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Biomedical subjects

Y Obata

Publications and source records attributed to Y Obata.

At least 109 records · Page 6Linked to original sources
PubMed1989

[Campylobacter pylori and diseases of the stomach].

In spite of extensive clinical studies the pathogenicity of Campylobacter pylori in various diseases of the stomach is still not fully elucidated. In peptic ulcer Campylobacter pylori has not provided a reasonable explanation for the localized and solitary development of ulcer lesion which is one of characteristic features of this clinical entity. Our previous clinical study revealed that relapse occurs mostly at or near the scar of the preceding ulcer lesion and occurs more often in red scar than in white scar in peptic ulcer. Therefore, the scar was chosen to investigate whether there is a correlation between Campylobacter pylori and relapse. Twenty patients with healed gastric ulcer were biopsied in duplicate at 4 different sites, namely at the center of and near the scar of the preceding ulcer lesion, in the body and pyloric antrum. One of the duplicate specimen was stained, and the other cultured. Number of the colony observed on the plate was highest at the scar center followed by near the scar or in the body, and the pyloric antrum showed the lowest. Campylobacter pylori was detected in 46.7% of red scar, and 20% of white scar. Campylobacter pylori may play a pathogenic role in some patients of peptic ulcer, but not in all. Namely Campylobacter pylori is one of factors which may cause in imbalance between offensive and defensive powers at gastric mucosa and may lead to development of ulcer lesion. In case of positive bacteriological test, therefore, as to presence of Campylobacter pylori, the preventive measure for relapse such as bismuth preparation may be considered.

Adult↗
PubMed1988

Antigenic phenotype and biological characteristics of two distinct sublines derived from a small cell lung carcinoma cell line.

Two sublines, SCLC-MOA1 (MOA1) and SCLC-MOA2 (MOA2), were established from the SCLC-MO cell line, which was originally derived from an oat cell type of small cell lung carcinoma (SCLC). SCLC-MO showed typical culture morphology of SCLC, growing as tightly packed floating aggregates, while both MOA1 and MOA2 grew as a monolayer. MOA2 showed markedly shorter culture doubling time and higher colony forming efficiency than SCLC-MO and MOA1. When transplanted into nude mice, both SCLC-MO and MOA1 showed intermediate cell type histology, while MOA2 showed a picture of large cell carcinoma as non-SCLC. As for biomarkers, SCLC-MO showed a transitional state between the classic and the variant types, while MOA1 was the variant type. In contrast, MOA2 lost the biomarker characteristic of SCLC, showing rather non-SCLC type. SCLC-MO expressed NE-150 neuroendocrine antigen, but lacked PE-35 panepithelial antigen which is generally present on SCLC. It lacked also OE-130 epithelial antigen which is generally absent from SCLC. Thus, the phenotype was NE-150+/PE-35-/OE-130-, which was different from the major phenotype of SCLC, NE-150+/PE-35+/OE-130-. MOA1 was weakly positive for PE-35, showing NE-150+/PE-35 +/- /OE-130-, while MOA2 was positive for OE-130, but lost NE-150, i.e., NE-150-/PE-35+/OE-130+, showing a non-SCLC phenotype. Thus, a good concordance was observed between the antigenic phenotype and the biological characteristics of these SCLC lines. The results altogether suggested that a part of large cell carcinoma in the tumor of the patient may be derived from SCLC. Karyotype analysis showed that there were several marker chromosomes including deletion of chromosome 3p shared by these three cell lines, supporting the belief that MOA1 and MOA2 originated from SCLC-MO. Southern blot analysis showed the amplification of the L-myc related gene, probably rearranged L-myc, in the primary SCLC tumor as well as in SCLC-MO and MOA1. Northern blot analysis showed the 2.2-kilobase transcripts hybridized with a L-myc probe were observed in SCLC-MO and MOA1, but not in MOA2. In contrast, the c-myc transcript was detected only in MOA2. The activity of the myc gene family may contribute to certain biological characteristics of SCLC.

Animals↗
PubMed1988

Influence of 5' flanking sequences on TL and H-2 expression in transfected L cells.

TL (thymus leukemia) antigens are encoded by genes in the major histocompatibility complex (MHC) of the mouse. Although similar in overall structure to other class I MHC antigens (H-2, Qa), TL expression is regulated in a highly distinctive fashion. In contrast to the broad distribution of H-2 and the intermediate distribution of Qa, TL expression is restricted to cells of T-cell derivation during development in the thymus and is lost when T cells migrate to the periphery. Some mouse strains do not express TL antigens on thymocytes (TL- strains), but leukemias occurring in these mice can have a TL+ phenotype, indicating activation of normally silent TL genes. In transfection studies with H-2 or TL genes in L cells (mouse fibroblasts), H-2 is expressed at high levels, whereas TL is poorly expressed. To identify genetic elements that regulate expression in transfected L cells, chimeric genes were constructed by transposing the 5' and 3' regions of TL and H-2 genes. Antigen expression was not influenced by transposing the cytoplasmic domain and 3' untranslated region. In contrast, interchanging the 5' flanking sequences and exon 1 had a marked influence on antigen expression, with 5' sequences from the H-2 gene increasing TL expression 10- to 50-fold, and 5' sequences from the TL gene markedly decreasing H-2 expression. With both the parental TL gene (p20-TL) and the highly expressed chimeric TL gene (construct 3), levels of TL mRNA and TL antigen correlated with the number of transfected gene copies. However, in cells transfected with equal copy numbers, much higher levels of TL mRNA and TL antigen were found in construct-3 transfectants than in p20-TL transfectants. In addition, there was marked heterogeneity in TL mRNA size in L cells transfected with p20-TL, in contrast to a more homogeneous transcript size in construct-3 transfectants. These results point to regulatory sequences in the 5' flanking region of class I genes that control proper initiation and processing of TL transcripts.

