Search PubMed⌕ Search

Biomedical subjects

S Abe

Publications and source records attributed to S Abe.

At least 595 records · Page 33Linked to original sources
PubMed1993

Interleukin 6-producing malignant mesothelioma.

Systemic amyloidosis of the amyloid A (AA) type, is occasionally associated with various neoplasms, but the cause is still unclear. We obtained interleukin 6 (IL-6)-producing cells designated YO from a primary culture of a malignant peritoneal mesothelioma of epithelial type obtained from a 62-year-old woman. Post mortem examination revealed that the patient had systemic amyloidosis of the AA type. The supernatant media of YO cells, as well as recombinant human IL-6, successfully induced nonneoplastic liver cells to produce serum AA (SAA). Our data suggest that IL-6 produced by the tumor cells may have played an important role in the paraneoplastic syndrome of AA amyloidosis in this patient.

Amyloidosis↗
PubMed1993

Cerebrocerebellar relationships in normal subjects and patients with dementia of the Alzheimer type: a SPECT study.

The relationships between blood flow in the cerebrum and the cerebellum was investigated in 21 normal subjects and 21 patients with dementia of the Alzheimer type (DAT). In normal subjects, only asymmetry in the frontal cortical blood flow was significantly correlated with asymmetry in the contralateral cerebellar blood flow. However, a significant correlation between asymmetry in the cerebral cortical blood flow in many areas and the blood flow in the contralateral cerebellum in DAT patients was observed. These results suggest the existence of a functional relationship between the cerebrum and the cerebellum in both normal and DAT groups, mediated by neuronal mechanisms through crossed fiber pathways. However, there are regional differences in the cerebrocerebellar relationship in normal resting and pathological states.

Aged↗
PubMed1993

Detection of reperfusion 30 and 60 minutes after coronary recanalization by a rapid new assay of creatine kinase isoforms in acute myocardial infarction.

We measured creatine kinase (CK) isoforms by a new immunoinhibition method to evaluate their usefulness in detecting early coronary reperfusion. Blood samples were collected at 15-minute intervals from 50 patients with acute myocardial infarction. CK isoforms were determined by a 10-minute immunoinhibition method with an autoanalyzer. Values for inhibited isoforms (MM3, MM2/2, and MB2/2) were divided by those of noninhibited isoforms (MM1, MM2/2, MB1, MB2/2, and BB) to calculate the isoform ratio. In the reperfused group the increase in the isoform ratio was 2.69 +/- 1.80 (SD) 30 minutes after reperfusion and 2.41 +/- 2.01 at 60 minutes, which was significantly higher than the corresponding values in the nonreperfused group (0.17 +/- 0.16 and 0.32 +/- 0.26, respectively). When an increase of 0.70 or more in the isoform ratio was used as the criterion for reperfusion, the sensitivity and specificity were 92% and 100% at 30 minutes and 100% and 100% at 60 minutes after recanalization, respectively. We conclude that the isoform ratio obtained by the new 10-minute assay of CK isoforms is useful for the noninvasive detection of reperfusion 30 and 60 minutes after recanalization in acute myocardial infarction.

Angioplasty, Balloon, Coronary↗
PubMed1993

Early detection of coronary reperfusion by rapid assessment of plasma myoglobin.

We assayed plasma myoglobin and creatine kinase to elucidate the usefulness of rapid assessment of myoglobin for detecting coronary reperfusion in 31 patients with acute myocardial infarction. Reperfusion was achieved in 20 patients by thrombolytic therapy or angioplasty, and it was not in 11 patients. Blood sampling was performed before and 43 +/- 15 (+/- SD) min after the start of treatment. In the reperfused group, blood samples were obtained before and 26 +/- 10 min after reperfusion. Myoglobin was assayed by a new quantitative test based on latex agglutination turbidimetry which required an assay time of 10 min. After treatment, the rate of increase of plasma myoglobin was significantly higher than that of plasma creatine kinase in the reperfused group (9.7 +/- 9.5 and 2.8 +/- 1.6-fold), but not in the occluded group (1.8 +/- 0.6 and 1.5 +/- 0.3-fold). When a 3.0-fold or greater increase in myoglobin (1.9-fold or greater increase in creatine kinase) was taken as evidence of coronary reperfusion, the sensitivity and specificity were 95% and 100% (70% and 82% in creatine kinase), respectively. In conclusion, using the rate of increase of myoglobin, as measured by latex agglutination turbidimetry, coronary reperfusion can be diagnosed within 1 h after reperfusion.

