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Biomedical subjects

Y Ushio

Publications and source records attributed to Y Ushio.

At least 217 records · Page 12Linked to original sources

Significance of elevated thrombin-antithrombin III complex and plasmin-alpha 2-plasmin inhibitor complex in the acute stage of nontraumatic subarachnoid hemorrhage.

Thrombin-antithrombin III complex (TAT) and plasmin-alpha 2-plasmin inhibitor complex (PIC) were examined in the acute stage in 51 patients with nontraumatic subarachnoid hemorrhage. TAT and PIC values were correlated with severity at the time of onset and with outcome. In the patients whose TAT levels were 25 ng/ml or more and PIC levels were 3.0 micrograms/ml or more (n = 16), only 25% had a good or fair outcome. In the patients with TAT levels less than 25 ng/ml or PIC levels less than 3.0 micrograms/ml (n = 35), on the other hand, 82.9% had a good or fair outcome. There were no significant differences in TAT and PIC levels between patients who experienced arterial spasm and those who did not. These results indicate that TAT and PIC values may reflect the severity of the brain damage induced by subarachnoid hemorrhage. It is speculated that marked coagulation and fibrinolytic disorders occur in the acute stage of subarachnoid hemorrhage.

Adult↗

Sequential changes in ischemic edema following transient focal cerebral ischemia in rats: magnetic resonance imaging study.

Sequential and regional changes in ischemic edema following various durations of focal cerebral ischemia were studied by magnetic resonance (MR) imaging in a rat unilateral intraluminal middle cerebral artery occlusion model. Occlusion was performed from 5 minutes to 5 hours. T2-weighted images were obtained chronologically 6 hours after onset of ischemia, on day 1 and day 7. An immunohistochemical study using antibodies to calcineurin and glial fibrillary acidic protein was performed to observe histological changes in the ischemic brain. The T2 high-signal-intensity areas representing ischemic edema were observed in the lateral striatum and/or the cerebral cortex by day 1 in all rats with 1- to 5-hour ischemia, and the areas were larger and detected earlier with longer durations of ischemia. In three of six rats with 15-minute ischemia and five of six rats with 30-minute ischemia, the T2 high-signal-intensity areas appeared transiently on day 1 in the dorsolateral striatum where loss of neurons expressing calcineurin immunoreactivity and associated gliosis were found. MR imaging in animal models of reversible focal ischemia can achieve sequential and noninvasive evaluation of dynamic regional changes in ischemic edema.

Animals↗

Occlusion of internal carotid artery and formation of anterior communicating artery aneurysm in cervicocephalic fibromuscular dysplasia--follow-up case report.

A 44-year-old female with cervicocephalic-fibromuscular dysplasia (FMD) suffered a subarachnoid hemorrhage 10 years after presenting with left impaired extraocular movement. Carotid and vertebral angiography had shown string-of-beads sign in the left external carotid artery and fusiform aneurysms in the left carotid cavernous portion and in the left vertebral artery. On admission, the left carotid angiogram showed complete occlusion of the left internal carotid artery and the right carotid angiogram showed a new anterior communicating artery aneurysm. The territory of the left middle cerebral artery was supplied from the right internal carotid artery via the anterior communicating artery and from the basilar artery via the posterior communicating artery. Occlusion of the main arteries is rare in the clinical course of FMD. We suggest that hemodynamic stress due to occlusion of the internal carotid artery contributed to formation of the anterior communicating artery aneurysm, possibly associated with intrinsic changes of the arterial wall induced by FMD.

Arterial Occlusive Diseases↗

Fenestration of the middle cerebral artery associated with an aneurysm--case report.

A 36-year-old female suddenly developed a severe headache. Computed tomography demonstrated subarachnoid hemorrhage in the left Sylvian fissure. Left carotid angiography revealed a fenestration at the distal portion of the M1 portion of the left middle cerebral artery, and an aneurysm arising from the proximal end of the fenestration. These findings were confirmed when the aneurysm neck was clipped. The embryonic origin of this lesion indicates that congenital factors may result in aneurysm formation.

