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K Moritake

Publications and source records attributed to K Moritake.

At least 55 records · Page 3Linked to original sources

[Effects of nilvadipine on membrane potential in cultured neuroblastoma-glioma hybrid NG108-15 cells].

Examination was made of the effects of nilvadipine on membrane potential in cultured neuroblastoma-glioma hybrid NG108-15 cells using the current clamp method. The NG108-15 cells line differentiates into neuronal cells following the addition of 1mM dibutyryl cAMP to the culture medium. This agent (nilvadipine) was found to inhibit both sodium and calcium current on the cell membranes of differentiated NG108-15 cells. The inhibitory effect was reversible in a dose-dependent manner between 10 and 100 microM. A substantial washing-time with normal saline, over 20 minutes, was needed for complete recovery from inhibition. The higher the concentration of nilvadipine, the more suppressive was the action on the membrane potential. A higher dose of nilvadipine, 100 microM, caused the disappearance of the peak membrane potential. This effect appeared irreversible, when cells were incubated in the presence of 100 microM nilvadipine for a longer time. Nilvadipine may thus exert inhibitory effect on the electrophysiological activity of neuronal cells, especially the calcium current of the membrane.

Animals↗

Chemotherapeutic effects of intra-arterial administration of ACNU in primary intracerebral non-Hodgkin's lymphoma.

The authors report five patients with primary intracerebral non-Hodgkin's lymphoma who were treated with several cycles of intra-arterial injection of 1-(4-amino-2-methyl-5-pyrimidinyl)-methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) at doses of 80 to 100 mg/m2/injection at several monthly intervals. There was no simultaneous use of steroids, and no patients had concomitant immunosuppression; no patient was human immunodeficiency virus positive. This therapy was initially used in four patients with advanced recurrent lymphoma. These patients experienced tumor progression despite our institutional standard therapy comprising cranial irradiation followed by repeated courses of systemic multi-agent chemotherapy (cyclophosphamide, vincristine, adriamycin, and prednisolone) more than 3 months previously. Based upon brain computed tomography scans and clinical neurologic examinations, three of the four cases showed partial responses ranging from 10 to 12 months in duration, whereas the other patient remained stable without worsening for 8 months. A fifth case was particularly noteworthy; this patient had no prior therapy and intra-arterial chemotherapy alone induced an 18-month, disease-free remission. No significant therapy-related complications nor neurotoxicity were seen. These results suggest that intra-arterial administration of ACNU may be a potential candidate for intracerebral lymphoma therapy.

Adult↗

Effects of nitro-L-arginine on endothelium-dependent relaxation of canine cerebral arteries.

1. The effect of NG-nitro-L-arginine (NO2Arg) on the relaxation of canine basilar artery was investigated and compared with those of middle cerebral and femoral arteries. 2. NO2Arg (10(-7)-3 x 10(-5) mol/L) inhibited the substance-P (Sub-P; 10(-12)-10(-8) mol/L) induced relaxation in the basilar artery precontracted with prostaglandin F2 alpha (PGF2 alpha; 10(-5) mol/L) or KCl (10(-2) mol/L) in a concentration-dependent manner and a ratio of the maximum inhibition by NO2Arg (3 x 10(-5) mol/L) was more than 90%. 3. The relaxation induced by A23187 (10(-9)-3 x 10(-6) was also abolished by NO2Arg (3 x 10(-5) mol/L), but that by glyceryl trinitrate (GTN; 10(-9)-3 x 10(-5) mol/L) was not, in the basilar artery precontracted with PGF2 alpha (10(-5) mol/L). NG-nitro-D-arginine (NO2ArgD; 3 x 10(-5) mol/L) did not affect the relaxation induced by Sub-P (10(-12)-10(-8) mol/L). 4. L-arginine (L-Arg; 3 x 10(-5)-10(-4) mol/L) did not inhibit Sub-P (10(-12)-10(-8) mol/L) induced relaxation in the basilar artery. Pretreatment of L-Arg (10(-4) mol/L) reversed the relaxation inhibited by NO2Arg (3 x 10(-6) mol/L) in the arteries. 5. NO2Arg (3 x 10(-5) mol/L) inhibited the Sub-P (10(-12)-10(-8) mol/L) induced relaxation in the canine middle cerebral artery as much as in the basilar artery.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Morphological changes of unmyelinated nerves in the cerebral arteries after removal of the pterygopalatine ganglion--an electron microscopic study.

