Search PubMed⌕ Search

Biomedical subjects

T Naruse

Publications and source records attributed to T Naruse.

At least 145 records · Page 8Linked to original sources
PubMed1995

Steroid-responsive pulmonary disorders associated with myelodysplastic syndromes with der(1q;7p) chromosomal abnormality.

We report three patients with pulmonary disorders associated with myelodysplastic syndromes (MDS). All three patients had symptoms of pyrexia and respiratory discomfort. One patient had pulmonary eosinophilia with bilateral pleural effusion, one had interstitial pneumonia, and one had bilateral pleural effusion caused by systemic vasculitis. Elevated C-reactive protein (CRP) levels, polyclonal hypergammaglobulinemia, and morphological abnormalities in peripheral blood were observed in all three patients. The bone marrow of these patients revealed trilineage dysplasia and eosinophilia. Cytogenetic analysis showed [46,XY,-7,+der(1q;7p)]. Antibiotic treatment was not effective. However, improvement was dramatic after corticosteroid treatment; CRP levels were reduced and the hypergammaglobulinemia was improved. These cases suggest that MDS with [-7,+der(1q;7p)] may be correlated with bone marrow eosinophilia and that an immunologic abnormality may be involved in the pulmonary disorders.

Adrenal Cortex Hormones↗
PubMed1995

Relationship between histamine receptors in the brain and diazepam-induced hyperphagia in rats.

We investigated whether histaminergic neurons in the brain are involved in diazepam-induced hyperphagia in rats. Pretreatment with intracerebroventricular (ICV) injection of either histamine H1-receptor antagonist, pyrilamine (10 and 30 micrograms) or histamine H2-receptor antagonist, famotidine (3 and 10 micrograms) did not affect only diazepam (1 mg/kg, subcutaneous, SC)-induced hyperphagia in nondeprived rats, but also spontaneous feeding in food-deprived rats. In addition, pretreatment with ICV injection of histamine H3-receptor antagonist, thioperamide, and histamine H3-receptor agonist, (R) alpha methylhistamine, enhanced and inhibited diazepam-induced hyperphagia (1 mg/kg, SC) in nondeprived rats, respectively. However, thioperamide and (R) alpha methylhistamine did not affect spontaneous feeding in food-deprived rats. These findings suggest that histaminergic neurons are not directly involved in diazepam-induced hyperphagia in rats. Furthermore, enhancement or inhibition of diazepam-induced hyperphagia by histamine H3-receptor antagonist or agonist may occur via histamine H3-receptors localized in the other neurons in the rat brain.

Animals↗
PubMed1995

Microsatellite polymorphism between the tumor necrosis factor and HLA-B genes in Behçet's disease.

Behçet's disease is associated with the HLA-B51 antigen. However, it has not yet been clarified if the HLA-B51 gene itself is the susceptibility gene related to this disease or if it is some other non-HLA gene in linkage disequilibrium with HLA-B51. Therefore, we screened one of the HSP70 genes, HUM70t (HSP70-Hom), around the class III region and the microsatellite sequence located between the HLA-B and TNF genes for genetic polymorphism in BD. A comparison between patients with BD and healthy controls revealed no significant difference in the frequency of the HUM70t polymorphism. In the microsatellite sequence, Tau-a, in the region between the HLA-B and TNF genes, the frequency of 14 repetitions of GT was increased significantly and that of 11 repetitions was decreased significantly in the patient group. Further, the allelic distributions of the B51 antigen-associated microsatellite polymorphism differed significantly between patients and healthy controls, and in the B51 antigen-negative subjects, analysis of the microsatellite polymorphism also revealed a significant difference in the haplotype frequency between the patient and control groups. These results suggest that the HLA-B51 gene may not be the primary locus responsible for BD, and implicate some other gene(s) located between the TNF and HLA-B genes.

Base Sequence↗
PubMed1995

Hypotensive effects of a new transdermal delivery system for clonidine (M-5041T) in spontaneously and renal hypertensive rats.

1. Antihypertensive effects of a new transdermal delivery system for clonidine (clonidine tape; M-50417) were investigated in spontaneously hypertensive rats (SHR), 2-kidney, 1-clip renal hypertensive rats (RHR) and deoxycorticosterone acetate/salt (DOCA/Salt) hypertensive rats. 2. M-5041T (0.5-4.5 mg/kg) elicited long-lasting hypotensive effects and bradycardia in a dose-dependent manner during 24 h patching in three hypertensive models compared with oral clonidine (100 mu g/kg). 3. The most hypotensive effect of M-5041T was observed in DOCA/salt hypertensive rats. 4. Co-administration of M-5041T with either trichloromethiazide (1 mg/kg, orally) or nifedipine (3 mg/kg, orally) at each dose without hypotensive effects per se induced significant hypotension in SHR. 5. Repeated administrations of M-5041T (1.5 mg/kg per day) for a consecutive 7 days produced significant hypotensive effects at postpatching 6 h, and recovered a postpatching 24 h in SHR. 6. Repetitive M-5041T administrations displayed no tolerance on the hypotensive effects and were devoid of any withdrawal syndrome. 7. These findings suggest that M-5041T may serve as an efficiently useful antihypertensive transdermal delivery system in humans.

