Biomedical subjects
Publications and source records attributed to S Waga.
A rare case of a solitary eosinophilic granuloma in the brain is reported. The mass, located in the right frontal lobe, mimicked a glioma not only grossly, but also by neuroimaging. The lesion was confirmed to be an eosinophilic granuloma by electron microscopy and immunohistochemical staining for S-100 protein and HLA-DR.
A case of mutism after removal of a vermian medulloblastoma from a 4-year-old girl is reported. Postoperatively, the patient was mute without disturbance of consciousness, language comprehension, or lower cranial nerve function. Computed tomography scans demonstrated no abnormal findings except for the surgical lesion in the posterior fossa. The mutism lasted for 78 days, followed by a period of dysarthria, but she gradually became fluent. The mechanism of "cerebellar mutism" is briefly discussed.
The binding of chromosomal protein HMG1 to a palindromic sequence that can form the cruciform structure in supercoiled DNA and the subsequent effect on the transcription of the sequence were examined with pBR322 and its derivative plasmids. The plasmid DNA under negative supercoiling showed a selective sensitivity to nuclease S1. HMG1 protected against the nuclease S1 digestion. The results of the filter binding assay indicated that the primary binding target of HMG1 is the single-stranded region within the cruciform in supercoiled DNA. In the transcription from pBR322 DNA in the absence of HMG1, intermediate transcripts of RNA-I, which are encoded from a DNA region containing the palindromic sequence that can form a cruciform, were accumulated with the increase in negative superhelical density whereas the full-length RNA-I was synthesized without an accumulation of intermediate transcripts in the presence of HMG1. The intermediates that accumulated in the absence of HMG1 were elongated to the final product by adding HMG1. These results suggest that the cruciform structure formed under negative supercoiling blocks transcription and that HMG1 can remove the block by altering the DNA conformation to allow the stalled RNA polymerase at the block to resume transcription.
The authors report a case of repeated brain metastases from hepatocellular carcinoma (HCC) in a 70-year-old male, who had underwent liver segmentectomy for HCC 5 years earlier. He developed intracerebral hemorrhage in the right parietal region, which was considered to be intratumoral because the metastatic tumor was detected in the same region. Total removal of the tumor and hepatic artery embolization followed by ethanol injection for recurrent HCC were performed. One month later, a metastatic tumor was discovered in the upper vermis and was totally removed. Both metastatic brain tumors were histologically verified as Edmondson grade 2 HCC. Four months later, multiple metastases to the left frontal region and the upper vermis occurred, and he died of pneumonia. Brain metastasis from HCC is rare; nine such cases have been reported in the literature, of which eight cases developed intracranial hemorrhage as in the present case.
A 58-year-old female was admitted to our hospital with nausea, vomiting, and gait disturbance of 1 year duration. Postcontrast computed tomographic scans demonstrated enhanced lesions in the left cerebellopontine angle (CPA), the retrosellar region, the right parasellar region, and the left parietooccipital convexity. The left parieto-occipital tumor was totally removed in the first operation and the left CPA tumor was partially removed in the second. The histological diagnosis of both tumors was xanthogranuloma. She also had cutaneous lesions (subcutaneous nodules without tenderness) and an ureteral stenosis possibly due to the retroperitoneal involvement. A skin biopsy demonstrated infiltration of xanthoma cells and foamy cells in the dermis. A gallium scintigram demonstrated an abnormal uptake in the thoracic cavity, liver, and bones. From these findings, systemic Weber-Christian disease was diagnosed. Another unique aspect was that the serum IgE levels were increased during postoperative hospitalization. This suggests that abnormal immunological conditions are related to this disease and that intracranial xanthogranulomas are a manifestation of systemic Weber-Christian disease.
The binding of DNA binding protein HMG1 to palindromic sequences that can form the cruciform structure in supercoiled DNA and the subsequent effects on the transcription of the sequence were examined. The results show that the cruciform structure formed under negative supercoiling is a block to transcription and that HMG1, which bound selectively to single-stranded region within the cruciform, can remove the block by altering DNA conformation to allow the stalled RNA polymerase at the block to resume transcription.
Explore the source record for details and available documents.
It seems generally accepted that meningiomas are benign tumors, and that malignant meningiomas are not common. The pathological criteria for judging whether meningiomas are malignant or not are controversial. Hemangiopericytic type, high cellularity, brain invasion, high mitotic rate, necrotic foci, and papillary type are regarded as histological characteristics of malignant meningiomas. Of a series of 105 patients with surgically treated meningioma, 25 patients demonstrated malignant characteristics (24%). The overall recurrence rate in our patients was 14%. The incidence of recurrence in 25 patients with pathologically malignant characteristics, and recurrence in 80 patients with pathologically benign characteristics were 32% and 9%, respectively. In comparison with benign meningiomas, recurrent factors in malignant ones included Simpson grade II operation, attachment of skull base, and no radiation-therapy. In conclusion, our criteria for malignant meningiomas have proved to be acceptable, and these cases should be treated with radiation therapy after surgery.
