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Biomedical subjects

K Ogata

Publications and source records attributed to K Ogata.

At least 361 records · Page 20Linked to original sources
PubMed1988

Expression of Fc receptors is suppressed in alveolar macrophages from patients with sarcoidosis.

To study the expression of Fc receptors in human alveolar macrophages (AM), the cells were collected from 12 healthy controls and 22 patients with sarcoidosis and the activity involved in binding to 125I-soluble immune complexes (IC) was investigated. The binding of 125I-IC was significantly suppressed in cells from the patients. A Scatchard plot analysis revealed that this suppression was due to a reduction in the number of Fc receptors on the surface membrane and not the result of a decrease in the binding affinity of the receptors. Rosette formation was observed by incubating AM with antibody-coated ox red blood cells. The presence of rosette forming cells was about 70% in the AM from healthy controls, while, a rate of only 50% was seen in those with sarcoidosis. These results indicate that the decrease of the 125I-IC binding in the AM from patients with sarcoidosis is to some extent the result of an increase in the population of the Fc receptor negative macrophages.

Adult↗
PubMed1988

Carrier detection in Japanese hemophilia A by use of three intragenic and two extragenic factor VIII DNA probes: a study of 24 kindreds.

The three factor VIII intragenic restriction fragment length polymorphisms (RFLPs), Bcll, Xbal, and Bgll and the two extragenic RFLPs, Bglll/DX13 and Taql/St14, were analyzed in 60 normal Japanese subjects and 24 families with hemophilia A. The allele frequencies were determined and the extent of linkage disequilibrium among the polymorphisms was assessed. In contrast to intragenic RFLPs of the factor IX gene, intragenic and extragenic RFLPs of the factor VIII gene in Japanese were similar to those observed in whites. As in whites, marked linkage disequilibrium severely compromised the value of the Bgll RFLP. The combination of the Bcll, Xbal, and Taql/St14 RFLPs gave 100% carrier detection in the hemophilia A families analyzed.

Asian People↗
PubMed1988

A liver-specific chromatin protein binding to the 5' far upstream region of the rat serum albumin gene.

Chromatin proteins which were extracted with 0.3 M NaCl from rat liver, brain, and kidney nuclei were examined by the protein blotting technique for their ability to bind to the 5' upstream regions of the rat serum albumin gene. A 110-kDa protein from liver nuclei bound specifically to the most upstream fragment (between approximately equal to -7.3 kbp and -2.0 kbp from the cap site) of the cloned albumin genomic DNA, whereas no proteins from kidney and brain bound to this fragment. It is possible that the 110-kDa protein is concerned with the tissue-specific expression of the albumin gene.

Animals↗
PubMed1988

DNA analysis of seven patients with hemophilia B who have anti-factor IX antibodies: relationship to clinical manifestations and evidence that the abnormal gene was inherited.

We have investigated genomic DNA samples of 24 patients with hemophilia B (factor IX deficiency), including seven patients with anti-factor IX antibodies (inhibitors), by molecular probes. Seventeen patients without inhibitors against factor IX and three patients with inhibitor showed no abnormalities in their restriction fragments generated by digestions of the genomic DNA by BamHl, EcoRl, Mspl, or Taql and hybridized with a factor IX cDNA probe (pHFIX). The remaining four patients with inhibitors were found to have gross deletions of the factor IX gene. Among those four patients, two were from the same family. Quantitative Southern blotting clearly showed that the abnormal gene was inherited in this family. DNA from the mother of another patient with deletion of the factor IX gene showed normal gene dosage, indicating that the mutation must have occurred at the mother's germ cells. The genomic DNA samples of four patients with gross factor IX gene deletions were found to lack the entire factor IX gene as analyzed with a factor IX cDNA as well as with a 3'-genomic factor IX fragment as probes. The hypoxanthine phosphoribosyltransferase (HPRT) gene probe, however, was found to hybridize with all of these DNA samples, indicating that the deletions in these genomic DNA samples had not extended to the region containing the HPRT gene locus in q27 proximal to the factor IX gene locus on the X chromosome. Several clinical characteristics were compared between inhibitor cases with gene deletion and inhibitor cases without obvious gene deletion.(ABSTRACT TRUNCATED AT 250 WORDS)

Chromosome Deletion↗
PubMed1987

Epitopes on proliferating cell nuclear antigen recognized by human lupus autoantibody and murine monoclonal antibody.

