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Biomedical subjects

Y Oba

Publications and source records attributed to Y Oba.

At least 37 records · Page 2Linked to original sources
PubMed1998

[alpha-thalassemia accompanied with Gilbert's syndrome].

A 15-year-old boy was admitted to our hospital because of microcytic hypochromic erythrocytosis and hyperbilirubinemia in October 1996. The laboratory findings were RBC: 597 x 10(4)/microliter, Hb: 13.1 g/dl, Ht: 40.8%, MCV: 70fl, MCH: 22pg, total bilirubin: 3.2 mg/dl (indirect: 2.2 mg/dl), s-Fe: 99 micrograms/dl, and ferritin: 25 ng/ml. Routine liver function tests were normal. There were no findings of hemolysis except for an increase in serum indirect bilirubin and reticulocytes. Decreased erythrocyte osmotic fragility was observed. The patient's mother and sister also showed microcytic hypochromic erythrocytosis. PCR analysis of genomic DNA from this patient, his mother, and his sister confirmed the diagnosis of the alpha-thalassemia trait. However, the bilirubin-UDP-glucuronosyltransferase 1 (B-UGT 1) gene mutation and the findings of the fasting test indicated the simultaneous presence of Gilbert's syndrome. The association of these two diseases in the same patient appears to be rare, especially in Japan because of the low incidence of thalassemia in this country. We concluded that the hyperbilirubinemia was caused by decreased bilirubin clearance, not by increased erythrocyte destruction.

Adolescent↗
PubMed1997

Inhibitory guanine-nucleotide-binding-regulatory protein alpha subunits in medaka (Oryzias latipes) oocytes--cDNA cloning and decreased expression of proteins during oocyte maturation.

We have previously shown that pertussis-toxin-sensitive inhibitory guanine-nucleotide-binding-regulatory proteins (G proteins) are involved in the signal transduction of steroidal maturation-inducing hormone (MIH) of rainbow trout (Oncorhynchus mykiss) oocytes, 17alpha,20beta-dihydroxy-4-pregnen-3-one (17alpha,20beta-DP) [Yoshikuni, M. & Nagahama, Y. (1994) Dev. Biol. 166, 615-622]. In this study, we obtained five different cDNA fragments of G protein alpha subunits from medaka (Oryzias latipes) intact ovarian follicles (three subtypes of G(i alpha), G(i alpha a), G(i alpha b) and G(i alpha c); two subtypes of G(s alpha), G(s alpha d), and G(s alpha e)). Using a newly developed extraction method for medaka oocyte RNA, we demonstrated that oocytes expressed both G(i alpha a) and G(i alpha c), but not G(i alpha b). Full-length cDNA clones for G(i alpha a) and G(i alpha c) were then isolated from a medaka ovarian follicle cDNA library. The predicted amino acid sequences of G(i alpha a) and G(i alpha c) exhibited significant similarity with G(i alpha1) and G(i alpha2) of other species, respectively. Both G(i alpha a) and G(i alpha c) possessed a specific Cys residue in the C-terminal region that was the site for ADP-ribosylation by pertussis toxin. G(o alpha), another G protein that is ADP-ribosylated by pertussis toxin, was not detected in oocytes, although it was expressed in brain tissue. Western blot analyses using a specific antibody against G(i alpha1) and G(i alpha2) subunit proteins revealed that in both medaka and rainbow trout G(i alpha) subunit protein (40 kDa) contents were abundant in plasma membranes of postvitellogenic immature oocytes, decreased in mature oocytes, and were absent in ovulated eggs. Furthermore, specific 17alpha,20beta-DP binding to plasma membranes was higher in postvitellogenic immature oocytes than in ovulated eggs. Taken together, these results suggest that G(i alpha a) and/or G(i alpha c) may be involved in the transduction of the signal from 17alpha,20beta-DP receptors during oocyte maturation of fish oocytes.

Amino Acid Sequence↗
PubMed1997

[Prevailing conditions and problems with blood transfusion tests as seen after analysis of Osaka Medical Association Survey].

We have analysed the results of the 1996 Osaka Medical Association Clinical Examination Quality Control survey. The number of participating clinical laboratories was 257 for ABO blood group system, 255 for Rh (D) antigen, and 250 for crossmatching. Five (5) clinical laboratories (1.9%) determined the ABO blood group by the antigens on red blood cells test only, and three (3) clinical laboratories (1.2%) showed errors when using antibodies in serum test. On the Rh(D) antigen tests, fifteen (15) clinical laboratories (5.9%) showed negative results without carrying out an antiglobulin test. Three (3) clinical laboratories (1.2%) were unable to detect the anti Dib antibody which showed 1:256 titerates using the antiglobulin test method. Moreover, it was apparent that thirty-four (34) clinical laboratories (13.6%) had problems with the test standards and other technical points, and further, two (2) clinical laboratories (0.8%) reported contradictory results due to confusing blood samples of donors and patients to be transfused. As a result, we consider it very important for preventing blood transfusion accidents that any technician carrying out blood transfusion tests makes correct decisions and determinations based on accurately performed test methods, and that a manual be prepared to avoid technical and administrative errors and that this manual be followed to the letter.

