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Biomedical subjects

A Shibata

Publications and source records attributed to A Shibata.

At least 217 records · Page 12Linked to original sources
PubMed1993

Frequency of presumed reentry with an excitable gap in sustained ventricular tachycardia unassociated with coronary artery disease.

In sustained ventricular tachycardia (VT) unrelated to coronary artery disease, the incidence of reentry with an excitable gap was examined, and rapid pacing was performed to entrain VT in 48 episodes in 42 consecutive patients. Coronary artery disease was excluded by coronary arteriography. The underlying heart diseases were postoperative congenital heart diseases (n = 5), dilated (n = 7) or hypertrophic (n = 4) cardiomyopathy, arrhythmogenic right ventricular dysplasia (n = 6) and miscellaneous heart diseases (n = 5), as well as no demonstrable heart disease (n = 15) in which 8 patients had verapamil-responsive VT. Except for 1 patient with hypertrophic cardiomyopathy, 48 morphologically distinct monomorphic sustained VTs were induced. Twenty-five VTs showed right bundle branch block morphology and 23 left bundle branch block morphology, and VT was entrained in 84 and 96%, respectively. The overall incidence of the entrainment was 89.6% (43 of 48 monomorphic VTs), and the frequency of the ability to entrain VT ranged between 33.3 and 100% in the subgroups. The lowest frequency was found in hypertrophic cardiomyopathy. In conclusion, most inducible monomorphic sustained VT unassociated with coronary artery disease was presumed to be reentry with an excitable gap.

Adolescent↗
PubMed1993

Characterization of T cells infiltrating the heart in rats with experimental autoimmune myocarditis. Their similarity to extrathymic T cells in mice and the site of proliferation.

A model of experimental autoimmune myocarditis, which resembles fatal giant cell myocarditis in humans, was previously established in rats immunized by s.c. injection of human cardiac myosin. We characterized herein the surface phenotype of lymphocytes infiltrating the heart and pericardial cavity as well as of mononuclear cells in various organs by using mAb in conjunction with immunofluorescence tests. Since profound thymic atrophy always accompanied the diseased states, attention was focused on characterization of T cells with properties similar to those of extrathymic T cells. In mice, extrathymic T cells were activated in association with thymic atrophy, expressed high levels of LFA-1 and IL-2R beta-chains, and contained a significant proportion of double negative CD4-CD8- T cells. In diseased rats, a large proportion of activated T cells that expressed high levels of LFA-1 and IL-2R was demonstrated in the pericardial effusion and heart tissue. Such T cells were rare in the other organs. Light scatter and microscopic observation revealed that activated lymphoblasts were most abundant in the pericardial effusion. Moreover, one-fourth of such T cells in the pericardial effusion displayed double negative phenotype. These cells in rats might correspond to the extrathymic T cells in mice. However, only a limited population of such activated T cells infiltrated the heart tissue. Concerning the location of such T cells mainly in the outer layer of the heart, it raised the possibility that extrathymic T cell differentiation in these autoimmune rats might occur in the pericardial cavity, and the differentiated cells then migrated to the sites of the cardiac lesion.

Animals↗
PubMed1993

Discordant and heterogeneous expression of GPI-anchored membrane proteins on leukemic cells in a patient with paroxysmal nocturnal hemoglobinuria.

