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H Mogami

Publications and source records attributed to H Mogami.

At least 109 records · Page 6Linked to original sources
PubMed1988

[Malfunction of gene expression as a possible cause of delayed neuronal death].

To clarify a possible cause of delayed neuronal death, synthesis of protein and ribonucleic acid (RNA) following transient forebrain ischemia was evaluated autoradiographically. Mongolian gerbils were subjected to transient forebrain ischemia for 5 minutes by occluding bilateral common carotid arteries. They were used for autoradiographic study at 1, 2, and 5 days after ischemia. Tracer dose of 14C-valine or 14C-uridine was injected intravenously, and animals were sacrificed 45 minutes thereafter. Brains were frozen and thin sliced for macroautoradiography. After the first autoradiogram was obtained, tissue sections were incubated in cold 5% trichloroacetic acid for 1 hour, dried and again used for autoradiogram. With this preparation we could differentiate the tracer incorporated into protein or RNA fraction from the total tissue radioactivity. In the different set of animals, microautoradiograms of 3H-valine and 3H-uridine was obtained to detect subcellular distribution of synthesized protein or RNA. At 1 day after ischemia, protein synthesis in the CA 1 region of the hippocampus was reduced by 57% of the sham control, but RNA synthesis was not reduced quantitatively. Microautoradiogram of 3H-uridine however, indicated that silver grains in the cytoplasms of the CA 1 pyramidal cells were much reduced as compared to sham controls, though the amount of silver grains in the nucleus was the same as sham controls. Therefore, synthesized RNA in the nucleus was not transported to the cytoplasm. At 2 days after ischemia, protein and RNA synthesis was preserved to the same level as sham controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

[Factors affecting the prognosis of brain tumors].

A variety of tumors with different histologic types are included in a group of brain tumors. Although each histologic type of tumor has its own range of malignancy, the prognosis seems to be affected by several clinical, histologic and cell-biological factors. For example, relative survival rate of patients with glioblastoma is lower if the patient is older than 50 or 60 years. The leptomeningeal dissemination of glioma cells is a sign of poor prognosis. The presence of necrotic foci in the astrocytic tumors suggests shorter astrocytic tumors suggests shorter survival. Using a monoclonal antibody to bromodeoxyuridine (BrdU), the growth activity of the tumor can be estimated by BrdU labeling index (BrdU-LI, %). Higher BrdU-LI is correlated with more malignant histologic features in astrocytic tumors. In meningiomas, higher BrdU-LI is correlated with a more frequent or rapid recurrence of the tumor. The significance of growth factor receptors and oncogene of growth factor receptors and oncogene products as a cell-biologic marker of malignancy was investigated with an immunohistochemical method. Transferrin receptor was demonstrated in all tumors, and epidermal growth factor in about 40% of astrocytic tumors. The immunoreaction to c-myc oncogene product was detected in most astrocytic tumors; with higher intensity in anaplastic astrocytomas and glioblastomas than in low-grade astrocytomas. The role of these markers in the prognosis of brain tumors is, however, still unclear. Total or subtotal resection of glioblastoma results in longer resection of glioblastoma results in longer survival. Both postoperative radiotherapy and chemotherapy are effective. However, maintenance of chemotherapy longer than longer than 2 years does not significantly improve the prognosis.

Age Factors↗
PubMed1988

[Postnatal cell proliferation in the rat cerebrum: immunohistochemical study with bromodeoxyuridine (BrdU)].

The postnatal cell proliferation in the rat cerebrum was studied immunohistochemically using a monoclonal antibody to bromodeoxyuridine (BrdU). Since BrdU, a halogenated analogue of thymidine, is incorporated into nuclear DNA during duplication, S-phase cells can be detected by demonstrating intranuclear BrdU. 200 mg/kg of BrdU was administered to normal Wistar rats intraperitoneally on the day of birth or intravenously 1, 2, 3, 5, 8 or 24 weeks after birth. Thirty minutes later, the brain was fixed by perfusion with ethanol, and the paraffin-embedded sections were processed for the avidin biotin peroxidase-complex method. BrdU-positive nuclei were counted among 500 to 10,000 cells in several regions of the brain to obtain the BrdU-labeling index (the number of BrdU-positive cells per 100 cells scored, LI, %). The present study demonstrated that (1) proliferating cells in the gray matter (cerebral cortex and caudate-putamen) are only few at birth (LI = 0.54-0.78%), which further decrease during the following few weeks, and disappear by adulthood, (2) in the white matter (corpus callosum), cell proliferation is relatively active within 1 week after birth (LI = 5.6-6.3%), but becomes inactive thereafter, (3) the proliferative activity of the cells in the subependymal layer of the lateral ventricle is very high at birth (LI = 15.5%), which somewhat decreases during the following few weeks, but still remains high in adulthood (LI = 7.5%). This kind of continued cell proliferation in the brain after birth seems important in the postnatal development of the normal cerebral structure, and in several pathologic processes such as tissue repair and the development of brain neoplasm.

