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Biomedical subjects

Y Kurimoto

Publications and source records attributed to Y Kurimoto.

At least 55 records · Page 3Linked to original sources
PubMed1994

[Clinical study on re-surgery of the combined valvular disease: simultaneous double valve replacement].

Between June, 1984 and December, 1993, 36 patients who underwent simultaneous double valve replacement for re-surgery of combined valvular disease were analyzed in this study. The indications for re-surgery were malfunction of mechanical valve in the aortic position, primary tissue failure of biological valve in the mitral position, deterioration of valvular disease and prosthetic valve endocarditis. Re-surgery was performed ranging from 4 to 15 years, with a mean period of 9.5 years, following initial operation. Early operative mortality was 5.5% (2 cases) and late mortality 8.3% (3 cases). There were no cardiac deaths during the late postoperative period. Despite of technical difficulty due to dissection of the adhesion around the heart and re-replacement of prosthetic valve, the operative mortality and morbidity were relatively low because of the improved operative technique and myocardial protection.

Adult↗
PubMed1993

2-Buten-4-olide (2-B4O) inhibits type II collagen-induced arthritis in Lewis rats.

2-Buten-4-olide (2-B4O) is an endogenous substance which suppresses appetite and/or food intake. We studied its effect on type II collagen-induced arthritis (CIA) in Lewis rats, an animal model for human rheumatoid arthritis. Bovine type II collagen with incomplete Freund's adjuvant was injected intradermally into Lewis rats to induce CIA. 2-B4O (50 or 100 mg/kg) significantly inhibited the expression of the clinical symptoms when administered i.p. daily from day 1 to 21 after immunization. Furthermore, administration of 2-B4O daily from day 15 to 21 significantly reduced the severity of symptoms in established CIA. In addition, the progression of soft tissue swelling and articular bone erosions were suppressed by daily administration of 2-B4O. 2-B4O also significantly suppressed the delayed-type hypersensitivity (DTH) response to type II collagen at doses of 50 and 100 mg/kg. Finally 2-B4O significantly inhibited the formation of anti-type II collagen antibody at a dose of 100 mg/kg, but not at 50 mg/kg. These results suggest that 2-B4O has the strong inhibitory effects and therapeutic usefulness effects on CIA through the suppression of immune responses to type II collagen.

4-Butyrolactone↗
PubMed1992

First isolation of gamma-L-glutamyl-gamma-aminobutyric acid from bovine brains.

We had obtained some immunohistochemical indications which suggested that peptide(s) containing GABA at the C-terminal could exist in specific neurons in brains. We therefore sought such GABA conjugate(s) by isolating an acidic GABA-dipeptide from bovine brains and determined its structure as gamma-L-glutamyl-gamma-aminobutyric acid (gamma-L-Glu-gamma Abu:GluGABA). Its gamma-linkage was determined by a mass-spectrometric (B/E linked scan SIMS) analysis; its chirality was established by a chiral column HPLC technique. This peptide is the first acidic GABA-peptide recognized in brain and the first brain peptide containing GABA at the C-terminal.

Animals↗
PubMed1992

[Benefit of the autoperfusion balloon catheter for emergency coronary artery grafting after failed percutaneous transluminal coronary angioplasty].

A 61-year-old man was operated on an emergent basis because of abrupt closure of left anterior descending coronary artery (LAD) following failed coronary angioplasty. At once abrupt closure occurred, Stack autoperfusion balloon catheter was placed across the coronary lesion to reestablish blood flow to the ischemic myocardial area with intraaortic balloon counterpulsation. Despite a longtime of 12 hours to cardiopulmonary bypass, the patient had been managed with excellent resolution of symptoms and ST elevation. Under a stable hemodynamic state, saphenous vein grafting to LAD was performed with minimal myocardial infarction. Stack catheter made it possible to perform the subsequent coronary bypass operation as a controlled, optimal revascularization procedure because of its passive autoperfusion effect.

Acute Disease↗
PubMed1992

[A case of acute renal failure due to left contracted kidney, complicated by right renal infarction].

A 46-year-old woman, who had been treated with anti-arrhythmic drugs and digitalis for mitral stenosis and paroxysmal atrial fibrillation, suddenly developed severe abdominal pain and nausea. There was tenderness around right CVA. BUN and serum-creatinine were elevated, 57 mg/dl and 4.5 mg/dl respectively. She was in acute renal failure (ARF). WBC, GOT, GPT, LDH were also elevated. Abdominal ultrasonography showed normal-size right kidney (12 cm) and atrophic left kidney (8.5 cm). Selective right renal angiography revealed right renal arterial embolism, suggesting that ARF developed from right renal infarction complicated by left atrophic kidney. Renal scintigram using 99mTc-DTPA indicated non-function type left kidney. Because of the high risk of surgery, she received anticoagulant therapy. Fifteen days later, BUN and serum-creatinine returned to 14mg/dl, 2.2mg/dl, respectively.

