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Biomedical subjects

M Fujiwara

Publications and source records attributed to M Fujiwara.

At least 361 records · Page 20Linked to original sources
PubMed1992

Endothelium-dependent contraction produced by acetylcholine and relaxation produced by histamine in monkey basilar arteries.

The present experiments were carried out to investigate the endothelium dependence of the responses to acetylcholine (ACh), arachidonic acid, and histamine in monkey basilar arteries. ACh and arachidonic acid caused endothelium-dependent contraction (EC) in both monkey and canine basilar arteries. The endothelium-derived contracting factor (EDCF) was probably thromboxane A2 (TxA2), as the EDC was attenuated by a cyclooxygenase inhibitor, TxA2 synthetase inhibitors, and TxA2 antagonists. On the other hand, histamine caused endothelium-dependent relaxation (EDR) in monkey and EDC in canine basilar arteries. The EDR in monkey basilar arteries was attenuated by a nitric oxide synthase inhibitor. The EDR and EDC were antagonized by tripelennamine but not by cimetidine, indicating that they are mediated by H1-receptors. From these results, we suggest that in the monkey basilar artery, either there are two types of endothelium (an EDCF type for ACh and arachidonic acid and an EDRF type for histamine) or there is a single type of endothelium with two types of signalling processes (one for EDC and one for EDR).

Acetylcholine↗
PubMed1992

Suppression of spontaneous murine lupus by inducing graft-versus-host reaction with CD8+ cells.

Splenic CD8+ (Lyt-2+) cells of C57BL/6 mice were injected into semiallogeneic (NZB x BXSB)F1 mice, which spontaneously develop lupus nephritis, in order to examine whether the disease was somehow modified by the occurrence of graft-versus-host reaction. The development of lupus nephritis in the F1 recipients was strongly inhibited and immunopathological parameters such as anti-DNA antibodies, circulating immune complexes (CIC) and splenic immunoglobulin-producing cells (IgPC) were markedly reduced. The injection of CD4+ (L3T4+) T cells into F1 recipients did not result in similar effects. These findings suggest that the development of autoimmune disease could be ameliorated by CD8+ cells responding to MHC class I antigens. The significance of the data is discussed in terms of the treatment of autoimmune diseases.

Animals↗
PubMed1992

A mosaic case of isodicentric chromosome 18.

A case of mosaicism of isodicentric chromosome 18 is reported. Dicentric chromosome 18 occurs rarely and only five cases of isodicentric chromosome 18 have been documented. A high resolution banding method revealed that the karyotype of the patient was mos 46,XX/46,XX idic(18)(pter-->q21.3::q21.3-->pter), and the ratio of normal and abnormal clones was 1:1. The clinical manifestations, resembling those of trisomy 18 syndrome, were affected by both partial trisomy 18pter-->q21.3 and partial monosomy 18q21.3-->qter.

Child↗
PubMed1992

In vivo lymphocyte-mediated myocardial injuries demonstrated by adoptive transfer of experimental autoimmune myocarditis.

BACKGROUND: To elucidate the mechanisms of immune-related myocardial injuries, we examined whether autoimmune myocarditis was passively transferable by use of humoral or cellular factors. METHODS AND RESULTS: Active myocarditis was elicited in Lewis rats by immunization with human cardiac myosin fraction in complete Freund's adjuvant. This experimental myocarditis was characterized by macroscopic features such as pericardial effusion, enlargement of the heart, and gray discoloration of the cardiac surface. Histologically, extensive myocardial necrosis and numerous inflammatory cell infiltrations were observed. Interestingly, multinucleated giant cells were frequently observed in the lesions. Transfer of the disease by the humoral factor was examined by use of fresh sera and immunoglobulin fraction of pooled sera from rats with severe myocarditis, and transfer by the cellular factor was tested by use of spleen cells and lymph node cells from the diseased rats. When naive Lewis rats were given 15.75 mg of immunoglobulin fraction, no particular change was observed in the hearts. Fresh sera also could not elicit myocarditis in recipient rats. In contrast, intravenous injection of spleen cells or lymph node cells that were cultured for 3 days in the presence of 1 microgram/ml of concanavalin A elicited severe myocarditis. The macroscopic and microscopic findings of passively transferred myocarditis are essentially the same as those found in actively induced myocarditis. Multinucleated giant cells were also observed in the lesions of transferred myocarditis. CONCLUSIONS: This study demonstrates direct evidence for in vivo lymphocyte-mediated myocardial injuries.