Administration, Cutaneous↗
PubMed1995

The kinetics of the pathogenic pronase-digested renal proximal tubular antigen and antibody in rat active Heymann nephritis.

We investigated the pathogenesis of active Heymann nephritis in the rat by conducting immunofluorescent and immunoblotting studies of the pathogenic antigen and the autoantibody, and by detecting this antigen-bound IgGs. Rat IgG was detected along the glomerular basement membrane (GBM) and significant proteinuria was observed 6 weeks after the injection of rat pronase-digested tubular brush border antigen. Circulating antibody which bound only to the brush border of proximal tubules of normal rat, appeared 2 weeks after antigen injection. Eluted antibody from nephritic kidney 6 weeks after immunization bound exclusively to the brush border of the proximal tubules of normal rat kidney. Monoclonal antibody against the nephritogenic 0.3 M antigen, which bound exclusively to the brush border in the normal rat, bound to the GBM in a fine granular fashion, as well as to the brush border from nephritic rats, indicating the deposition of nephritogenic 0.3 M antigen in the GBM of nephritic rats. On immunoblotting, both the circulating antibody and eluted antibody obtained from the nephritic kidney 6 weeks after immunization recognized the 0.3 M antigen. This antigen-bound IgG appeared in circulation at 2 weeks, becoming smaller in size at 4 weeks and disappearing 12 weeks after immunization. Thus, it is suggested that active Heymann nephritis in rats was induced by deposition of the circulating 0.3 M antigen-bound IgG complexes in the subepithelial space of GBM.

Animals↗
PubMed1995

Absence of tolerance to hypotensive effects of clonidine in spontaneously hypertensive rats.

Development of tolerance to the hypotensive effects of clonidine was investigated in spontaneously hypertensive rats (SHR). Clonidine (125 micrograms/kg/day) was administered subcutaneously for 5 weeks using an osmotic infusion pump. During the whole infusion period, significant hypotensive and bradycardiac effects were observed. Plasma clonidine concentrations were maintained relatively constant at about 2 ng/ml during the infusion period. On termination of treatment with clonidine, both the blood pressure and heart rate rapidly recovered to the control levels. These findings suggest that clonidine does not cause tolerance to its hypotensive effects in SHR with the present administration regimen.

Animals↗
PubMed1995

Inhibitory action of indomethacin on neutrophil infiltration in monosodium urate-induced pleurisy in rats.

The effects of indomethacin on the production of cytokines at inflammatory sites were investigated in the monosodium urate (MSU) pleurisy model characterized by both cellular influx and edema. Indomethacin (10 mg/kg) orally administered 0.5 hr prior to MSU injection into the pleural cavity significantly inhibited MSU-induced neutrophil accumulation in the cavity. In addition, the drug slightly enhanced the level of MSU-induced tumor necrosis factor production without affecting interleukin-1 production. Furthermore, indomethacin inhibited both the levels of MSU-induced rat cytokine-induced neutrophil chemoattractant (CINC/gro) and interleukin-6 (IL-6) production by 78.3% at 3 hr and 45.8% at 4 hr post-injection, respectively. Although intrapleural injection of CINC/gro induced neutrophil infiltration in a dose-dependent manner, IL-6 did not affect the action of CINC/gro on neutrophil influx. These findings suggest that the inhibitory action of indomethacin on neutrophil infiltration is, at least, partly mediated by a decrease in the MSU-induced CINC/gro content in this model.

Administration, Oral↗
PubMed1995

[Elderly non-hemophiliac patient with factor VIII inhibitor presenting various type hemorrhages].

A 81-year-old man who had been healthy without any history of abnormal bleeding, developed ecchymosis and hematuria in November, 1992 and was hospitalized in December, 1992. On admission, he developed widespread ecchymosis in his trunk and extremities, and subsequently ecchymosis of his cheek and neck, and also oral and pharyngeal hematoma. The laboratory data were as follows: whole blood clotting time, > 20 minutes; activated partial thromboplastin time (APTT), 108.6 seconds; Factor VIII activity, 4%. The level of Factor VIII inhibitor was high, 65.0 Bethesda Unit/ml. This inhibitor was a IgG type immunoglobulin, which had both kappa and lambda light chain. His serological and blood biochemical data of the blood were normal, and tests for autoantibodies were negative. The patient was treated with plasma exchange therapy, Prednisolone (PSL), Cyclophosphamide and Factor VIII concentrate. The hemorrhagic symptoms were improved, the inhibitor disappeared and the activity of Factor VIII returned to normal after one month. Follow-up was continued in the outpatient clinic for 5 months. After the dose of PSL was decreased, he developed bloody sputum and hematuria, and was readmitted in August, 1994. Factor VIII activity was 21% and the titer of Factor VIII inhibitor was 3.0 BU/ml. The hemorrhagic symptoms disappeared soon after increasing the dose of PSL, and the Factor VIII activity was normalized and the inhibitor could not be detected. These treatments appeared to offer effective control on severe hemorrhage in a patient with Factor VIII inhibitor.

