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M Kida

Publications and source records attributed to M Kida.

At least 73 records · Page 4Linked to original sources
PubMed1993

Human space experiments in SL-J: preparation and conducted.

This experiment investigated how human beings achieve visual stability during body movements, including fine motion on the ground. When humans are exposed to an environment with different gravity vectors, the programmed behavior on the ground must be changed, that is, it is reprogrammed. This is called habituation or familiarization. This experiment focuses on visual, vestibular and somatosensory perception coordination and how it changes in microgravity as compared to a 1-G environment. We examined these issues under microgravity during the mission Spacelab Japan [correction of Japane] (SL-J) mission with the cooperation of the Japanese Payload Specialist (PS), Dr. Mohri. In this paper we describe how the first human life science experiments were conducted and how the data processed is being.

Adaptation, Physiological↗
PubMed1993

[Comparison between ELISA and culture method for detection of Helicobacter pylori].

Detection of Helicobacter pylori (H. pylori) by ELISA was compared with that by the culture method in 115 patients with gastroduodenal diseases. Both the sensitivity and specificity were more than 85% for patients with histological gastritis with neutrophil infiltration. This indicated that the detection of H. pylori by ELISA is useful for the diagnosis of H. pylori-related gastritis. Although the sensitivity between the ELISA and culture method was 85%, the specificity was 58.8%. The false negative detection may have been caused by a sampling error during the endoscopic biopsy.

Adult↗
PubMed1992

Constitutional translocation t(4;22) (q12;q12.2) associated with neurofibromatosis type 2.

We report on a female patient with bilateral acoustic neurinomas and other tumors in the central nervous system (neurofibromatosis type 2: NF2) and the constitutional translocation, t(4;22) (q12;q12.2). The precise identification of the translocation breakpoint (q12.2) on chromosome 22 implies the refined localization of a gene responsible for NF2, and would provide a clue to its molecular characterization and to the isolation of the gene. Chromosomes of a paraspinal neurinoma from the patient were also analyzed, and the same karyotype as seen in cultured peripheral lymphocytes was found. The patient's father was also a carrier of the translocation, but he had no clinical symptoms of NF2, nor did other relatives. Several explanations are offered for the different expression of the translocation between the patient and her father.

Adult↗
PubMed1992

Protective effect of carteolol, a beta-blocker, on myocardial cellular damage in ischemic and reperfused pig hearts: assessment with gated in vivo 31-phosphorus magnetic resonance spectroscopy and electron microscopy.

To assess the effect of carteolol, a beta-blocker, on ischemia and reperfusion, changes in the ultrastructure of myocytes and energy metabolism were studied by 31P-NMR in 41 pig hearts without collateral circulation. The left anterior descending coronary artery was occluded for 20 min and reperfused for 120 min in three groups: seven pigs (group 1, no treatment with carteolol; group 2, pre-ischemia treatment with carteolol (10 micrograms/kg); group 3, post-ischemia treatment with carteolol before reperfusion). Other groups of five pigs were killed after 120 min of ischemia (group 4, no treatment; group 5, pre-ischemia treatment) or 20 min of ischemia (group 6, no treatment; group 7, pre-ischemia treatment). After 20 min of ischemia, ATP was higher in groups 2 (76 +/- 9% of the baseline value) than in group 1 (59 +/- 5%) and group 3 (60 +/- 10%). However, the difference disappeared after 30 min of ischemia. After 120 min of reperfusion, ATP showed much better recovery in group 2 (92 +/- 9%) than in groups 1 (66 +/- 7%) and 3 (68 +/- 10%). Ischemic injury, as viewed by light and electron microscopy, was milder in group 7 than in group 6 after 20 min occlusion, but the myocytes were almost normal after 120 min reperfusion in groups 1 to 3. The heart rate, blood pressure and rate pressure product showed no significant difference among the groups. These results indicate that pre-ischemia treatment with carteolol provided protection against ischemic cellular injury and accelerated the repletion of ATP during reperfusion, but the post-ischemia treatment did not lead to recovery of ATP. Therefore, the favorable effect during reperfusion of pre-ischemia treatment with carteolol depends on its protective effect during ischemia.

Adenosine Triphosphate↗
PubMed1992

Effects of chronic oral administration of nifedipine and diltiazem on occlusive thrombus of small coronary arteries in (NZW x BXSB)F1 male mice.

