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Y Koda

Publications and source records attributed to Y Koda.

At least 55 records · Page 3Linked to original sources
PubMed1998

Identification of a mutation (A1879G) of transferrin from cDNA prepared from peripheral blood cells.

We have prepared a transferrin (TF) cDNA from total RNA of peripheral blood cells of an individual with a TF B variant (TF Bv) phenotype to analyze the molecular basis for the TF Bv. The TF B variant allele (TF Bv) was found to contain an A to G transition at nucleotide 1879 in the coding region that may result in substitution of glutamic acid for lysine at codon 627 located in exon 16. In addition, a transient expression study by transfection of each plasmid containing TF C1, TF C2 or TF Bv cDNA into monkey kidney (COS7) cells indicated that the products from specific TF alleles were able to be identified respective phenotypes by isoelectrofocusing electrophoresis and immunoblotting analyses. Based on this nucleotide substitution, we also established a PCR-RFLP method to detect the TF Bv allele from genomic DNA. Thus, peripheral blood cells were useful as an alternative source for preparation of cDNA from human liver for the molecular analysis of TF polymorphism.

Animals↗
PubMed1998

The haptoglobin-gene deletion responsible for anhaptoglobinemia.

We have found an allelic deletion of the haptoglobin (Hp) gene from an individual with anhaptoglobinemia. The Hp gene cluster consists of coding regions of the alpha chain and beta chain of the haptoglobin gene (Hp) and of the alpha chain and beta chain of the haptoglobin-related gene (Hpr), in tandem from the 5' side. Southern blot and PCR analyses have indicated that the individual with anhaptoglobinemia was homozygous for the gene deletion and that the gene deletion was included at least from the promoter region of Hp to Hpr alpha but not to Hpr beta (Hpdel). In addition, we found seven individuals with hypohaptoglobinemia in three families, and the genotypes of six of the seven individuals were found to be Hp2/Hpdel. The phenotypes and genotypes in one of these three families showed the father to be hypohaptoglobinemic (Hp2) and Hp2/Hpdel, the mother to be Hp2-1 and Hp1/Hp2, one of the two children to be hypohaptoglobinemic (Hp2) and Hp2/Hpdel, and the other child to be Hp1 and Hp1/Hpdel, showing an anomalous inheritance of Hp phenotypes in the child with Hp1. The Hp2/Hpdel individuals had an extremely low level of Hp (mean+/-SD = 0.049+/-0. 043 mg/ml; n=6), compared with the level (1.64+/-1.07 mg/ml) obtained from 52 healthy volunteers having phenotype Hp2, whereas the serum Hp level of an individual with Hp1/Hpdel was 0.50 mg/ml, which was approximately half the level of Hp in control sera from the Hp1 phenotype (1.26+/-0.33 mg/ml; n=9), showing a gene-dosage effect. The other allele (Hp2) of individuals with Hp2/Hpdel was found to have, in all exons, no mutation, by DNA sequencing. On the basis of the present study, the mechanism of anhaptoglobinemia and the mechanism of anomalous inheritance of Hp phenotypes were well explained. However, the mechanism of hypohaptoglobinemia remains unknown.

Adult↗
PubMed1998

Distribution of H type 1 and of H type 2 antigens of ABO blood group in different cells of human submandibular gland.

We have examined the immunohistochemical distribution of H Type 1 and of H Type 2 substances of the ABO blood group system in human submandibular gland using either of the two anti-H monoclonal antibodies MAb 1E3 and MAb 3A5. MAb 3A5 was specific for H Type 2, and MAb 1E3 reacted with each of H Type 1-H Type 4 artificial antigens. We have developed a competitive inhibition method against H Type 2 and have obtained MAb 1E3, which is fairly specific for H Type 1 under certain conditions. Mucous cells from secretors were strongly stained by 1E3 and weakly by 3A5, whereas those from nonsecretors showed no reaction with 1E3 and 3A5. Serous cells from both secretors and nonsecretors were stained neither by 1E3 nor by 3A5. Striated and interlobular duct cells were strongly stained by 1E3 and by 3A5, regardless of the secretor status. These results indicated that the expressions of the H Type 1 and H Type 2 in different cell types of the submandibular gland were controlled by different genes. In addition, we have determined the acceptor specificity of two alpha(1,2)fucosyltransferases (H and Se enzymes) after transient expressions of the FUT1 and FUT2 in COS7 cells, and found that the H enzyme activity was similar for both Type 1 and Type 2 precursors, and that Se enzyme activity with the Type 1 precursor was higher than that with the Type 2 precursor. Expression of the H Type 1 antigen in mucous cells was found to be dependent on the Se gene, whereas expressions of the H Type 1 and H Type 2 antigens in striated and interlobular duct cells were dependent on the H gene. (J Histochem Cytochem 46:69-76, 1998)

