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T Nakadate

Publications and source records attributed to T Nakadate.

113 records · Page 7Linked to original sources
PubMed1979

Quantitative study on the liberation of tumor cells into the circulating blood.

A study was undertaken to investigate the mechanism of liberation of tumor cells into the blood stream in connection with the process of tumor growth, using three strains of ascites tumor such as Yoshida sarcoma (YS) with infiltrative growth pattern, AH100B with expansive one, and AH109A with intermediate one. For this experiment, a new method for the quantitation of the number of circulating tumor cells was devised. From its results, it was concluded as follows: (1) Tumor cells appear first in the circulating blood at the transitional phase from logarithmic growth to declining growth. (2) Tumor size is a macroscopical index of the risk of the liberation of tumor cells into the blood stream. (3) Tumor necrosis is a histological sign suggesting that the tumor growth phase is declining, namely, that hematogenous dissemination of tumor cells has begun already. (4) There is a striking difference in the frequency and number of tumor cells in the venous blood among these three tumor strains. The tumour strains in order of the number of the circulating tumor cells are YS, AH109A, and AH100B. (5) In YS and AH109A, the transition of the number of tumor cells liberated into the blood stream is closely related to the growth process of tumor tissue. (6) Liberated cells of AH109A and AH100B disappear promptly from the blood stream.

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PubMedDate not supplied

Inhibitory effect of beraprost sodium on formation of lipid peroxides in ischemia and recirculation-induced cerebral injury.

A cerebral injury was induced by the bilateral common carotid artery occlusion and recirculation in spontaneously hypertensive rats (SHRs). Employing this ischemia-recirculation rat model, the effects of beraprost sodium (beraprost) on (1) lipid peroxide formation, (2) the increase in the brain water content and (3) neurological signs were examined. In a dosage of 25 micrograms kg-1 or higher, beraprost, administered orally, significantly inhibited the formation of lipid peroxides in the brain and serum induced by cerebral ischemia and subsequent recirculation in a dose-dependent manner. Beraprost also alleviated ptosis and markedly inhibited abnormal running behaviour caused by the ischemia and subsequent recirculation. In addition, although administration of beraprost did not cause marked inhibition of the increase in the brain water content (used as an index of cerebral oedema) during the first 3 h after recirculation, it restored the normal brain water content within 24 h after recirculation. Therefore, this effect was observed evidently later than the effect of inhibition of lipid peroxide formation. Moreover, administration of beraprost resulted in improvement in the symptoms accompanying the ischemic treatment. These results suggest that beraprost is potentially useful for or treatment of the pathological state accompanying cerebral infarction.

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