[Hereditary angioneurotic edema with interesting radiographic findings in the small intestine].
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Biomedical subjects
Publications and source records attributed to H Otsuka.
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Eight hundred and twenty five infertility patients were investigated to reassess the association between uterine mild anomaly and menstrual disorder proposed as a new syndrome by Sørensen. A hysterosalpingogram we classified the shape of the uterine cavity into 4 types: Normal uterus, T-shaped uterus, arcuate uterus and others (included septate uterus, bicornuate uterus,--), and also classified the size of the uterine cavity into 3 groups; large uterus, medium-sized uterus and small uterus. After classification of uterine shape and size, menstrual disorder in each patient was reviewed and the correlation between uterine anomaly and menstrual disorder was examined. Five hundred and twenty eight out of 770 patients (68.6%) were assigned to normal uterus, 75(7.9%) to T-shape uterus, 148(19.2%) to arcuate uterus and 19(2.5%) to others. Their incidences of menstrual disorder were 31.4%, 37.2%, 39.2% and 42.1%, respectively, and no significant difference was found among them. There were 55 patients (7.3%) with a large uterus, 655(87.2%) with a medium-sized uterus and 41(5.5%) with a small uterus. The incidences of menstrual disorder were 16.4%, 35% and 34.1%, respectively, and there was significant difference in incidence between large uterus and medium-sized uterus. The uterine fundal depression index (FDI) was used as a parameter to evaluate uterine mild anomaly. The incidences of menstrual disorder were 29.8% in the FDI-0 group, 32.9% in the FDI-1 approximately 10 group, 42.7% in the FDI-11 approximately 20 group, 45.5% in the FDI-21 approximately 30 group and 22.2% in the FDI-over 31 group. However, it was difficult to find a difference in the pregnancy rate or delivery rate among different classifications of uterine shape, size or FDI. From these results, it can be said that mild uterine anomaly is hardly associated at all with menstrual disorder clinically.
An analysis of 105 autopsy cases (77 male, 28 female) of hepatocellular carcinoma (HCC) showed that 90 cases (85.7%) were associated with liver cirrhosis, of which 75 cases (83.3%) were of the macronodular type. Hepatitis B surface antigen (HBsAg) was detected with orcein stain in the hepatic tissue in 58 cases (55.2%). The incidence of HBsAg in cases of HCC patients with cirrhosis (58.9%) was higher, but not significantly, than that in those without cirrhosis (33.3%). The mean age of HBsAg-positive cases was five years less than that of HBsAg-negative cases, the age distributions therefore being significantly different.
To learn whether interferon could prevent the biochemical transformations induced by cloned herpesvirus thymidine kinase (TK) genes, LM(TK-) mouse fibroblast cultures were pretreated for 24 h with 2.4-40 international units (I.U.)/ml mouse alpha + beta interferon, and subsequently transformed to the TK+ phenotype with recombinant plasmids containing the herpes simplex virus type 1 (HSV-1) TK gene (pAGO and pMH110) and the marmoset herpesvirus (MarHV) TK gene (pMAR035). Mouse alpha + beta interferon inhibited transformation and the inhibition was interferon dose-dependent. Transformation was also inhibited when LM(TK-) cells were pretreated for 2-5 h with 40 I.U./ml interferon. Maximal inhibitions of TK+ colony formation were observed following a 9-20 h pretreatment period with interferon. In contrast, 40 I.U./ml interferon treatment for 20 h did not reduce the rate or extent of LM(TK-) cell growth. Experiments in which cultures were first treated with plasmid pAGO and only afterwards treated with interferon also showed that, as the interferon concentration used, interferon did not inhibit the outgrowth of transformated colonies. Enzyme assays showed that pretreatment with interferon inhibited the induction of TK activity in cells that had been transfected with pAGO DNA.
Glycolipids of erythrocytes from inbred mice, C3H/He and CDF1, were analyzed. Galactosylceramide, glucosylceramide, GM4 and GM2 were separated and their structures were established. Sialic acid of GM4 was exclusively N-acetylneuraminic acid, while GM2 contained only N-glycolylneuraminic acid. The fatty acid composition of GM4 was very similar to that of galactosylceramide, and a similarity was also found between that of GM2 and glucosylceramide. These results suggest that erythroid cells of mice have two separate biosynthetic pathways of gangliosides. One is the pathway to GM4 (NeuAc) from galactosylceramide, and the other is that for synthesizing GM2 (NeuGc) from glucosylceramide.
