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Articles by M Iida
Total Records ( 2 ) for M Iida
  T Shichita , T Ogata , M Yasaka , K Yasumori , T Inoue , S Ibayashi , M Iida and Y. Okada
 

Purpose: This study aimed to clarify the angiographic characteristics of radiation-induced carotid stenosis. Methods: We evaluated 11 carotid arteries of patients after radiotherapy (radiotherapy group) and 26 carotid arteries of age- and gender-matched patients without a history of radiotherapy (control group). All patients had carotid stenosis detected by digital subtraction angiography (DSA). We developed an original coordinate system on the DSA to determine the accurate length and location of the carotid lesion. Results: Radiation-induced carotid lesions were significantly longer than carotid lesions caused by atherosclerosis. The maximal stenosis of radiation-induced carotid lesions tended to be at the end of the stenotic area and within a wider range than the nonradiation-induced lesions, including in the proximal common carotid artery (CCA). Conclusions: Radiation-induced stenotic lesions seem to exist in a wide range of carotid artery, including the CCA, along the vessel, and show maximal stenosis near the end of the stenotic area.

  M Iida , T Sasaki and H. Komatani
 

To unravel the growth inhibition mechanism of Polo-like kinase 3 (Plk3), the effect of overexpression of Plk3 was examined in 293T cells. Cell rounding, changes in actin organization and cellular detachment were induced by Plk3 transfection in a kinase activity-dependent manner. Although apoptosis was not observed, Plk3 overexpression suppressed cellular growth in a long-term colony-forming assay. Because both Plk3 and Ras affect F-actin organization, the effect of co-transfection of Plk3 and Ras was evaluated. Adhesion was synergistically lost by co-transfection of these two genes, compared with transfection of Plk3 alone. Furthermore, overexpression of Plk3 caused long-term growth suppression in Ras-transformed NIH3T3. Collectively, Plk3 activation might cause cytoskeleton re-organization and result in growth suppression more pronouncedly in Ras pathway-activated cells.

 
 
 
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