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Biomedical subjects

H Mogami

Publications and source records attributed to H Mogami.

At least 199 records · Page 11Linked to original sources
PubMed1985

Immunohistochemical study of metastatic brain tumors with astroprotein (GFAP), a glia-specific protein. Tissue architecture and the origin of blood vessels.

Tissues from 12 metastatic tumors of the brain were studied immunohistochemically with an antiserum to a glia-specific protein, astroprotein (glial fibrillary acidic protein, GFAP). Emphasis was laid on demonstrating the tissue architecture of metastatic lesions incorporating brain-derived components (astrocytes and glial fibers). Of 12 samples, 11 manifested a number of irregular indentations at the tumor surface. These indentations, which contained astrocytic elements, extended into the tumor tissue in a tapering fashion. In seven cases, the deeper stromal portions of the tumor also contained astroprotein (GFAP)-positive elements. The presence of this glia-specific protein suggests that the stroma of the tumor tissue may in part be derived from preexisting brain tissue. This peculiar tissue architecture of the tumor supports the hypothesis that some of the blood vessels that are located in the stroma of the tumor tissue are also derived from the brain. These observations may be important in understanding the partial preservation of the blood-brain barrier in metastatic brain tumors and the mode of growth of the metastatic lesion, and in selecting the type of chemotherapy that will be most effective in controlling this central nervous system complication of systemic malignancies.

Astrocytes↗
PubMed1985

Circulatory disturbance of the spinal cord with epidural neoplasm in rats.

An experimental model of spinal epidural neoplasm was produced in rats by injecting Walker 256 carcinoma cell suspension anterior to the T12-13 vertebral body. With this model, spinal cord blood flow (SCBF) and its response to CO2 inhalation were estimated by the carbon-14-antipyrine autoradiography and the hydrogen clearance methods. In the early stages after tumor implantation, weakness, axonal swelling, and edema of the white matter were observed, while both SCBF and its response to CO2 inhalation remained normal. In the next stage, the tumor invaded the spinal canal and compressed the spinal cord epidurally. The edema of the white matter progressed, while the gray matter was morphologically intact. The SCBF and its response to CO2 inhalation were altered at both the compression area and caudally in the spinal cord. Changes in response to CO2 inhalation appeared earlier than the SCBF decrease. In the last stage, the SCBF decreased rapidly to the critical level, producing irreversible nervous tissue damage. Microangiographic studies revealed extensive obliteration of the spinal epidural venous plexus and patency of the larger nutritional vessels. From the data obtained, the progressive vascular pathophysiology related to spinal epidural neoplasm is as follows: 1) the vertebral venous plexus is compressed and obliterated in the early stages of the disease, and vasogenic edema appears in the spinal cord; 2) as the tumor grows, mechanical compression of the spinal cord is added and the circulatory disturbance increases; and 3) in the last stage, SCBF decreases rapidly to a critical flow level, and the loss of cord function becomes irreversible.

Angiography↗
PubMed1985

Immunohistochemical investigation of cerebral ischemia during recirculation.

Immunohistochemical methods for the determination of tubulin, creatine kinase BB-isoenzyme, and astroprotein-glial fibrillary acidic protein were used to investigate recovery of the ischemic lesion after temporary occlusion of a common carotid artery in the gerbil and the evolution of the postischemic lesion following reperfusion. One group of gerbils was followed from 15 minutes to one month after an ischemic period of 30 minutes, and another group was examined after 7 days following an ischemic period of 5 to 30 minutes. It was found that the postischemic lesion, visualized as loss of the immunohistochemical reaction for tubulin and creatine kinase BB-isoenzyme, evolved within 60 minutes after reperfusion in the hippocampus and cerebral cortex and within 3 hours in the caudoputamen and thalamus. Resolution of the preexisting ischemic lesion was possible only after an ischemic period of less than 10 minutes in the cerebral cortex and caudoputamen and less than 15 minutes in the thalamus. In the CA1-CA2 region of the hippocampus, the ischemic lesion already existed after an ischemic period of 5 minutes and was mostly irreversible. The immunohistochemical method of testing for different cellular and subcellular components was very useful for investigation of cerebral ischemia and may also be advantageous for investigation of other pathophysiological conditions of the nervous system.

