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Biomedical subjects

M Takeuchi

Publications and source records attributed to M Takeuchi.

At least 145 records · Page 8Linked to original sources
PubMed1990

In vitro production of B cell growth factor and B cell differentiation factor by peripheral blood mononuclear cells and bronchoalveolar lavage T lymphocytes from patients with idiopathic pulmonary fibrosis.

The activation of B lymphocytes and formation of immune complexes have been suggested to play an important role in the pathogenesis of idiopathic pulmonary fibrosis (IPF). To investigate the mechanisms of activation of B lymphocytes, we studied the production of B cell growth factor (BCGF) and B cell differentiation factor (BCDF) in patients with IPF and those with interstitial pneumonia associated with collagen vascular diseases (IP-CVD), in comparison with healthy controls. Culture supernatants of peripheral blood mononuclear cells from patients with IPF induced more IgM and IgA production by B lymphocytes than those from healthy controls, indicating a higher production of BCDF in the patients. Culture supernatants of T lymphocytes obtained from bronchoalveolar lavage fluids (BALF) of patients with IPF induced higher proliferation of B lymphocytes than those from healthy controls, indicating a higher production of BCGF. An increase in production of BCGF and BCDF was not observed in patients with IP-CVD. In the light of these results, it was suggested that there may be an imbalance in T lymphocyte subsets that release lymphokines like BCGF and BCDF in patients with IPF, and that the subsets may differ between blood and BALF. It remains to be elucidated whether the activation of B lymphocytes depending on T lymphocytes determines the development of disease in IPF.

Adult↗
PubMed1990

Immunohistochemical analysis of effects of cyclosporin A on gingival epithelium.

Cyclosporin A (CSA)-induced gingival overgrowth was immunohistochemically compared with that phenytoin-induced and nonspecific inflammatory gingiva, and CSA concentration was determined for dental plaque. Leu-6+ epithelial dendric cells (EDC) were found to significantly decrease in number in CSA-induced gingival overgrowth, while the ratio of HLA-DR+ EDC to Leu-6+ EDC did not change significantly. The expression of class II major histocompatibility complex antigens, such as HLA-DR, -DP and -DQ on keratinocytes did not change by CSA-treatment. Leu-4+ mononuclear cells in CSA-induced gingival overgrowth were located primarily in the connective tissue far outside the epithelium. CSA concentration was much higher in dental plaque than in blood and other tissues. Immune response thus appears to be suppressed in the epithelial layer of CSA-induced gingival overgrowth through decrease in Leu-6+ HLA-DR+ EDC and T cell infiltration, both due to CSA in dental plaque. DNA polymerase alpha was detected in much fewer basal keratinocytes of CSA- and phenytoin-induced gingival overgrowth. Epithelial hyperplasia may thus be not due to increased keratinocyte proliferation, but rather to enhanced keratinocyte life span.

Adolescent↗
PubMed1990

Chemical modification by 2,4,6-trinitrobenzenesulfonic acid (TNBS) of an essential amino group in 3-ketovalidoxylamine A C-N lyase.

3-Ketovalidoxylamine A C-N lyase of Flavobacterium saccharophilum is a monomeric protein with a molecular weight of 36000, and contains 32 amino groups and no cysteine or cystine residues. The enzyme was inactivated by 2,4,6-trinitrobenzenesulfonic acid (TNBS) following pseudo-first order kinetics. Substrate of the lyase, p-nitrophenyl-3-ketovalidamine, protected the enzyme against the inactivation, suggesting that the modification occurred at or near the active site. Although several amino groups were modified by TNBS, a plot of log (reciprocal of the half-time of inactivation) versus log (concentration of TNBS) suggested that one amino group has an essential role in catalysis.

Amino Acids↗
PubMed1990

Inhibitory effect of validamine, valienamine and valiolamine on activities of carbohydrases in rat small intestinal brush border membranes.

