Biomedical subjects

A Shibata

Publications and source records attributed to A Shibata.

At least 289 records · Page 16Linked to original sources

PubMed1992

Molecular characterization of the Entner-Doudoroff pathway in Escherichia coli: sequence analysis and localization of promoters for the edd-eda operon.

The nucleotide sequence of the entire Escherichia coli edd-eda region that encodes the enzymes of the Entner-Doudoroff pathway was determined. The edd structural gene begins 236 bases downstream of zwf. The eda structural gene begins 34 bases downstream of edd. The edd reading frame is 1,809 bases long and encodes the 602-amino-acid, 64,446-Da protein 6-phosphogluconate dehydratase. The deduced primary amino acid sequences of the E. coli and Zymomonas mobilis dehydratase enzymes are highly conserved. The eda reading frame is 642 bases long and encodes the 213-amino-acid, 22,283-Da protein 2-keto-3-deoxy-6-phosphogluconate aldolase. This enzyme had been previously purified and sequenced by others on the basis of its related enzyme activity, 2-keto-4-hydroxyglutarate aldolase. The data presented here provide proof that the two enzymes are identical. The primary amino acid sequences of the E. coli, Z. mobilis, and Pseudomonas putida aldolase enzymes are highly conserved. When E. coli is grown on gluconate, the edd and eda genes are cotranscribed. Four putative promoters within the edd-eda region were identified by transcript mapping and computer analysis. P1, located upstream of edd, appears to be the primary gluconate-responsive promoter of the edd-eda operon, responsible for induction of the Entner-Doudoroff pathway, as mediated by the gntR product. High basal expression of eda is explained by constitutive transcription from P2, P3, and/or P4 but not P1.

Aldehyde-Lyases↗

PubMed1992

Phase I/II study of recombinant human granulocyte-macrophage colony-stimulating factor in patients with advanced malignancy. The Multicenter Study Group.

The toxicity and hematologic effects of Escherichia coli-derived recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) were studied in 58 treatment cycles in Japanese patients with advanced malignancy as a phase I/II clinical trial. rhGM-CSF in doses from 30 to 250 micrograms/m2/day was administered by 24-hour continuous intravenous infusion, 8-hour intravenous, or a daily subcutaneous injection for 14 days. The most common adverse drug events (ADE) were fever, nausea/vomiting, diarrhea, skin eruption, and phlebitis. The frequency of moderate and severe ADE was 2.9, 14.7, 35.3 and 47.1% at 30, 60, 125, 250 micrograms/m2/day, respectively. In terms of administration routes, the frequency of ADE was 69% with 24-hour continuous intravenous infusion, 39.1% with 8-hour intravenous infusion and 16.7% with subcutaneous injection. Regarding the hematologic effects of rhGM-CSF, leukopenia improved in a dose-dependent manner. The appropriate dose level to be used in the phase II study was estimated to be in the range between 60 and 250 micrograms/m2/day.

Adult↗

PubMed1992

Incidence and mechanism of interruption of reentrant ventricular tachycardia with rapid ventricular pacing.

BACKGROUND: Information concerning the electrophysiological characteristics of the reentrant circuit is still limited. To understand the incidence and mechanism of pacing-induced interruption of ventricular tachycardia (VT), rapid pacing was performed to entrain VT, and the local electrogram at the VT origin and the surface electrocardiogram were analyzed. METHODS AND RESULTS: Among 25 patients, evidence of transient entrainment was confirmed in 20 patients, but the critical paced cycle length at which VT was interrupted was obtained in 13 patients when the paced cycle length was decreased in steps of 10 msec. During pacing at the critical cycle length (defined as block cycle length), changes in the local electrogram at VT origin were confirmed in all of the 13 patients; that is, 1) a change in morphology and 2) a change in the timing of activation: a sudden shortening in the stimulus to local electrogram time (third entrainment criterion by Waldo). The two changes mean that the exit is activated from a different direction (retrograde capture) because of an orthodromic block in the slow conduction zone. The QRS complex in the surface electrocardiogram showed a change in configuration from the fusion complex to the fully paced one at the same time when the exit was captured antidromically. CONCLUSIONS: Based on our observations in these patients, ventricular tachycardia interruption is very often associated with orthodromic block in the reentrant circuit at a critical cycle length of rapid pacing.