To investigate the participation of the pterygopalatine ganglion in the parasympathetic innervation of the cerebral arteries, Wallerian degeneration was evaluated in the unmyelinated nerves of the major cerebral arteries following the removal of the bilateral pterygopalatine ganglia in dogs. Several days after removal, transmission electron microscopy demonstrated typical features of degeneration in about one-third of the unmyelinated nerves, which are generally considered to be mostly autonomic, i.e., sympathetic and/or parasympathetic. Accordingly, removal of the pterygopalatine ganglion causes Wallerian degeneration of the sympathetic and/or parasympathetic nerves innervating the cerebral arteries. A supplementary study using monoamine fluorescence histochemistry demonstrated that there was no degeneration of the sympathetic nerves innervating the cerebral arteries. Therefore, the degenerated unmyelinated nerves are almost all parasympathetic. These experimental results support the concept that most parasympathetic nerves innervating the cerebral arteries originate in the pterygopalatine ganglion.

Animals↗

Role of histocompatibility antigen gene and protooncogene expressions in intracerebral tumorigenicity of mouse neuroblastoma.

The role of N-myc, c-src, and major histocompatibility complex (MHC, H-2 in the mouse) class I antigen gene expressions in dimethyl sulfoxide (DMSO)-induced differentiation and intracerebral tumorigenicity was examined using a mouse MNB85 neuroblastoma cell line. A fluorescence-activated cell sorter disclosed cell-surface MHC enhancement by DMSO, causing an increase in cytotoxic T-lymphocyte sensitivity. Southern blot analysis verified a single copy of the proto-oncogenes and MHC deoxyribonucleic acids in both untreated and DMSO-treated MNB85 cells. Northern blot analysis indicated that DMSO treatment induced a decrease in N-myc and an increase in c-src and MHC messenger ribonucleic acids. Nuclear run-off transcription assay revealed down-regulation of N-myc at a posttranscriptional level, contrasted with primary up-regulation of c-src at a transcriptional level. Immunoprecipitation after treatment with enzyme endo-beta-N-acetyl-glycoseamidase H proved that the terminal glycosylation of MHC heavy-chain gene products normally occurs in the Golgi apparatus of MNB85 cells. Intracerebral tumorigenicity assay showed that cells highly MHC-expressed by DMSO were less tumorigenic than untreated cells in association with DMSO-augmented cytotoxic T-lymphocyte susceptibility. These results suggest that proto-oncogenes may be linked to cellular differentiation, while cell-surface MHC gene expression influences intracerebral immunosurveillance.

Animals↗

Ossifying cementicular fibroma of the orbitofrontal bone in a child: case report.

A rare case of ossifying cementicular fibroma of the left orbitofrontal bone that developed in a 12-year-old boy is presented. A hard, painless mass that was incidentally noticed gradually enlarged over 2 years. Skull X-rays showed a well-demarcated lesion with mixed sclerotic and osteolytic radiolucent changes in the left orbitofrontal bone. Computed tomography revealed an expansile intradiploic multilocular mass that was separated by bony trabeculae. T1-weighted magnetic resonance imaging demonstrated a multi-cystic iso-intense mass with homogeneous contrast enhancement. Left external carotid angiograms revealed a vague tumor stain that was mainly fed by the middle meningeal artery. Systemic bone scintigrams revealed a single abnormal uptake in the lesion. The skull tumor was totally removed. Histological examination demonstrated two different characteristic findings that were composed of fibrous dysplasia and cementifying fibroma, although most of the tumor appeared to be a highly cementicular form of fibro-osseous lesion. The pathological diagnosis was a cementicular variant of fibrous dysplasia.