Three pseudo-aminosugars, validamine, valienamine and valiolamine, produced by Streptomyces hygroscopicus subsp. limoneus showed potent inhibitory action on rat small intestinal carbohydrase activities such as sucrase, maltase, glucoamylase, isomaltase and trehalase activities, but negligible action on lactase activity and pancreatic alpha-amylase activity. Where inhibition was seen, kinetic analysis showed fully competitive inhibition of the carbohydrase activities by all three inhibitors. Valiolamine has more potent carbohydrase inhibitory activity than validamine or valienamine, and the apparent Ki values of valiolamine for sucrase, maltase, glucoamylase, isomaltase and trehalase activities were 3.2 x 10(-7), 2.9 x 10(-6), 1.2 x 10(-6), 9.1 x 10(-7) and 4.9 x 10(-5) M, respectively, which are 10(-5) to 10(-3) times smaller than the apparent Km values.

Animals↗
PubMed1990

Inhibitory effects of flavonol glycosides on 12-O-tetradecanoylphorbol-13-acetate-induced tumor promotion.

The two-stage carcinogenesis by 7,12-dimethylbenz[a]anthracene and 12-O-tetradecanoylphorbol-13-acetate (TPA) in mice was inhibited by kaempferol and flavonol glycosides, whereas naringenin, a flavanone, had no effect. The induction of epidermal ornithine decarboxylase activity by TPA was also inhibited by kaempferol, whereas mauritianin, a kaempferol glycoside, failed to inhibit it. In addition, the effect of the flavonol glycosides on cell-mediated immunosuppression in the two-stage carcinogenesis, observed in terms of initiation after 14 weeks, was antagonized by mauritianin and myricitrin. Cell-mediated immunosuppression in the two-stage carcinogenesis was unaffected by kaempferol and naringenin. These results suggest that the inhibitory effects of flavonol glycosides may have been at least partly due to activation of immune responses against tumors.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1990

Increased accumulation of cytosine arabinoside in human leukemic cells and enhancement of its cell-killing activity by uridine.

The effects of uridine(UR) on the cell-killing activity of cytosine arabinoside(ara-C) against human leukemic cells, MOLT-4, and on ara-C accumulation in cells were studied. The 50% lethal dose(LD50) of ara-C as determined by clonogenic assay was decreased to 5.0 x 10(-8) mol from 9.0 x 10(-7) mol after 3 days exposure to 10(-3) mol of UR. The accumulation of 3H-ara-C at 24 and 48 h was significantly increased in culture medium containing 10(-8) mol of 3H-ara-C and 10(-3) mol of UR (5,129 +/- 123.5 vs 2,554 +/- 115.5 cpm/10(5) cells at 24 h, p less than 0.01, and 5,772 +/- 123.2 vs 1,372 +/- 51.8 cpm/10(5) cells at 48 h, p less than 0.01). It is noteworthy that cell-killing activity of ara-C against human leukemic cells was enhanced by the combination with a nucleoside(UR), but not with antileukemic agents.

Cell Survival↗
PubMed1990

Emesis-related biochemical and histopathological changes induced by cisplatin in the ferret.

Cisplatin is an effective antineoplastic agent that causes severe vomiting due to unknown mechanism. The ferret, an animal model useful in the determination of emetic activity, was used to clarify the emesis-related biochemical and histopathological changes that were induced by cisplatin. Cisplatin (5 to 10 mg/kg) was administered intraperitoneally and a 7-10 mg/kg i.p. dose evoked dose-dependent emesis in the ferret. Almost all cisplatin-vomiting episodes occurred within a 6 hour observation period. All ferrets receiving cisplatin in this study died within 3-5 days. Significant increases in ileal mucosal levels of serotonin and norepinephrine were observed in cisplatin-treated ferrets. There were no significant changes in the levels of serotonin and dopamine in the gastric mucosa. Also, karyorrhexis was observed in the epithelial cells of the ileum and in the lymph follicles of the spleen of cisplatin-treated ferrets. These significant biochemical and pathological changes in the ileum may play an important role in cisplatin-induced emesis.

Animals↗
PubMed1990

[Three-month oral subacute toxicity study of mofezolac (N-22) in rats].