Adult↗

Malignant trigeminal schwannoma associated with xeroderma pigmentosum--case report.

A 46-year-old male with xeroderma pigmentosum developed an intracranial malignant schwannoma originating from the second branch of the left trigeminal nerve. The tumor was subtotally removed and postoperative radiation therapy given, but the tumor recurred twice over 3 years, and extended to the third branch of the left trigeminal nerve and the ipsilateral facial nerve. Radical surgery and radiation therapy finally achieved a cure. This is the first case of malignant trigeminal schwannoma with xeroderma pigmentosum, although various other internal neoplasms including central nervous system tumors have been reported in xeroderma pigmentosum patients. Radical surgery and radiation therapy are effective for treating intracranial malignant schwannoma. Radiation therapy is considered safe for xeroderma pigmentosum patients.

Cranial Nerve Neoplasms↗

Expression and localization of messenger RNA and protein for monocyte chemoattractant protein-1 in human malignant glioma.

Expression of monocyte chemoattractant protein-1 (MCP-1) in human glioma cell lines and surgical specimens was studied by Northern blot analysis, reverse-transcription polymerase chain reaction, in situ hybridization, and immunohistochemistry. The samples tested consisted of 11 human glioma cell lines and eight specimens of human malignant glioma (seven from glioblastomas and one from a malignant ependymoma). Messenger ribonucleic acid (mRNA) of MCP-1 was detected by either Northern blot or reverse-transcription polymerase chain reaction analysis in all cell lines and tumor specimens examined. In vivo expression of MCP-1 mRNA and protein was found predominantly in glioma cells with large and pleomorphic nuclei rather than in areas of small nucleated glioma cells. Adjacent brain tissue did not produce a significant level of MCP-1 mRNA or protein. Tumor vessels with endothelial proliferation expressed a moderate level of MCP-1 protein. Macrophages were found among the glioma cells, and the degree of macrophage infiltration was grossly correlated with the level of MCP-1 expression. The study results suggest that MCP-1 produced by the glioma cells may mediate macrophage infiltration into the glioma tissue.

Aged↗

Visibility of epidermoid tumors on steady-state free precession images.

PURPOSE: To determine whether steady-state free precession sequences improve the MR visibility of epidermoid tumors in comparison with spin-echo images. METHODS: Patients were four women and three men with epidermoid tumors in the subarachnoid spaces. MR was performed with a 1.5-T superconductive unit. For steady-state free precession imaging, three-dimensional Fourier transform fast imaging with steady-state free precession (FISP) images were used (20-40/7 [repetition time/echo time], flip angle of 25 degrees). The visualization and contrast-to-noise ratio were compared in FISP images and spin-echo images. In one case, the images of FISP and fast low-angle shot were obtained with variable repetition times and flip angles to evaluate the best pulse sequences for the visualization of epidermoid tumors. RESULTS: The contrast-to-noise ratios between tumors and cerebrospinal fluid ranged from 7.9 to 17.5 (average was 12.9) on FISP images. The average of contrast-to-noise ratios on T1, T2, and proton density-weighted spin-echo images were 1.6, 2.0, and 4.2, respectively. Three-dimensional Fourier transform FISP images best showed central nervous system and demonstrated epidermoid tumors excellently. CONCLUSIONS: Epidermoid tumors in the subarachnoid spaces were better demonstrated on steady-state free precession (three-dimensional Fourier transform FISP) than on conventional spin-echo images.

Aged↗

Tumor-derived monocyte chemoattractant protein-1 induces intratumoral infiltration of monocyte-derived macrophage subpopulation in transplanted rat tumors.