We performed a flow cytometric analysis using monoclonal antibodies to decay accelerating factor (DAF) and CD59/membrane attack complex inhibitory factor (CD59/MACIF) in order to investigate the leukemic cells and erythrocytes from a patient with paroxysmal nocturnal hemoglobinuria (PNH) who developed acute myelocytic leukemia. In May 1990, the leukemic cells comprised 70% of the mononuclear cells in the bone marrow and 76% of those in the peripheral blood. They consisted of a mixture of positive and negative populations, including single DAF-positive cells. In August 1990, almost 100% of the peripheral mononuclear cells were leukemic blasts, and these consisted of a single population with reduced DAF expression. Single-color flow cytometric analysis showed that the leukemic cells lacked CD59/MACIF, while control leukemic cells (n = 3) expressed both DAF and CD59/MACIF. Leukemic blasts from this patient and six control patients expressed lymphocyte function-associated antigen 3 and FcIII receptors (CD 16) both before and after treatment with phosphatidylinositol-specific phospholipase C. The patient's erythrocytes lacking DAF and CD59/MACIF expression corresponded to the proportion of complement-sensitive cells at the onset of acute leukemia. These DAF- and CD59/MACIF-deficient erythrocytes disappeared almost completely with progression of the leukemia. In conclusion, it appears that the expression of glycosylphosphatidylinositol-linked membrane proteins by leukemic cells was heterogeneous and discordant in our patient, and that the leukemic cells were derived from the PNH clone because of their deficiency of CD59/MACIF. It is also suggested that DAF could compete more effectively than CD59/MACIF for a limited number of anchor molecules available on the proliferating leukemic cells.

Antigens, CD↗
PubMed1993

Defective signal transduction induced by thromboxane A2 in a patient with a mild bleeding disorder: impaired phospholipase C activation despite normal phospholipase A2 activation.

A patient with a mild bleeding disorder whose platelets responded defectively to thromboxane A2 (TXA2) was identified, and the mechanism of this dysfunction was analyzed. The platelets were defective in shape change, aggregation, and release reaction in response to synthetic TXA2 mimetic (STA2). When the platelet TXA2 receptor was examined with both a 125I-labeled derivative of a TXA2 receptor antagonist ([125I]-PTAOH) and [3H]-labeled TXA2 agonist ([3H]U-46619), the equilibrium dissociation rate constants (kd) and the maximal concentrations of binding sites (Bmax) of the platelets to both ligands were within normal ranges, suggesting that the binding capacity of their TXA2 receptor was normal. STA2 could not induce IP3 formation and intracellular Ca2+ mobilization, whereas these responses to thrombin were within normal ranges. GTPase activity was also decreased when the patient's platelet membrane was challenged with STA2. On the other hand, lysophosphatidylinositol formation, which is a direct indicator of phospholipase A2 (PLA2) activation, was found to be normal when the [3H]-inositol-labeled platelets were challenged with STA2. Thromboxane B2 (TXB2) was also produced in response to STA2. These results suggested that the abnormality in these platelets was impaired coupling between TXA2 receptor and phospholipase C (PLC) activation. Furthermore, it is also suggested that the activation of PLA2 and PLC are separable events in thromboxane-induced platelet activation.

Adult↗
PubMed1993

Effects of acetyl salicylic acid and cilostazol administration on serum thrombomodulin concentration in diabetic patients.

Serum thrombomodulin (sTM) is an endothelial cell marker which would reflect the endothelial damage. In order to examine whether some antiplatelet agents decrease the endothelial damage in diabetic patients, sTM concentrations were measured by enzyme-linked immunosorbent assay before and after oral administration of a daily 100 mg of cilostazol for 4 weeks in 9 diabetics or a daily 81 mg of acetyl salicylic acids (ASA) for 4 weeks in 8 diabetics. Basal concentrations of sTM were elevated in most of these patients as compared with healthy subjects. The sTM concentrations were decreased after administration of cilostazol from 28.1 +/- 7.1 ng/ml to 23.6 +/- 5.4 ng/ml (p < 0.01), and after ASA from 30.7 +/- 10.9 ng/ml to 27.9 +/- 11.6 ng/ml (p < 0.05). These results suggest that such drugs can decrease the endothelial damage, resulting in the reduced risk of diabetic vascular complications.

Aged↗
PubMed1993

Orphan peak analysis: a novel method for detection of point mutations using an automated fluorescence DNA sequencer.

Automated DNA sequencers draw the four-base profiles of a sample with four different colors, but it is also possible to draw the profiles of a base-specific reaction of four different samples with four colors. PCR-amplified DNAs from four individuals were subjected to a single base-specific sequencing reaction and the products were applied to a set of four lanes of an automated DNA sequencer. A base substitution in an individual was clearly identified as an individual-specific peak with a color specific for the individual. In this way, we analyzed more than 50 individuals and identified several polymorphic base substitutions. The sensitivity of this method was high enough to allow detection of the mutation/polymorphism even if samples from several individuals were applied to one lane. Thus, our method is applicable to screening of a large number of samples in an automated manner.

