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Biomedical subjects

H Mogami

Publications and source records attributed to H Mogami.

At least 91 records · Page 5Linked to original sources
PubMed1989

[Immunohistochemical study of c-myc oncogene product in human brain tumors].

C-myc oncogene is widely distributed in eukaryotic cells and is supposed to play an important role in the cellular proliferation and differentiation. Enhanced expression of this oncogene is reported in many kind of tumors, which is often associated with increased malignancy. It seems, therefore, important to study the expression of this oncogene in analyzing the cell biologic features of brain tumors. In the present paper we investigated the distribution of this oncogene product in paraffin-embedded tissue of various kind of brain tumors with a monoclonal antibody to synthetic c-myc peptide. The results demonstrated that c-myc product was detectable in most of the astrocytoma lineage. The immunoreaction within the cell nuclei was more intense in grade 3 and grade 4 astrocytomas than in grade 2 tumors. The expression in grade 4 tumors was, however, rather weaker that in grade 3 tumors. In benign, non-glial tumors like meningiomas and neurinomas, the nuclear immunoreaction was usually absent or only weak, although it was enhanced in a case of acoustic and spinal neurinomas associated with von Recklinghausen's disease.

Astrocytoma↗
PubMed1989

[Ischemic axonal injury and its recovery after focal cerebral ischemia].

After focal cerebral infarction by occluding the middle cerebral artery (MCA) of the rat, the neuronal death occurred in the ipsilateral thalamic neurons, because axons of the thalamic neurons were injured by infarction and retrograde degeneration occurred in the thalamic neurons. However, cortical neurons adjacent to the infarction survived despite their axons injured by ischemia. We employed immunohistochemical staining for 200 kilodalton (kD) neurofilament (NF), in order to study those responses of cortical and thalamic neurons against axonal injury caused by focal cerebral infarction. In the sham operated rats the immunoreactivity to the anti-200 kD NF antibody was only detected in the axon but not in the cell bodies and dendrites. At 3 days after MCA occlusion, axonal swelling proximal to the site of ischemic injury was found in the caudoputamen and internal capsule of the ipsilateral side. At 7 days after occlusion, cell bodies and dendrites of the neurons in the ipsilateral cortex and thalamus were strongly stained with anti-NF antibodies. At 2 weeks after occlusion these responses disappeared in the cortex, but lasted in the thalamus. These phenomena are caused by stasis of the slow axonal transport, because the NF is transported by slow axonal transport. In the cortical neurons impairment of slow axonal transport recovered in the early phase after injury, but in the thalamic neurons the impairment prolonged up to 3 weeks after occlusion. The early recovery of axonal transport from ischemia seemed to be essential for survival of neurons after ischemic axonal injury.

Animals↗
PubMed1989

[Antenatal detection of developing nervous system abnormalities and perinatal surgical management].

As the use of prenatal ultrasound sonographic study becomes more popular, it is likely that several fetal anomalies of the central nervous system will be diagnosed in utero more frequently and accurately. Obstetric sonogram correlates well with the results of postnatal CT scanning. Now, with improved diagnosis and support facilities for the newborn, neurosurgical intervention is being requested, as more concern is expressed for such fetus. We have experienced seven cases of fetal disorders of the central nervous system-meningocele, meningoencephalocele, myeloschisis, arachnoid cyst and maximal hydrocephalus. When diagnosed late in gestation (after the 2nd trimester), it may be reasonable to consider early delivery at the time of pulmonary maturity, and extrauterine management to decrease secondary damage to the developing central nervous system. The method of delivering a fetus must be tailored to suit each case. We present our program for the management of fetal hydrocephalus-placement of a subcutaneous low profile Ommaya's reservoir for neonate immediately after birth, and then subsequently conversion to a ventriculoperitoneal shunt three or four weeks later. As advances are made in antenatal diagnostic techniques and appropriate therapy, prognostic data on congenital abnormalities of the central nervous system will increase and become more pertinent.

Arachnoid↗
PubMed1989

[Neurofunctional disturbances as related to cortical ischemia and white matter ischemia].

