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N Koide

Publications and source records attributed to N Koide.

At least 181 records · Page 10Linked to original sources
PubMed1976

Approximately 70% of fucose-labeled glycopeptides from the cell surface and cellular material of rat.

Approximately 70% of fucose-labeled glycopeptides from the cell surface and cellular material of rat fibroblasts (3Y1B cells) were hydrolyzed by endo-beta-N-acetylglucosaminidase D in the presence of neuraminidase, beta-galactosidase and beta-N-acetylglucosaminidase. Structure of the susceptible glycopeptides were found to be very similar to non-membrane glycopeptides of the complex heteropolysaccharide unit, such as the sialylated glycopeptides of thyroglobulin. On the other hand, the resistant glycopeptides were also refractory toward endo-beta-N-acetylglucosaminidase H and alpha-mannosidase, and appeared to be a mixture of glycopeptides with unique structures.

Acetylglucosaminidase↗
PubMed1976

Characterization of mannose-labeled glycopeptides from human diploid cells and their growth-dependent alterations.

Mannose-labeled glycopeptides were prepared from human diploid fibroblasts harvested by brief pronase digestion. Combined use of endo-beta-N-acetylglucosaminidase H and D converted most of the mannose-label into arrays of oligosaccharides. They were separated by paper chromatography and were characterized by Sephadex G-25 column chromatography, by affinity column chromatography on concanavalin A-Sepharose, and by successive digestion with alpha-mannosidase and beta-mannosidase. The results indicated that mannose residues existed as clusters of various sizes, which we refer to as "oligomannosyl cores". The large oligomannosyl cores (approximately 7 to 8 mannosyl residues) were predominant in the glycopeptides from growing cells and were preferentially associated with neutral glycopeptides, similar to Unit A glycopeptides of thyroglobulin (mannose-N-acetylglucosamine unit). In glycopeptides from nongrowing cells, the ratio of the large oligomannosyl cores decreased, accompanying the increase of a small oligommanosyl core consisting of 3 mannosyl residues. The small core was preferentially associated with acidic glycopeptides.

Acetylglucosaminidase↗
PubMed1975

Structural studies of two ovalbumin glycopeptides in relation to the endo-beta-N-acetylglucosaminidase specificity.

Heterogeneities of the two ovalbumin glycopeptides, (Man)5(GlcNAc)2Asn and (Man)6(GlcNAc)2Asn, were revealed by borate paper electrophoresis of oligosaccharide alcohols obtained from the glycopeptides by endo-beta-N-acetylglucosaminidase H digestion and NaB3H4 reduction. The structures of the major components of the oligosaccharides were determined by the combination of methylation analysis, acetolysis, and alpha-mannosidase digestion. Based on the results, the whole structures of the major components of (Man)5(GlcNAc)2Asn and (Man)6(GlcNAc)2Asn were elucidated as Manalpha1 leads to 6[Manalpha1 leads to 3]-Manalpha1 leads to 6[Manalpha1 leads to 3[Manbeta1 leads to 4GlcNAcbeta1 leads to 4GlcNAc leads to Asn and Manalpha1 leads to 6[Manalpha1 leads to 3]Manalpha1 leads to 6[Manalpha1 leads to 2Manalpha1 leads to 3]Manbeta1 leads to 4GlcNAcbeta1 leads to GlcNAc leads to Asn, respectively. Since endo-beta-N-acetylglucosamini dase D hydrolyzes (Man)5(GlcNAc)2Asn but not (Man)6(GlcNAc)2Asn, the presence of the unsubstituted alpha-mannosyl residue linked at the C-3 position of the terminal mannose of Manbeta1 leads to 4GlcNAcbeta1 leads to 4 GlcNAcAsn core must be essential for the action of the enzyme.

Acetylglucosamine↗
PubMedDate not supplied

Clinicopathologic characteristics and postoperative outcome in Japanese and Chinese patients with thoracic esophageal cancer.

We evaluated the clinicopathologic findings and surgical results of 140 patients with thoracic esophageal cancer treated at Shinshu University, Japan (Shinshu group), and compared them with those from 1164 patients treated at Hebei Medical College, China (Hebei group) to determine if the two groups showed any differences. The Shinshu group had significantly higher incidences of elderly patients (>70 years of age), male patients, and tumors located at the lower esophagus (p < 0.01). In the Hebei group, although the depth of tumor invasion was more advanced, the incidence of nodal metastasis was significantly lower (p < 0.01). Operative death and postoperative complications were more frequent in the Shinshu group. Comparison of the postoperative survival curves revealed significantly longer survival of patients with pT2 or pT3 tumor in the Hebei group (p < 0.01), but there were no significant differences between the two groups when the lesions were classified by pTNM stage. This study demonstrated several differences between the patients in the two areas in regard to the clinicopathologic characteristics of thoracic esophageal cancer. The most important characteristic of the esophageal cancer in the Hebei group appears to be the low incidence of nodal metastasis.