OBJECTIVE: (NZWxBXSB)F1 male mice were used as a model to study the effects of chronic administration of nifedipine and diltiazem on small coronary artery disease and mortality. METHODS: 16 week old (NZWxBXSB)F1 male mice were given either nifedipine (n = 29) at 20 mg.kg-1.d-1 orally or diltiazem (n = 28) at 100 mg.kg-1.d-1 orally in two divided doses until they were 24 weeks old (ie, for 60 d). Age matched control mice were given an equivalent volume of vehicle (n = 30). Mice that died received immediate necropsy. After 60 d, all surviving mice were killed and hearts and kidneys were examined histologically. RESULTS: The survival rate at 24 weeks was significantly higher in mice given nifedipine than in the controls (71% and 47%, respectively, p less than 0.05). The number of mice with myocardial necrosis, scar formation, or both, the percentage of areas of the ventricular wall with myocardial necrosis and scar formation, and the number of mice with small intramyocardial arteries showing greater than or equal to 75% stenosis were all significantly lower in the mice given nifedipine than in the controls. In the mice given diltiazem, there were no such differences from the controls. There was no evidence of significant stenosis or thrombosis in the extramyocardial coronary arteries in any of the mice. Systolic blood pressure and the rate-pressure product at 24 weeks of age, as well as the histological score for glomerulonephritis changes, were significantly lower in mice given nifedipine or diltiazem than in the controls. CONCLUSIONS: Despite an equivalent improvement of systolic blood pressure, the double product, and renal disease in nifedipine treated and diltiazem treated mice, only nifedipine prevented small coronary artery disease and increased the survival of (NZWxBXSB)F1 male mice, suggesting that nifedipine prevents occlusive thrombi of small coronary arteries better than diltiazem.

Administration, Oral↗
PubMed1992

Automated homogeneous liposome immunoassay systems for anticonvulsant drugs.

We developed automated homogeneous immunoassays, based on immunolysis of liposomes, for measuring phenytoin, phenobarbital, and carbamazepine from serum. Liposome lysis was detected spectrophotometrically from entrapped glucose-6-phosphate dehydrogenase activity. The procedure was fully automated on a routine automated clinical analyzer. Within-run, between-run, dilution, and recovery tests showed good accuracies and reproducibilities. Bilirubin, hemoglobin, triglycerides, and Intrafat did not affect assay results. The results obtained by liposome immunoassays for phenytoin, phenobarbital, and carbamazepine correlated well with those obtained by enzyme-multiplied immunoassay (Syva EMIT) kits (r = 0.995, 0.986, and 0.988, respectively) and fluorescence polarization immunoassay (Abbott TDx) kits (r = 0.990, 0.991, and 0.975, respectively). The proposed method should be useful for monitoring anticonvulsant drug concentrations in blood.

Anticonvulsants↗
PubMed1991

Experimental and clinical studies on heater probe hemostasis for upper gastrointestinal bleeding with special reference to comparison with ethanol injection.

The hemostatic effects in patients with upper gastrointestinal bleeding was evaluated using an endoscopic heater probe method and ethanol injection method. The heater probe method was effective in 94.4% of patients with few complications. The ethanol injection method was effective in 86.5% of patients. The heater probe method is considered to be an effective and safe technique in the treatment of upper gastrointestinal bleeding.

Adolescent↗
PubMed1991

Failure to reduce infarct size by intracoronary infusion of recombinant human superoxide dismutase at reperfusion in the porcine heart: immunohistochemical and histological analysis.

Failure to Reduce Infarct Size by Intracoronary Infusion of Recombinant Human Superoxide Dismutase at Reperfusion in the Porcine Heart: Immunohistochemical and Histological Analysis. Journal of Molecular and Cellular Cardiology (1991) 23, 1287-1296. We quantitatively determined the extent of infarction and contraction band necrosis in porcine hearts, and analyzed the distribution of administered recombinant human superoxide dismutase (h-SOD) in the myocardium using a polyclonal antibody to h-SOD. After 1 hour of occlusion, h-SOD was infused for the first 30 min of reperfusion in SOD group, while pigs received only arterial blood in control group. The extent of infarction or contraction band necrosis was not significantly different between SOD group and control group. Positive staining by polyclonal antibody to h-SOD was detected only in the infarcted area in SOD group. Thus, h-SOD only entered irreversibly damaged myocytes and neither diminished reperfusion injury nor reduced infarct size in pigs.

