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Biomedical subjects

M Shimizu

Publications and source records attributed to M Shimizu.

At least 811 records · Page 45Linked to original sources
PubMed1994

Functional and immunoreactive thrombomodulin expressed by keratinocytes.

In an immunohistopathologic study using two monoclonal antibodies that recognize independent epitopes on human thrombomodulin, we detected expression of thrombomodulin on Malpighian-layer keratinocytes, but not on the basal or upper granular-layer keratinocytes. Western blotting and thrombomodulin-specific enzyme-linked immunosorbent assay performed on both shaved skin and cultured SV40-transformed keratinocytes showed the expression of full-length thrombomodulin, indistinguishable from endothelial thrombomodulin. Thrombomodulin was expressed by keratinocytes in 1 mM calcium but not in reduced calcium. A functional assay for thrombomodulin revealed that epidermal-derived thrombomodulin possessed cofactor activity for thrombin-catalyzed protein C activation. The limited pattern of expression of thrombomodulin in epidermis implies that this molecule may be a differentiation marker of keratinocytes in addition to being a potent anticoagulant in the skin.

Blotting, Western↗
PubMed1994

Neural blockade, urokinase and prostaglandin E1 combination therapy for acute digital ischemia of progressive systemic sclerosis.

To treat severe painful digital ulcers on progressive systemic sclerosis (PSS) patients, we developed a new combination therapy which included neural blockade, intravenous urokinase, and prostaglandin E1 infusion. All of these are already recognized treatments for circulatory disturbances in PSS. Although each of them alone has a limited effect on the painful ischemic attack in PSS; in stepwise combination, neural blockade for release of vascular spasm and pain, prostaglandin E1 for further vasodilatation, and urokinase for thrombolysis were effective in the treatment of digital ischemia in two PSS patients. This therapy reduced the necrotic areas predicted before therapy and saved fingers from amputation. It also relieved the intolerable digital pain and effected the recovery of digital function.

Adult↗
PubMed1994

Conversion of antinuclear antibody specificity as a marker of deterioration of cutaneous lupus erythematosus into lupus nephritis.

A 34-year-old male systemic lupus erythematosus patient (SLE) with cutaneous vasculitis developed renal failure after switching anti-nuclear antibody (ANA) specificity. He developed cutaneous lupus erythematosus with homogeneous and speckled type ANA and a high titer of anti-DNA antibody without renal involvement at 21 years of age. After developing lupus nephritis at the age of 27, the original ANA disappeared gradually. Two years later, a discrete speckled type ANA titer elevated abruptly to as high as 1:640 with low complementemia and without DNA antibody. Within five years, he suffered renal failure. This case of SLE suggests a direct correlation with ANA pattern and organ involvement.

Adult↗
PubMed1994

Increase in serotonin 1A receptors in the dentate gyrus as revealed by autoradiographic analysis following repeated electroconvulsive shock but not imipramine treatment.

The effects of repeated treatment with electroconvulsive shock (ECS) and imipramine on [3H]8-OH-DPAT binding to serotonin1A (5-HT1A) receptors in the rat brain were studied by quantitative autoradiographic analysis. A large number of binding sites for [3H]8-OH-DPAT were observed in the hippocampus, especially the dentate gyrus, CA1+CA2 field, dorsal raphe nucleus and septum. Repeated treatment with ECS, but not repeated imipramine treatment, significantly increased [3H]8-OH-DPAT binding sites in the dentate gyrus. These results suggest that the increase in [3H]8-OH-DPAT binding sites in the dentate gyrus may be important in ECS therapy for depressive illness.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1994

IgA deposits might not influence the production of extracellular matrix in glomeruli of ddY mice, a spontaneous animal model for IgA nephropathy.

Immunofluorescence studies were carried out to determine whether the expression of extracellular matrix (ECM) in glomeruli of ddY mice, a model for IgA nephropathy (Berger's disease), is influenced by treatment with a rat monoclonal antibody to murine CD4 molecules (mAb CD4). This mAb CD4 showed a selective decrease in the number of CD4+ T cells in the peripheral blood of ddY mice as described previously. The ddY mice were initially treated with intravenous injections, followed by weekly intraperitoneal injections of mAb CD4. In immunofluorescence, the mean intensity of IgA deposits in the renal glomerular mesangial areas and capillary walls of the treated ddY mice was significantly lower than that in saline-treated control mice at comparable ages. There was no significant difference in the distribution or intensity of ECM components, i.e. type IV collagen, fibronectin and heparan sulfate proteoglycan, in glomeruli between the mAB CD4-treated and the control ddY mice. In light microscopy, mesangial expansion in the treated ddY mice was milder than that found in the saline control mice. No significant differences in the average number of intraglomerular cells, levels of serum IgA and urinary protein between the treated and control ddY mice were observed. Thus, it appears that although CD4+ T cells modulate the amounts of glomerular IgA deposits, other factors may be involved in the expression of ECM in glomeruli of IgA nephropathy in ddY mice.