Adult↗
PubMed1993

Physiological correlates of abnormal behaviors in magnesium-deficient rats.

In order to elucidate the mechanism of behavioral alterations in magnesium-deficient rats, changes in the electroencephalogram (EEG) and electrocardiogram (ECG) were studied during auditory stimulation and correlated with the behavioral alterations. Weanling rats were fed either a Mg-deficient diet or a control synthetic diet for 2-3 weeks before the experiment. EEGs were recorded from the hippocampus and the sensorimotor and auditory cortices, and ECGs with a telemetry system. White noise with an intensity of 100 dB was given continuously to induce behavioral changes. The Mg-deficient rats developed consistent and graded behavioral changes in response to the stimulation, showing running-jumping behavior (stage 1), followed by tonic limb convulsion (stage 2) and finally by falling down on the floor (stage 3). The EEGs also showed consistent changes with spike activity, initiating in the hippocampus (stage 2) and then spreading to the neocortices bilaterally (stage 3). These findings indicate that the behavioral changes induced by auditory stimulation in the Mg-deficient rats are due to seizures arising in deeper brain structures, particularly in the limbic system, and projecting secondarily to the neocortices. The ECG changes, mainly consisting of marked bradyarrhythmia, occurred as early as the appearance of the EEG spikes, indicating that they were also related to the seizure. We conclude therefore that Mg deficiency in rats causes increased excitability of the central nervous system, resulting in seizures possibly originated in the limbic system, later developing secondary generalization, and also causing cardiac dysfunctions.

Acoustic Stimulation↗
PubMed1993

Light and electron microscopic study of remodeling and maturation process in autogenous graft for anterior cruciate ligament reconstruction.

We evaluated the remodeling process of autogenous patellar tendon graft for anterior cruciate ligament (ACL) reconstruction by means of light microscopic (LM) and electron microscopic (EM) examinations from the biopsy specimens obtained at the time of second-look arthroscopy. Twenty-one patients were examined at various times postoperatively (from 6 weeks to 15 months, mean 9.5 months), and the results were correlated with the morphology of normal patellar tendon and normal ACL. Our study showed that the graft was revascularized in the early postoperative period, fibroblastic remodeling took place, and the graft obtained gross similarity to the original ACL on their arthroscopic and LM appearances at approximately 1 year postoperatively. However, EM study showed that at both approximately 6 months and 1 year postoperatively the grafts consisted equally of active fibroblasts with a higher cytoplasm-to-nucleus ratio compared with normal ACL. Collagen fibrils of these grafts were of uniformly small diameter compared with normal patellar tendon and ACL. Our results with ultrastructural study suggest that the grafts were still immature even at 1 year postoperatively.

Adolescent↗
PubMed1993

Effects of isoprenaline on cytosolic calcium concentrations and on tension in the porcine coronary artery.

1. Using front-surface fluorometry and fura-2-loaded medial strips of the porcine coronary artery, cytosolic Ca2+ concentration ([Ca2+]i) and tension development were simultaneously monitored in an attempt to determine the mechanisms of vasorelaxation induced by l-isoprenaline (Iso). 2. Iso actively decreased [Ca2+]i of the strips at rest, both in the presence and absence of extracellular Ca2+. 3. In the presence of extracellular Ca2+, depolarization with high-external K+ solution induced an elevation of [Ca2+]i and tension of the rapid increase and sustained, steady-state type; both levels depended on external K+ concentration. When Iso was applied at the time of steady state of high-K(+)-induced [Ca2+]i elevation, there was an initial transient reduction (the first component) followed by a subsequent sustained reduction (the second component) of [Ca2+]i. For a given [Ca2+]i level during high-K+ depolarization, the tension developed in the presence of Iso was smaller than that in its absence. Thus, the [Ca2+]i-tension relationship during the steady state of high-K(+)-induced contraction was shifted to the right by Iso. Pretreatment with ryanodine, a compound which depletes Ca2+ stored in the sarcoplasmic reticulum, abolished the first component, but not the second sustained decrease in [Ca2+]i by Iso. 4. In the presence of extracellular Ca2+ (1.25 mM), histamine (Hist) induced an abrupt (the first component) and then sustained (the second component) elevations of [Ca2+]i, while the tension rose rapidly to reach the peak, and then, gradually declined. The second, but not the first, component of [Ca2+]i elevation depended on extracellular Ca2+. Iso inhibited both the first and the second components of [Ca2+]i elevation and the contraction induced by Hist, in a concentration-dependent manner (IC50, 2 x 10(-8) M for the first component, and 5 x 10(-8) M for the second component). Cumulative application of Hist (10(-7)-10(-4) M) increased [Ca2+]i and tension with the [Ca2+]i-tension relationship shifting to the left from that observed with high K+. The [Ca2+]i-tension relationship during the Hist-induced contraction shifted to the right by Iso. In contractions induced by a higher concentration (> or = 6 x 10(-5) M) of Hist, despite the negligible decrease in [Ca2+]i, Iso could relax the muscle in a concentration-dependent manner. 5. In the absence of extracellular Ca2+, Hist induced transient elevations of [Ca2+]i and tension, possibly due to a release of Ca2+ from intracellular stores, and with similar time courses to those of the first component observed in the presence of extracellular Ca2+.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Augmentation of murine tumor necrosis factor production by amphotericin B in vitro and in vivo.