Animals↗
PubMed1992

Syntheses and anti-inflammatory activity of novel oximes and O-acyloximes.

Novel oximes were prepared from the corresponding aldehyde or ketone in the usual way, and a number of oxime esters, O-lauroyl, O-2-pyridinecarbonyl, O-nicotinoyl, and O-isonicotinoyl oximes were synthesized by 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide (EDCI)-4-dimethylaminopyridine (DMAP) method or a mixed anhydride method, in our search for potent anti-inflammatory compounds. The anti-inflammatory activity of these compounds was assessed by the carrageenan-induced paw edema assay in rats. The oximes (4, 5, and 13), O-lauroyloxime 1L, O-nicotinoyloximes (1N, 2N, 3N, and 4N), O-isonicotinoyloxime 1I, and O-2-pyridinecarbonyloxime 7P showed higher anti-inflammatory potency than aspirin, a prostaglandin cyclooxygenase inhibitor.

Animals↗
PubMed1992

Effect of nebracetam on the disruption of spatial cognition in rats.

Central cholinergic hypofunction causes the disruption of spatial cognition, while cholinomimetics improve this disruption in rats. Scopolamine (0.5 mg/kg, i.p.) has also been reported to disrupt radial maze performance in rats. Nebracetam (WEB 1881 FU), a new nootropic candidate, was able to correct this scopolamine-induced disruption of spatial cognition at the dose of 10 mg/kg, p.o. Furthermore, nebracetam enhanced oxotremorine-induced tremors in mice. These results indicate that nebracetam has a cholinergic enhancing effect. The scopolamine-induced disruption of spatial cognition has been previously reported to improve not only by cholinomimetics but also by brain noradrenergic drugs such as L-threo-DOPS and amantadine. Nebracetam reversed the change of brain noradrenaline contents in the frontal cortex and hippocampus in which the noradrenaline content decreased by treatment with scopolamine. Nebracetam also decreased the delta 9-tetrahydrocannabinol (6 mg/kg, i.p.)-induced disruption of spatial cognition, which was reported to be related to the lymbic noradrenergic function. These results suggest that the cognitive enhancing effect of nebracetam involves not only cholinergic mechanisms but also involves lymbic and hippocampal noradrenergic mechanisms.

Animals↗
PubMed1992

A uniform alteration in serum lipid metabolism occurring during inflammation in mice.

The present study was designed to delineate changes in serum lipid levels following various kinds of tissue injury or inflammation such as contact sensitivity to picryl chloride, thermal burn, carrageenin-induced edema, the administration of turpentine oil, Freund's complete adjuvant (FCA), killed Bordetella pertussis (BP) or lipopolysaccharide (LPS). A uniform change in the serum lipid metabolism was observed in mice that received these inflammatory stimuli; that is, increases in total cholesterol, free cholesterol and phospholipid levels, a decrease in the ester ratio and a decline in lecithin: cholesterol acyltransferase activity as well as a decrease in albumin levels, which is an index of the acute-phase response. However, serum triglyceride levels were increased by treatment with the bacterial stimuli (FCA, BP and LPS) but decreased by treatment with the other stimuli. The serum free cholesterol and phospholipid levels were significantly correlated with the intensity of contact sensitivity, which was modified by treatment with cyclophosphamide. Indomethacin or dexamethasone suppressed carrageenin-induced edema and inhibited some of the alterations in lipid metabolism that developed during inflammation because each affected a part of the lipid metabolism. These findings suggest that, like the appearance of acute-phase proteins, the uniform change in serum lipid metabolism may be another sensitive index of the acute inflammatory response.

Animals↗
PubMed1992

Neurokinin A-stimulated phosphoinositide breakdown in rabbit iris sphincter muscle.

