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Biomedical subjects

T Murai

Publications and source records attributed to T Murai.

At least 163 records · Page 9Linked to original sources
PubMed1995

A new model to study repair of gastric mucosa using primary cultured rabbit gastric epithelial cells.

The process of wound repair was investigated using primary cultured rabbit gastric mucosal cells. A confluent monolayer gastric mucosal cell sheet consisting mainly of mucous cells was wounded to make a cell-free area of constant size. The changes in the cell-free area were analyzed quantitatively by image analysis. The wound recovered in 36-48 h in controls; wound repair was accelerated by the addition of fetal calf serum (FCS) and hepatocyte growth factor (HGF) to the medium and was retarded by inhibitors of cytoskeletal proteins. In the process of normal wound repair, 5-bromodeoxyuridine (BrdU)-positive cells appeared around the wound in 24-36 h but disappeared after complete repair. In the FCS- and HGF-treated group, BrdU-positive cells were mainly detected 12-24 h after wounding. In this model the wound was repaired in two steps: an initial cell migration stage and a later proliferation stage. In conclusion, FCS and some growth factors accelerate wound repair with the induction of both epithelial cell migration and proliferation. The cytoskeletal system plays an important role in normal gastric restoration.

Animals↗
PubMed1995

Effects of clonidine on intravenous sedation with midazolam.

The effect of clonidine, an alpha 2-adrenoceptor agonist, on intravenous (IV) sedation with midazolam was studied. Subjects were eight healthy adults; IV sedation was performed twice on each subject. In the control (CO) group, midazolam alone was administered. In the clonidine (CL) group, the subjects were given about 5 micrograms/kg of clonidine orally 2 hr before the initiation of sedation with midazolam. The following parameters were determined: dose of midazolam, changes in vital signs, recovery time, amnesia, and side effects. The average sedating dose of midazolam was 0.078 and 0.043 mg/kg in the CO and CL groups, respectively. Recovery times determined by stabilometry were 150 and 120 min in the CO and CL groups, respectively. Based on these results, the combined use of clonidine can reduce the dose of midazolam and shorten the recovery time. It is suggested that clonidine may be useful in IV sedation with midazolam.

Adrenergic alpha-Agonists↗
PubMed1994

Inhibition of growth of human tumor cells in nude mice by a metalloproteinase inhibitor.

The effects of a new metalloproteinase inhibitor, BE16627B [L-N-(N-hydroxy-2-isobutylsuccinynamoyl)-seryl-L-valine, MW: 375.2] isolated from microbial cultures, on human tumor cell growth in nude mice were investigated. BE16627B inhibited metalloproteinases in enzyme assays, as well as gelatinolysis and collagenolysis in cell cultures. BE16627B at 100 micrograms/ml showed no apparent cytotoxicity to human tumor cells in culture and its LD50 in mice was more than 1,000 mg/kg (i.p.). The effects of BE16627B on the in vivo growth of 2 human tumor cell lines were examined: HT1080 fibrosarcoma, which overproduces metalloproteinases, and HCT116 colon carcinoma, which barely secretes metalloproteinases. When BE16627B was administered to mice at 2 mg/mouse/day by an osmotic pump implanted s.c. for 3 weeks from 1 week after i.v. inoculation of HT1080 cells, the number and size of nodules of HT1080 cells on the lung surface were reduced to 24.3 and 46.4%, respectively, of those of controls, and the increase in lung weight due to tumor-cell growth was inhibited 85.5% without body-weight loss. Moreover, BE16627B inhibited 71.2% of the growth of HT1080 cells inoculated s.c. into mice under the same conditions, but did not significantly inhibit the s.c. growth of HCT116 human colon-carcinoma cells. Thus, BE16627B inhibited metalloproteinase-dependent human tumor-cell growth as well as lung colonization without showing cytotoxicity in nude mice.

Animals↗
PubMed1994

Opposite effects of midazolam and beta-carboline-3-carboxylate ethyl ester on the release of dopamine from rat nucleus accumbens measured by in vivo microdialysis.