Age Factors↗
PubMed1988

[Effect of ACNU against experimental brain tumor--immunohistochemical study using anti-BrdU monoclonal antibody].

We have studied the efficacy of intrathecal ACNU against experimental leptomeningeal tumors. In the present report, the effect of ACNU on the growth kinetics of the tumor was evaluated by the immunohistochemical technique using anti-BrdU monoclonal antibody. The experimental leptomeningeal tumor was developed by inoculation of Walker 256 carcinosarcoma cells into the cisterna magna of rats. Seven days after the inoculation of tumor cells, the animals were treated either by intravenous (15 mg/kg) or intrathecal (1.5 mg/kg) ACNU. Four, 12, 24, 48, 96 or 144 hours after treatment, the animals received intravenous BrdU (200 mg/kg). Thirty minutes thereafter, they were sacrificed and the brain was removed. L. I. was calculated by counting the immunoreactive tumor cells. L. I. of the tumor without treatment on the seventh day after inoculation was over 40%. L. I. began to decrease 24 hours after intravenous ACNU, and remained 11% up to 96 hours. On the other hand, L. I. already decreased to 20% 4 hours after intrathecal ACNU and remained to be low (17%) up to 48 hours. However, L. I. increased to 38% at 96 hours. Thus, the effect on the growth kinetics of the tumor differs between intravenous and intrathecal ACNU. These results are considered to be useful informations for determining the optimal dosage of the antineoplastic agent against the brain tumor and developing the effective combination chemotherapy.

Animals↗
PubMed1988

[Transplant-induced recovery from 6-OHDA lesions of the nigro-striatal dopamine neurons in mice].

Attempts to reconstruct the damaged nigrostriatal pathway in experimental models of Parkinson 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 behavior of C57BL/6 (H-2b) mice. The intraperitoneal administration of methamphetamine induced ipsilateral rotation at 7-20 turns/min. 11 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 60-th 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 C 3 H/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

[Distribution of epidermal growth factor receptor in glioma].

A monoclonal antibody (Amersham) to epidermal growth factor receptor (EGFR) was used for immunohistochemical study to confirm the presence of EGFR in the glioma tissue. Fresh surgical material was stored at -80 degrees C, and frozen sections were stained. Positive staining was demonstrated in 8 of 9 gliomas. In 2 of 8, more than 50% of tumor cells were positively stained. In 4 of 8, positive cells were seen scattered in the tissue. In the remaining 2 gliomas, few tumor cells were positively stained. The most representative staining was seen on the cytoplasmic membrane. But there were also nuclear and cytoplasmic stainings. The distribution of EGFR in the glioma cells suggests possible role of the epidermal growth factor in the proliferation of gliomas.

Adolescent↗
PubMed1988

[Effect of MX-2, a morpholino anthracycline derivative, against human and rat glioma cells and experimental leptomeningeal tumors in rats].

MX-2, a new morpholino anthracycline derivative, showed broad anti-neoplastic activity against experimental tumors. Molecular weight of MX-2 is 622.07, and it can cross blood-brain barrier because of its high lipid solubility. In this report, we described its in vitro and in vivo effects on brain tumors. The growth of rat 9L and human KNS-42 glioma cells were markedly inhibited by the medium containing more than 1 ng/ml of MX-2. The inhibitory concentration of MX-2 for 50% cell kill was 1.8 ng/ml for 9L cell and 18 ng/ml for KNS-42, respectively. These values were the almost same as those reported with P388 leukemia. In rats with meningeal carcinomatosis induced by intracisternal inoculation of Walker 256 carcinosarcoma cells, the median survival time was significantly prolonged. The increased life span was 40, 40, 40 (p less than 0.01), and 20% (p less than 0.05) in the animals given intravenous MX-2 of 1.5, 1.0, 0.75, and 0.375 mg/kg on day 1, 5, and 9 after tumor inoculation respectively. These results indicate that MX-2 may be a promising new antineoplastic agent for the treatment of malignant brain tumor.

Animals↗
PubMed1988

[Growth activity of meningeal carcinomatosis--immunohistochemical study using anti-BrdU monoclonal antibody].

