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Biomedical subjects

A Shibata

Publications and source records attributed to A Shibata.

At least 199 records · Page 11Linked to original sources
PubMed1994

Rat dilated cardiomyopathy after autoimmune giant cell myocarditis.

One of the possible causes of dilated cardiomyopathy is considered to be a sequel to myocarditis. Two mechanisms have been proposed in the process of progression of myocarditis into dilated cardiomyopathy: one is a persistent viral infection, and the other is an autoimmune myocardial injury. To clarify the possible part played by the autoimmune mechanism in the process, using an animal model, we investigated whether autoimmune myocarditis, exclusively not related to viral infection, might develop into dilated cardiomyopathy. Experimental autoimmune myocarditis was elicited in Lewis rats by immunization with cardiac myosin fraction. Rats of the control group were immunized with ovalbumin. The clinical course was observed over 4 months. Six rats from the myosin-immunized group died during the acute phase and the healing phase, and all those rats had severe myocarditis. All rats that survived until the end of the study showed enlarged and discolored hearts. Aneurysmal changes were observed in the right ventricle during thoracotomy. The ratio of heart weight to body weight of the myosin-immunized group was significantly higher than that of the control group (3.36 +/- 0.49 versus 2.69 +/- 0.06 g/kg, respectively; P < .005). The lengths of the anterior interventricular fissure and the posterior interventricular fissure of the hearts of the myosin-immunized group were significantly longer than those of the control group. The external diameter of the left ventricle of the myosin-immunized group was also significantly larger than that of the control group. Diffuse myocardial muscle loss and replacement fibrosis were the prominent histological findings of the rats of the myosin-immunized group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Novel mutations in the V2 vasopressin receptor gene in two pedigrees with congenital nephrogenic diabetes insipidus.

Novel mutations in the V2 vasopressin receptor gene were identified in two Japanese pedigrees with X-linked congenital nephrogenic diabetes insipidus. The V2 receptor belongs to the family of G-protein-coupled receptors that contain seven distinct transmembrane domains, and the V2 receptor gene is encoded by three exons. The coding regions amplified by polymerase chain reaction were directly sequenced. In a pedigree, one of four consecutive guanine sequences (nucleotides 528-531) in the second exon was deleted (528delG). This deletion mutation results in a frame shift beginning at codon 154 in the second intracellular domain and a premature termination at codon 161. In another pedigree, a missense mutation (A-->G) was identified at nucleotide position 310 in the second exon. This point mutation, H80R, changes a histidine at codon 80 in the second transmembrane domain to an arginine that is more positively charged than histidine under the neutral environment. Each mutation cosegregated with the phenotype of diabetes insipidus and supposed to be a cause for resistance to arginine vasopressin.

Adolescent↗
PubMed1994

Preparation and characterization of liposomes incorporating hydrophobic poly(amino acid)s with different secondary structure.

Incorporation of hydrophobic poly(amino acid) into liposomal membranes was achieved by the polymerization of N-carboxy anhydrides of amino acids in the egg yolk phosphatidylcholine (EyPC) bilayer under reduced pressure at 30 degrees C. The trapped volumes for the liposomes with and without polypeptides were 8.1-10.3 l mol-1 and 11.4 l mol-1, respectively. The permeability barrier abilities of liposomal membranes were lowered by the incorporation of polypeptides into the membrane bilayers. Water permeation across the membrane bilayer was more effective for the liposome with the alpha-helical polypeptide than for that with the beta-sheeted one.

Diffusion↗
PubMed1994

Radiofrequency current catheter ablation for ventricular tachycardia.