Individual non-glucuronidated . non-sulfated, glucuronidated and sulfated bile acids in serum were determined, i.e. lithocholic acid, deoxycholic acid, chenodeoxycholic acid, ursodeoxycholic acid, and cholic acid, by mass fragmentography. Glucuronic acid conjugates of lithocholic acid, deoxycholic acid, chenodeoxycholic acid, and cholic acid were synthesized via the Koenigs-Knorr condensation reaction. Deuterium labeled deoxycholic acid, lithocholic acid glucuronide, deoxycholic acid glucuronide, and deoxycholic acid sulfate were synthesized and used as internal standards. A serum sample of 1 ml including internal standards was purified with a Sep-Pak C18 cartridge. After the enzymatic cleavage of amino acid conjugates, bile acids were separated into three fractions, free, glucuronidated, and sulfated bile acids, using piperidinohydroxypropyl Sephadex LH-20 (Goto et al. (1978) Clin. Chim. Acta 87). Glucuronidated and sulfated bile acids were deconjugated by beta-glucuronidase treatment and solvolysis. Each fraction was converted to the hexafluoroisopropyl-trifluoroacetyl derivative and quantitated by mass fragmentography. The average concentrations of individual bile acid glucuronides from healthy fasting subjects (n = 9) were as follows; lithocholic acid 0.013 microgram/ml, deoxycholic acid 0.083 microgram/ml, chenodeoxycholic acid 0.078 microgram/ml, ursodeoxycholic acid 0.013 microgram/ml, and cholic acid 0.007 microgram/ml. Bile acid glucuronides occupied 7.8% of the total bile acids.
The presence of cholestanol had never been reported in cultured cells, but in the present study cholestanol was detected both in human and rat skin fibroblasts. The present study has shown that the origin of cholestanol in these fibroblasts was derived from de novo synthesis in the cells rather than from the fetal calf serum used in the growth medium. The activity of 5 alpha-cholestan-3-one reductase which is the enzyme catalyzing the final step in the biosynthesis of cholestanol was measured by mass fragmentography using deuterium labeled 5 alpha-cholestan-3-one as a substrate. The activity of this enzyme was also detected in the microsomal fractions of rat cerebrum and cerebellum as well as in the liver. These results suggest that cholestanol can probably be synthesized in extra-hepatic tissues as well as in the liver.
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The histogenesis of perianal squamous cell carcinomas induced by subcutaneous and intraperitoneal injection of 1,2-dimethylhydrazine dihydrochloride (DMH) and painting of methylazoxymethanol (MAM)-acetate on the anal region was investigated in 212 female BALB/c mice. Painting of MAM-acetate and injection of DMH induced similar benign and malignant tumors and hyperplastic lesions in the anal region. In chronological studies on animals given DMH subcutaneously, cystic or solid squamous lesions, foci of immature sebocytes, sebaceous hyperplasias and sebaceous adenomas were identified. These lesions seemed to be precursors of carcinomas that developed in the same region, and originated from hair follicles or sebaceous glands of the pilosebaceous complexes, but not from the anal mucosa. In mice treated with DMH, the incidence of perianal carcinomas was high in groups with high incidences of colon carcinomas.