We have developed an experimental model of leptomeningeal tumor by inoculating Walker 256 carcinosarcoma cells into the cisterna magna of rats. This model was considered to be useful in studying pathophysiology and treatment of malignant brain tumors. In this study, the growth kinetics of this experimental tumor was investigated by using the immunohistochemical technique with an anti-BrdU monoclonal antibody. Walker 256 carcinosarcoma was subcutaneously passaged in female Wistar rats. Seven days after subcutaneous inoculation, the tumor was aseptically removed and minced in Hank's medium by scissors to make single cell suspension of the tumor. The cell suspension was adjusted to 1 x 10(5) cells/ml. And 0.1 ml was inoculated percutaneously into the cisterna magna of female Wistar rats weighing 150 gr. Every day after tumor inoculation, the animal (5 on each day) was sacrificed 30 minutes after intravenous BrdU (200 mg/kg) and perfused by saline. Then, the brain was removed, fixed in ethanol and embedded in paraffin. Coronal sections of the brain 6 mu in thickness were cut and stained by the indirect immunoperoxidase (ABC) method. The anti-BrdU monoclonal antibody (Becton-Dickinson) was diluted in 1:100. The sections were counterstained by hematoxylin. Labelling index (L.I.) of the tumor was obtained by counting immunoreactive cells under the microscope. L.I. of the subcutaneous tumor 7 days after inoculation was 52.4%. In the tumor 1 to 3 days after inoculation, L.I. was still low and between 11.9 and 15.1%. Four or 5 days after inoculation, the tumor cells grew in several layers in the subarachnoid space. L.I. at this stage of the tumor growth was 26.6 to 34.8%.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Distribution of radiolabeled 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitros ourea hydrochloride in rat brain tumor: intraarterial versus intravenous administration.

To assess the rationale of intraarterial (i.a.) 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea chemotherapy, distribution of 14C-labeled 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)- 3-nitrosourea in rat glioma was studied after i.a. or i.v. infusion. Immediately after infusion, the tumor located in the hemisphere of intracarotid infusion received 4.6-fold higher radioactivity than the tumor located contralaterally to intracarotid infusion and 2.8-fold higher radioactivity than i.v. infusion. The difference was kept up to 30 min after i.a. infusion. Autoradiographic observation indicated rather uniform distribution of the tracer in the central portion of i.a. infusion. However, in the periphery of i.a. infusion, distribution of the tracer was nonhomogenous. The results indicate that i.a. 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea chemotherapy is useful when the tumor has high blood flow and is located in the center of an infused area.

Animals↗
PubMed1987

Intermediate filaments and anaplastic change of ENU-induced gliomass: immunohistochemical study with vimentin and astroprotein (GFAP).

To study the expression of two different subclasses of intermediate filaments in ethylnitrosourea-induced rat cerebral gliomas, the number of cells immunopositive for each subunit protein, vimentin and astroprotein (GFAP), was quantitatively analyzed. Vimentin is a subunit protein of non-specific intermediate filaments which appear transiently in immature glial cells, while astroprotein (GFAP) is a subunit protein of glial filaments, normally expressed in mature astrocytes. Although most normal astrocytes were negative for vimentin, many tumor cells showed weak to strong immunoreaction for vimentin. The expression of vimentin was more frequent and intense in anaplastic forms of gliomas than in benign forms. Accordingly, the vimentin/GFAP ratio [the number of vimentin-positive cells divided by the number of astroprotein (GFAP)-positive cells] was increased from 0.23 to 1.86, and from 0.26 to 1.85, respectively, as oligodendrogliomas and mixed gliomas become anaplastic. The present study demonstrated that the immunohistochemical study for those two subclasses of intermediate filaments can provide important informations on the cell biological nature of glial tumors.

Anaplasia↗
PubMed1987

The mechanism and overcoming of resistance in ACNU-resistant sublines of C6 and 9L rat glioma.

In order to study the mechanism of the resistance to chemotherapeutic agents, especially ACNU [1-(4-amino-2-methyl-5-pyrimidinyl) methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride), two variant cell lines (C6/ACNU and 9L/ACNU) resistant to ACNU were selected in vivo from rat C6 and 9L glioma, respectively. Uptake and efflux of ACNU in these resistant cells were studied with Ethylene[14C]ACNU. The result indicated that the resistance exhibited by both sublines were due to both the reduced uptake of the drug and the increased efflux. The study of the effects of oxidative phosphorylation inhibitor, DNP (2,4-dinitrophenol), on the uptake and retention of ACNU suggested that there is an active outward transport mechanism for ACNU in both glioma sublines and that enhanced activity of this efflux mechanism renders cells highly resistant to the cytotoxic action of ACNU. In an attempt to clarify the more detailed biochemical mechanisms of this active efflux system, we surveyed various membrane-modifying agents which potentiate the sensitivity of these resistant cells to ACNU. Among a number of membrane-modifying agents, reserpine was found to retain ACNU in the resistant cells and to enhance the action of ACNU on these resistant cell lines. It may be concluded that drugs such as reserpine may overcome a mechanism of ACNU resistance.

Animals↗