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M Ninomiya

Publications and source records attributed to M Ninomiya.

At least 73 records · Page 4Linked to original sources
PubMed1996

[Clinical characteristics of pulmonary embolism without definitive predisposing factors].

Patients with pulmonary embolism may have no definitive predisposing factors for thrombi. The clinical entity of chronic pulmonary embolism is also uncertain. This study clarified the clinical characteristics of pulmonary embolism without definitive predisposing factors. During the last 10 years, 36 consecutive patients were diagnosed as having pulmonary embolism (mean age 61 years, female 75%). Twenty-four patients (67%) had definitive predisposing factors ("definitive" group). Patients without definitive predisposing factors had the following characteristics. The onset of symptoms was out-hospital and insidious. The main symptom was exertional dyspnea without acute episode compatible with an embolism. In four patients (33%) there was a delay of over 2 years form the onset of symptoms to the diagnosis. Three patients had been treated for depression. Thrombolytic therapy caused an inadequate fall in mean pulmonary artery pressure from 41 +/- 11 to 24 +/- 8 mmHg and in three patients it remained over 30 mmHg. Deep vein thrombosis were found in four of nine patients in whom venography were performed 10 days after thrombolytic therapy, but only one patient showed thrombus in the "definitive" group. During the convalescent stage, all patients were treated with prophylactic warfarin. Home oxygen therapy was indicated in three patients and an inferior vena caval filter was implanted in two patients. One third of patients with pulmonary embolism in our institute had no definitive predisposing factors. In these patients, even with thrombolytic therapy, recovery of pulmonary hypertension was often insufficient and deep vein thrombosis persisted. Clinicians should be aware of this disease to avoid undue delay in its diagnosis.

Aged↗
PubMed1995

kappa-opioid agonist U50488 inhibits P-type Ca2+ channels by two mechanisms.

The effects of U50488, kappa-opioid agonist on P-type Ca2+ channels, were studied. U50488 inhibited depolarization-induced Ca2+ uptake into rat brain synaptosomes, which was sensitive to omega-Agatoxin IVA (omega-AgaIVA; P-type Ca2+ channel blocker) and inhibited P-type Ca2+ channel currents recorded from rat cerebellar Purkinje neurons by the whole-cell patch clamp method. Dynorphin A also inhibited P-type Ca2+ channel currents. The inhibition by U50488 was biphasic; high affinity component (21%, IC50 = 8.9 x 10(-8) M) and low affinity component (79%, IC50 = 1.1 x 10(-5) M). At low concentrations of U50488 (10(-6) M), P-type Ca2+ channel current inhibition was attenuated by norbinartorphimine (nor-BNI), kappa-opioid antagonist, and by dialysis of cells with a pipette solution containing guanosine 5'-O-(2-thiodiphosphate) (GDP-beta S). At high concentrations of U50488 (10(-5) M), P-type Ca2+ channel current inhibition was frequency-dependent. Thus U50488-induced current inhibition is mediated by two mechanisms. Its high affinity component is produced by activation of kappa-opioid receptors, whereas the low affinity component is due to its direct action on the P-type Ca2+ channel.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed1995

Human papillomavirus type 16-positive esophageal papilloma at an endoscopic injection sclerotherapy site.

Human papillomavirus infection is important for both the development of papilloma and the progression of the papilloma-carcinoma sequence in the cervix, larynx, lung, and colon. Esophageal squamous cell papilloma is rare but important as a possible precancerous lesion. Esophageal papilloma has previously been thought to develop mainly as a result of chemical irritation by chronic gastroesophageal reflux. However, a few recent studies suggested a role for papillomavirus infection in esophageal tumorigenesis, although the exact route of transmission and invasion of the virus has not been fully elucidated. A case of esophageal squamous papilloma at the site of endoscopic injection sclerotherapy (EIS) for varices is reported. Papilloma development was followed up clinically during a 2-year period, and the papilloma was removed by endoscopic mucosal resection. Histological examination of the tissue confirmed the diagnosis of squamous cell papilloma. DNA analysis of the tumor showed integration of papillomavirus type 16 but not types 18 and 33. The surrounding normal mucosa did not contain any of the three virus types. Injury such as ulceration resulting from EIS may have provided a locus susceptible to the viral infection. The clinical course after EIS should be monitored carefully to detect papilloma formation.