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To study the expression of SV40 tsA genomes that had been non-selectively introduced into mouse cells, SV40 tsA207 DNA was cleaved with BamH I and ligated to BamH I-cleaved plasmid pAGO DNA, which contains a functional HSV-1 thymidine kinase (TK) gene in the form of 2 kbp Pvu II fragment inserted at the Pvu II site of pBR322. Recombinant plasmids (11-12 kbp) were isolated and amplified in E. coli K12 strain RRI. Restriction nuclease analyses demonstrated that recombinant plasmids pSB15 and pSB10 contained intact SV40 genomes with the polarity of transcription oriented in the same direction (clockwise) or the opposite direction (counterclockwise), respectively, in relation to that of the HSV-1 TK gene. Cla I-cleaved pSB10 and pSB15 DNAs were used to transform LM(TK-) cells to TK+. Serological and disc PAGE analyses showed that clonal lines transformed by these plasmids all expressed the selected marker, HSV-1 TK. Molecular hybridization experiments showed that transformed clonal lines TF pSB10 C7 and TF pSB15 C10 had integrated intact SV40 genomes at one integration site, TF pSB10 C3 had integrated an SV40 genome with a small deletion near the BamH I site, but TF pSB15 Cl had integrated a plasmid from which most of the SV40 nucleotide sequences had been deleted. IF assays with hamster anti-SV40 tumor sera showed that TF pSB10 C7 and TF pSB15 C10 strongly expressed SV40 T antigens in over 90% of the cells, TF pSB10 C3 expressed SV40 T antigens in a minority of the cells, and TF pSB15 C1 did not express SV40 T antigens at all. [35S]-methionine labelling and immunoprecipitation experiments showed that, at 36.5 degrees C: (1) TF pSB10 C7 and TF pSB15 C10 expressed 92K and 20K mol. wt. species of SV40 T antigens and 50-55K cellular protein; (2) expression of all three was reduced in TF pSB10 C3 cells; and (3) TF pSB15 C1 expressed none of the SV40 T antigens, nor did parental LM(TK-) or TF 8-2 transformed cells (which contained the HSV-1 TK gene but not SV40 DNA). At 40 degrees C, labelling of the 50-55K cellular protein was markedly reduced in TF pSB10 C7 and pSB15 C10 cells. The results suggest that SV40 large T antigen (92K) induces and/or stabilizes the 50-55K cellular protein in these mouse cells.
Feeding experiments with 13C-labeled precursors followed by 13C NMR analysis of the antibiotic and its aglycon have established a polyketide mode of biosynthesis for chlorothricin, a metabolite of Streptomyces antibioticus. The acyl moiety is a substituted 6-methylsalicylic acid derived from four acetate units and a methyl group of methionine. The aglycon is comprised of ten acetate and two propionate units, leaving three carbon atoms, C-22, -23, and -24, unaccounted for. The two 2-deoxy-D-rhamnose moieties are derived from glucose with retention of the hydrogens at C-1, C-2, and C-6 and loss of H-3 and H-5. The hydrogen at C-4 of glucose is transferred intramolecularly to C-6 of the hexose, replacing the hydroxyl group at C-6 in an inversion mode, a result which implicates the thymidine 5'-diphosphate-glucose oxidoreductase reaction in this transformation.
To analyze the site of integration of the herpes simplex virus type I (HSV-I) thymidine kinase (TK) gene in biochemically transformed human cells, TK-HeLa-(BU25) cells were transformed to the TK+ phenotype by a cloned, 2 kbp Pvull fragment of HSV-I DNA. The transformed cells [HeLa(BU25)/TF pAGO PP3] were fused with mouse LM(TK-) cells, and human-mouse somatic cell hybrid clones (LH PP3 clones 1, 2, 3, 5 and 6) were isolated in HATG-ouabain selective medium. The HeLa(BU25)/TF pAGO PP3 cells and the LH PP3 hybrid clones expressed HSV-I specific TK activity and a herpesvirus-associated nuclear antigen, and contained herpesvirus nucleotide sequences. Molecular hybridization experiments were carried out to map the HSV-I and flanking cellular nucleotide sequences in the biochemically transformed cells. These experiments demonstrated that the HSV-I nucleotide sequences were integrated at a single site, and that the same cellular nucleotide sequences flanked the viral DNA in transformed HeLa(BU25)/TF pAGO PP3 and LH PP3 clone 5 cells. TK- revertant subclones isolated by growing the LH PP3 clone 5 cells in BrdUrd (and diphtheria toxin) failed to form colonies in HATG medium, but retained HSV-I nucleotide sequences. Isozyme analyses on 21 gene-enzyme systems representing 21 human chromosomes revealed that all of the LH PP3 clonal lines expressed human hexosaminidase B, which has been assigned to chromosome 5, and all were sensitive to diphtheria toxin, which is also a marker for chromosome 5. Chromosome analyses showed that chromosome 5 was the nly human chromosome present in mitoses of LH PP3 clone 5 cells and that human chromosome 5 was present in most of the mitoses of LH PP3 clone 1, 2, 3, and 6 cells. The latter clones also contained 1 or 2 additional human chromosomes in some of the cells. As expected from the molecular hybridization analyses, TK- revertants of LH PP3 clone 5 cells retained portions of chromosome 5 and expressed human hexosaminidase B. The results indicate that HSV-I nucleotide sequences were stably integrated in the biochemically transformed cells, most likely in human chromosome 5.
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