Animals↗
PubMed1985

[Extremely low-birth-weight infant with post-hemorrhagic hydrocephalus: surgical procedure and recognition by sonography].

In two infants admitted to the neonatal intensive care unit with birth-weight of less than 1,000 g, serial cranial real-time sonograms were obtained to determine the subependymal germinal matrix hemorrhage and follow up the post-hemorrhagic hydrocephalus, compared with computerized tomographic scan. This paper reports the results of the placement of a subcutaneous ventricular reservoir in these extremely low-birth-weight infants to resolve progressive post-hemorrhagic hydrocephalus and protect their cortical mantle until their risks of ventriculo-peritoneal shunting procedure are acceptable. In these infants, the hydrocephalus and increased intracranial pressure were controlled and following shunting procedure after their medical and anesthetic problems resolved.

Cerebral Hemorrhage↗
PubMed1985

[Bilateral, symmetrical hemorrhagic infarction of the basal ganglia and thalamus following neonatal asphyxia].

With the advancement of perinatal intensive care, the occurrence of subependymal germinal matrix hemorrhage (= GMH) in low-birth-weight (premature) infants has became a major concern in perinatal medicine. The pathophysiology of the GMH has long been controversial. The introduction of computed tomographic (= CT) scanning to perinatal medicine has revealed various pathological events heretofore unknown in newborn infants having respiratory and circulatory distress. At our serving the entire Osaka Prefecture, infants suffering from birth asphyxia with severe perinatal brain damage were found to have CT findings distinguishable from those of GMH. We report three asphyxiated newborn infant who had hemorrhagic infarction in bilateral caudate nucleus, striatum and thalamus on the CT scan. Reports of similar findings are rare, and ours is the first serial observation of such CT scan image in newborn infants. The mechanism of development and pathology of this pathological condition have been variously argued as pathophysiology of GMH. The present study lacks postmortem examination, however, the findings in serial CT scans in three infants and review of the literatures related to the pathology of neonatal asphyxia indicate the following course. The thrombosis in the internal cerebral veins led to severe swelling of the brain, and hemorrhage occurred with the reduction in the swelling, eventually resulting in diffuse leukomalacia. Etat marbré (status marmoratus), mentioned earlier, is considered to represent a milder stage of this pathologic course.(ABSTRACT TRUNCATED AT 250 WORDS)

Asphyxia Neonatorum↗
PubMed1985

[Nasopharyngeal paraganglioma extending to the middle cranial fossa].

A case report of a 15-year-old boy with a nasopharyngeal paraganglioma extended to middle cranial fossa is presented. We are reporting the fifteenth patient with a primary nasopharyngeal paraganglioma and reviewing the pertinent literature. The unusual initial presentation of oculomotor palsy and response to radiotherapy is described. The possible origin and radiosensitivity of this tumor discussed. Although the choice of therapy for this tumor remain controversial, the preferred treatment has been radiotherapy, in conjunction with surgical procedures for the mass of middle cranial fossa.

Adolescent↗
PubMed1985

[A case of multiple cerebral aneurysms caused by cardiac myxoma].

A case of neoplastic aneurysm caused by left atrial myxoma is reported. The patient was a 50-year-old woman who has been suffered from occasional vertigo and syncopal attack. She was admitted with a sudden loss of consciousness and cerebellar ataxia on December 1, 1983. Cerebral angiogram revealed multiple aneurysms in the periphery of both middle cerebral arteries and obstruction of the right superior cerebellar artery. Echocardiography displayed a cardiac myxoma in the left atrium. She suddenly died from recurrent cerebral embolism on January 7, 1984. The diagnosis was confirmed by the autopsy. The histopathological examination revealed that the wall of cerebral arteries were destroyed by the tumor cells of myxoma, and it caused cerebral aneurysms. We presented the detail of this case, and discussed about a mechanism and a treatment of neoplastic aneurysms.

