[Tests of gastric motility].
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Biomedical subjects
Publications and source records attributed to T Sekiguchi.
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STUDY DESIGN: This study demonstrated the chemonucleolytic effects of chondroitinase ABC and its histologic and biochemical background. OBJECTIVES: To determine the course of chondroitinase ABC action on normal rabbit discs, and to find its minimum effective dosage. SUMMARY OF BACKGROUND DATA: No previous study has assessed the chemonucleolytic action of chondroitinase ABC in a time- and dose-dependent manner. This study also investigated the biochemical causes of radiologic and histologic changes in the discs. METHODS: Rabbits were injected with 4 U of pharmaceutical-grade chondroitinase ABC intradiscally. They were radiologically and histologically observed, and biochemical analyses of the discs were conducted on days 1, 3, 5, 7, and 10 postinjection in the time course study. Different doses of chondroitinase ABC were injected, and radiologic observations and water content of the discs were measured in the dose-finding study. RESULTS: The time course study revealed that the chondroitin sulfate content of discs significantly decreased from day 1 postinjection until the end of the experimental period. The weight and water content of the nucleus pulposus decreased on day 3, and disc space narrowing was observed from the day after injection. The dose-finding study showed that a dose of 0.0002 U/disc still induced disc space narrowing and a decrease in water content. CONCLUSIONS: Chondroitinase ABC is estimated to have a chemonucleolytic effect at least by day 3 postinjection at a dose level of 0.0002 U/disc or higher in rabbits.
Three crystalline forms of 3-isopropylmalate dehydrogenase from the moderate facultative thermophile Bacillus coagulans were obtained by hanging-drop vapor-diffusion methods. One of them, which had crystallized under slightly milder conditions than the others, was suitable for X-ray analysis. Its asymmetric unit contains one dimeric molecule and the solvent content is higher than in other protein crystals. The crystal structure was solved in a preliminary manner by the molecular-replacement technique.
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BACKGROUND: The tsBN462 temperature-sensitive mutant hamster cell line exhibits cell cycle arrest and apoptosis at the restrictive temperature of 39.5 degrees C, due to a point mutation in the CCG1/TAFII250 gene, which encodes a component of the general transcription factor TFIID. RESULTS: We now report that CCG1/TAFII250 persisted as a complex with TBP and associated proteins (TAFs) in tsBN462 cells at the restrictive temperature. FACScan analysis revealed that the tsBN462 mutation resulted in a failure to progress out of G0 into G1. Using two-dimensional gel electrophoresis we observed a decrease in the synthesis of several proteins, starting in the middle of the G1 phase, becoming very pronounced during late G1. The expression of the immediate early genes c-fos, c-jun and c-myc was normally induced by serum treatment of quiescent cells at the restrictive temperature, whereas expression of cyclins A, D1 and D3 was reduced. Expression of the cyclin-dependent kinase (CDK) inhibitor proteins p21 and p27 was enhanced. Consistent with the decreased cyclin D and increased p21/p27 expression, we found that phosphorylation of Rb was decreased at 39.5 degrees C. Cyclin A-, E- and Cdk2-associated histone H1 kinase activity was reduced concomitantly with the increase in p21 protein. CONCLUSION: Decreased cyclin/Cdk kinase activity and decreased Rb phosphorylation are possible causes of G1 cell cycle arrest in tsBN462 cells at the restrictive temperature.
Changes in hyaluronan (HA) concentration and stainability were investigated in the rabbit cornea after wounds made by exposure to n-heptanol. The HA concentration in the cornea increased gradually until day 14 after wounding, and then decreased. The HA concentration returned to the normal level 56 days after wounding. In the normal control cornea, HA staining was observed in the epithelium and stroma. The intensity of HA staining in the epithelium and stroma increased until day 3 after wounding, when the epithelium had completely covered the defect. At day 28, when the thickness of the corneal epithelium returned to the normal level, the intensity of HA staining in the epithelium also decreased. However, staining in the stroma was still strong. HA staining in the stroma decreased by day 56 after wounding. In parallel experiments, the immunostaining for CD44, an HA receptor, and fibronectin (FN) was carried out in the same model. The immunostaining in the epithelium of both CD44 and FN was synchronistic with the HA staining during the early stages after wounding. These events suggest that HA, CD44 and FN cooperatively play important roles in corneal epithelial wound healing.