This report describes the effects of midazolam and beta-carboline-3-carboxylate ethyl ester (beta-CCE) on extracellular concentrations of dopamine in the nucleus accumbens of freely moving rats measured by in vivo microdialysis. The two compounds had opposite effects, midazolam (0.075 and 0.15 mg/kg i.v.) dose dependently decreasing, and beta-CCE (3 and 10 mg/kg i.p.) dose dependently increasing, dialysate concentrations of dopamine. Flumazenil (6 micrograms/kg i.v.) did not affect the efflux of dopamine but it prevented the effects of both midazolam and beta-CCE on dopamine efflux. N6-Cyclohexyladenosine (0.1, and 1 mg/kg i.p.), a selective adenosine A1 agonist, dose dependently increased the efflux of dopamine. This effect was blocked by 8-cyclopentyl-1,3-dipropylxanthine (25 mg/kg i.p.), a selective adenosine A1 receptor antagonist, a dose which given alone did not affect dopamine efflux; responses to midazolam were not affected. 3,7-Dimethyl-1-propargylxanthine (1 and 3 mg/kg i.p.), a selective adenosine A2 receptor antagonist, did not mimic the effects of beta-CCE. The results suggest that midazolam and beta-CCE modulate dopamine release in the nucleus accumbens by an action at the benzodiazepine binding site associated with the GABAA receptor complex.

Adenosine↗
PubMed1994

Hepatocyte growth factor accelerates the wound repair of cultured gastric mucosal cells.

Effects of hepatocyte growth factor (HGF) on gastric wound repair were assessed. Artificial wounds of uniform size were made by mechanical cell denudation in confluent rabbit gastric mucosal cell sheets. The changes in wound size were analyzed quantitatively. The wound repair process contained an initial migration stage and a later proliferation stage. The wound was completely repaired in 36 h in controls; this repair was accelerated by HGF with the induction of cell migration followed by proliferation and was retarded by tyrosine protein kinase inhibitor genistein. HGF might play some roles in gastric ulcer healing.

Animals↗
PubMed1994

Influences of aging and sex on renal pelvic carcinogenesis by N-butyl-N-(4-hydroxybutyl)nitrosamine in NON/Shi mice.

Influences of aging and sex on renal pelvic carcinogenesis induced by N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) were examined in 6-, 15 -and 45-week-old male and female NON/Shi mice. Histopathological examination revealed an age-related shortening of induction time for renal pelvic carcinomas in males, although actual incidences did not increase. The histological patterns of carcinomas induced in both renal pelvis and urinary bladder demonstrated male mice to be more prone to develop transitional cell carcinomas, while squamous cell carcinomas were more likely to arise in females. Moreover, the sex factor appeared to influence the progression of both renal pelvic and urinary bladder carcinomas.

Aging↗
PubMed1994

Inhibitors of tyrosine and Ser/Thr phosphatases modulate the heat shock response.

Following heat shock the expression of heat shock genes is regulated by the heat shock transcription factor, HSF, known to bind to arrays of the heat shock element, NGAAN, upstream of the heat shock genes. Phosphorylation of HSF is necessary for its activation. We report that the treatment of Chinese hamster HA-1 cells with 250 nM of okadaic acid (OA), a ser/thr phosphatase inhibitor, leads to an increase in activated HSF after heat shock. This is followed by the activation of the transcription of heat shock genes as assayed by the increase in the synthesis of beta-galactosidase in an HA-1 cell line containing the heat shock promoter ligated to the beta-galactosidase gene. To investigate the specificity of OA, we used other phosphatase inhibitors. We found that treatment of HA-1 cells with 500 microM of sodium vanadate, an inhibitor of tyr/phosphatases, resulted in a three to fivefold reduction in HSF activation and binding to the heat shock element following heat shock. Such reduction in HSF activation virtually abolished beta-galactosidase induction. Reduced HSP synthesis was further confirmed by SDS-PAGE and Western blot analysis using anti-HSP-70 and 28 antibodies. Sodium vanadate treatment of heat shocked cells greatly reduced levels of thermotolerance. These results show that ser/thr and specifically tyr/phosphatase inhibitors modulate the signal transduction pathway of HSF activation.

Animals↗
PubMed1994

Effect of phenacetin pretreatment on renal pelvic carcinogenesis by N-butyl-N-(4-hydroxybutyl)nitrosamine in NON/Shi mice of both sexes.