ABO Blood-Group System↗
PubMed1998

Assessment of aortic invasion by esophageal carcinoma using intraaortic endovascular sonography.

OBJECTIVE: Accurate preoperative assessment of aortic invasion by esophageal carcinoma is of great importance for planning surgery. We compared the accuracy of intraaortic endovascular sonography with that of CT in the diagnosis of aortic invasion by esophageal carcinoma. CONCLUSION: In this study, intraaortic endovascular sonography was sensitive in detecting aortic invasion; both sensitivity and specificity were 100%. Intraaortic endovascular sonography proved useful in detecting aortic invasion by esophageal carcinoma.

Aorta, Thoracic↗
PubMed1997

Missense mutation of FUT1 and deletion of FUT2 are responsible for Indian Bombay phenotype of ABO blood group system.

The Bombay phenotype fails to express the ABH antigens of ABO blood group system on red blood cells and in secretions because of a lack in activities of the H gene (FUT1)- and Secretor gene (FUT2)-encoded alpha (1,2)fucosyltransferases. In this study, we have examined the FUT1 and the FUT2 from three unrelated Indian individuals with the Bombay phenotype. These three individuals were found to be homozygous for a T725G mutation in the coding region of the FUT1, which inactivated the enzyme activity. In addition, we did not detect any hybridized band corresponding to the FUT2 by Southern blot analysis using the catalytic domain of the FUT2 as a probe, indicating that the three individuals were homozygous for a gene deletion in the FUT2. These results suggest that the T725G mutation of FUT1 and the gene deletion of FUT2 are responsible for the classical Indian Bombay phenotype.

ABO Blood-Group System↗
PubMed1997

Structure and expression of the gene encoding secretor-type galactoside 2-alpha-L-fucosyltransferase (FUT2).

The expression and secretion of ABO antigens in epithelial cells of glands are controlled by secretor-type alpha (1,2)fucosyltransferase activity. We have examined the expression of the secretor-type alpha(1,2)fucosyltransferase gene (FUT2) and a pseudogene of FUT2 (Sec1) in several tumor cell lines by northern blot and/or reverse-transcription-PCR (RT-PCR) analyses. Transcripts of FUT2 were found in total RNA from ovarian, gastric and colonic cancer cell lines but not from six leukemic cell lines, including erythroleukemic HEL cells, by RT-PCR. On the other hand, RT-PCR indicated that Sec1 was expressed in all these tumor cells, including all hematopoietic cells studied. Northern blot analysis indicated that FUT2 transcripts with a similar size (3.3 kb) were expressed in cancer cell lines. Rapid amplification of cDNA ends suggested that the entire FUT2 cDNA is 3.1-kb long and has two Alu repetitive elements in its 3' untranslated region, including an inverted repeat. The mRNA, therefore, may form a large stem-and-loop structure (1.2 kb). Each stem contains about 300 bases, the loop contains 640 bases, and the percentage of complementary nucleotide sequences in the stem region is 85%. The presence of a large stem-and-loop structure in the 3' untranslated region may regulate the level of the FUT2 transcript by affecting the stability of the mRNA.

Animals↗
PubMed1997

Structure and expression of H-type GDP-L-fucose:beta-D-galactoside 2-alpha-L-fucosyltransferase gene (FUT1). Two transcription start sites and alternative splicing generate several forms of FUT1 mRNA.