Acute Kidney Injury↗
PubMed1991

Ontogenesis of the cerebellofugal projection in the rat.

Ontogenesis of the cerebellofugal projection was studied in the rat by the tract-tracing method with WGA-HRP. The projection, forming a uniform front of compact fibre bundle tipped by growth cones, began entering the brainstem on embryonic day 17 (E17), grew rapidly and orderly with no random extension of fibers, and arrived at the most rostral part of the thalamus already by E18, distributing dense terminals to various brainstem and thalamic nuclei. The course and termination of this projection in prenatal animals was largely similar to normal adult projection although differences were found. Some projections increased postnatally, whereas some projections which were existent in embryos regressed with age and finally disappeared completely. The adult pattern of the projection was attained by 3 weeks of age. It is worth noting that the projections which appeared transiently are similar to those reported as aberrantly regenerated projections in kittens which are born in more mature state than rats and have no such projections at birth.

Aging↗
PubMed1991

The effect of interleukin 3 upon IgE-dependent and IgE-independent basophil degranulation and leukotriene generation.

Recent investigations have shown that the hematopoietic growth factor interleukin 3 (IL 3) enhances histamine release of mature human basophils. Furthermore, basophils exposed to IL 3 generate large amounts of leukotriene C4 in response to C5a, a basophil agonist which by itself is unable to promote lipid mediator formation. Also IL 3 renders the cells responsive to factors which do not otherwise induce basophil mediator release. Here we show in more detail how IL 3 affects the release of preformed and newly synthesized inflammatory mediators by basophils in response to antigen, anti-IgE, N-formyl-methionyl-leucyl-phenylalanine (FMLP) and C5a. In cells triggered by maximally effective concentrations of these agonists, IL 3 enhances histamine release, although it more profoundly affects leukotriene generation, in particular in response to stimuli which by themselves are inefficient or poor inducers of lipid mediator formation. This change in the mediator-release reaction occurs at low IL 3 concentrations, over the same concentration range of IL 3 of 0.01-1.0 U/ml regardless of which triggering agent is used as a second signal. Pretreatment of basophils with IL 3 results in a left shift of the dose-response curves for mediator release of both IgE-dependent and IgE-independent agonists by approximately one order of magnitude. IL 3 affects only the extent and not the time course of IgE-independent peptide-induced basophil degranulation. By contrast, histamine and leukotrienes are released more rapidly in response to IgE-dependent stimulation after IL 3 priming. IL 3 also shortens the lag time and increases the rate of leukotriene generation in basophils triggered by FMLP. The priming process induced by IL 3 does not require extracellular calcium. Basophils exposed to IL 3 release significant amount of mediators in response to C5a, even in EDTA buffers without addition of Ca2+/Mg2+, indicating that in the presence of IL 3 the Ca2(+)-dependent mediator release induced by C5a becomes partially Ca2+ independent. Thus, we find that IL 3 strongly affects the mediator profile, the amounts of mediators released, the dose-response curves and the kinetic of the release reaction in basophils stimulated with diverse agonists. The data further support the hypothesis that IL 3 plays an important role in inflammatory processes, in particular in hypersensitivity reactions.

Basophils↗
PubMed1991

Neurotropin inhibits experimental allergic encephalomyelitis (EAE) in Lewis rats.

The effects of Neurotropin, a substance extracted from the inflammatory dermis of rabbits inoculated with Vaccinia virus, for experimental allergic encephalomyelitis (EAE) in Lewis rats, a model for human multiple sclerosis (MS), was studied. The peptide defined by residues 68-84 (MB 68-84) which corresponds to the encephalitogenic portion of the guinea pig myelin basic protein (MBP) in complete adjuvant H37Ra (CFA) was injected into the hind foot pad of each rat. Neurotropin significantly suppressed the clinical and histological expression of actively induced EAE when administered i.p. daily from day 0 to day 6 after immunization. In addition, passive EAE induced by precultured spleen cells from rats immunized with MB 68-84 in CFA was also suppressed by daily administration of Neurotropin after cell transfer. Neurotropin treatment significantly suppressed the delayed-type hypersensitivity (DTH) response to MB 68-84. Furthermore, the ability of spleen cells from Neurotropin-treated rats to transfer EAE was significantly lower than that of saline-treated rats. It seemed that the suppression may be due to the inhibition of the activation by MB 68-84 of sensitized spleen cells, as demonstrated by proliferative response to MB 68-84. However, no difference was observed in Con A-induced proliferative response of the spleen cells between Neurotropin- and saline-treated rats. These findings indicate that Neurotropin inhibits EAE by suppressing the immune responses to encephalitogenic MBP with little non-specific suppression.

