esophagus under B-mode scanning, 300 mg/mL of Levovist was intravenously injected into the cubital vein at a rate of 1 mL/s under observation by CHA-mode scanning. Approximately 30 s after intravenous administration, interval-delay scanning was performed every second to visualize the area around the lower esophageal lumen. The degree of ultrasonographic enhancement was assessed as either no enhancement (negative); linear enhancement along the esophageal wall (weak) or full enhancement of the esophageal lumen (strong). Endoscopic evaluation of esophageal varices was also performed. RESULTS: The CHA enhancement around the lower esophageal lumen was identified in 21 of the 23 patients. Of these 21 patients, endoscopic assessments of varices were as follows: F0 in four patients, F1 in seven patients, F2 in three patients, and F3 in seven patients. Nine patients were red color sign (RCS)-positive. Regarding the relationship between ultrasonographic enhancement and endoscopic assessment, enhancement was identified as negative in all four F0 patients, negative in three and weak in three and strong in one of the seven F1 patients, weak in one and strong in two of the three F2 patients, and weak in two and strong in five of the seven F3 patients, respectively. Furthermore, of the nine RCS-positive patients, enhancement was recognized as strong in seven and weak in two patients. Ultrasonographic enhancement was identified as negative in all six healthy volunteers. CONCLUSIONS: By performing contrast-enhanced CHA ultrasonography using Levovist, ultrasonographic enhancement was detectable in all patients with varices categorized as F2 or above. Because the present method is easy to perform and causes less pain to patients compared to endoscopy, it is useful for following and assessing esophageal varices in patients with liver cirrhosis.

Aged↗
PubMed2002

Serum and tissue PIVKA-II expression reflect the biological malignant potential of small hepatocellular carcinoma.

A sensitive method for measuring the serum level of protein-induced by vitamin K absence or antagonist II (PIVKA-II) has become so widely available that it is now used for the clinical diagnosis of small hepatocellular carcinoma (HCC). It is known that serum PIVKA-II can be a prognostic indicator for HCC, but there have been no detailed investigations concerning the tissue expression of PIVKA-II. The present study assessed the relationship between serum or tissue PIVKA-II and the biological malignant potential of HCC. The subjects were 25 patients with histologically confirmed HCC, that were solitary and 3 cm or less in diameter. Tissue PIVKA-II was detected by immunostaining using MU-3 as the primary antibody. The biological malignant potential of the tumors was evaluated on the basis of the Ki-67 labeling index of HCC cells and the tumor arterial vascularity assesed by angiography and CO(2) enhanced ultrasonography. The recurrence-free period after treatment was also evaluated. Among the 25 patients, eight were positive for tissue PIVKA-II. Serum PIVKA-II levels were significantly higher in the tissue PIVKA-II-positive patients compared with the negative patients, but serum and tissue PIVKA-II expressions were not consistently parallel. Tumor cell proliferation was closely correlated with the tissue PIVKA-II expression, while the recurrence-free period was correlated with the serum PIVKA-II level. Tumor arterial vascularity showed a strong correlation with the expression of both serum and tissue PIVKA-II. In conclusion, serum and tissue PIVKA-II expression reflect the biological malignant potential of HCC and thus may be useful indicators for the prognosis of small HCC.

Journal Article↗