Influences of phenacetin (PH) pretreatment on renal pelvic carcinogenesis induced by N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) were examined in NON/Shi mice of both sexes. Histopathological examination revealed that PH pretreatment enhanced not only the induction of urinary tract carcinoma but also distant metastasis of renal pelvic carcinoma by BBN in male mice. The high incidence of urinary tract carcinoma by PH pretreatment might be due to hydronephrosis and epithelial proliferative lesions enhanced by PH, since a single treatment of PH induced hydronephrosis in all mice and simple hyperplasia in 70-80% of mice used.

Animals↗
PubMed1994

JM9 strains, a new type of group B streptococci from Japan.

JM9 strains isolated from human carriers and patients in several districts of Japan, represent a new serotype of group B streptococci (GBS, Streptococcus agalactiae). They were first detected in 1983 but are meanwhile prevailing among all other GBS serotypes in Japan. Outside of Japan, strains of this type have not been reported until now. In the present work, N-acetylneuraminic acid was detected in all strains investigated, by chemical analysis as well as by interaction with a sialic acid-binding lectin. This component is characteristic of all analyzed GBS type polysaccharides. In a chicken embryo model, all strains exhibited a very strong virulence. Examination of the antibiotic sensitivity revealed that all strains were susceptible to penicillin, cephalothin, clindamycin, mezlocillin, azlocillin, erythromycin, methicillin, chloramphenicol, tetracyclin, oxacillin and sulfamethoxazole/trimethoprim, whereas all strains were resistant against gentamicin, kanamycin and neomycin. Electron microscopic studies revealed for these strains relatively small capsules but unusually thick cell walls. By immunogold labelling, the type polysaccharide, the group polysaccharide, the lipoteichoic acid and in some strains, the protein R were localized.

Animals↗
PubMed1994

Identification of mK1, a true tissue (glandular) kallikrein of mouse submandibular gland: tissue distribution and a comparison of kinin-releasing activity with other submandibular kallikreins.

The protein structure, kinin-releasing activity, and tissue distribution of four major proteinases of mouse submandibular gland (mK22, mK9, proteinase F, proteinase P) were studied. When compared with the deduced amino acid sequence of each member of the tissue (glandular) kallikrein gene family, the amino acid sequence of proteinase F determined (approximately 40% of the total) was found to agree completely with the deduced amino acid sequence of mKlk-1. The proteinase P sequence, on the other hand, agreed with that of the product of mKlk-13, mK13 (prorenin-converting enzyme). Proteinase F had the strongest kininogenase activity for both low-molecular-weight and high-molecular-weight kininogen, while mK22 had 1/6 and 1/50 the activity of proteinase F for the respective kininogen substrate. Kininogenase activities of mK9 and proteinase P were less than 1/100 of the activity of proteinase F for both substrates. Acting on the two kininogen substrates, kallikreins mK22, mK9, and proteinase F, but not proteinase P, specifically released bradykinin, suggesting that the former three kallikreins strictly recognized peptide sequences around bradykinin in these substrate molecules but proteinase P recognized several sites in these molecules. Significant amounts of proteinase F, but not mK22 and others, were present in the urine, pancreas and digestive organs, as well as in the salivary glands. The present results revealed that the former proteinase F is identical to mK1, tissue/renal kallikrein, and confirmed its characteristics as a true kallikrein on the basis of its kinin-releasing activity and tissue distribution.

Amino Acid Sequence↗
PubMed1994

Decline of erythromycin resistance of group A streptococci in Japan.

Six hundred seventy isolates from children with Group A streptococcal infections from 1981 through 1990 were typed serologically and their antibiotic susceptibilities were determined. There were 479 isolates from patients with pharyngitis, 133 from those with scarlet fever, 35 from those with suppurative infection and 23 from those with nonsuppurative disease. The prevalent M serotypes were 12, 4, 1, 3 and 28. None of the 670 isolates were resistant to penicillin G and cephalexin. Resistance rates of isolates to erythromycin and lincomycin was 22.2% in 1981 and 1982, but a marked decrease was noted after 1983 and only one has been resistant since 1986. Nineteen of 21 erythromycin-resistant isolates were M type 12, and two others were M types 4 and 28. Chloramphenicol resistance was similar to that of erythromycin, and the tetracycline resistance rate decreased gradually from 60% to less than 20%.