Amyloid beta-Protein Precursor↗
PubMed1993

Preoperative diagnosis of malignant melanoma using the touch-fluorescence method.

We have developed a touch-fluorescence method using preparations from the outer surface of elevated and ulcerative malignant melanoma lesions. This method allows the demonstration of the melanogenic activity of melanoma cells within 30 min and has made it possible to definitively diagnose a lesion as malignant melanoma at the initial examination. In 21 cases clinically diagnosed as typical melanoma, 17 were definitively diagnosed as melanoma from the touch-fluorescence microscopic findings. Of the four cases in which no fluorescent tumor cells were found, two proved not to be melanoma. There was some correlation between the morbid types of primary melanoma and the configuration of fluorescent melanoma cells, the main cellular configuration of superficial spreading melanoma being round whereas that of nodular melanoma and acral lentigenous melanoma was pleomorphic. Based on the above results, this method was concluded to be extremely reliable for the preoperative diagnosis of elevated and ulcerative lesions of malignant melanomas, which are sometimes difficult to diagnose.

Adult↗
PubMed1993

Efficacy of amlodipine besilate therapy for variant angina: evaluation by 24-hour Holter monitoring.

The efficacy of amlodipine, a calcium antagonist, was investigated in 12 patients with variant angina. Amlodipine was administered at a dose of 5 mg once daily, and efficacy was assessed from the frequency of anginal attacks, the frequency of ST elevation or depression, and the extent of ST segment changes [ST segment elevation or depression (mm) x duration (seconds)] on the Holter ECG before and after treatment. The frequency of ST elevation during the observation period was 1.67 +/- 0.33 times/day (symptomatic attacks: 1.17 +/- 0.21/day; asymptomatic attacks: 0.50 +/- 0.19/day), and this significantly decreased to zero per day (both symptomatic and asymptomatic attacks) after treatment (p < 0.05). The extent of ST segment elevation during the observation period was 507.5 +/- 156.6 mm.sec/day (symptomatic: 382.5 +/- 102.9 mm.sec/day; asymptomatic: 125.0 +/- 62.0 mm.sec/day), and such changes were completely suppressed (both symptomatic and asymptomatic) by treatment (p < 0.05). The frequency of ST depression was 2.08 +/- 0.42 times/day (symptomatic: 0.25 +/- 0.13/day; asymptomatic: 1.83 +/- 0.37/day) during the observation period, while it was 1.50 +/- 0.36 times/day (symptomatic: 0.25 +/- 0.13/day; asymptomatic: 1.25 +/- 0.30/day) after treatment. Although anginal attacks remained unchanged, asymptomatic attacks tended to decrease (p = 0.07).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Catheter ablation with radiofrequency current of ventricular tachycardia originating from the right ventricle.

Catheter ablation of ventricular tachycardia (VT) with radiofrequency current would be safer than the conventional ablation with direct current shocks. Seven patients who had eight morphologically distinct symptomatic monomorphic VTs underwent catheter ablation with radiofrequency current. The mean age +/- SD was 52 +/- 16 years, and the mean cycle length of the clinical VT was 298 +/- 36 milliseconds. Sustained VT was induced by programmed stimulation with or without isoproterenol in four patients and developed during the infusion of isoproterenol alone in two patients. Of these, four VTs were entrained with rapid pacing. The ablation was attempted at the site of earliest activation through the distal electrode and the external patch electrode on the back during VT in seven episodes in six patients. In the other patient it was applied during sinus rhythm. Energy was 40 to 50 W in the first case and 30 to 40 W in the others, and was given for 30 seconds. All VTs were terminated within 6 seconds, 3.6 +/- 0.8 seconds after the application of the radiofrequency current. Additional current was given to one to four predetermined sites by mapping. The mean number of applications was 4.0 +/- 1.3 sites. Except in the first patient, VT was eliminated successfully and VT was not induced by programmed stimulation, by the administration of isoproterenol, or by treadmill exercise testing. VT did not recur during the follow-up period of 6.8 +/- 1.1 months.