By immunohistochemistry using anti-rat macrophage monoclonal antibodies RM-1, ED1, ED2, ED3, TRPM-3, and Ki-M2R, we studied transplanted rat tumors of 9L (rat gliosarcoma), Ad-2 (rat mammary carcinoma), and MT-P (rat malignant fibrous histiocytoma) cell lines to examine the distribution pattern of macrophages within and around the tumors. Most tumor-associated macrophages expressed RM-1, ED1, and Ia antigens, indicating activated macrophages. Based on differences in their immunophenotypical expression, these macrophages were distinguished into two major subpopulations. One expressed TRPM-3 and/or ED3, and the other was positive for ED2 and Ki-M2R. The former was considered to be monocyte-derived macrophages, whereas the latter showed the immunophenotype of tissue-fixed, resident macrophages. Infiltration and distribution patterns in the two macrophage subpopulations differed in the three different tumors. Monocyte-derived, activated macrophages infiltrated into 9L- and Ad-2-transplanted tumors, which markedly produced monocyte chemoattractant protein-1 (MCP-1). Additionally, numerous ED2- and Ki-M2R-positive macrophages were observed within the Ad-2-transplanted tumors, and some of them expressed TRPM-3. However, there were few macrophages in the MT-P-transplanted tumors that showed no MCP-1 production. In transplanted tumors of four MT-P/MCP-1 cell lines established by transfecting a rat MCP-1 gene expression vector (pCEP4/MCP-1) into the MT-P cell line, different levels of MCP-1 production were detected, which correlated well with the numbers of intratumorally infiltrated TRPM-3-positive macrophages. In contrast, ED2- and Ki-M2R-positive macrophages were not detected in any MT-P/MCP-1-transplanted tumors. MT-P/MCP-1-transplanted tumors exhibited lower growth rate than parental MT-P-transplanted tumors. These results indicate that tumor-derived MCP-1 induces intratumoral infiltration of monocyte-derived macrophages, but not macrophages with the immunophenotype of tissue-fixed, resident type. The former population of macrophages seems to have a suppressive effect on the growth of tumors.

Animals↗

[Chemotherapy of brain tumors].

Despite recent attempts to improve chemotherapeutic approaches for the treatment of malignant gliomas, results remain limited and palliative. The development of effective chemotherapy for tumors of the central nervous system (CNS) is complicated in that the blood-brain barrier (B.B.B.) hampers the penetration of most drugs into the brain and cerebrospinal fluid. The factors governing delivery in the brain are the drug's molecular weight, lipophilicity and degree of ionization. Now the standard therapy for malignant glioma is maximal tumor resection followed by combination radiotherapy plus chemotherapy. Nitrosoureas are representative drugs which easily cross the B.B.B.. It has been shown that nitrosourea compounds have an additive effect to radiotherapy. The toxicity profile of nitrosoureas is leukocytopenia and thrombocytopenia as a dose-limiting factor. Furthermore, the great heterogeneity of malignant glioma tissues offered a rationale for the use of multiple drugs. Many studies were reported to show a substantial advantage for the multidrug regimen over control series utilizing single drugs alone. Despite clear examples of the effectiveness of chemotherapy, we are still far from improving the cure rate for the vast majority of patients with primary malignancies of the CNS. Further improvement in patient survival may depend upon understanding and manipulating the pathways that regulate aberrant growth in these tumors. The development of new anticancer agents, which are sensitive to malignant glioma and can reach a high concentration in glioma tissue, is warranted.

Blood-Brain Barrier↗

[Upper cervical discitis: case report].

A 48-year-old man complained of severe neck pain. T1-weighted magnetic resonance imaging (MRI) after intravenous injection of Gadolinium disclosed homogeneously enhanced masses in the retropharyngeal soft tissue, in the inter-vertebral disc space between C3 and C4, and in the spinal epidural space behind the vertebral body. The symptoms of the patient improved smoothly after intravenous injection of antibiotics without surgical procedure. In this case, MRI was very important and useful in the prompt diagnosis of the disease.

Anti-Bacterial Agents↗

[Occlusion of the cervical internal carotid artery due to a dog bite wound: case report].