Adult↗
PubMed1995

Role of neutrophils in radical production during ischemia and reperfusion of the rat brain: effect of neutrophil depletion on extracellular ascorbyl radical formation.

A growing body of experimental data indicate that oxygen radicals may mediate the brain injury during ischemia-reperfusion. One potential source of oxygen radicals is activated neutrophils. To study the role of neutrophils in radical production during cerebral ischemia-reperfusion, we evaluated the effects of depletion of circulating neutrophils by administration of an anti-neutrophil monoclonal antibody (RP3) on radical formation in rats with 1-h middle cerebral artery (MCA) occlusion. In the present study, we employed a new electron spin resonance method coupled with brain microdialysis. The method uses the endogenous ascorbyl radical (AR) concentration as a marker of oxygen radicals and requires no spin-trapping agents. In the vehicle controls, extracellular AR decreased during MCA occlusion. After reperfusion, AR significantly increased at 30 min and 1 h, returned to near basal level until 2 h, and increased again at 24 h after reperfusion. In the rats treated with RP3, AR decreased during MCA occlusion to the same extent as in the vehicle control. However, RP3 treatment completely inhibited the increase in extracellular AR after reperfusion. RP3 treatment exerted no effect on the changes in extracellular ascorbate or tissue PO2 throughout the experimental period. In conclusion, neutrophils are a major source of oxygen radicals during reperfusion after focal cerebral ischemia.

Animals↗
PubMed1995

[Predictors for the massive thrombi occurring in the right coronary artery related to acute myocardial infarction].

Acute myocardial infarction (AMI) related to the right coronary artery (RCA) is associated with a lower reperfusion rate and higher reocclusion rate in the acute phase than AMI related to the left coronary artery. The greater susceptibility of the RCA to development of large thrombi makes successful reperfusion more difficult to achieve. This study investigated predictive factors for massive thrombus in the RCA before the selection of the treatment to achieve better rates of reperfusion. We classified 51 patients with AMI related to RCA into the massive (linear intraluminal radiolucency > 3 cm) thrombus group (9 patients) and the non-massive thrombus group (42 patients). 1) HISTORY: Patients in the massive thrombus group had a greater incidence of hypertension than the non-massive thrombus group, with more left ventricular hypertrophy (p < 0.05). There were no significant differences in other coronary risk factors. 2) RCA morphology: The maximum RCA diameter was significantly greater in the massive thrombus group than that in the non-massive thrombus group [proximal to the right ventricular branch, 4.2 vs 3.2 mm (median); distal to the right ventricular branch, 4.2 vs 3.4 mm, p < 0.05]. 3) Conditions of onset: The elapsed time was significantly longer in the massive thrombus group (15 hours) than that in the non-massive thrombus group (2.5 hours, p < 0.05). More massive thrombus cases were observed in summer (p < 0.05), but there was no evident correlation between massive thrombus formation and the onset time of day, weather, Hct and coagulation factor at the onset, left ventricular ejection fraction or left ventricular end-diastolic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

Role of cell adhesion molecules in brain injury after transient middle cerebral artery occlusion in the rat.