Aged↗
PubMed1995

[Clinical analysis of 14 patients with anti-myeloperoxidase antibody positive rapid progressive glomerulonephritic syndrome].

We investigated the clinical features and outcome of 14 patients with anti-myeloperoxidase antibody (MPO-ANCA) positive rapidly progressive glomerulonephritic syndrome. Underlying diseases included microscopic polyarteritis in 6 patients, idiopathic crescentic glomerulonephritis with lung hemorrhage in 2 patients, idiopathic glomerulonephritis in 3 patients, rapidly progressive glomerulonephritic syndrome without renal biopsy in 1 patient, crescentic glomerulonephritis associated with Sjögren syndrome and progressive systemic sclerosis in 1 patient and crescentic glomerulonephritis associated with sarcoidosis in 1 patient. Five patients were male (mean age, 59.2 years) and 9 were female (mean age, 54.0 years). On admission, most patients had anemia, leukocytophilia, and marked elevation of C-reactive protein (CRP). Average hemoglobin, white blood cell count and CRP levels on admission were 8.1 mg/dl, 11,500/mm3 and 14.7 mg/dl, respectively. Average serum creatinine was 4.0 mg/dl. All patients were treated with steroids either with or without cyclophosphamide. As the patients recovered clinically, the MPO-ANCA titers declined. Although most patients responded well to immunosuppressive therapy, some died of serious complications (such as acute respiratory distress syndrome, fungal infection, and pneumocystis pneumonia). The prognosis of patients with severe renal failure was especially poor. We conclude that early diagnosis, treatment and intensive care during immunosuppressive therapy are very important in the management of MPO-ANCA-positive rapidly progressive glomerulonephritis.

Adolescent↗
PubMed1995

Histamine excess symptoms in basophilic crisis of chronic myelogenous leukemia.

We encountered a patient with chronic myelogenous leukemia in basophilic crisis accompanied with histamine excess symptoms including bronchial asthma and gastric ulcer. The concentrations of histamine and histidine decarboxylase in leukemic cells containing granules typical for basophils were similar to those in mature basophils. His histamine excess symptoms rapidly disappeared concomitant with the reduction of blast cells after chemotherapy. We speculate that his histamine excess symptoms were induced by the leukemic cells.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1994

Multiple autoantibody production in a patient with splenic lymphoma.

We report on a patient with splenic lymphoma of B-cell origin who developed autoimmune hemolytic anemia (AIHA). IgM lambda M-protein, IgM anticardiolipin antibody (ACA), and lupus anticoagulant (LA) were detected in the serum, and direct Coombs' test showed autoantibodies of the IgG1 and IgG2 subclasses on red blood cells (RBC). In in vitro culture, tumor cells isolated from the spleen produced only IgM ACA, which was enhanced by IL-6 but not by IL-4 or IL-5. The levels of ACA and LA decreased after splenectomy and chemotherapy; the strength of the direct Coombs' test, however, did not change. These findings indicated that in this patient the lymphoma cells produced IgM lambda ACA, but not autoantibodies of the IgG1 and IgG2 subclasses against RBC. It was also suggested that IL-6 might at least partially stimulate the production of ACA.

Anemia, Hemolytic, Autoimmune↗
PubMed1994

Relationship between hypotensive effects and plasma concentrations of clonidine in spontaneously hypertensive rats: continuous treatment and sudden termination of clonidine infusion.

1. Clonidine was administered subcutaneously (62.5, 125 and 250 micrograms/kg/day) for 8 days using an osmotic infusion pump in spontaneously hypertensive rats (SHR). Clonidine, administered at 125 and 250 micrograms/kg/day at 48 hr after infusion, respectively, and thereafter were maintained at this level throughout the infusion period. 3. After terminating clonidine infusion, a rapid drug elimination from the plasma was manifested in both groups (125 and 250 micrograms/kg/day) with plasma clonidine levels, resulting in a decrease below 0.5 ng/ml at 4 and 6 hr, respectively. Four hours after terminating clonidine infusion at 125 and 250 micrograms/kg/day, transient but not remarkable increases in blood pressure and heart rate were observed only in the latter group compared with the values before termination. 4. These findings reveal that marked hypotensive effects were induced by relatively high doses (125 and 250 micrograms/kg/day) of clonidine in SHR, but no remarkable withdrawal symptoms after termination of clonidine infusion were observed. Therefore, unwanted withdrawal symptoms probably occur when an extremely high dose (250 micrograms/kg/day or more) of clonidine was infused for a long period (8 days or more) in SHR.

Animals↗