The effect of nonhistone protein HMG1 and HMG2 from pig thymus on the in vitro nucleosome assembly has been examined with plasmid pSV2-gpt DNA and pig thymus core histones in the presence of DNA topoisomerase I. In the absence of core histones, the direct binding of HMG proteins could induce negative superhelical turns in DNA at low ionic strength, but not at physiological ionic strength. The nucleosome formation in the higher histone-to-DNA ratios at physiological ionic strength was not facilitated by HMG proteins, in contrast to poly(L-glutamic acid). HMG proteins suppressed the nucleosome assembly in the moderate histone-to-DNA ratios, resulting in the reduction of fully supercoiled DNA topoisomers. The suppression by HMG proteins was not cancelled by poly(L-glutamic acid). These suggest that the highly acidic carboxy terminal of HMG proteins does not act as an assembly factor, and that the HMG proteins, on the contrary, suppress the nucleosome formation, probably by binding to DNA in a way to inhibit the assembly into core particles.
A case of malignant glioma, localized superficially in the cerebrum and composed of heavily lipidized tumor cells, is described. Microscopically, the lipid-laden tumor cells were GFAP-positive and exhibited marked cellular and nuclear pleomorphism. In the present case the tumor was superficially located in the cerebral hemisphere, as opposed to the usual deep localization described by Kepes and Rubinstein, and others.
We present 6 cases with dissecting aneurysm of the intracranial vertebral artery who developed subarachnoid haemorrhage (SAH). The following procedures were performed in this series; trapping of the involved artery in 2, proximal occlusion of the vertebral artery with detachable balloon in 2, and proximal clipping of the vertebral artery in 2. Proximal occlusion of the vertebral artery in 4 and trapping of the vertebral artery in one gave excellent results. We believe the treatment of choice is proximal occlusion of the vertebral artery, either by open surgery or by interventional neuroradiological procedures.
A 12-year-old girl with transverse myelopathy, massive pleural effusion and ascites as the presenting features of systemic lupus erythematosus (SLE), is described. All these features developed within a week, but other manifestations of SLE such as malar rash and arthritis were not seen during the illness. Investigations revealed positive direct Coombs' test, high titer of antinuclear antibodies, elevation of serum anti-DNA antibodies, depressed complement activity, thrombocytopenia and proteinuria, indicating that she had SLE. A week after starting treatment with prednisolone 35 mg/day, the thrombocytopenia improved, and following an increase in dosage to 60 mg/day the pleural effusion and ascites diminished after two weeks, and the serological abnormalities improved after two months. The neurological disturbances were unchanged in spite of injections of methylprednisolone 1 g/day for three days from the 89th day of her illness. Review of other cases reported to be improved neurologically, suggested that the earlier initiation of corticosteroids in higher dosage might be beneficial in transverse myelopathy in SLE.
We studied the effects of acetylcholine and calcium ionophore A23187 on human basilar artery rings. Among 11 arteries, both agents produced significant relaxations in five, A23187 but not acetylcholine caused a response in six, and neither agent was effective in four. After rubbing off the endothelium, the relaxations induced by both agents were significantly attenuated. Indomethacin (a cyclooxygenase inhibitor) and AA861 (a specific inhibitor of 5-lipoxygenase) did not but SKF525A (an inhibitor of cytochrome P450-dependent monooxygenase) did significantly inhibit the acetylcholine-induced relaxation in human basilar arteries. On the other hand, AA861 inhibited while neither indomethacin nor SKF525A had any effect on the A23187-induced relaxation. Our results suggest that different mechanisms may be involved in acetylcholine and A23187-induced relaxations in human basilar arteries.
Multi-level cervical spondylosis and ossification of the posterior longitudinal ligament (OPLL) are well-documented causes of myelopathy. The choice of surgical procedures remain controversial. Between January 1983 and December 1987, we have performed anterior cervical vertebrectomy in 45 patients with cervical myelopathy caused by multi-level spondylosis and OPLL. They consisted of 19 patients with cervical spondylosis, 12 with OPLL, and 14 with combined lesions of both cervical spondylosis and OPLL. There were 32 men and 13 women. The mean age was 55 years, ranging from 35 to 70 years. In all of our 45 patients, anterior vertebrectomy, discectomy, removal of posterior osteophytes and OPLL, and interbody fusion were done for progressive myelopathy refractory to conservative treatment. In 2 of 45 patients, 5 vertebral bodies were resected; in 3 patients, 4 vertebral bodies were resected; in 12 patients, 3 vertebral bodies were resected, in 19 patients, 2 vertebral bodies were resected; and in 9 patients, 1 vertebral body was resected. Thirty-nine of 45 patients (87%) had good results. Neurological signs did not improve in 5 patients (11%). One patient died because of agranulocytosis secondary to treatment with antibiotics. In conclusion, cervical cord compression caused by lesions located principally in the anterior aspect of the spinal canal may be completely relieved via anterior vertebrectomy, discectomy, removal of the calcified ligament, and fusion.