Animals↗
PubMed1994

Brain ischemia decreases phosphatidylcholine-phospholipase D but not phosphatidylinositol-phospholipase C in rats.

BACKGROUND AND PURPOSE: Phosphatidylcholine (PC)-phospholipase D (PLD) is an important intracellular signaling pathway in response to a variety of agonists, but little is known about the effects of brain ischemia on the PC-PLD system. We thus have examined the effects of global cerebral ischemia on PLD in rats. METHODS: We have examined the effects of global ischemia (decapitation or four-vessel occlusion) on PLD and PLC activity in the membrane fraction of rat brains. We measured the PLD and PLC activity in detergent-mixed micelle assay systems using 3H-labeled exogenous substrate. RESULTS: The results demonstrate that basal PLD activity showed a gradual decrease with increased duration (5 to 30 minutes) of ischemia by decapitation in the hippocampus; after 30 minutes of ischemia, PLD activity was significantly decreased compared with the control. Lineweaver-Burk plots showed that the apparent Vmax value of PLD in ischemia was one half of that in the control without changes in Km value. Ischemia by decapitation significantly decreased PLD activity in the brain stem as well as the hippocampus, whereas in four-vessel occlusion study, ischemia significantly decreased PLD activity in the hippocampus but not in the brain stem. Lowered temperature (30 degrees C and 22 degrees C) during ischemic incubation did not reverse the ischemia-induced PLD activity decrease. In contrast to PLD, ischemia by decapitation had no effect on basal phosphatidylinositol-phospholipase C activity or the amount of phospholipase C beta 1 in the membrane fractions from 30-minute ischemic hippocampus by immunoblots probed with the antibody. CONCLUSIONS: These results suggest that PC-PLD is one of the target enzymes of ischemia; its decrease may cause a perturbation of PC hydrolysis and/or disorders of intracellular transduction of signals or choline metabolism for acetylcholine formation in brain.

Animals↗
PubMed1994

Anti-inflammatory constituents of topically applied crude drugs. V. Constituents and anti-inflammatory effect of Aoki, Aucuba japonica Thunb.

The Et2O-soluble fraction of the MeOH extract of the leaves of Aucuba japonica Thunb. showed an anti-inflammatory effect when topically applied to rats. E-Phytol, phytone, bis(2-ethylhexyl)phthalate and friedelin were isolated as active anti-inflammatory components inhibiting carrageenin-induced paw edema. The most effective, E-phytol, inhibited histamine-induced paw edema more potently than the compound 48/80-induced edema, suggesting that the mechanism of action is due to inhibition of the H1 receptor.

Administration, Topical↗
PubMed1994

Radiological and histological analysis of the structural changes in the rat parotid gland following release of Stensen's duct obstruction.

Sialography is the preferred method for diagnosis and treatment planning in obstructive sialadenitis. Although many experimental studies have reported changes following duct obstruction, those following release of obstruction have not been examined. The present study was undertaken to clarify: (1) the relationship between sialographic and histological changes; (2) the effects of duration and pressure of obstruction on gland recovery; (3) the possibility of establishing those sialographic features which indicate the prognosis for gland recovery. Stensen's ducts of rat parotid glands were obstructed for two different periods and at three different pressures in order to induce varying degrees of degenerative changes in the gland. The structural alterations resulting from release of obstruction were investigated by means of qualitative and quantitative microsialography and histology. Gland structure was assessed visually from the latter and classified into six groups: normal, recovery, and slight, moderate and severe degeneration and fibrous. Microsialograms were evaluated based on these groups. Qualitatively, microsialograms of the operated glands had a stricture in the obstructed region and dilation of the major ducts. Histological differences between recovery and degeneration glands were reflected in the morphology of peripheral ducts. The former showed a branch-like morphology similar to that of the normal group, and the latter contained small granule-like structures. Quantitatively, dilation of major ducts in the recovery group decreased compared with the other operated groups. There were no distinct sialographic features in the degeneration and fibrous groups which correlated with the degree of degeneration observed histologically. Duration and pressure of obstruction were highly predictive for prognosis for recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Isolation of porcine reproductive and respiratory syndrome (PRRS) virus from Heko-Heko disease of pigs.

Porcine reproductive and respiratory syndrome (PRRS) virus was isolated at high frequency from the sera and lungs of pigs affected with Heko-Heko disease. In addition, a considerable amount of Mycoplasma hyorhinis (Mhr) was also isolated from the lungs. Inoculation of gnotobiote pigs with the first isolate of PRRS virus resulted in the reproduction of proliferative and interstitial pneumonia. The virus was recovered from the inoculated pigs for long periods. Superinfection with PRRS virus and Mhr appeared to produce more serious pneumonia than inoculation with PRRS virus alone. In this study, the presence of PRRS virus was confirmed in Japan, and the PRRS virus was considered as being the most important pathogen for Heko-Heko disease.