A three-month oral subacute toxicity study of mofezolac (N-22), a non-steroidal anti-inflammatory agent, was performed using dose levels of 6, 20, 60 and 200 mg/kg in rats, and recovery was also assessed one month after withdrawal. 1. Toxic signs caused by N-22 administration, observed only in the 200 mg/kg group, were as follows: soiling around the mouth and/or nose, piloerection, anemia, diarrhea, emaciation and decreased spontaneous locomotor activity. Nine males and thirteen females in the 200 mg/kg group excreted bloody diarrhea and died of general exhaustion between weeks four and thirteen of study. 2. In the 200 mg/kg group, decrease in food consumption and suppression of body weight gain were noted in males from about week four and in females from about week six after initiation of administration, and increase in water consumption was noted in males from about week seven. 3. Urinary examination revealed a decline in urinary pH in males of the 20 mg/kg and above groups and elevation of urobilinogen levels in males of the 60 and 200 mg/kg groups. 4. Hematological examination showed decreases in erythrocyte count (RBC), hematocrit value (Ht) and hemoglobin concentration (Hb) and increase in reticulocyte rate in both sexes of the 200 mg/kg group and an increase in neutrophil rate in males of the 200 mg/kg group. 5. Biochemical examination demonstrated a decrease in chloride (Cl-) in males receiving the 20 mg/kg or above doses and a decrease in calcium (Ca++) in males of the 60 and 200 mg/kg groups. Moreover, there were decreases in cholinesterase (ChE) activity, total protein (TP) and albumin (Alb) values, as well as increases in blood urea nitrogen (BUN), uric acid (UA) and potassium (K+) in both sexes of the 200 mg/kg group, along with elevations in GOT and lactate dehydrogenase (LDH) activities in females of the 200 mg/kg group. 6. The absolute and/or relative organ weights for liver, kidneys, spleen and adrenals were increased in the 200 mg/kg group. 7. On pathological examination, perforating ulceration in the jejunum and ileum, turbid ascites, adhesion and inflammatory changes in capsules of the abdominal organs, splenomegaly, mesenteric lymph node hyperplasia and inflammatory changes in the thoracic cavity were observed in dead animals of the 200 mg/kg group. Similar pathological changes were observed in a few survival cases of the 200 mg/kg group. 8. After a one month recovery period, the above-mentioned changes had mostly recovered, indicating that they were reversible.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1990

[Three-month subacute oral toxicity study of mofezolac (N-22) in dogs].

Mofezolac (N-22) is a new developed analgesic and anti-inflammatory agent. A subacute oral toxicity test of N-22 was carried out at dose-levels of 0, 2, 6 and 20 mg/kg/day using male and female beagle dogs. Treatment for 3 months was followed by 1 month recovery period except in the case of both sexes receiving 20 mg/kg/day. The results obtained from the present study were as follows. 1. Observation of general conditions revealed vomiting, sporadic bloody feces, anemia, recumbency and hyposthenia in both sexes receiving 20 mg/kg/day. Anemia or erosion of tongue was observed in each female receiving 6 mg/kg/day. 2. Respectively 3 dogs of both sexes receiving 20 mg/kg/day died during dosing period. In these animals, perforating ulcers were observed in the pars pylorica ventriculi or duodenum, and loss of blood, peritonitis and aggravation of general exhaustion were considered as causes of death. 3. Body weight tended to decrease in both sexes receiving 20 mg/kg/day, and food and water consumption levels decreased in males receiving 2 mg/kg/day or above and females receiving 2 mg/kg/day. 4. Urinalysis demonstrated an increasing tendency for specific gravity of urine and a decreasing tendency for urine volume in males receiving 2 mg/kg/day or above. 5. Hematological examination showed decreases in red blood cell count and Hb concentration in males receiving 2 mg/kg/day or above, and in Ht values in males receiving 6 mg/kg/day or above. 6. Serum biochemical examination revealed decreases in total protein and albumin in both sexes receiving 20 mg/kg/day. 7. There were no remarkable changes in hepatic and renal function, ophthalmological findings or electrocardiogram. 8. In the organ weights, significant decrease in thymus weights was observed in the dead animals receiving 20 mg/kg/day. 9. Pathologically, the dead animals receiving 20 mg/kg/day were found to exhibit peritonitis with perforating ulcers in the pars pylorica ventriculi or duodenum. In the surviving animals of this group, scar ulcers in the pars pylorica ventriculi and small intestine were evident on necropsy, and histopathology revealed neutrophils infiltration and thrombosis in blood vessels in the thickened submucosal stomach tissues. Moreover, localized hepatocyte necrosis and intrasinusoidal cellular infiltration in liver, as well as interstitial cellular infiltration, degeneration and dilatation of the renal tubules in the kidney were observed. In females receiving 6 mg/kg/day, the changes in kidney were similar to those in surviving animals receiving 20 mg/kg/day, and male of the group showed atrophy of thymus.(ABSTRACT TRUNCATED AT 400 WORDS)

Administration, Oral↗
PubMed1990

Croconazole metabolism in rats.