Adult↗
PubMedDate not supplied

Assessment of proliferative activity of glandular cells in hyperfunctioning parathyroid gland using flow cytometric and immunohistochemical methods.

The proliferative activity of epithelial cells in hyperfunctioning parathyroid glands was estimated by flow cytometric and immunohistochemical procedures. A total of 30 parathyroid glands, 29 hyperfunctioning glands, and 1 normal gland were studied. The pathology of the 29 glands was determined to be hyperplasia in 19 and adenoma in 10. The S-phase cell population was expressed in terms of the S-phase fraction (%SPF) calculated from the histogram by DNA flow cytometry and in terms of the BrdU immunostaining labeling index (BrdU LI). Cells in all stages of the cell cycle were studied by Ki-67 immunostaining and expressed in terms of the labeling index (Ki-67 LI). Both BrdU LI and Ki-67 LI values were low, ranging from 0% to 0.58% and from 0.21% to 2.62%, respectively. The BrdU LIs were lower than the Ki-67 LIs, ranging from one-sixth to one-twelfth of the values depending on the disease. There were significant correlations between the two indices (p < 0.001). The %SPF determined by flow cytometry was consistently higher than both the BrdU LI and the Ki-67 LI. This discrepancy cannot be explained precisely, and further improvements are required for the flow cytometric analysis of %SPF. The cell cycle study by BrdU and Ki-67 immunohistochemistry suggested that the glandular cells of the hyperfunctioning parathyroid were characterized by low proliferative activity. No evidence of rapid cell turnover rate assumed from the flow cytometric study could be observed in the hyperfunctioning parathyroid gland.

Adenoma↗
PubMedDate not supplied

Time-dependent increases in syndecan-1 and fibroglycan messenger RNA expression in the infarct zone after experimentally induced myocardial infarction in rats.

BACKGROUND: Syndecan-1 and fibroglycan, heparan sulphate proteoglycans, play important roles in extracellular matrix formation via their biological functions. OBJECTIVE: To examine experimentally the sequential changes in syndecan-1 and fibroglycan messenger RNA (mRNA) expression after acute myocardial infarction. MATERIALS AND METHODS: The left coronary arteries of male Sprague-Dawley rats were ligated and the hearts were excised on days 1-14, 28 and 42. Syndecan-1 and fibroglycan mRNA expression in the infarct and non-infarct zones and in sham-operated hearts was determined by reverse transcriptase-polymerase chain reaction. Amplified products were quantified by densitometry of the electrophoresed bands stained with ethidium bromide and standardized relative to the glyceraldehyde 3-phosphate dehydrogenase or beta-actin mRNA expression. Northern hybridization was also performed in the infarct and non-infarct zones on day 3. RESULTS: Expression both of syndecan-1 and of fibroglycan mRNA began to increase on day 2. The expression attained maximum levels on day 3. The maximum levels of syndecan-1 and fibroglycan expression were, respectively, sevenfold and fivefold the preligation level and the level in the sham-operated hearts. The levels remained elevated until day 14, whereupon they declined gradually, returning to the control levels by around day 42. Northern blotting also demonstrated that there was an increased expression both of syndecan-1 and of fibroglycan mRNA in the infarct compared with that in the non-infarct zone on day 3. CONCLUSION: Our results demonstrated that there are sequential increases in the expression both of syndecan-1 and of fibroglycan mRNA in the infarct zone after experimentally induced myocardial infarction in rats, suggesting that these proteoglycans play some role in the pathological course of infarction.

Animals↗
PubMedDate not supplied

Loss of heterozygosity and analysis of mutation of p53 in hepatocellular carcinoma.

Thirty-six hepatocellular carcinoma (HCC) tissues obtained from 34 patients were classified according to histological diagnosis into six well-differentiated HCC, 20 moderately differentiated HCC and 10 poorly differentiated HCC. High molecular weight DNA was prepared from each tumour and the corresponding non-tumour tissue. Loss of heterozygosity (LOH) on chromosomes 4q, 5q, 10q, 11p, 16q, 17p, mutation of the p53 gene and polymorphism of intron 25 of the retinoblastoma (RB) gene were simultaneously analysed. The patients were composed of three cases of small HCC (the diameter of which was < 3 cm) and 31 cases of advanced HCC. Twenty-nine of 34 (85.3%) patients analysed had been exposed to hepatitis B virus and/or hepatitis C virus. The frequencies of LOH on seven chromosomes were 57.9% in 17p13.3, 45.1% in 17p, 45.1% in 11p, 41.9% in 5q, 41.9% in 16q24, 29.0% in 4q, 25.8% in 10q in advanced HCC (four of well differentiated, 18 of moderately differentiated and nine of poorly differentiated carcinoma). In contrast, LOH was observed on 4q, 5q, 16q and 17p in 33% (1/3) of the small HCC (two of well differentiated and one of moderately differentiated carcinoma). The mutation of the p53 genes and polymorphism of the RB gene were present in 25.8% (8/31) and 12.9% (4/31) of the advanced tumours, respectively, but the mutation was not found in small HCC. LOH on every chromosome and the p53 mutation were observed more frequently in more advanced tumours, and the genetic changes accumulated with the increase of the histopathological grade.(ABSTRACT TRUNCATED AT 250 WORDS)

Blotting, Southern↗
PubMedDate not supplied

Is 2-propyl-4-pentenoic acid, a hepatotoxic metabolite of valproate, responsible for valproate-induced hyperammonemia?