Activated neutrophils appear to be directly involved in tissue injury after focal cerebral ischemia and reperfusion. Intercellular adhesion molecules-1 (ICAM-1) and CD11/CD18 integrins have been implicated in ischemia-reperfusion induced neutrophil endothelial adhesion and transmigration. We therefore investigated the roles of CD11a/CD18 (LFA-1) and ICAM-1 in cerebral ischemia-reperfusion injury by using monoclonal antibodies, WT1 (anti-CD11a), WT3 (anti-CD18), and 1A29 (anti-ICAM-1). Rats were subjected to 1 h of middle cerebral artery occlusion (MCAO). Individual antibodies were administered at a dose of 5 mg/kg intraperitoneally at 15 min before ischemia and immediately after reperfusion. Rats were killed at 24 h after reperfusion, and brain edema, neutrophil infiltration and infarct size were measured. Sustained enhancement of ICAM-1 expression on capillaries was observed up to 24 h (beginning between 1 and 3 h after reperfusion). While, leukocytes began to infiltrate into the ischemic hemisphere between 6 and 12 h after reperfusion. Treatment with individual antibodies against cell adhesion molecules reduced edema formation and infarct size in addition to neutrophil accumulation 24 h after reperfusion. These results strongly implicate the invasion of neutrophils in the development of post-ischemic brain injury, and suggest that interactions between CD11a/CD18 and ICAM-1 contribute to neutrophil infiltration into the ischemic brain.

Animals↗
PubMed1994

Diverticulum of the superior vena cava.

A 14-year-old girl underwent operation with the diagnosis of diverticulum of the superior vena cava. Microscopic findings revealed a diverticulum with venous architecture. This represents a rare case of a giant diverticulum of the superior vena cava.

Adolescent↗
PubMed1994

Glutamate efflux via the reversal of the sodium-dependent glutamate transporter caused by glycolytic inhibition in rat cultured astrocytes.

[3H]L-Glutamate uptake in cultured rat astrocytes was completely reduced by 30 min preincubation with 1 mM of iodoacetic acid, a glycolytic inhibitor. This treatment significantly reduced the energy charge potential, but did not cause membrane destruction in the cultured astrocytes. To examine the effect of iodoacetic acid on the glutamate release, [3H]L-glutamate was preloaded into astrocytes in the presence of methionine sulfoximine, a glutamine synthetase inhibitor, and the total intracellular radioactivity was measured after 30-min treatment with 1 mM iodoacetic acid for comparison with non-treated astrocytes. During the treatment, about 40% of the total intracellular glutamate content was effluxed. This efflux could be decreased by reducing the extracellular potassium ion concentration. The intracellular sodium concentration, measured with a sodium ion-sensitive fluorescent probe (sodium-binding benzofuran isophtalate), gradually increased to 30 mM on addition of 1 mM iodoacetic acid. These results indicate that the glutamate efflux via reversal of the Na(+)-dependent transporter occurred during glycolytic inhibition, and which may be caused by intracellular Na+ overload. Such an iodoacetic acid-induced Na+ overload could be completely diminished by pretreatment with 1 microM 5-[N- ethyl-N-isopropyl]amiloride, a selective Na(+)-H+ antiporter inhibitor, but even this did not stop the iodoacetic acid-induced glutamate efflux. The intracellular pH, measured by a pH-sensitive fluorescent probe [2',7'-bis(carboxyethy)-5,6-carboxy-fluorescein], was gradually decreased to 7.1 by the iodoacetic acid treatment. On the other hand, iodoacetic acid-induced intracellular acidosis was more rapid and severe in the presence of 5-[N-ethyl-N-isopropyl]amiloride. These results suggest that the reversal of the Na+-dependent glutamate transporter may be caused by not only intracellular Na+ overload but also intracellular acidosis.

ATP-Binding Cassette Transporters↗
PubMed1994

Inhibitory effects of (-)-epigallocatechin gallate on spontaneous hepatoma in C3H/HeNCrj mice and human hepatoma-derived PLC/PRF/5 cells.