Animals↗
PubMed1994

Days required for 75% suppression of ventricular premature contractions by antiarrhythmic agents obtained from continuous in-hospital ECG monitoring.

To determine the number of days required to obtain 75% suppression of ventricular premature contractions (VPCs) by antiarrhythmic agents, which was expressed as t1/4, we performed 32 in-hospital continuous all day ECG monitoring trials in four groups of 28 symptomatic patients (ages; 54 +/- 20 years-old) with frequent VPCs. Nine patients had no organic heart disease (group 1, 11 trials), nine had valvular heart disease (group 2, 10 trials), three had dilated cardiomyopathy (group 3, 3 trials) and seven had myocardial infarction within two to four weeks onset (group 4, 8 trials). All patients were monitored by ECG telemetry with an arrhythmia analyzer, which could count hourly and daily VPCs. Class I antiarrhythmic agents were given in 18 trials, class II in two trials and class I+ class II in 12 trials. Plasma concentrations of the antiarrhythmic agents were monitored in 11 trials. In 21 trials, t1/4 could be obtained; ten (91%), six (60%), three (100%) and two trials (25%) in the four groups, respectively (p < 0.05). The value of t1/4 in the four groups was 6 +/- 6, 7 +/- 6, 14 +/- 11 and 13 +/- 2 days, respectively (mean 8 +/- 7 days; N.S.). Immediate response to the initial antiarrhythmic agent administration, expressed as percent VPC count after three hours, correlated significantly with t1/4 (r = 0.696, p = 0.0006), but ejection fraction, patient's age, control VPC counts or plasma antiarrhythmic agent level did not correlate with t1/4. In conclusion, t1/4 is a useful index for the evaluation of VPC suppression, revealing wide inter-individual variations and can be roughly estimated from the immediate response to the initial antiarrhythmic agent administration.

Adolescent↗
PubMed1994

Type IV collagen in hypertrophic cardiomyopathy.

Basement membrane of myocytes from patients with hypertrophic cardiomyopathy who died suddenly, seemed to be discontinuous by immunohistochemical methods. With the use of the sandwich immunoassay technique, we determined the frequency of type IV collagen and its influence on functional abnormality in 31 patients with hypertrophic cardiomyopathy and controls. Hypertrophic cardiomyopathy exhibited significantly increased serum type IV collagen compared with controls. A significant correlation was observed between serum type IV collagen and fractional shortening (r = -0.42 p < 0.05), and end-diastolic volume (r = 0.40 p < 0.05), DT (r = -0.50 p < 0.05). These data suggest that serum type IV collagen enhances clusters of cell-surface type IV collagen, including an alteration of the cytoskeleton, which may account for functional abnormalities in hypertrophic cardiomyopathy. Considering the fact that microscopic examination is unable to resolve the structure of the myocardial basement membrane, measurement of serum type IV collagen is thought to be useful in the diagnosis of myocardial basement membrane injury and the progression of hypertrophic cardiomyopathy.

Aged↗
PubMed1994

Detection of anomalous origin of the left coronary artery by transesophageal echocardiography and magnetic resonance imaging.

Anomalous origin of the left coronary artery can lead to angina pectoris, acute myocardial infarction or even sudden death, especially during exercise. We present a patient in whom the anomalous origin of the left coronary artery from the posterior aortic (non-coronary) sinus produced ischemic chest pain. The anomaly was identified by transesophageal echocardiography (TEE) and magnetic resonance imaging (MRI) as well as by coronary angiography. TEE and MRI are useful for detecting anomalies of the coronary artery both clearly and noninvasively and for evaluating the mechanism of ischemia.

Chest Pain↗
PubMed1994

Uptake of remnant like particles (RLP) in diabetic patients from mouse peritoneal macrophages.

To investigate whether the remnant like particles (RLP), separated from serum by an immunoaffinity gel mixture of anti-apo B-100 and apo A-I monoclonal antibodies, are relevant to the initiation or progression of atherosclerosis, the incorporation of RLP into mouse macrophages was studied using histochemical and biochemical techniques. Remnant lipoproteins such as RLP are reported to contain a large quantity of chyloniron and very low density lipoprotein (VLDL) remnants, especially in diabetic patients. The RLP separated from the sera of 32 diabetic patients were found to be predominantly taken up into macrophages harvested from mouse abdominal cavities by the staining method applying oil red O. Furthermore, using 14C-oleate to prove the uptake of lipoproteins by macrophages, the uptake of RLP-VLDL, a VLDL fraction of RLP by ultracentrifugation, was the next highest to that of the oxidized LDL, which suggests that RLP-VLDL is also aggressively taken up by macrophages. The degree of uptake of RLP-VLDL by macrophages was positively correlated with HbA1c of these diabetic patients (r = 0.556, p < 0.01), irrespective of the ways of the treatment of diabetes. In conclusion, RLP can contribute to the foaming of macrophages, which in turn may explain the acceleration of atherosclerosis in diabetic patients.

Aged↗