ABO Blood-Group System↗
PubMed1986

Ectopic adrenocorticotropin syndrome caused by lung cancer that responded to corticotropin-releasing hormone.

ACTH responses to corticotropin-releasing hormone (CRH) were studied in three patients with the ectopic ACTH syndrome caused by lung cancer. Plasma ACTH responded to synthetic CRH in two of three patients. Tumor tissues obtained from these two patients contained CRH and ACTH. In one patient, tumor ACTH secretion was stimulated by CRH in vitro. Tumor CRH was immunologically, chromatographically, and biologically similar to hypothalamic CRH. In addition, multiple forms of immunoreactive beta-endorphin were present in plasma and the tumor extracts. From these results, we conclude that some patients with the ectopic ACTH syndrome have tumors that produce both ACTH and CRH and that CRH can stimulate ACTH secretion by such tumors. Other patients with the ectopic ACTH syndrome do not have ACTH responses to CRH. Therefore, procedures other than CRH testing are needed to differentiate patients with Cushing's syndrome due to ectopic ACTH/CRH production from those with Cushing's disease, since the latter also usually have ACTH responses to CRH.

ACTH Syndrome, Ectopic↗
PubMed1975

Metabolic activities of histones in rat liver and spleen.

Synthesis and turnover of histone I and II in normal rat liver and spleen were studied by Amberlite CG 50 column chromatography. Histone I was separated into three or four subfractions, each of which showed a different rate of incorporation of [3H]lysine. This was verified by a more shallow gradient chromatography developed by Kinkade and Cole [3] for very lysine-rich histone (F1), which showed tissue specific differences between liver and spleen in both the elution pattern and synthetic rates. These subfractions were distinguished from each other by dodecylsulphate electrophoresis. The turnover, or disassociation of histone I and II in chromatin was measured by double-labelling of normal rat liver with [3H] and [14C]lysine. A good correspondence was found between the synthesis and turnover patterns of individual histone I fractions, while the histone II synthesized was conserved for over a month. From consideration of the turnover in relation to the cell population of normal liver tissue, which consists of a very small fraction of growing cells and a very large fraction of resting ones, it was concluded that turnover of histone I must occur even in resting cells. When DNA synthesis in the spleen was completely inhibited by hydroxyurea, the synthesis of histone II was inhibited but that of histone I was only partially inhibited. The remaining synthesis seemed to occur in cells in the resting state. It was concluded tentatively, the continuous replacement of very lysine-rich histones of chromatin must occur even in resting cells in which DNA synthesis has ceased. The biological significance of disassociation of histones from chromatin was discussed.

Animals↗
PubMed1975

Interaction of aflatoxin B1 with DNA.

The interaction of aflatoxin B1 with DNA was investigated. In the presence of native DNA the absorption spectrum of the toxin showed an obvious spectral shift in the region of 300-420 nm with an isosbestic point at 376 nm. DNA-bound aflatoxin is hydrolyzed in alkaline media more easily than the free toxin. The hydrolized form has a labile structure and can decompose further. The bound toxins are easily dissociated by heat as well as by salt, and all toxin molecules are released from DNA which remains double-stranded. Aflatoxin can bind to thermally denatured DNA as well, with an accompanying spectral shift which depends on the particular preparation of denatured DNA, and there was an isosbestic point at 380 nm. The complex of toxin and denatured DNA was stabilized by salt up to 0.1 M. Thus it was concluded that aflatoxin was bound with denatured DNA in a different form from native DNA. The number of binding sites of DNA was estimated by constructing Scatchard plots based on both spectral analysis and equilibrium dialysis. However, these show no definite value but fall in the region of 0.07 to 0.013, that is one toxin molecule per 80-140 nucleotide of native DNA. Several lines of evidence suggest the possibility that aflatoxin exists in aqueous solution as aggregates. The mechanism of the binding was discussed. It is noteworthy that the number of binding sites of DNA doubles by the presence of histones.

Aflatoxins↗
PubMed1974

Selective removal of histones from calf-thymus nucleohistone with sodium dodecylsulfate.

Calf-thymus nucleohistone studied by a newly developed ;SDS gradient' centrifugation technique showed that histones dissociate sequentially when treated with increasing concentrations of sodium dodecylsulfate. Histones F2a1 and F2a2 were dissociated first at about 0.03% sodium dodecylsulfate, and F1 was removed lastly by the highest concentration of sodium dodecylsulfate (0.06% or more). A DNA-histone F1 complex, which consisted of DNA and all of the histone F1 and completely lacked other histones, was obtained by sedimenting nucleohistone through 0.05% sodium dodecylsulfate. Results of equilibrium gel filtrations in 0.05% sodium dodecylsulfate revealed that the binding of sodium dodecylsulfate to nucleohistone caused new binding sites to be available for the detergent which presumably was accompanied with dissociation of histones from DNA. This result indicates that no redistribution of histone F1 on DNA should occur in the presence of 0.05% sodium dodecylsulfate.

Binding Sites↗