Murine peritoneal macrophages were preincubated with amphotericin B (AMPH) and were then stimulated with bacterial lipopolysaccharide or streptococcal preparation (OK432). These macrophages produced a large amount of tumor necrosis factor. When administered to mice, the priming activity of amphotericin B for tumor necrosis factor production in vivo was also observed.

Amphotericin B↗
PubMed1993

Acute myocardial infarction without warning: clinical characteristics and significance of preinfarction angina.

We investigated the clinical characteristics of acute myocardial infarction (AMI) not preceded by angina in 256 patients with first AMIs. Complications, including sustained ventricular tachycardia or ventricular fibrillation, pump failure and cardiac rupture, were more frequent in patients with AMI not preceded by angina (group 1, n = 92) than those preceded by angina (group 2, n = 164). The in-hospital mortality rate was higher in group 1 than in group 2. Poor preexisting collateral channels or lack of ischemic preconditioning may be responsible for the poorer outcome in group 1 patients.

Aged↗
PubMed1993

Serial changes in plasma concentration of plasminogen activator inhibitor-1 before and serially after thrombolytic therapy for acute myocardial infarction.

Plasminogen activator inhibitor-1 (PAI-1), which is secreted from vascular endothelial cells, plays an important role in regulating fibrinolysis. We measured the plasma concentrations of tissue-type plasminogen activator (t-PA), PAI-1 and t-PA PAI complex before and serially after thrombolytic therapy for acute myocardial infarction to clarify the relationship between thrombolytic therapy and PAI-1. Plasma concentrations of t-PA, PAI-1 and t-PA PAI complex before thrombolytic therapy were 11.6 +/- 5.5, 27.0 +/- 13.0 and 7.3 +/- 5.4 ng/ml, respectively. t-PA and t-PA PAI complex increased to 25.0 +/- 5.3 and 14.3 +/- 6.5 ng/ml immediately after drug administration; however, the level of PAI-1 decreased slightly immediately after thrombolytic therapy. The PAI-1 level increased again several hours after therapy, especially in patients showing apparently successful reperfusion. All values returned to normal 4-7 days after thrombolytic therapy. Not only augmented antifibrinolytic activity suggested by increased PAI-1 but also augmented fibrinolytic activity suggested by increased t-PA was observed in patients with acute myocardial infarction. These abnormal findings persisted several days after coronary thrombolytic therapy.

Aged↗
PubMed1993

Inflammatory endotracheal polyp resolved after antibiotic treatment.

We describe a rare case of asymptomatic inflammatory endotracheal polyp resolved by antibiotic treatment. Histological examination of biopsy specimens showed an inflammatory polyp consisting of fibrovascular stroma and sparse lymphocyte infiltration. The size of the polyp was unchanged during 3 months without any treatment and its etiology was unclear. Although a bacterial organism was never proven, the polyp decreased remarkably under treatment with an oral antibiotic (ciprofloxacin) and did not recur for 6 months. Antibiotic treatment may be of value for inflammatory tracheobronchial polyps in cases of unclear etiology.

Ciprofloxacin↗
PubMed1993

Diagnostic accuracy of single photon emission computed tomography in Alzheimer's disease.