To investigate the association between valproate metabolism (VPA) and VPA-induced hyperammonemia together with the contribution of VPA hepatotoxicity risk factors such as young age, polypharmacy, and high serum VPA levels to VPA-induced hyperammonemia, plasma ammonia (NH3) levels, serum levels of VPA and its metabolites, and biochemical parameters were determined in 98 patients treated with VPA (53 monopharmacy cases and 45 polypharmacy cases). In monopharmacy patients, plasma NH3 levels did not depend on age, VPA dosage or serum levels. Serum level of 2-propyl-4-pentenoic acid (4-en) showed a negative correlation with plasma NH3 level in the monopharmacy group. In polypharmacy patients, plasma NH3 levels, serum glutamic pyruvic transaminase, and gamma-glutamyl-transpeptidase were significantly higher, while level/dose VPA ratio, 2-en-VPA serum level, and bilirubin were significantly lower than those in monopharmacy patients. These results suggest that young age and relatively high VPA serum levels within the therapeutic range were unlikely to be risk factors for common hyperammonemia associated with VPA therapy and that 4-en was not causally related to this adverse effect. The decreased serum level of 2-en-VPA in polypharmacy patients may be a reflection of a certain mitochondrial dysfunction, which might be a mechanism of the increased NH3 levels. The changes in biochemical parameters in polypharmacy patients were considered results of the enzyme-inducing activity of coadministered antiepileptic drugs (AEDs).

Adolescent↗
PubMedDate not supplied

Associations between risk factors for valproate hepatotoxicity and altered valproate metabolism.

The effects of three risk factors for valproate (VPA) hepatotoxicity (i.e., young age, polypharmacy, and high VPA serum level) on the metabolism of VPA to its monounsaturated metabolites [2-en-VPA (2-en), 3-en-VPA (3-en) and 4-en-VPA (4-en)] were investigated in 106 patients treated with VPA (56 cases of monotherapy and 50 cases of polytherapy). In the monotherapy group, there was a significant negative correlation between age and 4-en/VPA ratio. In the same group, the 4-en/VPA ratio showed a significant positive correlation with serum VPA level, while 3-en/VPA and 2-en/VPA ratios showed significant negative correlations. In patients greater than 10 years, the 4-en/VPA ratio was significantly higher, while the 2-en/VPA ratio was significantly lower in the polytherapy group than in the monotherapy group. Our results indicate that all three risk factors clearly increase the metabolic conversion of VPA to 4-en, the most toxic VPA metabolite, and that polytherapy and high VPA serum level result in the inhibited beta-oxidative metabolism of VPA to 2-en. These altered VPA metabolic profiles are strikingly similar to the abnormal VPA metabolism previously reported in cases with fatal hepatic failure. Although VPA-induced fatal hepatotoxicity has been regarded as an idiosyncratic reaction, it is possible that these three factors enhance susceptibility to VPA hepatotoxicity by altering the metabolism of VPA.

Age Factors↗
PubMedDate not supplied

A case of Zollinger-Ellison syndrome produced by gastrinoma in the duodenum accompanied with multiple endocrine neoplasia type 1.

A case of Zollinger-Ellison syndrome produced by gastrinoma in the duodenum accompanied by multiple endocrine neoplasia type-1 (MEN-1) is reported. A 46 year-old female underwent distal gastrectomy due to gastric ulcer 5 years ago. As ulceration of the residual stomach recurred, further examination was performed. Hyperprolactinemia, hypergastrinemia, primary hyperparathyroidism, pancreatic tumor, and duodenal carcinoid were evident, and the diagnoses of Zollinger-Ellison syndrome and MEN-1 were established. The origin of the gastrin secretion was suspected to be from the pancreatic tumor, so sampling of the portal blood was performed. As lesion on the gastrinoma in the pancreas could not be identified, total parathyroidectomy was performed for primary hyperparathyroidism. The level of the gastrin secretion, however, remained high. Partial resection of the duodenum for the duodenal carcinoid and a distal pancreatectomy were carried out concurrently. Immunohistochemical study of the anti-gastrin antibody revealed duodenal tumor cells. Initially, the gastrinoma was thought to be in the pancreas, however, the lesion accompanied with MEN-1 and the Zollinger-Ellison syndrome had occurred in the duodenum.

Duodenal Neoplasms↗