UNLABELLED: Radiofrequency current catheter ablation was attempted for 17 morphologies of ventricular tachycardia (VT) in 14 patients. Five patients had underlying heart disease. The site of VT origin was determined as the earliest site of ventricular activation, or by pacing within the area of slow conduction. In 15 VTs, ablation was performed during VT, and 12 VTs (80%) were terminated within an average of 5.4 +/- 4.2 seconds. After ablation, 14 VTs (14/17 = 82%) of 11 patients (11/14 = 79%) could not be induced by electrical stimulation. Radiofrequency ablation appeared to be more effective in VTs without underlying heart disease (91%), and in VTs originating from the right ventricle (100%). Successful ablation sites usually showed a normal local electrograms during VT. Ablation in the slow conduction area was attempted in 3 VTs, and 2 VTs became noninducible. The mean number of applications of radiofrequency current for each VT origin was 7.7 +/- 6.4 at 20-50 Watts. In 4 patients, application of radiofrequency current was required 10 or more times because of a possible large arrhythmogenic area, or because of reinduction of VT, even though VT was terminated by radiofrequency current. No major complication was observed except for complete right bundle branch block in 1 patient. IN CONCLUSION: (1) Radiofrequency catheter ablation was considered to be effective and safe, especially for VT without underlying heart disease or VT originating from the right ventricle. (2) Ablation during VT was considered to be useful for identifying the proper ablation site and to avoid creating an unnecessary lesion.

Adult↗
PubMed1994

Evidence for slow conduction areas during pacing in patients with sinus rhythm, and their relation to the site of VT origin.

UNLABELLED: In 52 patients with reentrant monomorphic sustained ventricular tachycardia (VT), the site of VT origin was determined by endocardial mapping and the interval from stimulus artifact to the onset of QRS complex (St-QRS) was measured during pace-mapping. Eleven patients had remote myocardial infarction (group 1), 25 patients had other underlying heart diseases (group 2), and 16 had idiopathic VT (group 3). At St-QRS interval of 40 msec or longer was defined as abnormal. (1) Long St-QRS interval: Thirteen sites with long St-QRS intervals were detected in 13 (25.0%) of 52 patients: 5 patients in group 1 (45.5%), 7 (28.0%) patients in group 2 and one (6.3%) in group 3. (2) Local electrogram: The local electrogram at sites with a long St-QRS interval was wide and 113 +/- 38 msec in duration during sinus rhythm which increased to 159 +/- 64 msec during VT (p < 0.05). In sinus rhythm, an abnormally prolonged local electrogram was observed in 11 of 13 sites with a long St-QRS interval, and mid-diastolic potential or continuous activity was observed in 3 sites during VT. (3) Relation to VT origin: At sites with a long St-QRS interval, concealed entrainment was observed in 3 patients, and the earliest activated local electrogram during VT in 5 patients. CONCLUSION: Sites with a long ST-QRS interval were observed in 25% of the patients with VT, and their incidence tended to be higher in patients with ischemic heart disease. Such sites were associated with abnormal local electrograms and some of the sites were considered to be the active limb of the reentry circuit.

Adolescent↗
PubMed1994

Clinical value of electrophysiologic study in patients with nonsustained ventricular tachycardia.

Electrophysiologic study (EPS) was performed in 68 consecutive patients with nonsustained ventricular tachycardia (VT) detected by ambulatory monitoring. The study group consisted of 11 patients with coronary artery disease, 11 patients with idiopathic cardiomyopathy or myocarditis, 2 patients with valvular heart disease, 1 patient with post atrial septal defect repair and 43 patients with a normal heart. Syncope or presyncope was found in 34 percent of these patients. EPS was performed after all antiarrhythmic drugs were withdrawn for more than 5 days. Nonsustained VT, sustained VT, and ventricular fibrillation were induced in 21%, 4%, and 4% respectively. VT was induced more frequently in patients with organic heart diseases but it was not related to the history of syncope. Ejection fraction in the inducible patients was not different from that of the noninducible patients. During the mean follow up period of 31 months, there was no cardiac death. The results suggest that the prognosis of patients with nonsustained VT is good and the clinical significance of their EPS findings seems to be limited.

Adolescent↗
PubMed1994

Effect of digoxin on exercise performance in mildly symptomatic patients with idiopathic dilated cardiomyopathy and sinus rhythm.