The expression of the ABO antigens on erythrocyte membranes is regulated by H gene (FUT1)-encoded alpha(1,2)fucosyltransferase activity. We have examined the expression of the FUT1 in several tumor cell lines, including erythroid lineage and normal bone marrow cells, by Northern blot and/or reverse transcription-polymerase chain reaction (RT-PCR) analyses. RT-PCR indicated that bone marrow cells, erythroleukemic cells (HEL), and highly undifferentiated leukemic cells (K562) that have erythroid characteristics expressed the FUT1 mRNA while four leukemic cell lines did not. The FUT1 mRNA was also demonstrated in gastric, colonic, and ovarian (MCAS) cancer cell lines by RT-PCR. Northern blot analysis indicated that a 4. 0-kilobase FUT1 transcript was expressed in some of these tumor cell lines. Rapid amplification of 5' cDNA end (RACE) analysis suggested that the FUT1 transcript had several forms generated by two distinct transcription start sites and alternative splicing. The results of RT-PCR using specific primers for each starting exon suggested that two transcription initiation sites (exon 1A and exon 2A) of the FUT1 were identified in gastric cancer cells and in ovarian cancer cells. Only exon 1A was identified as a transcription start site in another gastric cancer cell line, two colonic cancer cell lines, and in K562 cells, whereas only exon 2A was identified in HEL cells and in bone marrow cells. These two transcription start sites were located 1.8 kilobases apart. Therefore, two distinct promoters appeared to be present in the FUT1. The distinct promoters of the FUT1 and alternative splicing of the FUT1 mRNA may be associated with time- and tissue-specific expression of the FUT1.

Alternative Splicing↗
PubMed1997

Switch from conventional to high-flux membrane reduces the risk of carpal tunnel syndrome and mortality of hemodialysis patients.

The use of a high-flux membrane, which eliminates larger molecular weight solutes with better biocompatibility, has steadily increased since the discovery of beta-2 microglobulin (beta 2m) amyloidosis in 1985. The long-term effects of a dialyzer membrane on morbidity and mortality are not completely understood. To examine the membrane effect as a factor of carpal tunnel syndrome onset and mortality, multivariate Cox regression analysis with time-dependent covariate was conducted on 819 patients from March 1968 to November 1994 at a single center. Two hundred and forty-eight of the patients were either switched from the conventional to high-flux membrane or treated only with a high-flux membrane. Fifty-one patients underwent a CTS operation and 206 died. Membrane status (on high-flux or on conventional) was considered as time-dependent covariate and risk was adjusted for age, gender, type of renal disease and calendar year of dialysis initiation. The relative risk of CTS was reduced to 0.503 (P < 0.05) and mortality 0.613 (P < 0.05) by dialysis on the high-flux membrane, compared to the conventional membrane. Serial measurements of beta 2m indicated significantly lower beta 2m to persist in patients on the high-flux membrane. The high-flux membrane decreased the risk of morbidity and mortality substantially. Larger molecule elimination was shown important not only for preventing beta 2m amyloidosis, but for prolonging survival of dialysis patients as well.

Adult↗
PubMed1997

Two missense mutations of H type alpha(1,2)fucosyltransferase gene (FUT1) responsible for para-Bombay phenotype.

BACKGROUND AND OBJECTIVES: Rare individuals (Bombay and para-Bombay phenotypes) fail to express the A, B and H antigens on erythrocyte membranes because of a lack in the H gene (FUT1)-encoded alpha(1,2)fucosyltransferase activity. In this study, we have found a para-Bombay individual (Bmh) who expressed B and H antigens in saliva but not on red blood cells. The FUT1 alleles of this person contained two single base changes (T460C and G1042A) in the coding region relative to the wild type allele. These substitutions may result in changes in two amino acid residues (Y154H and E348K). MATERIALS AND METHODS: Since the T460C and G1042A mutations destroy endonuclease RsaI and AvaI sites, respectively, we tested for these mutations using PCR-RFLP. RESULTS: Our findings indicated that this para-Bombay person was homozygous for the T460C and G1042A mutations, and that neither of these mutations was found in 136 randomly selected Japanese individuals. The measurement of the alpha(1,2)fucosyltransferase activity after transient expression of the FUT1 alleles in COS-7 cells indicated that the H-deficient allele-encoded enzyme had no detectable activity. Moreover, transfection by chimera FUT1 allele contains only the T460C mutation, or only the G1042A mutation, and yielded 1.0 or 9.3%, respectively, of the activities compared to transfection by the wild type allele. CONCLUSIONS: These results suggest that the two mutations in combination are responsible for the inactivation of the FUT1-encoded enzyme activity.