Child↗

A case of sellar chordoma mimicking a non-functioning pituitary adenoma with survival of more than 10 years.

A rare case of sellar chordoma occurring in a 67-year-old woman who survived for more than 10 years is presented. Clinical signs and symptoms masqueraded as a non-functioning pituitary adenoma with visual disturbance and hypopituitarism. Initial computed tomography (CT) showed an intrasellar mixed dense mass with suprasellar extension, accompanied by non-homogeneous contrast enhancement. Partial removal of the mass was accomplished via right fronto-temporal craniotomy. Histological examination revealed a typical chordoma with no malignancy. After postoperative irradiation, the patient was discharged with clinical improvement. Serial CT and magnetic resonance imaging 8 years after treatment disclosed a regrowth of the intrasellar lesion, which extended to the sphenoid sinus and clivus, accompanied by non-homogeneous contrast enhancement. The patient underwent subtotal removal of the recurrent tumor through a sublabial transsphenoidal approach. Histological examination confirmed the previous diagnosis. Immunohistochemical study demonstrated positive cytoplasmic expression of vimentin, epithelial membrane antigen, keratin and S-100 protein, in contrast with a lack of appearance of carcinoembryonic antigen. After reoperation, she completely recovered and has survived for more than 10 years with good quality of life.

Adenoma↗

[Empty sella syndrome].

An empty sella is defined as a sella which, regardless of its size, is completely or partly filled with cerebrospinal fluid (CSF). Empty sella is occasionally found as a normal anatomical variation, which is referred to as primary empty sella. On the other hand, empty sella is also seen after surgery, irradiation or medical treatment of pituitary adenoma, which is called secondary empty sella. Magnetic resonance imaging (MRI) is useful in diagnosing empty sella. Primary empty sella is usually free from clinical symptoms but sometimes associated with headache, obesity, visual disturbance, non-traumatic CSF rhinorrhea and pituitary insufficiency. These associated findings constitute the empty sella syndrome. CSF rhinorrhea, visual disturbance and severe increased intracranial pressure are the indications for surgical treatment. Non-symptomatic cases require no treatment but periodical follow up is necessary.

Adenoma↗

[Effect of enalaprilat, an angiotensin converting enzyme inhibitor, on the membrane potential of cultured neuroblastoma-glioma hybrid NG108-15 cells].

The effect of enalaprilat on the membrane potential of cultured neuroblastoma-glioma hybrid NG108-15 cells was investigated using the current clamp method. The NG108-15 cell line characteristically differentiates into neurons after addition of 1 mM dibutyryl cAMP to the culture medium. First it was found that enalaprilat inhibits both sodium and calcium currents in the cell membrane of differentiated NG108-15 cells. At concentrations between 10 and 100 microM, this inhibitory effect was reversible and transient, and occurred in a dose-dependent manner. Prolonged washing with normal saline (> 20 min) was needed to completely reverse the inhibitory effect of enalaprilat. The higher the concentration of enalaprilat, the greater its suppressant action on the membrane potential, and at high concentrations (100 microM), enalaprilat caused the peak membrane potential to disappear. When cells were incubated with enalaprilat, 100 microM, for longer periods, however, this inhibitory effect appeared to become irreversible. These findings suggest that enalaprilat has an inhibitory effect on the electrophysiological activity of neurons especially on membrane calcium currents.

Animals↗

[Effects of interferon-gamma on cytotoxicity of murine activated macrophages against murine glioma cells].