Adult↗
PubMed1993

Different effects of various hematopoietic growth factors on myelomonocytic cell line (KY-821) and its drug-resistant sublines.

Human myelomonocytic leukemic cell line, designated as KY-821, and its sublines KY-Ra, KY-VCR, and KY-MTX, which were resistant to cytosine arabinoside, vincristine, and methotrexate, respectively, were compared for response to various hematopoietic growth factors. Cells of KY-Ra and KY-VCR proliferated in response to natural interleukin-1 (nIL-1), whereas the proliferation of KY-821 and KY-MTX was inhibited. Unexpectedly, recombinant IL-1 alpha and IL-1 beta had no effect on the proliferation of each cell line. The effect of nIL-1 was partially deleted by an addition of optimal anti-IL-1. Supernatants of each cell line had no IL-1 activity. Interferon gamma (IFN gamma) and tumor necrosis factor alpha (TNF alpha) also had an inhibitory effect for KY-821 and KY-MTX, but lacked such effect in KY-RA and KY-VCR. nIL-1, IFN gamma and TNF alpha could not differentiate between any of the cell lines but IFN gamma and TNF alpha induced monocytic surface antigens. In addition, there was no difference in the number of IL-1 and TNF alpha receptors in each cell line. These results indicate that there is a difference in biological effects between nIL-1 and recombinant IL-1 species and acquirement of resistance for some types of drugs may associate closely with different responses to hematopoietic growth factors, probably through altered postmembranous transduction.

Animals↗
PubMed1993

Induction of surface antigen recognized by new monoclonal antibody, YU311, on 1-beta-D-arabinofuranosylcytosine-resistant human leukemic cell line.

A new monoclonal antibody, YU311, against an antigen expressed on 1-beta-D-arabinofuranosylcytosine(ara-C)-resistant human leukemic cell line with decreased deoxycytidine kinase activity was generated. YU311 reacted with ara-C-resistant human leukemic cell line (KY-Ra), but not with its parental cell line (KY-821) which was sensitive to ara-C. YU311 recognized the 92-kDa membrane protein. Furthermore, YU311 inhibited the growth of KY-Ra in suspension medium with and without ara-C. In immunocytochemistry, there was no difference in expression of usual differentiation antigens between KY-Ra and KY-821. These findings indicate that antigenic change could occur in ara-C-resistant human leukemic cells with stable expression of differentiation antigens and that the 92-kDa membrane protein may be one of the membrane proteins which regulate cell growth of KY-Ra.

Animals↗
PubMed1993

Effects of cyclosporine, prednisolone and aspirin on rat autoimmune giant cell myocarditis.

OBJECTIVES: Preventive effects of cyclosporine, prednisolone and aspirin on autoimmune giant cell myocarditis in rats were investigated. BACKGROUND: The therapeutic efficacy of immunosuppressants for human myocarditis is controversial. Although harmful effects of immunosuppressive therapy on experimental viral myocarditis have been reported, the effects on autoimmune myocarditis have not been investigated. Recently, a novel experimental autoimmune myocarditis model characterized by congestive heart failure and multinucleated giant cell has been established. Using this model, the preventive effects of cyclosporine, prednisolone and aspirin on autoimmune myocarditis were investigated. METHODS: Lewis rats were immunized with cardiac myosin in complete Freund's adjuvant on days 0 and 7. In experiment 1, four groups of seven rats each were established. Rats in each group received for 21 days intraperitoneal injections of either 1) phosphate-buffered saline solution, 1 ml/day (control); 2) cyclosporine, 20 mg/kg body weight per day (cyclosporine 20); 3) prednisolone, 4 mg/kg per day; or 4) aspirin, 15 mg/kg per day. In experiment 2, two additional groups (five rats each) received for 21 days an injection of cyclosporine, 1 or 5 mg/kg per day (cyclosporine 1 and cyclosporine 5, respectively). All rats were killed on day 21, when histopathologic studies were performed and the titers of antimyosin antibodies were measured. RESULTS: The rats in the control, prednisolone and aspirin groups became ill and immobile in week 3. In comparison, rats in the cyclosporine 5 and 20 groups were still active until death was induced. Heart weight/body weight, lung weight/body weight and liver weight/body weight ratios in the rats in the cyclosporine 5 and cyclosporine 20 groups were significantly lower than those in the control group, and no differences were detectable among rats in the control, prednisolone and aspirin groups. The rats in the latter three groups and the cyclosporine 1 groups showed severe myocarditis with multinucleated giant cells. However, myocarditis was effectively prevented in the rats in the cyclosporine 5 and 20 groups. The histologic scores in each group were 2.91 in the control group, 2.14 in the prednisolone group, 2.91 in the aspirin group and 0.02, 2.58 and 0.07, respectively, in the cyclosporine 20, 1 and 5 groups. Production of antimyosin antibodies was remarkably suppressed in rats in the cyclosporine 5 and 20 groups in comparison with values in all other groups. CONCLUSIONS: Autoimmune myocarditis is preventable by cyclosporine but not by prednisolone or aspirin in usual dosages.