The immune epitopes of proliferating cell nuclear antigen (PCNA), also called cyclin, were analyzed by determining the reactivity between PCNA peptide fragments and anti-PCNA antibodies from lupus patients, murine monoclonal antibody (19A2), and rabbit anti-NH2-terminal peptide antibody. Limited digestion of PCNA/cyclin with Staphylococcus aureus V8 protease resulted in several peptide fragments. Five fragments of 30, 20, 15, 14, and 13 kDa were reactive with rabbit anti-NH2-terminal peptide antibody denoting that they contained the NH2-terminal peptide. The 30- and 20-kDa fragments reacted with 19A2 but the others did not. Lupus sera reacted with 17- and 15-kDa peptide fragments allowing their classification into three groups. Two of eight sera (type A) reacted only with the 17-kDa fragment. Two others (type B) reacted with both the 17- and 15-kDa fragments and the remaining four sera (type C) reacted only with the 15-kDa fragment. The sera reacting with the 15-kDa fragment also reacted with the 20-kDa fragment, but the sera reactive only with the 17-kDa fragment did not, indicating that the 17-kDa fragment was not a degradation product of 20-kDa fragments. The 19A2 epitope resided in the region between 15 and 20 kDa from the NH2 terminus, whereas there was at least one distinct epitope on each 15- and 17-kDa peptide, which were recognized by lupus autoantibodies.

Animals↗
PubMed1987

Molecular cloning and nucleotide sequence of cDNA specific for rat ribosomal protein L5.

cDNA clones specific for rat ribosomal protein L5, which is the protein moiety of 5S RNA protein particles, were isolated by using a mixture of tetradecamer deoxyribonucleotide probes reflecting the amino acid sequence of the N-terminal portion of L5. A cDNA clone (pRL5-1) lacking the 3'-terminal region of L5 was isolated by hybrid-selected translation and shown to be L5-specific by the identity of the deduced amino acid sequence and that of the N-terminus of protein L5. pRL5-1 was then used to select another clone (pRL5-2) by colony hybridization which contained the entire coding region, 3'-non-coding region and poly(A) addition signal. The nucleotide sequence of L5-specific cDNA was determined by using these two clones. It contained a total of 1069 base pairs: 123 base pairs in the 5'-non-coding region, 894 base pairs in the coding region and 52 base pairs in the 3'-non-coding region. The poly(A) addition signal appeared at the 33rd nucleotide after the termination codon. The amino acid sequence deduced from this nucleotide sequence consists of 296 amino acids. The homology of amino acid sequence between L5 and other 5S RNA-binding proteins is discussed.

Amino Acid Sequence↗
PubMed1987

Rat ribosomal protein L35a multigene family: molecular structure and characterization of three L35a-related pseudogenes.

The rat ribosomal protein L35a gene comprises a multigene family which contains 15-20 members as shown by the Southern blot analysis using L35a cDNA as a probe. We isolated 15 independent clones which contained distinct genes from a rat genomic library. Analysis of the restriction sites showed that all of them lacked the intervening sequences. Thermal stability of the hybrid molecules between these genes and the cDNA indicated that the similarity of the genes to the cDNA sequence varied. The nucleotide sequences of three genes gRL35a-A, gRL35a-B and gRL35a-G were determined. They shared some characteristics; namely: they lacked the intervening sequences, they contained (A)-rich tracts, and they were flanked by direct repeats. Two genes, gRL35a-A and gRL35a-B, contained a sequence completely identical to that of the cDNA. The nucleotide sequence of the 5' flanking region of gRL35a-B showed a significant homology with that of the same region of mouse ribosomal protein L32-related unmutated processed genes. Although this region of gRL35a-B contained the sequences homologous to the TATA box and the CCAAT box, gRL35a-B was not transcribed in an in vitro assay system. Thus, the L35a gene family comprises mostly processed pseudogenes. Further, Southern blot analysis in various animals indicated that the multigene construction of this ribosomal protein gene was a feature of mammalian genes. The origin and the evolutionary aspect of processed pseudogenes are discussed.

Animals↗