We evaluated regional cerebral blood flow (rCBF) by means of hydrogen clearance method as well as [14C]-iodoantipyrine autoradiographic method, cortical auditory evoked potentials (AEP), somatosensory evoked potentials (SEP) induced by forelimb (median nerve) stimulation (SEP-F), and SEP induced by hindlimb (tibial nerve) stimulation (SEP-H) in cats after occlusion of the left middle cerebral artery (MCA) under alpha-chloralose anesthesia. According to the degree of ischemia, the experimental animals were divided into two groups. One was the critical ischemia which was defined as permanent total suppression of AEP, and low residual blood flow in the auditory cortex. And the other was the non-critical ischemia which included transient suppression and spontaneous recovery of the cortical sensory evoked potentials, and high residual blood flow (greater than 15 ml/100 g/min). In one cat with transient suppression of three kinds of sensory evoked potentials, the [14C]-iodoantipyrine (IAP) autoradiograph revealed only a limited ischemic area of subcortical white matter. In the critical ischemia group, ischemia of the primary sensory cortex ranged from the mostly affected primary auditory cortex (supplied by the MCA) to the least affected hindlimb projection area within primary somatosensory cortex (supplied by the ACA). The forelimb projection area of the primary somatosensory cortex (supplied by both ACA and MCA) showed a mild or moderate reduction of rCBF after occlusion. The [14C]-IAP autoradiograph showed severe reduction of the white matter including the somatosensory pathway in the wide range. However, rCBF in the thalamus and hindlimb projection area within somatosensory cortex was almost intact in the cat with ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Antitumor efficacy of FK 973 on malignant glioma cells].

FK 973, a new substituted dihydrobenzoxazine, was obtained by chemical modification of a novel antibiotic which was isolated from the fermentation products of streptomyces sandaensis No. 6897. FK 973 had cytotoxic effects against in vitro cultured human and murine glioma cells. The concentration of FK 973 required to inhibit cell growth by 50% was 0.06-5 micrograms/ml, after 2-day exposure of this drug against human glioblastoma (ONS-6, 12, 23, and ONS-12/ACNU), human medulloblastoma (ONS-76, 81), human neuroblastoma (ST), and murine glioblastoma (RSV-M glioma). FK 973 showed antitumor efficacy in the meningeal gliomatosis models by RSV-M glioma cells. The median survival time (MST) of models treated by FK 973 (i.t.) was 30 days. However, the MST of control group was 23 days. In the in vitro neurotoxicity test, FK 973 proved to be slightly more toxic than ACNU and MTX, but it had no crucial problems, compared with ADM.

Animals↗
PubMed1989

[Astrocytic proliferation in the brain adjacent to infarcted lesion: immunohistochemical study of astroprotein (GFAP) and bromodeoxyuridine (BrdU)].

Although cerebral infarction is a destructive process of nerve cells and brain tissue, the nature is not exclusively disintegrating but also includes active cellular reaction which may modify the progression of tissue damage. Most prominent cellular reaction in the area surrounding infarction can be recognized as a trophic or proliferative change of glial cells. In the present study we produced a focal cerebral ischemia in Mongolian gerbils and investigated the dynamic change of astrocytes in the brain adjacent to thalamic infarction. Using immunohistochemical methods, astrocytes were identified with the antibody to astroprotein (GFAP) and the DNA synthesizing (S phase) cells were detected with the antibody to bromodeoxyuridine (BrdU). The posterior communicating artery of a gerbil was occluded by coagulation through the trans-tympanic bulla approach under general anesthesia with ketamine hydrochloride (80 mg/kg, i.p.). Thirty min after intravenous administration of BrdU (200 mg/kg), animals were sacrificed by transcardiac perfusion with 75% ethanol on days 1, 2, 3, 5 and 7 post-infarction. Ethanol-fixed, paraffin-embedded blocks were cut coronally into 6 microns-thick sections at the level of dorsal hippocampus. Double-labeled immunohistochemical technique (avidin biotin peroxidase-complex method) was carried out with each antibody using 3,3'-diaminobenzidine tetrahydrochloride and 4-chloro-1-naphthol as chromogens. The population of GFAP-positive cells and their S-phase fraction (the number of BrdU-positive nuclei divided by the number of GFAP-positive cells expressed in per cent, %) were examined. The data demonstrated that the regional GFAP-positive cells increased continuously between days 1 to 5 (105.9 to 528.8 cells/mm2) postinfarction (44.6 cells/mm2 in normal brain).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[A case of repeated hematomyelia caused by cavernous hemangioma in the spinal cord].

A case is reported of repeated hematomyelia caused by cavernous hemangioma in the spinal cord. A 47-year-old woman first noticed a sudden onset of numbness in her thigh and then it gradually disappeared. Four months after the onset, she began to experience weakness and numbness in both of her legs, and difficulty in voiding and defecating. She recovered gradually for several months, but felt numbness in both legs. Myelography showed swelling at Th5 level. T2-weighted MRI showed a reticulated core of mixed intensity with rims of decreased intensity. During the subsequent operation, a dark brown lesion was detected at Th5 level, which consisted of multicystic cavities with old hematoma. But there were no abnormal vessels, or active bleeding. This lesion was almost completely removed and was diagnosed as cavernous hemangioma.