Adolescent↗
PubMed1994

Increased insulin sensitivity in patients with aldosterone producing adenoma.

OBJECTIVE: Primary aldosteronism is a recognized endocrine cause of glucose intolerance. A blunted insulin response to glucose in patients with primary aldosteronism is well known, but insulin sensitivity has not been thoroughly determined. We investigated insulin sensitivity and insulin secretion in patients with aldosterone producing adenoma. DESIGN: Glucose tolerance and insulin responses to glucose were evaluated using a standard 75 g oral glucose tolerance test in patients with aldosterone producing adenoma before and after surgery, and in control subjects. Parameters for insulin resistance (HOMA-R) and pancreatic beta-cell function (HOMA-beta F) were derived from a homeostasis model assessment. PATIENTS: Fifteen patients with aldosterone producing adenoma and 41 control subjects with normal glucose tolerance matched for age and body mass index, were studied. Eight patients were re-evaluated after surgical removal of the adenoma. In 5 patients 125I-insulin binding to erythrocytes was also measured. MEASUREMENTS: Plasma glucose was measured by a glucose oxidase method. Plasma insulin, aldosterone and renin activity were measured by radioimmunoassay. RESULTS: Both fasting plasma glucose and insulin were lower in the patients than in the controls. Although the areas under the curve for plasma glucose during the oral glucose tolerance test did not differ, that for plasma insulin was less in the patients with hyperaldosteronism. Insulin sensitivity was increased in the patients, as evidenced by decreased HOMA-R compared with controls, while HOMA-beta F was comparable between the groups. 125I-insulin binding to erythrocytes was higher in 5 patients than in 19 normal controls. After surgical removal of adenoma, neither fasting plasma glucose nor the glucose area under the curve during the oral glucose tolerance test changed. However, fasting plasma insulin and the insulin area under the curve increased significantly. HOMA-R increased and HOMA-beta F remained unaltered. CONCLUSION: Insulin sensitivity was increased in untreated patients with aldosterone producing adenoma. Enhanced insulin receptor binding may contribute to this increased insulin sensitivity.

Adenoma↗
PubMed1994

Identification and characterization of a chromosomal virulence gene, vacJ, required for intercellular spreading of Shigella flexneri.

Intercellular spreading of shigellae is a prerequisite for shigellosis, although the molecular mechanisms underlying the phenomenon are still largely obscure. To elucidate some of these mechanisms, we performed random Tn10 insertion mutagenesis in Shigella flexneri YSH6000T and found a chromosomal locus in the NotI-J segment responsible for bacterial spreading. The locus affected in the mutant, designated vacJ, was neither involved in the invasion of epithelial cells nor in intracellular movement, but was required for intercellular spread. The vacJ mutant was capable of forming bacterium-containing membranous protrusions within the infected cell, but had diminished ability to move from the protrusions into the cytoplasm of the adjacent epithelial cells. Cloning and sequencing of the vacJ region indicated that the vacJ gene encoded a 28.0 kDa protein possessing a signal peptide at the N-terminus, which contained the motif characteristic of lipoproteins. The analysis of the vacJ product indicated that VacJ was exposed on the bacterial surface. The vacJ gene was distributed among shigellae and enteroinvasive Escherichia coli, and the constructed vacJ mutants failed to spread intercellularly, indicating that vacJ is a chromosomal gene essential for the pathogenicity of shigellae.

Amino Acid Sequence↗
PubMed1994

Effect of nicotine in migration and proliferation of rabbit gastric mucosal cells in a culture cell model.

The aim of this study was to assess the effects of nicotine on the gastric epithelial restoration using primary cultured rabbit gastric mucosal cell model. Confluent monolayer mucosal cell sheets consisting of mainly mucous cells were wounded using a rotating silicon tip. The process of restoration was monitored, and the size of wound was measured and analysed quantitatively. Artificial wounds recovered in 36 h in controls. The nicotine treatment (10(-5), 10(-4) and 10(-3) mol/L) did not cause any effects on the process of wound repair. Bromodeoxyuridine (BrdU) positive cells appeared around the wound 24-36 h after injury and then disappeared after the complete repair in controls and also in nicotine-treated groups. However, in the morphological observation, numerous vacuoles were detected in parietal cells of nicotine-treated groups. This effect of nicotine was reversible by removing nicotine from the medium. Present data suggest that nicotine has no direct effects on the mucosal restoration but might have an effect on the structure and function of parietal cells.