Adolescent↗

PubMed1992

Temporal bone findings in keratitis, ichthyosis, and deafness syndrome. Case report.

In 1981, the term KID syndrome was suggested for patients with congenital ichthyosis associated with deafness and keratitis. We had a chance to examine the temporal bone of an infant with this syndrome. This patient showed no auditory brain stem response in either ear. Temporal bone studies revealed cochleosaccular abnormality. These findings are offered as a possible explanation for the patient's deafness. The pathologic inner ear findings of congenital deafness syndromes associated with ichthyosis have been heretofore reported in Refsum's syndrome and in a case with universal alopecia. In these cases, the temporal bone pathologic findings were a result of cochleosaccular abnormality. From our case and previous reports, it is suggested that the deafness associated with congenital ichthyosis might be the result of cochleosaccular abnormality.

Cochlea↗

PubMed1992

Prolongation of canine epidural anesthesia by liposome encapsulation of lidocaine.

The purpose of our study was to produce a long-acting lidocaine by using a liposome that would entrap the drug. Egg yolk phosphatidylcholine and cholesterol were used as liposome materials. After epidural administration, the pharmacodynamics and pharmacokinetics of liposomal and free lidocaine were studied in 20 dogs. Two percent liposomal or free lidocaine (3.0 mL) was injected into the lumbar epidural space. Nerve blocking effects were estimated by measuring somatosensory evoked potentials. Recovery time from the epidural block in the liposomal lidocaine group (170 +/- 49.5 min) was approximately three times longer than that in the free lidocaine group (61 +/- 18.1 min). The areas under the drug concentration-time curves (AUC0-infinity) and time to maximal concentration (Tmax) in the liposomal lidocaine group were significantly larger than those in the free lidocaine group. These results suggest that the prolongation of epidural blockade by liposomal lidocaine is caused by a slow release of the drug from liposomes. The present study suggests that liposomal lidocaine can be used as a long-acting local anesthetic.

Amines↗

PubMed1992

Effects of long-term xamoterol in idiopathic dilated cardiomyopathy.

In prospective study, the beta 1-partial agonist xamoterol (200 mg daily) was given to 26 patients with idiopathic dilated cardiomyopathy (DCM) in addition to conventional therapy with digitalis, diuretics and vasodilators. The patients were followed for 35 +/- 15 months (6-53 months). Cardiothoracic ratio (CTR), left ventricular end-diastolic dimension (LVDD) and exercise heart rate decreased, and exercise duration, fractional shortening (FS) and ejection fraction (EF) increased after xamoterol therapy. Twenty-one patients survived and one patient dropped out at 7 months. Twelve of the 20 patients improved their NYHA functional class. Blood norepinephrine concentration (NE), LVDD, FS, EF and pulmonary capillary wedge pressure (PCWP) after xamoterol were significantly better in survivors than in non-survivors. Survival rate at 3 years was 83%. The results suggest that adjunctive xamoterol therapy in DCM has a beneficial effect on hemodynamics and symptoms. Prognosis will be satisfactory if improvement in parameters such as NE, LVDD, FS, EF and PCWP is seen during xamoterol therapy.

Adrenergic beta-Agonists↗

PubMed1992

Importance of coronary artery spasm in alcohol-related unexplained syncope.

To examine the role of coronary artery spasm in patients with syncope after alcohol ingestion, we performed an intracoronary ergonovine provocation test in 7 male patients (39 to 73 years old, mean 54 years) with alcohol-related syncope which remained unexplained despite noninvasive cardiovascular and neurological examinations. No patients had structural heart disease or significant coronary artery stenosis. Ergonovine was continuously infused into each coronary artery at a rate of 10 micrograms/min for up to 5 min. Coronary artery spasm with ST-segment elevation was induced in 4 of 7 patients. Chest pain before syncope or history of chest pain were not present in 3 of 4 patients with a positive ergonovine test. Multivessel coronary artery spasm was induced in 3 patients. One patient presented with triple vessel coronary artery spasm progressing to near syncope as a result of profound hypotension and ventricular tachycardia during provocation. Coronary artery spasm was promptly relieved by intracoronary isosorbide dinitrate infusion. All patients with a positive ergonovine test were treated with calcium antagonist and did not experience syncope during follow-up. These results suggest that coronary artery spasm is one of the important causes of syncope after alcohol ingestion.

Adult↗

PubMed1992

Acute hemodynamics of pimobendan in chronic heart failure. A comparative crossover study of captopril and pimobendan.