The purpose of this investigation was to evaluate the effect of digoxin on aerobic performance in mildly symptomatic patients with congestive heart failure and sinus rhythm. Ten patients (8 men and 2 women) with idiopathic dilated cardiomyopathy (ejection fraction 17 to 33%, mean 27 +/- 4%) who were stable and mildly symptomatic with maintenance digoxin and diuretic therapy were studied. All patients underwent maximal symptom-limited ergometer exercise with analysis of respiratory gases during maintenance digoxin therapy, 4 weeks after digoxin withdrawal, and 4 weeks after digoxin readministration. Exercise capacity was assessed by peak oxygen uptake and anaerobic threshold. Serum digoxin concentration was 1.0 to 1.8 (mean 1.3 +/- 0.2) ng/ml during digoxin therapy, and less than the detectable level after digoxin withdrawal. No patients showed clinical deterioration after digoxin withdrawal. Peak oxygen uptake after digoxin withdrawal (23.7 +/- 3.0 ml/kg/min) did not differ significantly from that during maintenance digoxin therapy (23.8 +/- 2.5 ml/kg/min) or after digoxin readministration (24.1 +/- 2.9 ml/kg/min). The anaerobic threshold after digoxin withdrawal (14.9 +/- 2.5 ml/kg/min) did not differ significantly from that during maintenance digoxin therapy (15.0 +/- 2.1 ml/kg/min) or after digoxin readministration (14.9 +/- 2.2 ml/kg/min). No differences in heart rate and diastolic blood pressure were observed during exercise, but systolic blood pressure during exercise was significantly higher with digoxin therapy (p < 0.05). These results suggest that digoxin has no effect on aerobic performance in mildly symptomatic patients with idiopathic dilated cardiomyopathy and sinus rhythm.

Adult↗
PubMed1994

Clinical and angiographic characteristics of patients with multivessel coronary spasm in variant angina. Significance of progressive course of angina and disease activity.

The purpose of this study was to investigate the incidence of multivessel coronary spasm and compare the clinical characteristics between patients with and without multivessel coronary spasm. In variant angina, it is controversial whether coronary hyperreactivity to vasoconstrictor stimuli is localized to a segmental lesion in only one coronary artery. Moreover, the clinical characteristics of patients with multivessel coronary spasm have never been investigated. Sixty-three patients (51 men and 12 women; mean age, 56 years; range 35-72 years) with variant angina and documented ST-segment elevation during a spontaneous attack underwent spasm provocation testing with selective intracoronary injection of ergonovine. All but 4 patients who experienced spontaneous attacks during cardiac catheterization had induced coronary spasm associated with ST-segment elevation and chest pain. Multivessel coronary spasm was found in 27 (43%) of 63 patients. By univariate analysis, a high frequency of angina (> or = 3 times/week), occurrence of a spontaneous attack within 24 hours after withdrawal of medication, a long history of angina and a progressive course of angina were significantly associated with multivessel coronary spasm. Multivariate analysis indicated a positive correlation between multivessel coronary spasm and progressive angina. Multivessel coronary spasm was found in 43% of patients with variant angina. Patients with multivessel coronary spasm have some unique clinical features. These results may increase the understanding of the pathophysiology and natural course of variant angina.

Adult↗
PubMed1994

Procainamide-induced changes in reentrant ventricular tachycardia with special reference to the tachycardia-interrupting critical paced cycle length during transient entrainment with rapid pacing.

With rapid ventricular pacing, sustained ventricular tachycardia (VT) is often entrained and interrupted at a critical paced cycle length. In this paper, the possible mechanism and determinant of the critical cycle length interrupting VT are addressed. Sixteen consecutive patients underwent rapid ventricular pacing in 18 morphologically distinct sustained VTs before and after procainamide. The VT morphology was identical before and after the drug. The VT origin was determined by endocardial mapping as the earliest site of activation of VT and an electrode catheter was located at the site. Rapid pacing was performed to entrain VT and repeated in 10 msec decrements of cycle length until VT was interrupted at a critical paced cycle length which was defined as the block cycle length. The effective refractory period was measured at the pacing site. The paced QRS duration and the local conduction time were measured and used as indices of conduction time in the normal myocardium. VT was entrained and interrupted in all patients. At the block cycle length, initial constant fusion was replaced abruptly by the fully paced QRS complex. At the same time, the local electrogram at the site of VT origin showed changes in the morphology and the timing of activation which were identical to those of the fully paced beat. This loss of fusion and the changes in the local electrogram were considered to be a result of orthodromic block and the block cycle length was assumed to represent the cycle length at which 1:1 conduction fails in the area of slow conduction. After procainamide, both the VT cycle length and the block cycle length were prolonged to a similar degree (p < 0.001) but the relative degree of change varied from patient to patient. The paced QRS duration and the conduction time were prolonged by procainamide but in smaller degrees than the cycle length of VT or the block cycle length (p < 0.02-01). The effective refractory period at the pacing site and the QT interval showed small changes after procainamide. The postrepolarization refractoriness rather than the duration of action potential can be responsible for the procainamide-induced prolongation of the block cycle length, and the block cycle length might be used as a new index to characterize the electrophysiologic property of the VT circuit and also the action of antiarrhythmic drugs.