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

Possible absence of common polymorphisms in coagulation factor IX gene in Japanese subjects.

Four distinct intragenic polymorphisms in the coagulation factor IX gene which have been reported to be important for family diagnosis of Caucasian hemophilia B were studied in 51 normal Japanese subjects (21 males and 30 females). High-molecular-weight DNA prepared from peripheral blood lymphocytes were digested with endonuclease, Ddel, Mspl, Taql or Xmnl, and were studied by Southern blot analysis with factor IX complementary DNA as a probe. None of the minor fragments produced by these enzymes was found in the normal Japanese DNA samples tested, although the probe detects minor allelic forms in control Caucasian DNA samples. Our data suggest that the frequent polymorphic sites found in Caucasians are possibly absent in the Japanese population.

Asian People↗
PubMed1987

Clonal T cell population in angioimmunoblastic lymphadenopathy and related lesions.

The arrangements of the T cell receptor (TCR) beta genes were studied in lymph node specimens with the histological characteristics of angioimmunoblastic lymphadenopathy with dysproteinemia (AILD), AILD-like T cell lymphoma (AILD-T), T-zone lymphoma, or Lennert's lymphoma. Eight of 11 cases with AILD or AILD-T showed clonal rearrangements of TCR beta genes: all three AILD cases showed clonal rearrangements of TCR beta genes, while five of 8 AILD-T cases exhibited clonal rearrangement patterns. Malignant lymphoma evolved in one AILD case showed the same rearrangement band of TCR beta genes as its primary AILD lesion. The rearrangement of TCR beta genes was also observed in 2 out of 3 cases with T-zone lymphoma and 2 out of 2 cases with Lennert's lymphoma. None of the cases studied, except one AILD-T case, exhibited clonal rearrangements of immunoglobulin heavy chain genes. The results suggested that a significant proportion of AILD, AILD-T, T-zone lymphoma and Lennert's lymphoma cases are malignancies of peripheral T cell origin.

Adult↗
PubMed1987

[Serological and immunomolecular markers for the diagnosis of hematopoietic tumors].

The analysis of cell surface markers with monoclonal antibodies has recently been developed and has been proved to be valuable in the diagnosis and classification of hematopoietic tumors. Occasionally, however, such serological studies have been shown to be inconclusive in identifying cell lineage and or clonal proliferation. In order to overcome these problems, two new approaches were introduced in our laboratory. First, T cell receptor and immunoglobulin gene rearrangement analysis as a means of immunomolecular marking was carried out. Second, a double immunoenzymatic staining technique for determining the surface phenotypes of proliferating lymphocytes using a monoclonal antibody against DNA polymerase alpha together with those detecting lymphocyte membrane antigens was developed. The results revealed by these techniques strongly suggested that some CD2-, CD5+, CD7+ ALL cases are of T cell origin and that AILD may be a neoplastic disease derived from either of the subsets of peripheral T cells.

Antibodies, Monoclonal↗
PubMed1987

[Basic evaluation of measurement of the serum level of squamous cell carcinoma-related antigen (SCC) and its value following irradiation of cancer of the uterine cervix].

The measurement of the serum level of squamous cell carcinoma-related antigen (SCC) purified from liver metastasis of cancer of the uterine cervix by an RIA kit is basically evaluated. The results of sensitivity, the recovery test, dilution test and variance test are good enough for clinical application. In gynecological disorders, the positive rate is high (62% [29/47]) in patients with cancer of the uterine cervix. Furthermore, the rate and level are related with the clinical staging. The changes of the serum SCC level in irradiated patients with cancer of the uterine cervix were a good reflection of the effectiveness of the treatment.

Antigens, Neoplasm↗
PubMed1986

Molecular basis of a unique tumor antigen of radiation leukemia virus-induced leukemia B6RV2: its relation to MuLV gp70 of xenotropic class.

Hybridomas secreting monoclonal antibodies that reacted with the B6 radiation leukemia virus (RadLV)-induced leukemia B6RV2 were produced by fusion of BALB/c NS-1 myeloma cells with spleen cells from (BALB/c X B6)F1 mice immunized with B6RV2. By direct and absorption analyses with 28 B6 and BALB/c leukemias, the monoclonal antibodies NU7-4 and NU7-99 were shown to react only with B6RV2, indicating that they recognized an individually distinct antigen on B6RV2 that was identified previously with conventional (BALB/c X B6)F1 anti-B6RV2 serum. Another monoclonal antibody, NU1-132, showed relatively restricted reactivity with B6 RadLV leukemias. These three monoclonal antibodies all precipitated material of approximately 80,000 daltons, which is the same size as that precipitated by anti-xenotropic MuLV gp70 serum. Sequential immunoprecipitation analysis revealed that the molecules precipitated by NU7-4 were not removed by pretreatment of NU7-99 or NU1-132 and that the molecules precipitated by NU7-99 were not removed by NU7-4 or NU1-132. The molecules precipitated by NU1-132 were partially removed by pretreatment with NU7-4, but not with NU7-99. The molecules precipitated by these three monoclonal antibodies were removed by pretreatment with anti-xenotropic gp70. These results suggested heterogeneity of the xenotropic MuLV gp70-related molecules expressed on B6RV2 and a possible relation between serologically defined unique tumor antigens and gp70-related molecules.

Animals↗