Specific [3H]-substance P binding was saturable and of high affinity (KD = 2.5 nM) with a Bmax of 725 fmol/mg protein in the isolated rabbit iris sphincter muscle. The competition for [3H]-substance P binding was in the order of eledoisin greater than substance P greater than kassinin greater than neurokinin B greater than neurokinin A greater than physalaemin. In the same preparation, neurokinin A, as well as substance P induced a concentration-related accumulation of [3H]-inositol phosphates (IPs), and the maximum increase was about 200% of the control at 10(-4) M. [D-Arg1, D-Trp7,9, Leu11]-substance P (SP) and [D-Pro2, D-Trp7,9]-SP (10(-3) M) inhibited substance P or neurokinin A (10(-4) M)-induced phosphatidylinositol 4,5-bisphosphate (PIP2) hydrolysis significantly. [D-Arg1, D-Pro2, D-Trp7,9, Leu11]-SP (10(-3) M) also inhibited neurokinin A (10(-4) M)-induced PIP2 hydrolysis significantly. Neurokinin A and substance P produced concentration-related contractions in normal Ca(2+)-containing medium. The contractile response was weaker in Ca(2+)-free medium, and there was no response in 0.2 mM EGTA medium. In Ca(2+)-free medium, the basal level of [3H]-IPs accumulation was smaller than that in normal medium, and neurokinin A and substance P significantly increased PIP2 hydrolysis. In the 0.2 mM EGTA containing medium, neurokinin A and substance P did not stimulate the PIP2 hydrolysis.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Impairment of endothelium-dependent relaxation in aorta from rats with arteriosclerosis induced by excess vitamin D and a high-cholesterol diet.

The present investigation was undertaken to characterize the relaxing responsiveness in aortic strips from rats with arteriosclerosis, which was produced by excess vitamin D2 (VD) administration followed by treatment with or without a high-cholesterol diet for 6 weeks (VD + CHOL and VD group, respectively). This arteriosclerotic aorta was characterized by medial calcification and intimal cell proliferation. Helical strips of thoracic aorta were suspended in oxygenated Krebs-Henseleit solution. Under precontraction with noradrenaline, endothelium-dependent relaxations to acetylcholine were significantly attenuated in the VD and VD + CHOL as compared with the control. Relaxation to calcium ionophore A23187 was also significantly attenuated in the VD + CHOL. However, the relaxing responses to acetylcholine and A23187 in aortas from rats fed a high-cholesterol diet alone remained unaffected. Nitroglycerin caused an equal degree of relaxation in aortas from control and arteriosclerotic rats. There was a significant negative correlation between the relaxing response to acetylcholine and the calcium content in the aorta. These results indicate that in arteriosclerotic rat aortas, the endothelium-dependent relaxation to acetylcholine is impaired in proportion to the degree of calcification, and such impairment is facilitated by cholesterol feeding but can not be attributed to hypercholesterolemia or vascular cholesterol deposition.

Acetylcholine↗
PubMed1992

Analysis of swinepox virus antigens using monoclonal antibodies.

Seventeen monoclonal antibodies (MAbs) against swinepox virus (SPV) were produced and characterized. These MAbs were classified into eight groups (A through H) on the basis of the molecular weight of the polypeptides which they recognized and the staining patterns of antigens in SPV-infected cells by the indirect immunofluorescent (IF) technique. The MAbs belonging to groups A, B, C and G recognized late antigens in cytoplasmic inclusion bodies with molecular weights of 97 kD, 65 kD, 48 kD and 15 kD, respectively. The MAbs belonging to groups D and H respectively recognized 35 kD and 12 kD late antigens, which first appeared in cytoplasmic inclusion bodies and spread to the cytoplasms and surface membranes of the infected cells. The MAb of group F recognized an 18 kD late antigen with granular distribution in the cytoplasm. The MAbs of group E recognized a 32 kD early antigen. Although all the MAbs belonging to the six groups (A, D through H) were specific for SPV, some of those belonging to groups B and C showed cross-reactivity with members of the other genera of poxviridae. An MAb in group B, SP14, cross-reacted with orf and rabbit fibroma viruses. Two MAbs in group C, SP24 and SP32, cross-reacted with vaccinia, cowpox, ectromelia, and rabbit fibroma viruses. These findings indicate that at least two SPV antigens contain cross-reactive epitopes with different genera of poxviridae.

Animals↗
PubMed1992

Histological characteristics of lupus nephritis in F1 mice with chronic graft-versus-host reaction across MHC class II difference.

Renal lesions at the chronic phase of MHC class-II-disparate graft-versus-host reaction (GVHR) were examined. To induce GVHR, C57BL/6 (B6) spleen cells were injected twice into either (B6 x bm12)F1 (class-II-disparate), (B6 x bm1)F1 (class-I-disparate) or (bm1 x bm12)F1 mice (class-I + II-disparate). For comparison, (C57BL/10 x DBA/2)F1 (BDF1) mice injected with DBA/2 spleen cells were also used. (B6 x bm12)F1 and BDF1 recipients showed marked elevation of anti-DNA antibodies, circulating immune complexes (CIC) and the number of immunoglobulin producing cells (IgPC). At 20 weeks after cell injection, severe immune complex glomerulonephritis (ICGN) was observed in (B6 x bm12)F1 recipients, but was far less severe in (bm1 x bm12)F1 recipients and was not observed in (B6 x bm1)F1 recipients. ICGN was also observed in BDF1 recipients at 12 weeks after cell injection. By immunofluorescent microscopy, IC deposition was detected along the capillary loops and also in the mesangial area in (B6 x bm12)F1 recipients, while BDF1 recipients showed only a capillary pattern. By light microscopy, the renal lesion of (B6 x bm12)F1 recipients appeared similar to those of BDF1 recipients. Histologically, (B6 x bm12)F1 recipients serve as a good model for lupus glomerulonephritis induced by class-II-disparate GVHR.