Animals↗
PubMed1991

Hypertrophy of surviving myocytes overlying the infarct in human old myocardial infarctions with abnormal Q waves.

The time course of hypertrophy of surviving myocytes overlying the infarct after the onset was examined and the hypertrophy was analyzed in relation to the transmural extent of infarct in 34 autopsied hearts with Q wave infarction. The 34 hearts were divided into 4 groups according to the length of time between the onset of infarction and death. This was less than 5 days in group 1 (n = 10), 20-30 days in group 2 (n = 7), 40-60 days in group 3 (n = 7), and 12-24 months in group 4 (n = 10). To clarify the regional hypertrophy of myocytes overlying the infarct, the size of the surviving myocytes in the outer third of the left ventricular wall in the 1-cm wide central zone of the infarct was compared with that of the myocytes in the outer third of the left ventricular wall without infarction (control wall) in the same heart. To exclude factors which stimulate the hypertrophy of the whole left ventricle, the ratio of the monocyte diameter in the infarcted wall to that in the control wall was examined. It was 1.0 +/- 0.0 (mean +/- SD) in group 1, 1.0 +/- 0.1 in group 2, 1.2 +/- 0.1 in group 3, and 1.3 +/- 0.1 in group 4. The ratio was significantly higher in group 3 than in group 1 and 2, and was highest in group 4. In group 4, the corrected percentage transmural extent of infarct indicating the original transmural extent of infarct at the acute stage was 63 + 8%, and this transmural extent correlated positively with the ratio of myocyte diameter.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1991

Expression and distribution of atrial natriuretic peptide in human hypertrophic ventricle of hypertensive hearts and hearts with hypertrophic cardiomyopathy.

To investigate the ventricular expression of atrial natriuretic peptide (ANP) in human hypertrophic hearts, we conducted an immunohistochemical study of 130 endomyocardial biopsy specimens obtained from the right side of the ventricular septum (RVB), left ventricular free wall (LVB), or both from a total of 80 patients: 44 patients with hypertrophic cardiomyopathy (HCM), 14 with apical hypertrophic cardiomyopathy (APH), 13 with hypertensive hearts (HHD), and nine without hypertrophy (controls). No patients had apparent congestive heart failure. ANP was not seen in ventricular myocytes in controls but was identified in biopsy specimens of hypertrophic hearts, and its distribution was characteristic in each hypertrophic group: 15 RVB (37%) and two LVB (7%) of the HCM group, one RVB (7%) and two LVB (18%) of the APH group, and zero RVB (0%) and five LVB (46%) of the HHD group. Clinical data (including echocardiographic, hemodynamic, and angiographic data) were not directly related to ventricular ANP expression in HCM, APH, or HHD with one exception. In HHD patients, LVB specimens with ANP showed greater ventricular wall thickness than LVB specimens without ANP. According to histological data, however, the ANP-present RVB specimens of HCM or ANP-present LVB specimens of HHD had greater myocyte size than did the ANP-absent specimens. In addition, in HCM patients, the ANP-present RVB specimens showed more severe fibrosis and myofiber disarray than did the ANP-absent specimens. We conclude that a failing state and hemodynamic overload are not likely to be indispensable for ANP expression in human hypertrophic ventricles and that ventricular ANP expression occurs as a response to disease-specific changes: hemodynamic overload in HHD and histological changes such as myocardial fiber disarray, hypertrophy of myocytes, and fibrosis in HCM, which may reflect the characteristic distribution of intraventricular ANP.

Adult↗
PubMed1991

Ischemic preconditioning preserves creatine phosphate and intracellular pH.