Acute hemodynamics of pimobendan were compared to captopril in a crossover trial in patients with chronic heart failure (NYHA II-III). Heart failure had been stabilized by conventional therapy with diuretics and digitalis for more than 2 weeks. Patients receiving vasodilators were excluded. The hemodynamics were analyzed using a Swan-Ganz catheter at the bedside during drug administration. Following an intravenous injection of 2.5 mg of pimobendan, there was a significant increase in heart rate and decrease in mean pulmonary artery pressure, total pulmonary resistance, mean arterial pressure, systemic vascular resistance and mean right atrial pressure 2 hours after the injection. Captopril (12.5 mg, orally) significantly decreased mean arterial pressure, systemic vascular resistance and double product 2 hours after administration. In this study, the inotropic effect was evaluated through the relation between the stroke volume index and diastolic pulmonary artery pressure, and also between the stroke volume index and mean arterial pressure. Although decreases of diastolic pulmonary artery pressure and mean arterial pressure were seen with both drugs, the differences in stroke volume index were not significant. In comparison with captopril, the acute hemodynamics of pimobendan are characterized as follows: 1) the systemic arteriovasodilating effects of the two drugs were equal, 2) the pulmonary arteriovasodilating effect of pimobendan was marked, 3) a venodilating effect, documented through a decrease of mean right atrial pressure, was seen only with pimobendan. This study concluded that pimobendan is a stronger arterio-venodilator than captopril.

Aged↗

PubMed1992

Successful transseptal catheter electrical ablation of sustained ventricular tachycardia of possible intramuscular origin.

Low-energy electrical ablation at 100 joules was attempted via a catheter in a patient with sustained ventricular tachycardia (VT) refractory to drug therapy. The patient was a 17-year-old woman who had undergone complete surgical correction of a double outlet right ventricle at the age of 9. The first episode of VT appeared at the age of 17. It was refractory to procainamide and lidocaine and it was sustained until termination with direct countershock. Two different QRS morphologies of VT were documented in the electrophysiologic study and one was identical to the VT observed in the clinical course. Conventional drug therapy failed to prevent induction of VT and catheter electrical ablation was attempted. The earliest activation site during the clinical episode of VT was localized to the right ventricular side of the interventricular septum (site 14-15), but pacing from this site resulted in a slightly different QRS morphology from that of VT. At the left ventricular side of this site (site 2), pacing during VT resulted in a QRS morphology identical to that of VT but the electrogram of this site did not precede the onset of the surface QRS complex. From these findings, the origin of VT was considered to be in the muscular layer of the interventricular septum. The method of transseptal shock using two catheters was applied and direct countershock at 100 joules successfully ablated the VT.

Adolescent↗

PubMed1992

Possible intramural site of reentrant circuit in ventricular tachycardia of nonischemic cause. Pre and intraoperative mapping studies.

A patient with a drug-refractory sustained ventricular tachycardia (VT) of nonischemic cause was mapped for the site of VT origin. The intraoperative mapping showed the earliest site of activation of VT on the epicardial surface at which the initial deflection of the local electrogram preceded the onset of the QRS complex of VT by 45 msec. The endocardial mapping could not indicate the site at which the electrogram was found prior to the onset of the QRS complex of VT. However, at the earliest site of the endocardial mapping, VT was entrained without change in the configuration of the QRS complex. After cessation of the rapid pacing, VT resumed at the intrinsic rate and the first post-paced return cycle was identical to each paced cycle length. The interval from the stimulus to the orthodromically captured local electrogram at the pacing site was identical to the cycle length of VT. Catheter ablation from the endocardial side and a cryoablative procedure from the epicardial side failed to eradicate the VT. These findings suggest an intramural site of VT origin and reentrant circuit of which the exit and the entrance face the epicardial and the endocardial surfaces, respectively.

Cardiac Pacing, Artificial↗

PubMed1992

Intraventricular concealed double tachycardia: a case report.

An electrophysiologic study was performed on a patient with ischemic sustained ventricular tachycardia (VT). During pacing at the right ventricular apex, ventricular double potential was recorded at the left ventricular apex. Sustained VT was induced by double extra stimuli from the right ventricular apex. Three types of VTs with different QRS morphologies were observed, and each VT was changeable to other types. The interval between one of the two potentials and the surface QRS was constant during all VTs, but the other potential showed dissociation from the surface QRS. During this dissociation, an intrinsic rhythm of the potential was sometimes shorter than the cycle length of the VT. The mechanism of a block between the VT and a bystander could hardly explain these electrophysiologic findings. Concealed double ventricular tachycardia was considered to be the likely mechanism.