1. Following subcutaneous administration of 1-(2-(3-chlorobenzyloxy)phenyl)vinyl)-1H-imidazole (croconazole) to rats, four metabolites were identified by comparison of their mass and n.m.r. spectra, g.l.c., and t.l.c. with those of synthetic compounds and enzyme hydrolysis. These compounds are o-hydroxyacetophenone sulphate (M1S), 1-(1-(2-hydroxyphenacyl)vinyl)-1H-imidazole sulphate (M12S), 2-(3-chlorobenzyloxy)phenacyl alcohol (M2), and 2-(3-chlorobenzyloxy)benzoic acid (M9-1). 2. At 10 mg/kg dosing of croconazole the elimination rate of the unchanged drug from plasma was faster in male than in female rats. 3. The percentage of excretion of M12S in 24 h urine was 17% for males and 7.5% for females, and that of M1S was 6.6% for males and 6.5% for females. The percentage of excretion of M2 in 24 h bile was 14% for males and 22% for females, and that of M9-1 was 3.7% for males and 1.6% for females.

Animals↗
PubMed1990

Active and passive cutaneous anaphylaxis in WBB6F1 mouse, a mast cell-deficient strain.

WBB6F1 mouse, a mast cell-deficient strain, was tested for active and passive cutaneous anaphylactic reactions. Active cutaneous anaphylaxis was not produced in mice which had been immunized for 1 to 2 weeks by an intraperitoneal injection of bovine serum albumin with either adjuvant, Freund's complete adjuvant or Bordetella pertussis organisms, even though circulatory IgE and IgG1 antibodies were raised. Passive cutaneous anaphylaxis (PCA) was also absent, when the mice had been sensitized with allogeneic IgE or IgG1 monoclonal antibodies. However, obvious PCA was produced when allogeneic or xenogeneic hyperimmune serum was employed. These findings indicate that mast cells are not necessarily needed for the production of PCA. Some mechanism quite different from the well-elucidated mechanism, i.e., IgE- or IgG1 antibody-triggered histamine release from mast cells, seems to be operative.

Animals↗
PubMed1990

[The mechanism of speech perception using multichannel cochlear implant].

The mechanism of speech perception in patients with Australian multi-channel cochlear implant was investigated. 1) Vowel recognition abilities of patients were sufficient with this implant, whereas, consonant recognition abilities were insufficient. 2) Although the cochlear hair cells were functionally damaged, cochlear nerves had the ability to characterize frequency. 3) The signals from the implanted material were very simple compared to those from normal cochlea, however these patients could understand speech well, perhaps due to aid from the central nervous system.

Adult↗
PubMed1990

[Study of a monoclonal antibody against new epithelial membrane antigens of transitional cell carcinoma].

Immunizing mice with a transitional cell cancer (TCC) tissue in the renal pelvis, we produced a monoclonal antibody (EH14) against new epithelial antigens. After the mice were immunized repeatedly, their splenic cells were harvested and fused with NS/1 myeloma cells. The normal kidney tissue of the same patient was used on Dot blots to select the hybridoma. A a result, one hybridoma whose antibody (EH14) reacted very strongly with TCC but only faintly with normal kidney tissue or normal bladder mucosa was obtained. On immunohistochemistry, EH14 stained all of the 29 TCC tissues. EH14 also stained uterus cancer (7/7) and gastric cancer (6/6) as well as the normal squamous cell and many types of the normal epithelium. All of the lymphnodes containing metastatic bladder cancer were strongly stained with EH14. EH14, however, did not stain interstitial tissues, muscles and sarcomas. The molecular weight of the antigen recognized by EH14 was 14KD and 28 KD on Western blot analysis, and the antigen was stable with formalin or ethanol. The antigen was not the same as that reported previously, and may be useful as a histological marker of TCC.