Fine granules or capsules of azithromycin (AZM) were given to 32 pediatric patients for the treatment of the following diseases: pharyngitis in three cases; tonsillitis in one; bronchitis in six; pneumonia in six; mycoplasmal pneumonia in 14; pertussis and enteritis in one, each. Effectiveness of AZM was evaluated in 30 cases and the drug was rated "excellent" in 18 patients, "good" in 11 and "fair" in one, resulting in a total efficacy rate of 96.7%. Three strains of bacteria were isolated from 3 patients as the causative organisms including: Streptococcus pneumoniae, Haemophilus influenzae and Haemophilus parainfluenzae, from three different patients, respectively. One patient complained of mild diarrhea, another patient mild urticaria. Abnormal laboratory test results were reported as follows: one patient showed a slight decrease in leukocyte count, three patients showed slight increases in eosinophils, and one patient had slight elevations in GOT and GPT. The above results suggest that AZM is a useful antibiotic drug in the treatment of pediatric patients with various bacterial infections.
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A temperature-sensitive (ts) mutant of the BHK21 cell line derived from golden hamsters, tsBN462 has a mutation in the gene encoding the largest subunit of the TFIID complex, TAFII250/p230/CCG1, and arrests in the G1 phase at the nonpermissive temperature, 39.5 degrees C. We found that tsBN462 cells underwent apoptosis following growth arrest at 39.5 degrees C, suggesting a role for CCG1 as a repressor of apoptosis. By electron microscopic observation, tsBN462 cells at 39.5 degrees C showed characteristic features of apoptosis. Apoptosis was not suppressed by expression of Bc1-2 or the adenovirus E1B 19 kDa protein. Cell death was suppressed completely by expression of wild-type CCG1 and partially by wild-type p53, a growth suppressor protein. Cell cycle arrest induced by p53 may help survival of tsBN462 cells at 39.5 degrees C. Apoptosis was accelerated in SV40 large T antigen-transformed tsBN462 cells at 39.5 degrees C where SV40 large T antigen formed a complex with p53, implying that the apoptosis of tsBN462 cells at 39.5 degrees C occurred in a p53-independent manner. Our results suggest that CCG1/TAFII250 is required for the expression of factors regulating apoptosis.
Endoscopic ultrasonography of the lower esophagus was performed in 25 patients with reflux esophagitis and 13 age-matched controls. Thickening of the esophageal wall and abnormalities of its architecture were detected. As these morphological changes became more extensive, the lower esophageal sphincter pressure and the decrease of sphincter pressure on relaxation were both progressively reduced. There was a significant correlation between morphological abnormalities and lower esophageal function. Our results suggest that inflammatory damage to the muscle layer of the lower esophagus may impair lower esophageal sphincter function further, especially in patients with advanced esophagitis.
The effects of biotin on ammonia concentration in blood and brain were evaluated in hyperammonemic rats and mice. Rats were injected with 5 mmol/kg BW of ammonium acetate, and mice were injected with 10 mmol/kg BW. Increases in blood ammonia levels in rats 15-30 min after ammonia loading were prevented by treatment with 0.2 ml/100 g BW of biotin or 0.04 ml/100 g BW of arginine-glutamate with statistical significance. Blood ammonia levels after ammonia loading were lower, although not significantly, in the arginine glutamate-treated rats than in the biotin-treated animals. In mice also, increases in blood and brain ammonia levels after ammonia loading were prevented by the administration of biotin. The decrease in brain glutamate and aspartate after ammonia loading was lower and the brain glutamine level was higher in biotin-treated mice than in the controls. These findings indicate the protective effect of biotin against ammonia intoxication.
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A 37-year-old Japanese man was admitted with delirium and hyperammonemia. He was diagnosed as having type II citrullinemia because of an elevated citrulline level on amino acid analysis and very low hepatic argininosuccinate synthetase activity. He also showed a low neutrophil count and a low serum level of granulocyte colony-stimulating factor. Reduced production of this cytokine and/or impairment of its feedback regulation by the neutrophil count may have played a role in the neutropenia of this patient.
We report a rare case of benign esophagobronchial fistula associated with achalasia. The fistula healed spontaneously after esophagocardioplasty with a gastric patch, suggesting the utility of this procedure.