Female↗
PubMed1985

[Immunohistochemical study of ethylnitrosourea-induced rat gliomas with vimentin and astroprotein (GFAP)].

Expression of two different types of intermediate filaments, vimentin filaments and glial filaments, was studied immunohistochemically in experimental rat gliomas. Although vimentin filaments are most commonly seen in mesenchymal cells, recent immunocytochemical study demonstrated that this type of filaments can be recognized also in glial cells during early cell differentiation and in tumor cells of epithelial origin. In the present communication, distribution of vimentin filaments in rat glial tumors was investigated and compared with that of glial filaments by using specific antiserum to each protein subunit, vimentin and astroprotein (GFAP). Ethylnitrosourea (50 mg/kg) was injected subcutaneously into 3 day-old Wistar rats. After four to ten months, brains of animals were removed, fixed in 95% ethanol and embedded in paraffin. Peroxidase-antiperoxidase method was carried out on 6 micron-thick sections. In normal portion of the brain, immunoreaction for vimentin was noted in ependymal cells and in vascular endothelial cells but not in astrocytes. This distribution contrasted with that of astroprotein (GFAP), which distributed in astrocytes but not in normal ependymal cells. These findings confirmed that the two antisera used in the present study do not crossreact to each other. In contrast to the absence of vimentin immunoreaction in normal astrocytes, a number of tumor cells showed positive reaction to the antiserum to vimentin. Mixed glioma with astrocytoma and oligodendroglioma had both astroprotein (GFAP)-positive and negative cells. Well developed cellular processes were noted in astroprotein (GFAP)-positive cells (astrocytoma cells). Weak immunoreaction for vimentin was noted in those cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

CT findings in patients with gliomas, surviving more than 10 years.

After reviewing the latest CT scans of 23 mostly low grade glioma patients who survived more than 10 years after treatment, it was suggested that loss of the original tumour bulk and frequently the presence of porencephalic cavity replacing the original tumour, with a smooth lining which is not contrast-enhanced is essential to assume a clinical "cure" in the case of intrinsic cerebral gliomas. In the case of gliomas growing within the ventricle or subarachnoid space, tissue with calcium deposit but without contrast-enhancement was noted, although the number of cases was limited.

Adolescent↗
PubMed1984

Normalization of thyroid stimulating hormone levels in acromegalic patients after selective adenomectomy.

Changes in TSH secretion in six acromegalic patients were studied before and after transsphenoidal adenomectomy (Hardy's method) and compared to normal subjects and six patients with prolactinoma. Basal serum GH levels ranging from 5 to over 250 ng/ml before adenomectomy decreased to below 5 ng/ml after the operation, and the abnormal responses of GH to TRH observed initially in three of the six patients almost disappeared in the post-adenomectomy period. The response of serum TSH to TRH in acromegalic patients improved in each of the six patients after the operation. The TRH-stimulated TSH secretion in patients with prolactinoma of a size and grade similar to those in acromegalic patients was not so extremely low as that in the acromegalic subjects. As indicators of thyroid function, serum triiodothyronine (T3), thyroxine (T4), T3-uptake levels and free T4 indices did not change significantly after adenomectomy as compared with those before the operation in five of the six patients tested. Serum T3, T4 and T3-uptake levels and free T4 indices before adenomectomy were normal or subnormal in each patient except for a high serum T4 level and free T4 index before the operation in only one patient. Thus, it is difficult to conclude that the function of thyrotrophs was decreased by pressure upon the intact pituitary gland by the tumor, or that the thyroid gland also became hypertrophic secondary to the elevated GH, resulting in a large quantity of thyroid hormone being secreted, which caused a suppression of TSH secretion by negative feedback.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