Animals↗
PubMed1990

[Inhibitory factors of calcium oxalate crystal growth in urinary macromolecules].

We studied the inhibitory effect of urinary glycosaminoglycans (GAGs), in the natural form, on calcium oxalate crystals. Control urine was collected from five healthy subjects and filtered by 5 microns and 0.22 micron membranes. The urine was cut off by a membrane of 30,000 M.W. and the remaining urine was fractionated into three groups by anion-exchange chromatography on DEAE-cellulose: peak A contained only protein, peak B both protein and GAGs and peak C only GAGs. Peak A and peak B were fractionated again through a Sephacryl S-200 gel column. Each fractionated sample was examined for the inhibitory effect on calcium oxalate crystal growth using the 14C-oxalate seeded crystal growth assay in a metastable solution developed by Koide et al. GAGs were determined by two-dimensional electrophoresis on cellulose acetate membrane. SDS-polyacrylamide electrophoresis was used to determine the molecular weights of proteins. Peak A was found to have many kinds of proteins which had low inhibitory effects. Peak B had three kinds of proteins such as those with molecular weights of 130,000, 45,000 and 35,000 as well as uronic acid. These proteins and uronic acid had high inhibitory effect and the highest inhibitory effect was found in the fraction of around 50,000 M.W. where protein and uronic acid were contained. The molecular weight of this protein was 42,000 by SDS electrophoresis. Uronic acid was a keratan sulphate by a two-dimensional electrophoresis. In peak C there were mainly chondroitin sulphate and a small amount of heparan sulfate which had high inhibitory effect.(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium Oxalate↗
PubMed1990

Studies on inhibitors of rat mast cell degranulation produced by microorganisms. I. Screening of microorganisms, and isolation and physico-chemical properties of eurocidins C, D and E.

Microorganisms producing anti-inflammatory substances were screened by the inhibitory effect on mast cell degranulation. Three new compounds related to pentaene macrolide eurocidins, eurocidins C, D and E, have been isolated from the culture broth of Streptoverticillium eurocidicum IFO 13491 as the inhibitors. Their molecular weights and molecular formulae were estimated as 781.89 and C39H59NO15 for eurocidin C, 795.92 and C40H61NO15 for eurocidin D, and 779.92 and C40H61NO14 for eurocidin E, respectively.

Animals↗
PubMed1990

Trehalase inhibitors, validoxylamine A and related compounds as insecticides.

Validoxylamine A showed a potent inhibitory activity against insect trehalase in a competitive manner with a Ki value of 4.3 x 10(-10) M. The other validoxylamines and validamycins also exhibited the activity in vitro. Injection of these compounds to young last instar larvae of the tobacco cutworm, Spodoptera litura, elicited the morphological abnormality followed by death after the cessation of feeding. Validoxylamine A showed 100% mortality at a dose of 10 micrograms/ last instar larva.

Animals↗
PubMed1990

[Retinal degeneration after intravitreal injection of ornithine. 1. Early change after administration].

Retinal damage 1 to 7 days after intravitreal injection of 1-ornithine hydrochloride solution into monkey eyes was investigated. Clinically the retinal pigment epithelium (RPE) showed edema, and hyperfluorescence on fluoroangiograms, predominantly in the equatorial region at 3 to 7 days. No retinal changes were seen at the posterior pole. Histopathologically, RPE in the equatorial region showed severe damage 24 hours after injection, becoming liquefactively necrotic and degenerated at 3 to 7 days. Early changes in RPE consisted of an increase in the number of secondary lysosomes, disappearance of basal infolding, destruction of most of the smooth endoplasmic reticulum, shortening of microvilli, and marked swelling of mitochondria. These RPE changes were seen slightly in the posterior pole. There were slight changes in the inner retina including photoreceptors. In eyes injected intravitreally by hi-osmosis of 3.5% NaCl solution, with equivalent osmolarity to ornithine solution, mild changes of microvilli and mitochondria were seen, but not necrotic changes. Our experiment showed that intravitreal injection of a small amount of 1-ornithine hydrochloride induced severe RPE damage. Selective toxicity of ornithine to RPE appeared mainly in the equatorial region.

Animals↗