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Kenichi Amagasaki, Tsuneo Shimizu, Yoko Suzuki and Toshiyuki Kakizawa

✓ 28-year-old woman presented with mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS). The diagnosis was based on the results of molecular genetic analysis, which indicated a typical point mutation at the nucleotide pair 3243. Xenon computerized tomography scans obtained during the strokelike episodes revealed the lesion responsible for the symptoms to be an area of focal hyperperfusion, and scans obtained after the episodes revealed an area of hypoperfusion. Pathogenesis of the strokelike episodes appears to be metabolic dysfunction, although the involvement of a vascular event cannot be excluded.

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Kenichi Amagasaki, Shoko Abe, Saiko Watanabe, Kazuaki Naemura and Hiroshi Nakaguchi

This 31-year-old woman presented with typical right trigeminal neuralgia caused by a trigeminocerebellar artery, manifesting as pain uncontrollable with medical treatment. Preoperative neuroimaging studies demonstrated that the offending artery had almost encircled the right trigeminal nerve. This finding was confirmed intraoperatively, and decompression was completed. The neuralgia resolved after the surgery; the patient had slight transient hypesthesia, which fully resolved within the 1st month after surgery. The neuroimaging and intraoperative findings showed that the offending artery directly branched from the upper part of the basilar artery and, after encircling and supplying tiny branches to the nerve root, maintained its diameter and coursed toward the rostral direction of the cerebellum, which indicated that the artery supplied both the trigeminal nerve and the cerebellum. The offending artery was identified as the trigeminocerebellar artery. This case of trigeminal neuralgia caused by a trigeminocerebellar artery indicates that this variant is important for a better understanding of the vasculature of the trigeminal nerve root.

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Kenichi Amagasaki, Hiromichi Yamazaki, Kimie Ohmori, Hidehito Koizumi, Kazuhiro Hashizume and Nobuo Sasaguchi

✓ This 55-year-old man presented with malignant intravascular lymphomatosis, a rare vascular disorder of the central nervous system characterized by proliferation of malignant lymphoma cells. The clinical manifestations were focal neurological signs and progressive dementia. Angiography demonstrated stenoses of the cortical veins. Postmortem examination revealed infiltration of tumor cells into the lumen and vascular wall, although the stenoses were caused primarily by fibrin thrombi. To the authors' knowledge this is the first case of malignant intravascular lymphomatosis associated with venous stenosis.

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Kenichi Amagasaki, Tsutomu Yagishita, Shinichi Yagi, Katsuhiro Kuroda, Kazuyuki Nishigaya and Hideaki Nukui

✓ This 47-year-old man was admitted to the hospital with disturbance of consciousness due to subarachnoid hemorrhage caused by a ruptured dissecting aneurysm of the left anterior cerebral artery (ACA). Conservative treatment resulted in improvement in the patient's consciousness; however, repeated rupture occurred during the chronic stage. Endovascular coil embolization of the parent artery was successful. Serial angiography demonstrated all stages in the development of the aneurysm. Follow-up angiography demonstrated an incidental dissecting aneurysm of the right vertebral artery. This aneurysm was also treated by endovascular embolization. No new neurological deficit appeared during or after the treatment.

Multiple dissecting aneurysms are rare, especially those involving both supra- and infratentorial regions. A ruptured dissecting aneurysm of the ACA is also an uncommon vascular disorder. This case shows that rebleeding may occur, even during the chronic stage, and thus appropriate treatment for the prevention of subsequent bleeding is essential. Incidental dissecting aneurysms can be treated using the endovascular technique, but further study is necessary.

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Lei Zhang, Eiji Sato, Kenichi Amagasaki, Atsuhito Nakao and Hirofumi Naganuma

Object

Malignant glioma cells secrete and activate transforming growth factor–β (TGFβ) and are resistant to growth inhibition by that factor. Nevertheless, the mechanism underlying this effect remains poorly understood. In this study, the mechanism of the resistance to growth inhibition induced by TGFβ was investigated.

Methods

The authors examined the expression of downstream components of the TGFβ receptor, including Smad2, Smad3, Smad4, and Smad7, and the effect of TGFβ1 treatment on the phosphorylation of Smad2 and the nuclear translocation of Smad2 and Smad3 by using 10 glioma cell lines and the A549 cell line, which is sensitive to TGFβ-mediated growth inhibition. The expression of two transcriptional corepressor proteins, SnoN and Ski, and the effect of TGFβ1 treatment on the expression of the SnoN protein and the cell cycle regulators p21, p15, cyclin-dependent kinase–4 (CDK4), and cyclin D1 were also examined.

Expression of the Smad2 and Smad3 proteins was lower in the glioma cell lines than in the A549 cell line and in normal astrocytes. In particular, Smad3 expression was low or very low in nine of the 10 malignant glioma cell lines. Expression of Smad4 was low in four glioma cell lines, and expression of the Smad7 protein was similar when compared with protein expression in the A549 cell line and in normal astrocytes. The levels of Smad2 phosphorylation after TGFβ1 treatment were lower in glioma cell lines than in the A549 cell line, except for one glioma cell line. Seven of the 10 glioma cell lines exhibited lower levels of nuclear translocation of Smad2 and Smad3, and two cell lines that expressed very low levels of Smad3 protein showed no nuclear translocation. All glioma cell lines expressed the SnoN protein and its expression was unaltered by treatment with TGFβ1. Three glioma cell lines expressed high levels of the Ski protein. The expression of the p21cip1, p15INK4B, CDK4, and cyclin D1 proteins was not altered by TGFβ1 treatment, except in one cell line that displayed a slight increase in p21 protein. Overall, the expression of the Smad2 and Smad3 proteins was low in the glioma cell lines, the phosphorylation and nuclear translocation of Smad2 and Smad3 were impaired, and the TGFβ receptor signal did not affect the expression of the SnoN, p21, p15, cyclin D1, and CDK4 proteins.

Conclusions

These results suggest that the ability to resist TGFβ-mediated growth inhibition in malignant glioma cells is due to abnormalities in the TGFβ signaling pathway.