The inhibitory effect of (-)-epigallocatechin gallate (EGCG), a main constituent of Japanese green tea, on spontaneous hepatoma in C3H/HeNCrj mice was investigated. A total of 72 mice were divided into three groups; the control group without EGCG, and two experimental groups receiving 0.05% (w/w) or 0.1% EGCG in drinking water. EGCG reduced the incidence of hepatoma-bearing mice from 83.3% (control) to 56.0% (0.05% EGCG) and 52.2% (0.1% EGCG), and also reduced the average number of hepatomas per mouse from 1.83 (control) to 0.72 (0.05% EGCG) and 0.91 (0.1% EGCG) at week 65. Ridit analysis of the distribution of the number of hepatomas in each group revealed that EGCG significantly increased the rate of mice without hepatoma in the two EGCG groups as compared to the control. EGCG did not affect body weight gain, food consumption or any serum biochemical parameter. EGCG inhibited the growth and secretion of alpha-fetoprotein by human hepatoma-derived PLC/PRF/5 cells without decreasing their viability. These results indicate that EGCG may be a practical, nontoxic preventive agent against human hepatoma.

Animals↗
PubMed1994

Role of alpha-toxin in Clostridium perfringens infection determined by using recombinants of C. perfringens and Bacillus subtilis.

Clostridium perfringens type A strains which differed in alpha-toxin (phospholipase C [PLC]) productivity were inoculated intraperitoneally or intravenously into mice, and then their 50% mouse lethal doses (LD50) were determined. Strain NCTC 8237 produced ninefold higher PLC activity than strain 13. The mean LD50 for the former was 1 log unit lower than that for the latter. Two isogenic strains were constructed from strain 13: strain 13(pJIR418 alpha) (pJIR418 alpha contains the plc gene), which produced ninefold higher PLC activity than strain 13; and strain 13 PLC-, which showed no PLC productivity at all because of transformation-mediated gene disruption. The mean LD50 for strain 13(pJIR418 alpha) was 1 log unit lower than those for strain 13 PLC- and strain 13. These results indicate that PLC functions as a virulence-determining factor when it is produced in a sufficient amount. Such a difference in LD50 was also observed between Bacillus subtilis with and without the cloned plc gene. Inoculation of B. subtilis PLC+ intravenously into mice caused marked thrombocytopenia and leukocytosis. Mice inoculated with B. subtilis at 2 LD50 died because of circulatory collapse. Histological examination revealed that intravascular coagulation and vascular congestion occurred most prominently in the lungs. These results suggest that PLC plays a key role in the systemic intoxication of clostridial myonecrosis, probably by affecting the functions of platelets and phagocytes.

Animals↗
PubMed1994

Correlation between myeloperoxidase-quantified neutrophil accumulation and ischemic brain injury in the rat. Effects of neutrophil depletion.

BACKGROUND AND PURPOSE: Neutrophils have been implicated in the pathogenesis of ischemia-reperfusion injury. The aim of the present study was to evaluate the correlation between neutrophil infiltration into ischemic tissues and brain injury after transient focal ischemia. METHODS: We evaluated the effects of depletion of circulating neutrophils by administration of an antineutrophil monoclonal antibody (RP3) on brain edema formation, infarct size, and neutrophil infiltration (myeloperoxidase [MPO]-quantified) in rats with 1 hour of middle cerebral artery (MCA) occlusion. RESULTS: In the cerebral cortex perfused by the anterior cerebral artery (ACA area), there was a significant increase in MPO activity only 24 hours (P < .05) after reperfusion. In the cerebral cortex perfused by the middle cerebral artery (MCA area) and caudate putamen, MPO activity was significantly increased at 12 (MCA area, P < .01; caudate putamen, P < .05), 24 (MCA area, P < .05; caudate putamen, P < .01), and 72 hours (MCA area, P < .01; caudate putamen, P < .05) and returned to near-normal level by 168 hours after reperfusion. Brain MPO activity after transient MCA occlusion correlated well with the appearance of neutrophils. Depletion of neutrophils by RP3 treatment completely inhibited the increase in MPO activity in the ischemic brain after 24 hours of reperfusion. In addition, treatment with RP3 significantly attenuated the postischemic increase in brain water content at 24 hours after reperfusion. RP3 also significantly reduced the size of infarct area. CONCLUSIONS: These results indicate that the increase in brain MPO activity after transient focal ischemia virtually reflects the neutrophil infiltration and that neutrophil infiltration into the ischemic brain is implicated in postischemic brain injury.