BACKGROUND: Ischemic preconditioning slows ATP depletion and ultrastructural damage during the final episode of ischemia. To define the influence of creatine phosphate (CP) and intracellular pH (pHi) on this effect, CP and pHi were serially measured in porcine hearts without collateral circulation by using 31P-NMR spectroscopy and ultrastructural examination. METHODS AND RESULTS: Farm pigs weighing 12-15 kg were anesthetized with Fluothane. The control group underwent a single occlusion (20 minutes or 60 minutes); the preconditioned group underwent four episodes of 5-minute occlusion and 5-minute reperfusion followed by a sustained occlusion (20 minutes or 60 minutes). After ischemic preconditioning, CP increased to 115 +/- 11% (p less than 0.05) of preischemic value and ATP decreased to 84 +/- 8% (p less than 0.05) of preischemic value, but pHi returned to preischemic value. At 5 and 10 minutes of sustained ischemia, CP was significantly preserved in the preconditioned group (control group, 19 +/- 3% versus preconditioned group, 29 +/- 4% at 5 minutes; control group, 5 +/- 3% versus preconditioned group, 11 +/- 3% at 10 minutes; p less than 0.05). At 15 and 20 minutes of sustained ischemia, ATP was significantly preserved in the preconditioned group (control group, 64 +/- 3% versus preconditioned group, 73 +/- 3% at 15 minutes; control group, 51 +/- 7% versus preconditioned group, 62 +/- 2% at 20 minutes; p less than 0.05). At 10, 15, 20, and 25 minutes of sustained ischemia, pHi was significantly higher in the preconditioned group (control group, 6.5 +/- 0.05 versus preconditioned group, 6.7 +/- 0.1 at 10 minutes; control group, 6.3 +/- 0.05 versus preconditioned group, 6.6 +/- 0.06 at 15 minutes; control group, 6.1 +/- 0.1 versus preconditioned group, 6.4 +/- 0.1 at 20 minutes; control group, 6.0 +/- 0.2 versus preconditioned group, 6.3 +/- 0.1 at 25 minutes; p less than 0.05). Ultrastructural changes were milder in the preconditioned group at 20 minutes of sustained ischemia. CONCLUSIONS: In addition to ATP and ultrastructure, preconditioning preserved CP and pHi during sustained ischemia. These protective effects might be due to overshoot phenomenon of CP and/or reduced ATP consumption. The relatively longer period of preservation of pHi, which probably is the result of reduced ATP consumption, indicates its greater contribution to reducing infarct size than that of CP and ATP.

Adenosine Triphosphate↗
PubMed1991

Relation between myoglobin and cardiac dysfunction in myocarditis--immunohistochemical study of endomyocardial biopsy specimens.

To investigate the mechanism of cardiac dysfunction in myocarditis, myoglobin, an intracellular oxygen-transport, was immunohistochemically examined in biopsy specimens obtained from the right side of the ventricular septum and left ventricular free wall in 58 patients with myocarditis and 19 controls. Sections 4 microns thick were stained by the indirect immunoperoxidase method using a polyclonal antibody to human myoglobin as the primary antibody. Under light microscopy, the intensity of myoglobin immunoreactivity in the tissue section was semiquantitatively classified from grade 0 to grade 3. Then, the grade of myoglobin staining was compared with clinical, hemodynamic and histopathologic parameters. In right and left ventricular specimens, the grade of myoglobin staining was positively correlated with ejection fraction, but inversely with left ventricular end-diastolic and end-systolic volume indices. The percentage of myocytes with grade 0 was correlated with the number of mononuclear cells in the specimens. In addition, the grade of myoglobin staining in right ventricular specimens was positively correlated with the duration of illness but inversely correlated with the number of mononuclear cells. In 4 patients who had serial biopsies, the ejection fraction was improved and the grade of myoglobin staining was increased in the convalescent stage. These results indicate that myoglobin staining reflects the intensity of myocarditis and a decrease of myoglobin may be important as one of the pathogenetic factors of cardiac dysfunction in myocarditis.

Adolescent↗
PubMed1991

[Mechanism of protective effects of ouren-gedoku-to and san'ou-syashin-to on the gastric mucosa].

Ouren-Gedoku-To (OGT) and San'ou-Syashin-To (SST), traditional Chinese prescriptions, have been used to treat peptic ulcer. In order to elucidate the mechanism of the protective effects of OGT and SST on the gastric mucosa, we studied their effects on gastric mucosal lesions, ion permeability and prostaglandin synthesis using ulcer experimentally induced in rats by saturation with acidic test solution after taurocholate treatment. Both OGT and SST inhibited taurocholate-induced gastric mucosal lesions in a dose-related manner. These prescriptions dose-dependently inhibited not only the increase of hydrogen and sodium ion net fluxes but also possible hydrogen ion back diffusion into the gastric mucosa during saturation with acidic test solution. SST induced a significant increase in gastric mucosal prostaglandins synthesized from 14C labeled arachidonate. These results suggest that both OGT and SST by strengthening the gastric mucosal barrier demonstrate their protective effects on the gastric mucosa and that this effect of SST is attributable to the increased ability of the gastric mucosa to synthesize prostaglandin.