A rare case of traumatic occlusion of the carotid artery at the neck caused by a dog bite is reported. A 10-year-old boy presented delayed onset of left hemiparesis after a dog-bite wound in the right neck. CT scan revealed a cerebral infarction in the right basal ganglia, and IV-DSA disclosed complete occlusion of the right internal carotid artery at the neck. The patient was treated conservatively and his left hemiparesis improved, but impaired visual acuity remained on the right side. Repeated IV-DSA 12 days later showed recanalization of the right internal carotid artery. The mechanisms of the traumatic occlusion of the internal carotid artery were discussed with reference to the literature.

Angiography, Digital Subtraction↗

[Neurocutaneous melanosis--a case report].

Neurocutaneous melanosis is a rare congenital phacomatosis characterized by the presence of large or multiple congenital melanocytic nevi and benign or malignant pigmented cell tumors of the leptomeninges. A 14-month-old boy was admitted with a recent history of vomiting and drowsiness. He was found to have multiple congenital melanocytic nevi. Gd-enhanced MRI showed ventriculomegaly and leptomeningeal enhancement in the ambient cistern. CSF cytology revealed abnormal cells with pigmented granules. A diagnosis of hydrocephalus with malignant neurocutaneous melanosis was made. The patient was treated with combination chemotherapy (DAV therapy, ACNU intrathecal perfusion therapy, interferon beta therapy) while controlling intracranial pressure by CSF drainage, but in spite of treatment he died due to rapid progression of leptomeningeal infiltration. Postmortem examination revealed meningeal malignant melanomas predominantly at the base of the brain and benign meningeal melanosis over the cerebral cortex. Newborn infants or infants with large or multiple congenital melanocytic nevi should be carefully followed, especially for the first two years. When hydrocephalus or convulsions occur in patients with skin lesions, Cd-enhanced-MRI and careful CSF cytology studies should be performed to detect meningeal abnormalities.

Humans↗

[Mixed angioma of the brain: report of two cases].

Clinical features of two patients with mixed angiomas are presented. One patient with a cerebral venous angioma with arterial components was successfully treated with radiation therapy; and the other, who had a common draining vein with cerebellar arteriovenous malformation and venous angioma, was treated with surgical removal of the arteriovenous malformation. These two cases suggested that there is a similarity between the pathogenesis of arteriovenous malformation and venous angioma in the brain.

Adult↗

Quantitative study of monocyte chemoattractant protein-1 (MCP-1) in cerebrospinal fluid and cyst fluid from patients with malignant glioma.

BACKGROUND: Monocyte chemoattractant protein-1 (MCP-1) is a 76-amino acid protein that attracts monocytes. In vitro studies have reported high levels of MCP-1 messenger RNA expression, as well as the presence of MCP-1, in malignant glioma cells. PURPOSE: Our purpose was to determine whether an MCP-1 assay could be used in a clinical setting 1) to differentiate malignant from benign gliomas and from nontumor disorders of the central nervous system and 2) to detect subarachnoid dissemination of glioma cells. METHODS: MCP-1 levels in cerebrospinal fluid (CSF) and cyst fluid were measured with a sandwich enzyme-linked immunosorbent assay (ELISA) that we had previously developed. We measured MCP-1 levels in CSF samples from 19 patients with malignant glioma (glioblastoma, 10; anaplastic astrocytoma, six; anaplastic oligodendroglioma, two; and ependymoblastoma, one), nine patients with benign glioma, and seven patients with nontumor disorders of the central nervous system. Cyst fluids from four patients with malignant glioma (anaplastic astrocytoma) were also tested. The correlation between MCP-1 concentration in the CSF and subarachnoid dissemination of malignant glioma cells was also studied. RESULTS: The MCP-1 concentration (mean +/- SE) in CSF samples from patients with malignant glioma (2.3 +/- 0.4 ng/mL) was significantly higher than that from patients with benign glioma (0.6 +/- 0.1 ng/mL) (P < .01) or from patients with no tumor (0.5 +/- 0.1 ng/mL) (P < .01). Furthermore, CSF samples from patients with subarachnoid dissemination of malignant glioma contained significantly higher amounts of MCP-1 than those from patients without dissemination (P < .05). Cyst fluids from four of the patients with malignant glioma contained high concentrations of MCP-1. CONCLUSIONS: These results indicate that MCP-1 is produced by malignant glioma in vivo as well as in vitro and suggest that testing for MCP-1 in CSF may be useful in the clinic to differentiate malignant glioma from benign glioma and to detect subarachnoid dissemination of the tumor cells. IMPLICATIONS: The MCP-1 ELISA in CSF may lead to more accurate diagnosis of malignant glioma and detection of subarachnoid dissemination of tumor cells, facilitating selection of patients with these conditions for appropriate therapy.