Animals↗
PubMed1993

Lymphoplasmacytic lymphoma in a stallion.

Lymphoplasmacytic lymphoma found in a 6-year-old Anglo-Arabian stallion was investigated histologically, immunohistochemically and ultrastructurally. The animal showed a large mediastinal mass and generalized lymph node involvement. The neoplastic cells were in various differentiation stages of small lymphocyte, centrocyte, centroblast, immunoblast and plasma cell. Some neoplastic cells showed positive cytoplasmic reactivity for mu and lambda chains. There were well developed rough endoplasmic reticulum (RER) and Golgi complexes in plasmacytoid cells, and slightly developed RER or a few long strands of RER in medium-sized to large lymphoid cells. These findings suggest that this neoplasm is of B-cell origin.

Animals↗
PubMed1993

Pharmacological studies on a new dihydrothienopyridine calcium antagonist. 1st communication: comparative studies on the cardiovascular effects of methyl-4,7-dihydro-3-isobutyl-6-methyl-4-(3-nitrophenyl)thieno[2,3- b]pyridine-5-carboxylate and its two enantiomers in experimental animals.

Antihypertensive effects in conscious spontaneously hypertensive rats (SHR), cardiovascular effects in anesthetized dogs, and calcium antagonistic effects in the rabbit isolated basilar arteries and guinea-pig isolated coronary arteries of S-312 (methyl-4,7-dihydro-3-isobutyl-6-methyl-4- (3-nitrophenyl) thieno [2,3-b] pyridine-5-carboxylate) and its two enantiomers were comparatively investigated. The antihypertensive effect in SHR and hypotensive effect in anesthetized dogs of S-312-d (CAS 120056-57-7) were approximately 2 times more potent than those of S-312, but these effects of S-312-l were very weak even at 10 to 100 times higher doses. Increases of vertebral blood flow in dogs with S-312 and S-312-d were almost corresponding. The IC50 concentrations of S-312-d, S-312, S-312-l in the rabbit isolated basilar arteries contracted with high K+ solution were 1.4 x 10(-10) mol/l, 2.2 x 10(-10) mol/l, and 4.6 x 10(-9) mol/l, respectively. The relaxing effect of S-312-d in the isolated coronary arteries was most potent, followed by those of S-312 and S-312-l. It is concluded that the cardiovascular and calcium antagonistic effect of S-312-d are mainly responsible for those effects of S-312.

Animals↗
PubMed1993

Pharmacological studies on a new dihydrothienopyridine calcium antagonist. 4th communication: prophylactic and therapeutic effects of S-(+)-methyl-4,7-dihydro-3-isobutyl-6-methyl-4-(3-nitrophenyl)thieno[2, 3- b]pyridine-5-carboxylate in stroke-prone spontaneously hypertensive rats.