ABO Blood-Group System↗
PubMed1996

Plasma endothelin-1 level in athletes after exercise in a hot environment: exercise-induced dehydration contributes to increases in plasma endothelin-1.

We investigated whether dehydration due to exercise contributes to the increase in plasma endothelin-1 (ET-1) concentration. We measured the plasma concentration of ET-1 before and after exercise in a hot environment (about 30 degrees C). Five male intercollegiate Kendo (Japanese fencing) players entered the present study. Each athlete participated in 15 min of Kendo fighting, followed by 5 min of rest and another 15 min of Kendo fighting (i.e., total exercise 30 min), with or without oral intake of 700 ml of water. Body weight and left atrial diameter, a parameter that reflects changes in circulating plasma volume, were significantly decreased after exercise under both conditions. However, the decreases in both values were significantly greater after exercise without water intake than after exercise with water intake, indicating that dehydration and decreased circulating plasma volume were more marked after exercise without water intake. The extent of the increase in plasma ET-1 concentration appeared to be closely related to the extent of exercise-induced dehydration; the greater the dehydration, the greater the increase in plasma ET-1 concentration. These findings suggest that exercise-induced dehydration may contribute to increases in plasma ET-1 concentrations.

Adult↗
PubMed1996

Measurement of ABH blood group substances in human saliva by immunoassay using artificial antigens as standard substances.

Introducing artificial antigens (trisaccharide-albumin complexes for A, B and H activities) as reference substances for immunoassay, blood group substances, A, B, and H in human saliva were measured. A good correlation between hemagglutination inhibition titers and concentrations of A, B, and H in saliva was demonstrated. Since the anti-H 1E3 used showed the specificity for both H type 1 and H type 2 chains and anti-H 224 for H type 2 chain, we measured H type (1 and 2) and H type 2 separately, and found 10- to 20-fold higher concentration of H type (1 and 2) compared with that of H type 2 in human saliva. The H type 2 was not found in all the saliva samples from nonsecretors irrespective of ABO subtypes. The results suggest that about 90% of A and B blood group substances in human saliva is also type 1 chain.

ABO Blood-Group System↗
PubMed1996

Molecular basis for secretor type alpha(1,2)-fucosyltransferase gene deficiency in a Japanese population: a fusion gene generated by unequal crossover responsible for the enzyme deficiency.

About 20%-25% of Caucasian individuals are nonsecretors who fail to express soluble A, B, H, and Lewis b histo-blood group antigens in secretory organs and secretory fluids because of the absence of the Secretor gene (FUT2)-encoded alpha(1,2)-fucosyltransferase (Se enzyme) activity. Recently, the FUT2 and a pseudogene have been isolated, and an Se enzyme-deficient allele (se) caused by a nonsense mutation (G428A, se1) in Caucasians has also been reported. Although we were unable to find the se1 allele, we have found a missense mutation (A385T, se2) and two nonsense mutations (C571T, se3 and C628T, se4) in the Japanese Se enzyme-deficient alleles. In addition, we have found a fusion gene, which consisted of the 5'-region of the pseudogene and the 3'-region of the functional FUT2, as a Se enzyme-deficient allele (se5). The DNA sequence analysis of the fusion gene indicated that the crossover region corresponded to regions between bases 253 and 313 of the pseudogene and between bases 211 and 271 of the FUT2. This finding suggested that the fusion gene was generated by homologous but unequal crossover. A population study on 141 randomly selected Japanese has indicated that the se2 is a common Se enzyme-deficient allele in the Japanese population. The results suggest that Se enzyme-deficient alleles are race specific.