Adolescent↗

Neuronal induction of 72-kDa heat shock protein following methamphetamine-induced hyperthermia in the mouse hippocampus.

By means of an immunohistochemical technique, we examined the neuronal induction of 72-kDa heat shock protein (HSP72) in response to methamphetamine-induced hyperthermia in the mouse hippocampus. Strong HSP72 immunoreactivity (ir) was found in the neurons of hippocampus proper, particularly in the CA1/2 and medical CA3 subfields, at 10 h after drug injection. By 18 h, those neurons still revealed HSP72-ir, while neurons of the dentate gyrus also appeared positive for HSP72. At this stage, intense HSP72-ir was first detected in non-neuronal cells, i.e. glial and vascular endothelial cells. At 24 h, no apparent HSP72-ir was found in the hippocampal neurons, while only non-neuronal cells still revealed immunoreactivity for HSP72. In addition, no morphological evidence of cell degeneration or loss was noted in the CA1 sector or other hippocampal regions at 5 days after hyperthermic insult. In conclusion, (1) methamphetamine-induced hyperthermia per se is a stressful stimulant causing neuronal induction of HSP72 in the hippocampus neurons, particularly of CA1/2 and medial CA3 sectors, but does not prove fatal to the cells; (2) there is a cell type-specific difference in response to hyperthermic insult by inducing HSP72 and the timing of the induction response in the hippocampal formation; and (3) the animals that underwent drug-induced hyperthermia may be useful as an experimental model for the study of the protective mechanism of heat shock proteins against subsequent harmful stimuli.

Animals↗

Changes of immunoreactivity for synaptophysin ('protein p38') following a transient cerebral ischemia in the rat striatum.

We assessed the chronological change of the expression of synaptophysin, an integral glycoprotein on the presynaptic vesicles, after a transient cerebral ischemic insult in the rat. The ischemic lesion was consistently localized in the dorsolateral part of the striatum, which was clearly visualized by a depletion of calcineurin immunostaining or increases of immunoreactivities for glial fibrillary acidic protein and tyrosine hydroxylase. Immunoreactivity for synaptophysin was transiently increased in the ischemic lesions from 3 to 7 days after cerebral ischemia. Thereafter, synaptophysin immunostaining in the damaged areas gradually decreased and finally almost disappeared one month after surgery. Because synaptophysin is located in the presynaptic vesicle, and thought to be involved in presynaptic functions such as vesicle-membrane fusion and release of neurotransmitters, present findings suggest that loss of the postsynaptic site after ischemic insult induces a transient increase of the presynaptic functions, followed by a decrease of functional presynaptic activity or trans-synaptic retrograde degeneration of axon terminals.

Animals↗

Cellular colocalization of calcium/calmodulin-dependent protein kinase II and calcineurin in the rat cerebral cortex and hippocampus.

An immunoperoxidase technique was used to locate multifunctional Ca2+/calmodulin-regulated protein phosphatase (calcineurin) and kinase (CaM-kinase II) in the rat cerebral cortex and hippocampus. Immunoreactivities for both enzymes were highly concentrated in the brain regions, where pyramidal-shaped neurons revealed strong immunoreactivities in their perikarya and dendrites. Serial thin section analysis using the polyethylene glycol embedding procedure disclosed that the cellular distribution of calcineurin immunolabelling in the cerebral cortex and hippocampus was similar to that of CaM-kinase II. The present findings suggest that the phosphatase and kinase may interact with each other in such neuronal subsets.

Animals↗