Aged↗

PubMed1992

Capability of various cytokines to induce quiescent myeloid leukemia cells to the proliferative stage.

In order to investigate the capability of cytokines to induce myeloid leukemia cells from G0 phase to the proliferative stage, blasts from 9 patients with AML and 1 patient with CML-MC were cultured with various cytokines (IL-3, GM-CSF, IL-3 + GM-CSF, G-CSF) for 48 hours or 96 hours in a serum-free culture system. Cells were analyzed by two-color flow cytometry, using PI and the monoclonal antibody Ki-67. The percentage of cells in G0 phase was reduced significantly when the cells were cultured with IL-3 (p < 0.01), GM-CSF (p < 0.01), and IL-3 + GM-CSF (p < 0.01) for 48 hours, as compared with the percentage of cells in G0 phase before culture. Moreover, the percentage of cells in S phase increased significantly when the cells were cultured with IL-3 (p < 0.01), GM-CSF (p < 0.02), and IL-3 + GM-CSF (p < 0.01) for 48 hours, as compared with the percentage of cells in S phase before culture. It is well known that many drugs which are widely used in the treatment of acute leukemia are cytotoxic mainly to proliferating cells, so that if quiescent G0 phase cells can be induced to the proliferative stage, the treatment of acute leukemia would become more effective. The present findings showed that a considerable variation was observed among individual patients in the induction of the G0 component to the proliferative stage.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

PubMed1992

Vincristine-resistant human leukemia cell line: new monoclonal antibodies to a 65kDa membrane protein.

A vincristine-resistant human myelomonocytic leukemic cell line (KY-VCR) was established. KY-VCR exhibited approximately a 2.5 x 10(6)-fold increase in resistance to vincristine compared to the parental cell line. KY-VCR showed a decreased uptake and, an increased efflux of vincristine, and cross-resistance to Adriamycin and Actinomycin D. The M(r) 200,000 membrane glycoprotein was overexpressed in KY-VCR. Furthermore, two antibodies, designated TO73 and TO77, preferentially reacting with KY-VCR were obtained. Enzyme linked immunosorbent study indicated that both antibodies recognized the same epitope and TO77 the wide portion. Immunoprecipitation analysis demonstrated that the antibodies recognized M(r) 65,000 membrane protein, which was distinct from overexpressed glycoprotein in KY-VCR. The induction of membrane protein identified by the antibodies may play a role in drug resistance. KY-VCR cells and two antibodies to them may be very useful for the study of drug resistance and prediction of drug efficacy.

Antibodies, Monoclonal↗

PubMed1992

Diastolic mitral regurgitation in intact mitral valve detected by color Doppler echocardiography in a patient with acute aortic regurgitation.

A 38-year-old man was admitted with coingestive heart failure due to infective endocarditis. Echocardiography with color Doppler imaging revealed severe aortic regurgitation, mitral valve premature closure and diastolic mitral regurgitation. The flow of the diastolic mitral regurgitation was directed to the posterior wall of the left atrium through just behind the posterior mitral leaflet. The diastolic mitral regurgitation was observed only in the period of late diastole and no mitral regurgitation could be detected in the systolic phase. After successful aortic valve replacement, the diastolic mitral regurgitation disappeared completely.

Adult↗

PubMed1992

Risk factors and the effects of xamoterol in idiopathic dilated cardiomyopathy.

A long-term follow-up study was performed for 110 patients with idiopathic dilated cardiomyopathy (DCM) for 34 +/- 12 months (range 3-122 months). Thirteen patients died of heart failure, 15 of sudden death and one of non-cardiac death. The 3- and 5-year survival rates were 78 and 62%, respectively. The important factors in predicting the 3-year survival rate were left ventricular end-diastolic volume index (LVEDVI > or = 150 ml/m2 = 66%, < 150 ml/m2 = 93%, p < 0.01), myocardial cell diameter (> 25 microns = 42%, < or = 25 microns = 87%, p < 0.05) and sustained ventricular tachycardia (VT present = 32%, absent = 85%, p < 0.01). In a prospective study, 26 patients with DCM were given a beta 1-partial agonist, xamoterol (200 mg daily) and were followed for 35 +/- 15 months (6-53 months). The cardiothoracic ratio, left ventricular end-diastolic dimension and exercise heart rate decreased, and the exercise duration, fractional shortening and ejection fraction increased after xamoterol therapy. The 3-year survival rate was 83%. These results suggest that the important factors in predicting the survival rate of DCM patients were LVEDVI, myocardial cell diameter and the occurrence of VT. Adjunctive xamoterol therapy in DCM had a beneficial effect on hemodynamics and symptoms.