To determine whether the detection of parietotemporal functional abnormalities as demonstrated by single photon emission computed tomography (SPECT) can be employed as a diagnostic marker for Alzheimer's disease (AD), we studied 219 patients with neurologic disorders including 56 with AD and 25 healthy controls. The diagnostic sensitivity (parietotemporal hypoperfusion present in AD patients) was 82%, and the specificity (parietotemporal hypoperfusion absent in non-AD patients and controls) was 89%. These results suggest that SPECT imaging provides an accurate and sensitive diagnostic test for AD.

Aged↗
PubMed1993

Inhibition of IgE-mediated leukotriene generation and bronchoconstriction in primates with a new 5-lipoxygenase inhibitor, E6080.

The inhibitory effects of a novel compound, 6-hydroxy-2-(4-sulfamoylbenzylamino)-4,5,7-trimethylbenzothiazo le hydrochloride (E6080) on IgE-mediated reactions in vitro and in vivo were determined in rhesus monkeys. E6080 inhibited both antigen- and anti-human IgE-induced leukotriene C4 generations from lung fragments at similar concentrations: the IC50s of E6080 were 1.11 and 0.96 microM, respectively. AA861 also inhibited both leukotriene C4 generations with IC50s of 0.79 and 0.76 microM, respectively. All 9 monkeys demonstrating positive cutaneous reactivity against Ascaris antigen at < 10(-7) g protein/0.1 ml showed reproducible bronchoconstriction upon aerosolized antigen challenge, but 5 monkeys demonstrating weak or no reactivity to the antigen at levels > 10(-5) g protein/0.1 ml showed no significant bronchoconstriction. The high responder monkeys showed a marked increase in lung resistance (RL 335.3 +/- 85.3%, n = 11) and a decrease in dynamic lung compliance (67.7 +/- 4.2%, n = 11) after antigen challenge following pretreatment with diphenhydramine. These pulmonary changes lasted for more than 30 min. E6080 at oral doses of 3 and 10 mg/kg showed dose-dependent inhibition of both pulmonary changes. Ten milligrams per kilogram of E6080, administered 1.5 h prior to antigen challenge, significantly inhibited the changes in both parameters, while 3 mg/kg showed significant inhibition of only the RL change. These results demonstrate that E6080 inhibited immunologically stimulated leukotriene production in the lung, resulting in inhibition of the antigen-induced airway response in primates.

Animals↗
PubMed1993

Myocardial infarct size can be estimated from serial plasma myoglobin measurements within 4 hours of reperfusion.

BACKGROUND: An early estimation of infarct size is useful for the appropriate early treatment of patients with acute myocardial infarction. We evaluated how early and how accurately infarct size could be estimated from serial plasma myoglobin (Mb) measurements in patients with successful reperfusion. METHODS AND RESULTS: We measured plasma Mb and creatine kinase (CK) in 35 patients in whom reperfusion therapy was successfully performed. Blood samples were collected at 15-minute intervals for 2 hours after reperfusion, at 30-minute intervals for the subsequent 2 hours, and at 3-6-hour intervals until 52 hours after reperfusion. Plasma Mb was measured by a newly developed turbidimetric latex agglutination assay. Total Mb and CK release (sigma Mb, sigma CK) were calculated with a one-compartment model. The mean chord motion in the most hypokinetic 50% of the infarct-related artery territory was calculated from follow-up ventriculograms as an index of the severity of regional hypokinesis. There were significant correlations between sigma Mb and sigma CK (r = 0.89), between log sigma Mb and the severity of regional hypokinesis (r = -0.85), and between log sigma CK and the severity of regional hypokinesis (r = -0.74). The time required for the cumulative Mb release curves to reach a plateau was 64 +/- 28 minutes. An additional 53 +/- 14 minutes was required to calculate the disappearance rate constant of Mb, and 15 minutes was necessary for the assay. Therefore, the total time required for sigma Mb to be available was 132 +/- 40 minutes, significantly shorter than the time required for sigma CK, 24.3 +/- 9.1 hours (p < 0.001). The infarct size could be estimated from the sigma Mb in 34 of 35 patients within 4 hours of reperfusion. CONCLUSIONS: Infarct size can be estimated accurately 4 hours after reperfusion by calculating the sigma Mb in patients with successful reperfusion.

Clinical Enzyme Tests↗