Animals↗
PubMed1990

Clinicopathological study of myocardial infarction with normal or nearly normal extracardiac coronary arteries. Quantitative analysis of contraction band necrosis, coagulation necrosis, hemorrhage, and infarct size.

In order to clarify the pathogenesis of acute myocardial infarction (MI) in hearts with normal coronary arteries, infarct size, and the extent of contraction band necrosis (CBN), coagulation necrosis, and hemorrhage were quantitatively examined using an image analyzer in 5 autopsy cases of MI with normal or nearly normal extracardiac coronary arteries. One patient died 40 h after acute MI. A second patient with acute MI due to severe spasm of segment 6, confirmed by cineangiography, died three days later. The third patient had already suffered a subarachnoid hemorrhage, and died 10 h after the onset of acute MI. The fourth patient had aortic stenosis and regurgitation. She developed acute MI due to total occlusion of segment 6, confirmed by cineangiography 4 h after the onset, and died 61 days later. Autopsy revealed old anteroseptal MI with normal coronary arteries and valvular thrombi. The fifth patient had a malignancy, and died one day after the onset of acute MI. Autopsy revealed multiple occlusive thrombi in the small intramural coronary arteries of the left ventricular wall supplied by segment 14, without any stenosis in the feeding vessel. Most infarcts were localized in the territory supplied by 1 or 2 of the 3 epicardial coronary arteries, and coincided with the clinically diagnosed infarct site. The infarct size ranged from 3%-26% of the left ventricular wall, and infarcts were generally localized to the inner third of the wall (67 +/- 20%). Histological examination of the four patients with acute MI revealed diffuse CBN (86 +/- 14% of the infarcted area) and/or hemorrhage.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Protective effect of verapamil in ischemic porcine hearts: analysis of ultrastructural and metabolic changes using in vivo 31P-NMR spectroscopy.

To assess the protective effect of verapamil on ischemic myocardium, the changes in high energy phosphates, inorganic phosphate, and intracellular pH were serially and quantitatively measured in ischemic porcine hearts without collateral circulation using 31P-NMR spectroscopy, together with ultrastructural examination. Twenty-six farm pigs weighing 11 to 14 kg were anesthetized with fluothane and were divided into control (C) group and verapamil pretreatment (V) group. In V group 0.2 mg/kg of verapamil was administered for 20 mins before occlusion of the anterior descending coronary artery. 31P-NMR spectra were serially obtained throughout the experiment, and ultrastructural examination was done at 20-min occlusion and at 120-minute occlusion in each group. At 10-min ischemia, creatine phosphate was significantly preserved in V group (C/V = 11 +/- 4%/16 +/- 5% P less than 0.05). At 20 min ischemia, ATP was significantly preserved (C/V = 60 +/- 9%/73 +/- 8% P less than 0.05), and intracellular pH was significantly higher in V group (C/V = 6.4 +/- 0.2/6.6 +/- 0.1 P less than 0.05). Morphologically, clumping of the nuclear chromatin, mitochondrial swelling and decrease in glycogen were milder in V group at 20 min ischemia. However, these beneficial effects disappeared at 120 min ischemia. Thus pretreatment with verapamil attenuated depletion of high energy phosphates, progression of acidosis, and ultrastructural changes. There was no significant difference of rate pressure product and regional blood flow between hearts with and without pretreatment of verapamil. Therefore, this protective effect may be due to the energy sparing effect or other direct subcellular effect of verapamil on ischemic myocyte.

Angiography↗
PubMed1990

Bone metastasis from gynecologic carcinomas: a clinicopathologic study.

Between 1948 and 1984, autopsies were performed on 305 patients with primary carcinomas of the cervix, endometrium, ovaries, fallopian tubes, vulva, and vagina. Skeletal metastases were detected premortem and at autopsy in 49 cases (16.1%): cervix, 20 (40.8%); endometrium, 17 (34.7%); ovary, 7 (14.3%); vulva, 4 (8.2%); fallopian tube, 1 (2%). There were no cases of osseous metastasis from vaginal carcinoma. The incidence and sites of metastasis from these gynecologic carcinomas were correlated with their clinical and histopathologic classifications. This clinicopathologic study, based on autopsy data, demonstrates that osseous metastases are not uncommon, are significantly greater than clinically appreciated, and correlate with advanced anatomic stage and histopathologic type and grade.

Autopsy↗