ABO Blood-Group System↗
PubMed1996

[Transjugular intrahepatic portosystemic shunt: a new therapy for portal hypertension].

Thirty-five patients with portal hypertension due to liver cirrhosis secondary to chronic viral hepatitis underwent transjuglar intrahepatic portosystemic shunt for the last 3-year period. Shunts were successfully completed in 31 of 35 patients at 89%. Portal vein pressure was markedly reduced on average in the all cases until 6 months after TIPS. The endoscopic findings of varices much improved in 90% of the patients. Long-term patency rates of TIPS were 97% after 4 weeks, 79% after 6 months, 76% after a year and 55% after 2 years, respectively. The authors concluded that TIPS was an effective and reliable means of lowering portal pressure, improving endoscopic findings of varices and controlling of refractory ascites.

Esophageal and Gastric Varices↗
PubMed1996

PCR analysis of Lewis-negative gene mutations and the distribution of Lewis alleles in a Japanese population.

Three mutations in the Lewis-negative gene, T59G, G508A and T1067A, have been detected by means of a polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in 149 unrelated Japanese individuals. We found three common Lewis alleles-Le (without the T59G, G508A, and T1067A mutations), le1 (with the T59G and G508A mutations), and le2 (with the T59G and T1067A mutations) in a Japanese population. In addition, we also found one rare Lewis-negative allele, le3 (only with the T1067A mutation). The allele frequencies of Le, le1, le2, and le3 were 0.607, 0.275, 0.114, and 0.003, respectively. Our results were in accordance with those expected by the Hardy-Weinberg equilibrium. Some statistical parameters of forensic interest were also calculated.

Alleles↗
PubMed1995

Portal vein reconstruction using an internal jugular vein as a graft: report of a case.

We report the case of a 41-year-old man with pancreatic carcinoma invading the portal vein who was successfully treated by portal vein resection combined with pancreatoduodenectomy and reconstruction using an autointernal jugular vein. The internal jugular vein is an ideal graft for portal vein replacement because it has sufficient length, a well-matched diameter, and there is no venous insufficiency after unilateral resection. Nevertheless, this is the first report of portal vein reconstruction using the internal jugular vein as a graft.

Adenocarcinoma↗
PubMed1995

Detection of T to G mutation at position 59 in the Lewis gene by mismatch polymerase chain reaction.

Recently, we discovered the missense mutations of T to G at position 59 and of G to A at position 508 in one of the Lewis-negative (le) genes (Koda et al. 1993). In the present study, we report a method to detect the mutation at position 59 using mismatch PCR amplification and endonuclease MspI digestion. For this mutation, we found that 7 out of 12 Lewis-negative, and none of 15 Lewis-positive individuals were homozygous, while 4 out of 12 Lewis-negative, and 4 out of 15 Lewis-positive individuals were heterozygous. These results indicate that the mutation at position 59 is a common mutation in the le genes.

Base Sequence↗
PubMed1995

A plasmid encoding enzymes for nylon oligomer degradation: nucleotide sequence and analysis of pOAD2.

The entire nucleotide sequence of nylon oligomer degradative plasmid pOAD2 from Flavobacterium sp. KI723T1 was determined. pOAD2 comprises 45519 bp, with a 66.6 mol% G+C content. The precise loci of the four nylon oligomer degradation genes, namely nylA (6-aminohexanoate-cyclic-dimer hydrolase gene), nylB (6-aminohexanoate-dimer hydrolase), nylB' (a gene having 88% homology to nylB) and nylC (endo-type 6-aminohexanoate oligomer hydrolase), and five IS6100 elements were identified on this plasmid. Comparison of the sequence of pOAD2 with those in the GenBank and EMBL databases revealed that the deduced amino acid sequences from eight regions of pOAD2 had significant similarity with the sequences of gene products such as oppA-F (oligopeptide permeases), ftsX (filamentation temperature sensitive), penDE (isopenicillin N-acyltransferase) and rep (plasmid incompatibility). A functional map of pOAD2 is presented.

Amidohydrolases↗