Animals↗
PubMed1993

Dystrophin negative skeletal and myocardial muscle cells in a carrier of Duchenne's muscular dystrophy.

A 47-year-old woman whose elder son had typical Duchenne's muscular dystrophy (DMD) was diagnosed as the manifesting carrier of the disease. She had developed congestive heart failure but had no evidence of skeletal muscular atrophy. Histological observation of the cardiac muscle revealed a mosaic pattern of dystrophin negative fibres detected by immunofluorescence analysis.

Cardiac Output, Low↗
PubMed1993

Evaluation of oral anticoagulant therapy by measuring plasma prothrombin fragment 1 + 2.

To assess the degree of haemostatic system activation, plasma levels of prothrombin fragment 1 + 2 (F1 + 2), a direct indicator for thrombin generation in vivo, were measured in 49 patients with thrombotic disease undergoing long-term warfarin therapy (Thrombotest values < or = 40%). In these patients, vitamin K dependent coagulation factors (factors II, VII, IX and X) were decreased together with the anticoagulant proteins C and S, but the mean plasma concentration of F1 + 2 was significantly decreased compared with 48 healthy subjects. In warfarin-treated patients, F1 + 2 was positively correlated with the Thrombotest value, factors II, VII, IX and X. When analysed according to the intensity of anticoagulation, patients with Thrombotest values less than 30% showed a significant decrease in F1 + 2, but the mean F1 + 2 level was normal in patients with Thrombotests higher than 30%. These findings indicate that long-term oral anticoagulant therapy suppresses thrombin generation approximately in parallel to the decrease in coagulation factors, and levels of F1 + 2 lower than healthy subjects are observed when Thrombotest values are less than 30%.

Administration, Oral↗
PubMed1993

Coronary artery spasm is a major cause of sudden cardiac arrest in survivors without underlying heart disease.

BACKGROUND: The role of coronary spasm in underlying disease-free patients who were resuscitated from sudden cardiac arrest remained uncertain. This study investigated the cause of cardiac arrest, and the etiologic and prognostic differences were compared between patients with underlying heart disease (group I) and those patients without underlying heart disease (group II). METHODS: Twenty-five survivors of sudden cardiac arrest were classified into two groups according to the presence or absence of underlying heart disease. To investigate the cause of cardiac arrest, we performed ergonovine testing and electrophysiologic study. Fifteen of the patients had underlying heart disease, while 10 did not. RESULTS: Electrophysiologic abnormalities were found in 13 of the 15 patients in group I. In group II, spontaneous attack of coronary spasm occurred in four patients during the observation period, and coronary spasm was induced in three of the remaining six period of 32 +/- 23 months, whereas no patients in group II had recurrence of sudden cardiac arrest at a median follow-up of 32 months (range, 10 to 72 months). CONCLUSIONS: Electrophysiologic study identified a potential cause in 13 of 15 patients with underlying heart disease. Coronary spasm was involved in the pathogenesis of sudden cardiac arrest in survivors without identifiable underlying heart disease.

Adolescent↗