Animals↗
PubMed1992

Evaluation of the effect of PTCR/PTCA by 99mTc-MIBI myocardial imaging in acute and old myocardial infarction.

This study is to clarify the ability of technetium-99m-Hexakis-2-methoxyisobutyl isonitrile(MIBI) myocardial scintigraphy for assessment of the effect of PTCR/PTCA as compared with conventional thallium-201 myocardial scintigraphy (201Tl). 99mTc-MIBI (740-888MBq) was injected before emergency PTCR/PTCA, and the initial imaging was performed immediately after PTCR/PTCA in 4 patients with acute myocardial infarction (AMI). On the other hand, in 2 patients with old myocardial infarction (OMI), 201Tl and MIBI myocardial imagings were performed before and one week after rescue PTCA. The defect area on the follow-up MIBI imaging was smaller than that on the initial MIBI imaging in 2 patients with successful emergency PTCR/PTCA. But in the other 2 AMI patients with unsuccessful reperfusion, the defect area did not significantly decrease after PTCR/PTCA. Reperfusion was successful in one of the two patients with OMI. In both the two patients with OMI, the MIBI defect area did not significantly decrease after rescue PTCA. MIBI myocardial scintigraphy is a useful noninvasive method for evaluating the effect of emergency PTCR/PTCA for myocardial salvage in patients with AMI, because MIBI is a kit type agent, and it does not redistribute.

Aged↗
PubMed1992

Immune regulation by brain cells in the central nervous system: microglia but not astrocytes present myelin basic protein to encephalitogenic T cells under in vivo-mimicking conditions.

The antigen-presenting capability of various types of brain cell, such as primary mixed glial cells, astrocytes and microglia, was examined under conditions in which Ia antigen expression on the cultured cells mimicked that in the central nervous system (CNS) of rats with experimental autoimmune encephalomyelitis (EAE). In the CNS of rats with EAE, microglia but not astrocytes express Ia antigens. To produce such conditions, cultured brain cells were treated with various concentrations of interferon-gamma (IFN-gamma). It was revealed that in vivo-like conditions were produced when cultured brain cells were treated with less than 100 U/ml IFN-gamma. Under such conditions, microglia presented an antigen, myelin basic protein (MBP), to MBP-specific T-cell lines. Astrocytes, on the other hand, did not show antigen-presenting ability, but rather suppressed T-cell proliferation. Primary mixed glial cells, mainly comprising astrocytes and microglia, were also weak antigen-presenting cells (APC). These findings suggest that brain cells comprising various types of cell with regard to APC function do not up-regulate the proliferation of encephalitogenic T cells in vivo, although a particular type of brain cell, i.e. microglia, show antigen-presenting capability.

Animals↗
PubMed1992

[A case of painless myocardial injury probably caused by coronary artery spasm].

A 53-year-old male was admitted to the hospital due to electrocardiographic ST-segment elevation in V1-4 with ST-segment depression in the inferior leads, which suggested acute myocardial infarction. He had a cough and a slight fever without chest pain. Serum creatine kinase and its myocardial band were slightly elevated but creatine kinase value did not exceed twice the normal upper limit. Emergent coronary arteriography (CAG) revealed intact coronary arteries. The CAG in a chronic stage again revealed intact coronary arteries. Intracoronary administration of acetylcholine of 100 micrograms to the left coronary artery and 50 micrograms to the right coronary artery provoked diffuse spasm in the right and left coronary arteries. The electrocardiogram (ECG) during the right coronary artery spasm revealed ST-segment depression in the inferior leads with ST-segment elevation in V2 and V3, which resembled the ECG finding at the time of the patient's admission. With intracoronary isosorbide dinitrate, the spasm and ST-segment elevation were resolved. These findings strongly suggest that coronary spasm can cause myocardial injury indicated by a slight elevation of serum creatine kinase value.

Coronary Angiography↗