Adolescent↗
PubMed1994

Intracoronary acetylcholine-induced prolongation of the QT interval and Torsade des Pointes in long QT interval syndrome.

A 75-year-old female had syncopal episodes from Torsade des Pointes (TdP). Her electrocardiogram showed a prolonged QT interval which was not associated with electrolyte imbalances or drug therapy. Similar electrocardiographic abnormalities were found in three family members. Electrophysiologic study showed a mildly prolonged effective refractory period of 260-290 msec, but no tachyarrhythmia was induced. Coronary arteriography was normal but intracoronary acetylcholine unexpectedly induced a prolongation of the QT interval and TdP. Direct action of acetylcholine on the ventricular muscle was suggested.

Acetylcholine↗
PubMed1994

Morphological analysis of multinucleated giant cells occurred in experimental autoimmune myocarditis.

Our previous study reported the rich existence of multinucleated giant cells in an autoimmune myocarditis experimentally induced in rats. The present study investigated the histochemical and ultrastructural characteristics of these giant cells. Histochemistry for an acid phosphatase clearly demonstrated multinucleated giant cells dispersed at the inflammatory foci. Ultrastructurally, the giant cells were shown to be single cells, but not clustered cells. Their ultrastructural characteristics were very similar to the basic features of macrophages, except that the giant cells were poor in lysosomes and phagosomes. It was noticeable that some macrophages possessed three or more nuclei, displaying an intermediate form between mononuclear macrophages and multinucleated giant cells. These findings suggest that the giant cell in the experimental autoimmune myocarditis is a single multinucleated cell, and possibly derived from macrophages by cell-to-cell fusion.

Acid Phosphatase↗
PubMed1994

Female siblings with Pendred's syndrome.

Female siblings with Pendred's syndrome were admitted to our clinic. The abnormality of the acoustic structure was examined by MRI. Bilateral enlargement of the vestibular aqueduct and a prominently marked endolymphatic sac were found on MRI. These findings seemed likely to represent a Mondini deformity. Acoustic structure in Pendred's syndrome was examined here by MRI for the first time. We examined their HLA-DR locus as a genetic marker using the affected sib-pair method preliminary. HLA typing might be a diagnostic criteria of Pendred's syndrome, although the present siblings possessed 2 HLA genes in common.

Adolescent↗
PubMed1994

Plasma urokinase-type plasminogen activator in patients with leukemias.

Plasma levels of urokinase-type plasminogen activator (u-PA) were measured with an enzyme-linked immunosorbent assay in patients with leukemias. As compared with healthy subjects (0.73 +/- SD 0.17 ng/ml), plasma u-PA antigen level was markedly elevated in patients with acute promyelocytic leukemia (APL) (1.76 +/- 0.89 ng/ml) at disease onset. Mean u-PA concentrations in patients with other acute nonlymphoblastic leukemia (0.57 +/- 0.51 ng/ml), acute lymphoblastic leukemia (0.77 +/- 0.82 ng/ml) and chronic myelocytic leukemia in blastic crisis (1.30 +/- 1.35 ng/ml) were not significantly elevated, but some of them showed an elevation of plasma u-PA. Plasma u-PA values were correlated with some of the fibrinolytic parameters such as FDP and D-dimer. Plasma u-PA antigen was decreased after the administration of antileukemic drugs in patients with APL. These results suggest that the coagulopathy in patients with various leukemias may in part be associated with u-PA release from the leukemic cells, especially in patients with APL.