Animals↗
PubMed1990

Effect of a non-protein fraction from an extract of the inflamed skin of rabbits inoculated with vaccinia virus (Neurotropin) on Meth A-induced delayed type hypersensitivity.

The effect of a non-protein fraction from an extract of inflamed skin of rabbits inoculated with vaccinia virus (Neurotropin, NSP) was studied on Meth A tumor-induced delayed type hypersensitivity (Meth A-DTH) in BALB/c mice. NSP enhanced the Meth A-DTH. NSP also enhanced the DTH suppressed with 5-fluorouracil (5-FU). Moreover, NSP inhibited the fatal effect of 5-FU and restored the decrease of body weight caused by 5-FU. However, NSP reduced partially but significantly the suppression of the tumor growth by 5-FU. NSP may be useful for cancer treatment in combination with chemotherapeutic agents, if NSP does not inhibit their antitumor activity.

Animals↗
PubMed1990

Growth factors, lipid mediators and effector cells.

Hematopoetic growth factors stimulate the proliferation of leukocyte precursors in bone marrow cultures, but some also augment the responsiveness of mature effector cells. For example, granulocyte-macrophage colony-stimulating factor (GM-CSF) enhances superoxide production and cytotoxicity of neutrophils stimulated by diverse agonists. We show that preexposure of neutrophils to GM-CSF is absolutely required for the induction of leukotriene B4 and platelet-activating factor (PAF) synthesis by a soluble agonist, C5a or N-formyl-methionyl-leucine-phenylalanine (FMLP). Lipid mediator synthesis occurs very rapidly after triggering with the second signal, and under identical conditions superoxide release is enhanced. Interleukin-3 (IL-3), another hematopoetic growth factor, enhances granule release and more profoundly leukotriene C4 (LTC4) synthesis in basophils stimulated by immunoglobulin-E (IgE)-dependent or -independent agonists. Sequential stimulation with IL-3 and C5a results in the production of large quantities of LTC4, while neither factor alone induces the release of lipid mediators. We conclude that a major function of these cytokines is to allow lipid mediator synthesis in effector cells after triggering with agonists which by themselves do not induce the production of bioactive lipids. We also propose that lipoxygenase metabolites and PAF represent an autocrine response amplification pathway in effector cells which might explain the enhanced responsiveness of cells primed by these cytokines.

Animals↗
PubMed1989

The neutrophil-activating peptide NAF/NAP-1 induces histamine and leukotriene release by interleukin 3-primed basophils.

IgE-independent mediator release from basophils is considered an important event in inflammation, particularly in nonallergic immediate hypersensitivity and in allergic late-phase reactions. This study demonstrates that after exposure to IL-3, basophils release histamine and leukotrienes in response to the neutrophil-activating peptide NAF/NAP-1. Thus, the sequential action of two pure cytokines can promote basophils mediator release. In the presence of IL-3, NAF/NAP-1 functions like a "histamine-releasing factor" and may therefore not only induce cellular infiltration but also provoke symptoms of hypersensitivity reactions.

Basophils↗
PubMed1989

Interleukin 3-dependent mediator release in basophils triggered by C5a.