We present an unusual case of a spinal dural arteriovenous malformation (AVM) which produced compression radiculopathy of the left S1 nerve root. The nerve root was compressed by epidural vessels, draining vessels, and the nidus, without the characteristic myelographic findings of a dural AVM. No feeding vessels could be identified. It is important to consider the possibility of a spinal dural AVM in middle-aged patients who suffer lumbosacral radiculopathy, even if myelography does not demonstrate the characteristic findings.
The effect of hypercholesterolemia on vascular responsiveness was studied in isolated rabbit arteries. The arteries of animals maintained on a cholesterol-rich (1%) diet for 6 months had more pronounced intimal lesion than those receiving the diet for 3 months. The aortas were more severely damaged than the carotid or basilar arteries. Segments of the arteries were mounted in organ chambers for isometric tension recording or for measurement of the endothelium-derived relaxing factor. Endothelium-independent relaxation induced by glyceryl trinitrate was not affected even in the most severely damaged arteries; endothelium-dependent relaxation in response to acetylcholine (ACh) and A23187 was progressively inhibited as the degree of fatty streak formation increased. In the carotid arteries, mean (+/- standard deviation) relaxation induced by 10(-5) M of ACh (expressed as a percentage of the maximum relaxation induced by 10(-4) M of papaverine) decreased from 87.33% +/- 6.30% in control tissues to 60.90% +/- 4.64% in vessels from animals subjected to 6 months of hypercholesterolemia (p less than 0.01); in the aortas, mean relaxation due to 10(-5) M of ACh was 85.08% +/- 8.03% in control tissues and 41.35% +/- 13.68% in hypercholesterolemic tissues (p less than 0.01). In the carotid arteries, mean relaxation induced by 10(-7) M of A23187 decreased from 95.81% +/- 3.58% in control tissues to 55.95% +/- 2.81% in hypercholesterolemic tissues (p less than 0.01); in the aortas, relaxation in response to 10(-7) M of A23187 was 73.73% +/- 4.35% in control tissues and 29.35% +/- 6.77% in hypercholesterolemic tissues (p less than 0.01). Intimal lesions were not produced in the basilar arteries even in rabbits with 12 months of hypercholesterolemia, and endothelium-dependent relaxation was preserved.
A 58-year-old female suffered frequent attacks of unconsciousness due to vertebrobasilar insufficiency. She had a slight left hemiparesis, dysarthria, gait disturbance, and decreased vibration sense. Angiography revealed remarkable stenoses of the bilateral vertebral artery origin with inadequate collateral flow from the anterior circulation. Percutaneous transluminal angioplasty (PTA) was performed on the more severely narrowed left vertebral artery through transfemoral approach. This was followed by PTA on the right one through transbrachial approach after an interval of 3 weeks. The procedure cleared off the signs and symptoms; neuroradiological studies including angiography and Xe-CT scan confirmed the improvement. PTA has been performed on stenotic lesions at the origin of the vertebral artery and the common carotid artery with more safety than on stenotic lesions of the other cerebral arteries, because of the smooth luminal non-ulcerated lesions of the former. In spite of the possibility of restenosis after PTA, in selected cases, PTA leads to good results, less complications and shorter stay in hospital. These factors are of major benefit to the patients. In the future, PTA may be an alternative method for treating arterial stenotic lesions in the field of neurosurgery.
It has been reported that endothelium-derived relaxing factor (EDRF) possesses chemical and pharmacological properties that are indistinguishable from those of nitric oxide (NO). Moreover, NO is the active chemical species responsible for endothelium-independent vasodilation produced by nitrogen oxide-containing substances including glyceryl trinitrate (GTN). Both EDRF and GTN activate soluble guanylate cyclase and consequently increase cyclic GMP level in various artery preparations. However, there have been few reports regarding cyclic GMP accumulation induced by EDRF or GTN in canine cerebral arteries. Therefore, it was investigated whether EDRF and GTN cause vasodilation through the common pathway mediated by cyclic GMP in the canine basilar artery. The relaxation responses induced by EDRF or GTN were studied in the canine basilar artery by an isometric tension-recording method. EDRF was induced by calcium ionophore A 23187. A 23187 did not relax the vascular tissue in the absence of the endothelial cells. On the other hand, GTN did induce relaxation in either the presence or absence of endothelial cells. FeSO4 at 3 X 10(-5) M reversed A23187-induced relaxation, but not GTN-induced relaxation (N = 10). Since Fe2+ is able to catalyse the formation of O2- in oxygenated phosphate buffer, these findings suggest that Fe2+ antagonizes EDRF by inactivating it via the generation of O2-. By the addition of 10(-5) M methylene blue, both A 23187- and GTN-induced relaxations were reversed (N = 8). Moreover, pretreatment with 10(-5) M methylene blue augmented contractile responses to 3 X 10(-6) M prostaglandin F2 alpha (N = 5).(ABSTRACT TRUNCATED AT 250 WORDS)