Female↗
PubMed1989

[Ischemia-induced neurotrophic activity detected in the peri-infarcted brain tissue].

In the experimental ischemia induced by occlusion of the rat middle cerebral artery, axons of both cortical and thalamic neurons were affected. However, cortical neurons survived thereafter and thalamic neurons died because of retrograde degeneration. The fate in these two groups of neurons was remarkably different and may be related to neurotrophic activity induced by ischemia. To detect ischemia-induced neurotrophic activity, fetal cortical neuron was cultured and neurotrophic activity was detected by applying tissue extract to the culture system. Fetal neurons obtained from 17 days rat embryo were cultured for 24 hours at 3.75 x 10(4) cells per 15 mm well in modified Eagle's minimum essential (MEM) supplemented by 10% fetal bovine serum (FBS), then for next 3 to 7 days with Dulbecco's modified Eagle's medium/Ham's nutrient mixture F-12 (DME/F-12) supplemented with insulin 5 mg/l, transferrin 10 mg/l, progesterone 6.3 micrograms/l, Na2SeO3 5.2 micrograms/l. The tissue extract was obtained from the rat subjected to ischemia and homogenized with DME/F-12. The homogenate was centrifuged at 100,000 g for 90 minutes and the supernatant was obtained. Application of peri-ischemic cortical extract improved neurons' survival by 50% as compared to extract of the contralateral side. However, the thalamic extract of the ischemic side had no neurotrophic activity as compared to the contralateral side. The activity was detected in the extract obtained at 8 days after ischemia but not detected in the extract obtained at 4 days after ischemia. The neurotrophic activity was disappeared by heating the extract at 90 degrees C for 10 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

[Extracellular purine catabolites and tissue nucleotides and purine catabolites during progression and recovery of ischemia].

During progression and recovery of ischemia, extracellular purine catabolites were measured and compared with purine catabolites and adenine nucleotide levels in the tissue. Ischemia was induced by bilateral occlusion of the common carotid arteries in gerbil. Extracellular purine catabolites were sampled by in vivo brain microdialysis technique, and tissue adenine nucleotides and purine catabolites were extracted from in situ frozen and lypholized brain tissue. These metabolites were measured with simple method of isoclatic condition by HPLC system. Ischemia depleted tissue ATP and ADP, whereas AMP and purine catabolites accumulated strikingly. In parallel, extracellular purine catabolites increased as consecutive degradation on the biochemical metabolic pathway in the same animal. Levels of tissue ATP and adenosine normalized in the recovery phase of ischemia immediately. However, extracellular purine catabolites during the recovery are much higher than those during the progression of ischemia. These data indicated extracellular high levels of purine catabolites during the ischemic insult, and especially adenosine as neuromodulator which may turn off spontaneous neuronal activity and exert antiepileptic effects during the recovery rather than the progression of ischemia.

Adenine Nucleotides↗
PubMed1988

Transplant-induced recovery from 6-OHDA lesions of the nigrostriatal dopamineneurones in mice.

Attempts to reconstruct the damaged nigrostriatal pathway in experimental models of Parkinson's disease have thus far been carried out in animals with neurotoxically induced dopamine deficiency. Our study established that unilateral 6-hydroxydopamine (6-OHDA) lesions of the nigrostriatal dopamine (DA) neurons produced a well-characterized functional asymmetry in the behaviour of the C57BL/6 (H-2b) mice. The intraperitoneal administration of methamphetamine induced ipsilateral rotation at 7-20 turns/min 1 x 10(6) syngenic DA-rich cells of embryonic ventral mesencephalon were stereotaxically transplanted in the caudate-putamen. A complete recovery of methamphetamine-induced rotational response was produced around the 60th day after the syngenic cell suspension graft. And a complete compensation of the rotational response was also brought about with the DA-rich cells from embryonic ventral mesencephalon (crown-rump length; 10-13 mm) of allogenic C3H/HeN (H-2k) mice. The FACS IV analysis revealed no H-2 (Kk and Iak) antigens before transplantation of these embryonic cells. Immunohistochemistry showed that the dopaminergic fibers had grown predominantly into the ipsilateral caudate-putamen. These results provide evidence of integration of syngenic and allogenic grafts and host tissue. And the immunological response in the transplanted brain are under investigation.

Animals↗
PubMed1988

Intrathecal ACNU--a new therapeutic approach against malignant leptomeningeal tumors.