Animals↗
PubMed1994

[Serotype and antibiotic susceptibility of isolates from children with group A streptococcal infection; observation for 10 years].

Six hundred and seventy isolates from children with group A streptococcal infections from 1981 through 1990 were typed serologically and their antibiotic susceptibilities were determined. Productivity of streptococcal pyrogenic exotoxins was also investigated in some isolates. Four hundred and seventy-nine strains were isolated from patients with pharyngitis, 133 from those with scarlet fever, 35 from those with suppurative infection and 23 from those with non-suppurative disease. With immediate treatment (antibiotics were started at the same day throat swabs were taken) for 10 days, 5.3% of the patients with pharyngitis including scarlet fever had relapses and 13.4% of those patients had recurrences. Of the episodes of recurrences 15.7% were due to the same M serotype strains. Six patients had two episodes of scarlet fever. M type of isolate was different in the first and the second episode of each patient. Pyrogenic exotoxin type was unprecedented in the second episode of 4 out of 6 patients. M-typable and T-typable rates of isolates were 90.7% and 97.3%, respectively. Coincidence between M and T types was 73.3% (83.0% if including strains with the same and mixed T-type). Prevalent M-serotypes were 12 and 4, but M1, 3, or 28 was the most prevalent type of isolates in certain years. None of the 670 strains was resistant to penicillin G and cephalexin. Resistant rate of isolates to erythromycin and linecomycin was 26.5% in 1981 and 18.4% in 1982. But a marked decrease has noted since 1983 and only one has been resistant since 1986.(ABSTRACT TRUNCATED AT 250 WORDS)

Child↗
PubMed1994

Bullous pemphigoid sera induce bullous-pemphigoid-like lesions in neonatal mice pretreated with a limited dose of ultraviolet B irradiation.

The role of bullous pemphigoid (BP) autoantibodies (Abs) in the pathogenesis of BP is unclear. Lack of a confirmed experimental animal model prevents studies of the pathogenetic role of BP Abs. We hypothesized that some alterations of BP antigens (BP Ags) will be necessary for causative binding of BP Abs to the Ags. To cause an artificial and reproducible alteration, neonatal mice were irradiated with ultraviolet B (UVB). After the irradiation of 600 mJ/cm2 of UVB, BP serum was intraperitoneally injected. When the BP sera, which recognized only the 230-kD BP Ag, or both 230- and 180-kD BP Ags, were transferred into the UVB-treated mice, erosions and vesicles appeared in 14-78% of the animals. Histopathological examination revealed subepidermal blister formation in the mice treated with UVB and BP sera. Electron microscopy demonstrated that the separation occurred at the level of the lamina lucida. Human IgG and C3 were deposited at the dermal-epidermal junction. Control animals to which healthy sera were injected after the same dose of UVB irradiation showed degeneration of the upper epidermis but no apparent dermal-epidermal cleft formation histopathologically. These results suggest that BP antibodies play a pathogenetic role in vivo. This animal model can contribute to a study of the pathogenesis of BP.

Animals↗
PubMed1994

Radioimmunoassay of conjugated 1 beta-hydroxycholic acid in dried blood spots for diagnosis of congenital biliary atresia.

Radioimmunological measurement of conjugated 1 beta-hydroxycholic acid in dried blood spots obtained from newborns at 4-5 d after birth has been carried out to investigate a diagnostic utility for congenital biliary atresia. The method allowed the determination of this bile acid, with a detection limit of 50 pg in one disc (3 mm i.d.), and showed good reproducibility with inter- and intra-assay coefficients with variations of 3.5-7.7% and 6.3-8.8%. With the analysis, a relatively high concentration of this substance was observed in the patients, as compared to normal subjects, averaging 1.63 ng/disc in the former and 0.97 ng/disc in the latter.

Bile Acids and Salts↗