I Yamada

Moyamoya disease: diagnostic accuracy of MRI

Our purpose was to evaluate the diagnostic accuracy of MRI in moyamoya disease. We studied 30 patients with this disease, comparing MRI and angiographic findings. The diagnostic value of MRI was evaluated for occlusive lesions, collateral vessels, and parenchymal lesions. In all patients bilateral occlusion or stenosis of the supraclinoid internal carotid artery and proximal anterior and middle cerebral arteries was clearly shown by MRI, and staging of the extent of occlusion agreed with angiographic staging in 44 (73%) of 60 arteries. MRI, particularly coronal images, clearly showed basal cerebral moyamoya vessels in 54 hemispheres, and 45 of a total of 71 large leptomeningeal and transdural collateral vessels were identified. MRI also showed parenchymal lesions in 48 (80%) hemispheres, and the extent of occlusion in the anterior and posterior circulations respectively correlated with white matter and cortical and/or subcortical infarcts.

MRI in spontaneous cerebrospinal fluid rhinorrhoea.

We studied two patients with spontaneous cerebrospinal fluid (CSF) rhinorrhoea with MRI and other imaging modalities. T2-weighted images proved most useful for the detection and localisation of the CSF leakage. MRI appeared to provide an accurate and noninvasive method for preoperative investigation of spontaneous CSF rhinorrhoea.

The killing effect of 4-S-cysteaminylphenol, a newly synthesised melanin precursor, on B16 melanoma cell lines.

We have examined the killing effect of 4-S-cysteaminylphenol (4-S-CAP), a newly synthesised melanin precursor, on B16 melanoma cell lines possessing different melanin-producing activities and found it to be particularly effective in heavily melanised melanoma cells, but less so in moderately melanised melanoma cells, and having no effect on amelanotic melanoma cells and nonmelanoma cells. Thus, it was found that the killing effect of 4-S-CAP is highly dependent upon the synthesis of melanin and tyrosinase in melanoma cells, suggesting that 4-S-CAP may become toxic to melanoma cells only after oxidation by tyrosinase. The killing activity of 4-S-CAP also was found to be associated with a profound inhibition of the thymidine incorporation in pigmented melanoma cells, as compared to the uridine and leucine incorporation. Further, the inhibition of DNA synthesis was most pronounced in heavily melanised melanoma cells, less so in moderately melanised melanoma cells, and not seen in amelanotic melanoma cells. As a possible mechanism that might account for this action, it may be that 4-S-CAP is oxidised by tyrosinase to the o-quinone form via the catechol derivative and that some of the quinones then conjugate with sulfhydryl enzymes including DNA polymerase, thus exerting a killing activity for pigmented melanoma cells. Thus, 4-S-CAP appears to provide a new, effective cytotoxic agent for rational chemotherapy of malignant melanomas.

The effect of L-dopa on the potentiation of radiation damage to human melanoma cells.

Since L-dopa (L-3,4-dihydroxyphenylalanine) has been shown to possess a selective toxicity for melanoma cells both in vitro and in vivo, we have examined the combined effect of L-dopa and radiation on human melanoma cells. It was found that the combined use of L-dopa potentiated the radiation cytotoxicity to HMV-I human melanoma cells, compared with the response seen in non-melanoma HeLa S3 cells. In HMV-I cells during their exponential phase, L-dopa decreased the shoulder width of the radiation survival curve significantly. In addition, L-dopa significantly inhibited the repair of potentially lethal damage (PLD) in HMV-I cells during their plateau phase. When the distributions of the G1, S, and G2-M cells were measured 24 h after combined L-dopa and radiation treatment, there was significant increase in the accumulation of cells in the G2-M phase of the cell cycle, compared to cells that received either L-dopa or radiation treatment only.