Enzyme-Linked Immunosorbent Assay↗
PubMed1994

Low expression of the deoxycytidine kinase (dCK) gene in a 1-beta-D-arabinofuranosylcytosine-resistant human leukemic cell line KY-Ra.

Molecular change of the deoxycytidine kinase (dCK) gene in a 1-beta-D-arabinofuranosylcytosine-resistant human leukemic cell line (KY-Ra) was investigated. KY-Ra showed the same restriction pattern of genomic DNA and the same nucleotide sequences of the dCK gene as the parental cell line. However, the amount of deoxycytidine kinase mRNA was markedly decreased in KY-Ra compared to the parental cell line. This is the first report showing that the down regulation of dCK gene expression may be affected by a different mechanism than mutation.

Base Sequence↗
PubMed1994

Angina-linked syncope and lack of calcium antagonist therapy predict cardiac arrest before definitive diagnosis of vasospastic angina.

BACKGROUND: Several prognostic factors have been identified in patients with vasospastic angina; however, factors that would predict potentially fatal cardiac arrest during the period between the onset of angina and its definitive diagnosis remain unknown. We investigated the predictive value of the clinical findings that are available when a patient is hospitalized after a cardiac arrest but before a definitive diagnosis of vasospastic angina is made. METHODS: We compared the clinical findings in 11 patients who experienced cardiac arrest before vasospastic angina was definitively diagnosed (group I) with 81 patients with vasospastic angina without cardiac arrest (group II). The definitive diagnosis of vasospastic angina was made on the basis of results of coronary spasm provocation test or ECGs during spontaneous attacks, or both. RESULTS: The incidence of angina-linked syncope was significantly higher in group I than in group II (six out of 11 versus nine out of 81, P < 0.005). Significantly fewer group I patients were receiving calcium antagonists than group II patients (three out of 11 versus 63 out of 81, P < 0.005). Serious arrhythmias were significantly more common in group 1 than in group II (seven out of 11 versus 12 out of 81, P < 0.005). Logistic regression analysis of the eight clinical variables available when first seen in the hospital indicated that angina-linked syncope and the lack of calcium antagonist therapy were independently related to risk of cardiac arrest. CONCLUSIONS: From the clinical findings available, a history of angina-linked syncope and lack of calcium antagonist therapy were found to be independent predictors of cardiac arrest before a definitive diagnosis had been made. Patients who have suspected vasospastic angina may benefit from early treatment with calcium antagonists if they have a history of angina-linked syncope.

Aged↗
PubMed1994

The therapeutic significance of myeloperoxidase detectable only by electron microscopy in acute leukemia.

The lineage assignment is a prerequisite for successful therapy of acute leukemia because the optimal therapeutic agents and schedules are quite different between acute myeloid leukemia (AML) and acute lymphoid leukemia (ALL). The most reliable marker for AML has been thought to be myeloperoxidase (MPO). We describe here two patients who were initially diagnosed with ALL owing to the negative light microscopic reaction for peroxidase and the positive reaction of T-lymphoid markers. While these patients were successfully treated by ALL-directed therapy and survived in remission for more than 5 years, ultrastructural study using preserved specimens retrospectively revealed that some blasts had MPO-positive granules. We suggest that some cases of acute leukemia with MPO-positive blasts detected only by electron microscopy, especially when accompanied by T-lymphoid markers, will benefit from ALL-directed therapy.

Acute Disease↗
PubMed1993

Absence of linkage disequilibrium at amyloid precursor protein gene locus in Japanese familial Alzheimer's disease with 717Val-->Ile mutation.

To date, eleven independent FAD pedigrees with the 717Val-->Ile mutation have been identified. Interestingly, five pedigrees were of Japanese origin and four were of British origin. The apparent ethnic prediction of this mutation raises the possibility that there is a founder effect in these two island nations. We did not observe any significant linkage disequilibrium in any locus of APP and GT12 loci in the five Japanese FAD pedigrees with the 717Val-->Ile mutation. A founder effect would probably not be present in Japanese FAD pedgrees with the 717Val-->Ile mutation.

Alleles↗