The anaphylatoxin C5a is a potent trigger for basophil degranulations, but in contrast to IgE-dependent basophil activation, it does not result in the synthesis of sulfidoleukotrienes (leukotriene C4/D4/E4). Thus, degranulation and the generation of lipid mediators are separately regulated cellular responses. Exposure of human blood basophils to the cytokine IL-3 alone does not induce the release of histamine in cells from most donors and never leads to the generation of LTC4, indicating that IL-3 is not a direct agonist for basophil mediator release. However, preincubation of basophils with IL-3 enhances the degranulation response to C5a. Most importantly, IL-3 "primes" basophils to release large amounts of leukotriene C4 after challenge with C5a (mean of 50 gp LTC4 per nanograms cellular histamine), while neither peptide alone is capable of inducing the formation of bioactive lipids. This effect is dose dependent, occurring at IL-3 concentrations considerably lower than are required to stimulate the growth of bone marrow progenitor cells. IL-3 affects the extent but not the time course of basophil degranulation, and leukotriene release of cells sequentially exposed to IL-3 and C5a occurs very rapidly concomitant with degranulation. A preincubation of the basophils with IL-3 is strictly required for C5a-induced LTC4 synthesis, but not for an enhancement of degranulation. Priming for C5a-induced lipid mediator generation occurs rapidly after exposure of the cells to IL-3, starting at 1 min and reaching maximal effects at 5 min, but this altered state of responsiveness is relatively long lasting. Cell fractionation studies indicate that the basophil is the source of lipid mediators and that IL-3 affects the basophil response directly. This study demonstrates that IL-3 is a potent modifier of effector functions of mature basophils; this is possibly of greater in vivo significance than its growth factor properties. The large amounts of LTC4 formed after triggering of IL-3-primed basophils may not only enhance but also qualitatively change the pathophysiological consequences of complement activation, and this might be important in the pathogenesis of immediate type hypersensitivity reactions, shock syndromes, and inflammation.

Basophils↗
PubMed1988

Immunomodulating effect of neurotropin on delayed type hypersensitivity response in mice.

Effect of Neurotropin on the delayed type hypersensitivity (DTH) response to sheep red blood cells was examined in mice. Neurotropin suppressed the high DTH responses in ddY and BALB/c mice, while it enhanced the low DTH response in C57BL/6 mice when administered after sensitization. In addition, Neurotropin exerted a suppressive effect on the enhanced DTH response by cyclophosphamide pretreatment in C57BL/6 mice, but had a restorative effect on the suppressed DTH response in ddY mice loaded with restraint stress.

Adjuvants, Immunologic↗
PubMed1986

Usefulness of intravenous dipyridamole combined with pacing stress for detection of myocardial ischemia in coronary artery disease.

In order to establish a more clinically useful diagnostic method to detect myocardial ischemia, a stress test of 0.56 mg/kg of intravenous dipyridamole (D), an atrial pacing (P) and the combination of both (D + P) were administered to 14 patients with significant coronary stenosis and 8 patients with normal coronary arteriogram. The effects on regional coronary hemodynamics and myocardial metabolism were subsequently studied. Treadmill exercise tests in 15 patients and thallium-201 exercise myocardial scintigraphy in 14 patients were also performed at another time. When the uptake ratio of myocardial lactate less than 0% was used as an indicator of myocardial ischemia, 100% (12/12) of sensitivity and 100% (6/6) of specificity were obtained with (D + P)-test in diagnosis of significant coronary stenosis and its sensitivity was significantly higher than that with P-test (43%) or with D-test (31%). Even though sensitivity and specificity of exercise electrocardiogram (70% and 50%) or thallium-201 exercise myocardial scintigram (88% and 80%) in diagnosis of coronary stenosis were not significantly lower than those of (D + P)-test respectively, myocardial ischemia could also be detected with (D + P)-test in two patients at the region perfused by the infarct-related artery, which had not been detected by thallium-201 exercise myocardial imaging. We conclude, (D + P)-test combined with investigation of myocardial lactate metabolism is quite useful to detect myocardial ischemia.

Aged↗
PubMed1981

[Effect of neurotropin (NSP) on allergic reactions (author's transl)].

A study was carried out to examine the effect on neurotropin (NSP) on the 4 types of allergic reactions classified by Coombs and Gell. 1) Type 1: NSP inhibited 48-hr homologous passive cutaneous anaphylaxis (PCA) as well as antigen-induced degranulation of rat mesenterium mast cells. The drug also inhibited both experimental asthma and histamine release from lung tissue in guinea pigs, as mediated by IgE antibody. 2) Type 2: NSP slightly suppressed the increase in urinary protein levels caused by nephrotoxic nephritis in rats and showed a tendency to inhibit Forssman shock in guinea pigs. NSP had an anticomplement activity in vitro but did not inhibit the reversed cutaneous anaphylaxis in rats. 3) Type 3: NSP suppressed an increase in the urinary protein level of rats with glomerulonephritis, as induced by immune complex. 4) Type 4: NSP slightly inhibited the increase in the urinary protein level in glomerulonephritic rats pretreated with IgG. However, the drug did not affect picryl chloride-induced contact dermatitis in mice. We conclude that NSP inhibits allergic reactions used in the present study except for reversed cutaneous anaphylaxis and contact dermatitis, and the most potent activity is seen in the case of Type 1 reaction.

Animals↗