We studied the effects of mouse IFN-gamma on the cytotoxic activity of murine activated macrophages (M phi) against mouse VM-Glioma cells (H-2b). Activated M phi were obtained from peritoneal exudate cells of mice from four strains, C57BL/6 (H-2b), C3H/He(H-2k), DBA/2 (H-2d), and BALB/c (H-2d), following intraperitoneal injection of (1) LPS 200 micrograms, (2) BCG 200 micrograms, (3) C. parvum 200 micrograms, or (4) MDP 350 micrograms 7 days prior to 20-hr 51Cr release-assay. Of the various combination of mouse strains and activating agents tested, that of activated M phi of the C3H/He mouse with induction by LPS had the most tumoricidal effect against the glioma cells, which was not MHC restricted. Although LPS-activated M phi underwent marked loss of cytotoxicity following initiation of in vitro culture, this 24 hr pretreatment with IFN-gamma inhibited this reduction in tumoricidal effects in a dose-dependent fashion. On the other hand, 24 hr pretreatment of target cells with IFN-gamma did not increase their susceptibility to lysis by activated M phi. These findings suggest that IFN-gamma augments the in vitro tumoricidal activation of M phi; This effect appears to be unrelated to any influence of IFN-gamma on target sensitivity to lysis by macrophages.

Animals↗

Clinical analysis of post-traumatic vomiting.

Post-traumatic vomiting was clinically analyzed. One hundred and forty seven patients with head injury came to our hospital consecutively from April 1991 to August 1991. Of 147 patients, 26 exhibited vomiting post-traumatically. The incidence of loss of consciousness, that of fractures on plain X-ray films, and that of traumatic intracranial lesions demonstrated on CT were compared between two patient groups, i.e., a group of patients with post-traumatic vomiting and another one without it. None of them were revealed to be significantly different between the two groups, respectively. It was concluded from the results that the existence of post-traumatic vomiting implied neither severe traumatic impact nor serious intracranial damage. The plausible mechanisms of post-traumatic vomiting are discussed, taking account of the statistical data on the patients' age, sites of impact, and past histories.

Adolescent↗

Primary intracerebral malignant lymphoma associated with different histological types of carcinoma: report of two cases.

Two rare cases with histologically proven multiple primary neoplasms are described: an association of intracerebral malignant lymphoma with hepatocellular carcinoma in one case and with squamous cell carcinoma of the uterine cervix in the other. Therapeutic problems pertinent to the coexistence of primary intracerebral malignant lymphoma and neoplasms of a different histological type are discussed.

Aged↗

A morphological and ultrastructural investigation of normal mouse brain tissue after intracerebral injection of tumor necrosis factor.

Morphological and ultrastructural changes in normal mouse brain tissue were investigated after intracerebral stereotactic injections of tumor necrosis factor (specific activity: 2.0 x 10(6) U/mg protein) into the right frontal lobe. The mice received either a single infusion or multiple tumor necrosis factor infusions in three different dose groups (10, 100, or 500 U). Compared with sham-treated control mice that received adjusted intracerebral injections of purified albumin, the tumor necrosis factor-treated mice in all dose groups did not show any specific in vivo behavioral abnormalities during the 2 months of study following the infusions. Histological studies revealed hemorrhage attributable to the mechanics of the intracerebral infusions, a thickening of the arachnoid membranes, a reactive gliosis, and neutrophilic and/or mononuclear cell infiltration along the infusion pathway. A local neutrophilic response was prominent 1 day after tumor necrosis factor injection. An immunohistochemical analysis indicated that the mononuclear cell infiltration consisted of lymphocytes and macrophages. Except for the transient neutrophilic infiltration, these histological alterations did not differ from those seen in the sham-treated control groups, and most nonspecific reactive changes disappeared within 8 weeks after the injections. Furthermore, an ultrastructural study showed no apparent pathological changes in the cytoplasmic organelles of neuronal, glial, and endothelial cells in the tumor necrosis factor-injected mouse specimens. These results suggest that the tumor necrosis factor injections caused no specific toxicity and did not alter the parenchymal and stromal cells comprising normal mouse brain tissue.

Animals↗