Pharmacokinetics, toxicity and therapeutic efficacy of intrathecal ACNU, 3-[4-amino-2-methyl-5-pyrimidinyl)methyl)-1-(2-chloroethyl)-1-nitroso urea, were studied in rats to determine if it is a new and effective method for the treatment of malignant leptomeningeal tumors. Pharmacokinetics of intracisternally administered ACNU was studied by macroscopical autoradiography using 14C-labeled ACNU. It was demonstrated that intracisternally administered ACNU distributed in the subarachnoid space and subpial layer of the brain in high concentration and was rapidly eliminated into the systemic circulation. The diffusional transport of ACNU into the deeper part of the brain was limited. More than 3.0 mg/kg of intracisternal ACNU induced progressive loss of the weight of body in normal rats, and 80% of the rat given 6.0 mg/kg died. Increase of capillary permeability, neuronal loss and gliosis were observed in the marginal layer of the brain facing to the subarachnoid space in the rat given more than 3.0 mg/kg of ACNU. Systemic and local toxicity was not observed in the rat given less than 1.5 mg/kg. Therapeutic effect of intrathecal ACNU against leptomeningeal tumors was evaluated in the rat with meningeal carcinomatosis induced by intracisternal inoculation of Walker 256 carcinosarcoma cells. The median survival time of the rat treated with 1.5 mg/kg of intracisternal ACNU once on day 2 or on day 5 after tumor inoculation was significantly prolonged by 173%, and 214% at maximum, respectively, as compared with that of the untreated animal. These findings suggest that intrathecal ACNU may be of value for clinical trial against leptomeningeal tumors.

Animals↗
PubMed1988

Effects of phenytoin on cell-mediated immunity.

The effects of phenytoin on cellular immunity were examined in murine models. Fresh splenocytes were obtained from mice which had received 1 mg/day of phenytoin i.p. for 28 days. The serum concentration of phenytoin in these animals was 10-20 micrograms/ml. The proliferative response of splenocytes to mitogens was assessed by 3H-thymidine incorporation. The cytotoxic activities of cells such as natural killer (NK) cells, cytotoxic T lymphocytes (CTL), and lymphokine-activated killer (LAK) cells were estimated by a 4-h 51Cr release assay. The 3H-thymidine incorporation of splenocytes was reduced significantly (P less than 0.01) in phenytoin-treated mice. The NK and CTL activities of splenocytes from phenytoin-treated mice were significantly suppressed. However, the LAK activity of phenytoin-treated mice was equal to that of control mice.

Animals↗
PubMed1988

An adoptive immunotherapy of patients with medulloblastoma by lymphokine-activated killer cells (LAK).

An adoptive immunotherapy of 6 patients with medulloblastoma by lymphokine-activated killer (LAK) cells is described. They were from 2 to 9 years in age and had cerebrospinal fluid (CSF) dissemination of the tumours. All patients underwent the whole-neuraxis irradiation and chemotherapy. After the usual treatments, they were submitted to an adoptive transfer of one-haplotype identical LAK cells. The LAK cells were induced from peripheral blood lymphocytes (PBL) of their relatives with human recombinant interleukin-2 (rIL-2). 3 - 15 x 10(9) LAK cells were transferred intrathecally in 2-3 months. In 3 of 6 patients, neurological signs were improved and malignant cells had never been detected on CSF cytology after the adoptive immunotherapy. One among these 3 patients showed complete response in 20 months. Thus, this is an attractive approach for the treatment of medulloblastoma with CSF dissemination of the tumour which current therapeutic intervention can not cure.

Cerebellar Neoplasms↗
PubMed1988

Regional differences in inhibition and recovery of protein synthesis after transient hindbrain ischaemia of gerbils.

Regional protein synthesis was estimated autoradiographically in a model of transient hindbrain ischaemia of gerbils. In studies of 5 min ischaemia followed by 5 min recirculation, incorporation of [14C]valine into the TCA-insoluble protein fraction was not affected. In studies of 15 min ischaemia followed by 5 min recirculation, incorporation of the tracer into the protein fraction was severely depressed in the ischaemic lesion of the brain stem and cerebellum. However, the granular layer of the cerebellar cortex had partially preserved protein synthesis. When recirculation time was extended to 2 h after 30 min ischaemia, protein synthesis of the cerebellar cortex almost recovered to the full level of the control. However, in the pontine grey matter, inferior colliculus and vestibular nucleus, a significant reduction in protein synthesis persisted. These results indicate that protein synthesis in the pontine grey matter, inferior colliculus and vestibular nucleus are selectively inhibited by ischaemia. Further its recovery after recirculation is slow. The cerebellar cortex is less vulnerable to ischaemia, and recovery is relatively fast. The regional heterogeneity of protein synthesis is neither due to the degree of ischaemia in this model nor the extent of postischaemic hypoperfusion. Factors that influence protein synthesis in this ischaemic model are discussed.

Animals↗