Adolescent↗

PubMed1992

[Acute hemodynamic effects of pimobendan and captopril: a comparative study in the same patients with chronic heart failure].

In this study, the acute hemodynamic effects of pimobendan (2.5 mg), a new drug, was compared with that of captopril (12.5 mg) in the same 8 patients with chronic heart failure (NYHA class II-III); 3 with dilated cardiomyopathy and 5 with regurgitant valvular heart disease. The hemodynamics were serially assessed before and after drug administration for at most 6 hours. Pimobendan reduced mean blood pressure, mean pulmonary artery pressure, pulmonary capillary wedge pressure, right atrial pressure, total systemic vascular resistance, and total pulmonary vascular resistance but it increased heart rate. By contrast, captopril reduced mean blood pressure and double product. No significant changes were noted in the cardiac index, stroke volume index, AV-O2 difference or the arterial oxygen pressure between the 2 drugs. In conclusion, pimobendan seems to function as a strong arterio-veno-dilator rather than as an inotropic agent in patients with chronic heart failure.

Aged↗

PubMed1992

[Clinical evaluation of effects of KRN8601 (rhG-CSF) on neutropenia].

Clinical effects of KRN8601 (recombinant human granulocyte colony-stimulating factor:rhG-CSF) were studied in 26 patients with chronic neutropenia including 4 Kostmann's disease, 1 Shwachman's syndrome, 1 Lonsdale's syndrome, 1 glycogen storage disease Ib-associated, 6 chronic benign, 5 chronic hypoplastic, 2 cyclic, 4 autoimmune and 2 miscellaneous neutropenia. The patients were given rhG-CSF intravenously at doses of 20-540 micrograms/m2 or subcutaneously at doses 20-400 micrograms/m2, over the periods of 2-32 weeks. Increases in neutrophil counts occurred after rhG-CSF administration in 23 of the 26 patients. Patients with Kostmann's disease, Shwachman's syndrome and chronic hypoplastic neutropenia responded poorly compared to patients with other types of neutropenia. There were no serious side effects which caused interruption of the study. These results indicated a beneficial effect of KRN8601 in various types of chronic neutropenia.

Adolescent↗

PubMed1992

Behaviour of tissue plasminogen activator, plasminogen activator inhibitor 1 and their complex in various disease states.

Plasma levels of tissue plasminogen activator (t-PA) antigen, plasminogen activator inhibitor 1 (PAI-1) antigen and t-PA/PAI-1 complex were measured in plasmas from 18 healthy subjects and 75 patients with various diseases (28 patients with haematological malignancies, 20 with thrombotic diseases, five with infectious diseases, four with liver diseases, ten with bleeding disorders and eight miscellaneous conditions). In addition, we studied ten patients with bleeding disorders after DDAVP infusion and 18 healthy subjects after venous occlusion. Plasma levels of t-PA antigen, PAI-1 antigen and t-PA/PAI-1 complex were increased in the patients compared with the healthy subjects. t-PA/PAI-1 complex levels correlated well with t-PA antigen levels and molar concentrations of t-PA antigen were similar to those of the t-PA/PAI-1 complex. Venous occlusion induced an increase in both t-PA antigen and PAI-1 antigen and the molar concentration of the t-PA/PAI-1 complex was equivalent to that of t-PA antigen. Following DDAVP infusion, the levels of t-PA antigen and t-PA/PAI-1 complex increased but PAI-1 antigen levels decreased, and the increase of t-PA antigen was greater than that of t-PA/PAI-1 complex. These findings indicate that PAI-1 antigen exceeds t-PA antigen in healthy subjects and in patients with various diseases. We conclude that part of the t-PA/PAI-1 complex is rapidly cleared from the circulation and that free t-PA increases after DDAVP infusion.

Adult↗