The prophylactic and therapeutic effects of S-312-d (S-(+)-methyl-4,7-dihydro-3-isobutyl-6-methyl-4-(3-nitrophenyl)thieno[2, 3- b]pyridine-5-carboxylate, CAS 120056-57-7) were compared with those of nimodipine or nicardipine using male stroke-prone spontaneously hypertensive rats (SHRSP). The survival rate of SHRSP was dose-dependently increased by once a day oral administration of S-312-d (0.3, 1, and 3 mg/kg) or nimodipine (10 mg/kg), while all non-treated SHRSP fed with high Na+ diet died within 40 days after the start of the experiment. All SHRSP treated with 3 mg/kg S-312-d survived during the 60-day experiment periods. Marked decreases of body weights and various neurological symptoms were also inhibited with S-312-d or nimodipine. Moderate diuretic effects were observed with S-312-d at doses of 1 and 3 mg/kg. The appearance of urinary occult blood in control SHRSP was markedly inhibited with S-312-d at 1 mg/kg and nimodipine at 10 mg/kg. Histological examination of the brain of SHRSP showed that cerebral stroke lesion including edema, hemorrhage, and/or softening was dose-dependently inhibited with S-312-d. Once a day oral administration of S-312-d (1, 3, or 10 mg/kg) dose-dependently increased the body weights and improved the neurological symptoms of diseased SHRSP. The appearance of proteinuria and of occult blood in the urine of SHRSP were also markedly inhibited with S-312-d or nicardipine. Histological examination of the brain of SHRSP showed that the arbitrary neurotoxic index (ANI) for stroke lesion dose-dependently decreased with S-312-d at 1, 3, and 10 mg/kg as follows: 4.8, 3.0, 2.3. The ANI for non-treated SHRSP was 7.6. The therapeutic effects of nicardipine (ANI 3.9) at 10 mg/kg corresponded to those of S-312-d at 3 mg/kg. Thus, S-312-d can be recommended for the treatment of cerebral insufficiency or vasospasm following stroke as well as in essential hypertension.

Animals↗
PubMed1993

Effects of a novel calcium antagonist, S-(+)-methyl-4,7-dihydro-3-isobutyl-6- methyl-4-(3-nitrophenyl)thieno[2,3-b]pyridine-5-carboxylate (S-312-d), on ischemic amino acid release and neuronal injury in stroke-prone spontaneously hypertensive rats.

The effects of a novel dihydrothienopyridine Ca antagonist S-(+)-methyl-4,7-dihydro-3-isobutyl-6-methyl-4-(3-nitrophenyl)-thieno [2,3-b]pyridine-5-carboxylate (S-312-d), on the amount of amino acid release during cerebral ischemia and delayed neuronal death in the hippocampal CA1 region of stroke-prone spontaneously hypertensive rats were studied and compared with those of nimodipine. The released amino acids were measured by high-performance liquid chromatography after microdialysis. Cerebral ischemia was produced by occlusion of the bilateral common carotid arteries for 20 min. Intraduodenal administration of 0.3 mg/kg of S-312-d at 60 min before the carotid occlusion significantly decreased the ischemic release of glutamate and taurine, but did not influence their basal release. However, nimodipine did not inhibit the ischemic glutamate release even at a dose of 10 mg/kg. Similar peripheral hemodynamic effects were observed before and during bilateral carotid occlusion in groups treated with S-312-d or nimodipine. During the carotid occlusion, almost no cerebral blood flow was observed in either group. Therefore, the inhibitory effect of S-312-d on ischemic amino acid release probably arises from its potent direct action on neuronal cells. The neuronal cell densities of the CA1 subfield at 7 days after 20-min bilateral carotid occlusion significantly decreased in the vehicle-control group compared with the sham-operated group. Intraperitoneal administration of 0.1 mg/kg of S-312-d at 60 min before ischemia prevented the decrease of neuronal cell density compared with the vehicle control. These results show that S-312-d can offer marked neuronal protective effects against ischemic injury.

Amino Acids↗
PubMed1992

Pathoanatomy of lumbar disc herniation as demonstrated by computed tomography/discography.

Computed tomography/discography was performed in 378 patients (403 discs) with lumbar disc herniation receiving intradiscal therapy. The grade of disc degeneration defined by the Dallas discogram description correlated closely with age. The most common herniation routes ran through the central portion of the posterior aspect of the disc (48.9%), through the paracentral portion (18.6%) and through the entire central portion (9.7%), with these directions parallel to the sagittal plane. However, the intraforaminal and extraforaminal routes (4.2%) passed obliquely to the sagittal plane. The development of these herniation routes has been well explained by the findings of earlier histopathologic and biomechanical studies. Computed tomography/discography was very useful in observing the detailed features of HNP such as the range, site of maximum protrusion and protrusion size.

Adolescent↗