[Radiological study of sm-Esophageal cancer (author's transl)].
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Biomedical subjects
Publications and source records attributed to T Kikuchi.
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We describe a method for determination of guanidino compounds in plasma and erythrocytes. The compounds are separated by liquid chromatography, the concentrations in the effluent being estimated fluorometrically (Trans. Am. Soc. Artif. Intern. Organs 24: 61, 1978). Guanidinoacetic acid, guanidinosuccinic acid, guanidinobutyric acid, guanidine, methylguanidine, taurocyamine, and arginine can be detected and quantitated in both plasma and erythrocytes from healthy individuals. The method was also applied to patients in chronic renal failure. Guanidinosuccinic acid, creatinine, guanidine, and methylguanidine are substantially increased in the plasma and erythrocytes of the uremic patient. Guanidino compounds can be effectively extracted from plasma with 0.5 volume of 300 g/L trichloroacetic acid, from erythrocytes with five volumes of 120 g/L trichloroacetic acid.
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The labeling of m7GpppN1mpN2p caps with L-[methyl-3H]methionine on short (100-500 nucleotides) heterogeneous nuclear RNA (hnRNA) chains of HeLa cells is increased 2-3 times but the labeling of caps on longer (greater than 2000 nucleotides) hnRNA chains is decreased by approximately 80% by treatment of the HeLa cells with 5,6-dichloro-1-beta-D-ribofuranosylbenzimidazole (DRB). The experimental conditions were as follows: HeLa cells were treated with 75 muM DRB for 40 min before labeling and also during the 30-min pulse of L-[methyl-3H]methionine; actinomycin D (0.05 microgram/mL) was used to suppress ribosomal RNA synthesis. Control cells received no DRB. The RNA was separated in Me2SO gradients to ensure no aggregation. Labeling of cells with [3H]uridine for 10 min and separation of RNA by these techniques reconfirmed the findings [Tamm, I., Hand, R., & Caliguiri, L. A. (1976) J. Cell Biol. 69, 229-240; Sehgal, P. B., Darnell, J. E., Jr., & Tamm, I. (1976) Cell 9, 473-480] that 70-80% of the synthesis of hnRNA (GREATER THAN 1000 NUCLEOTIDES) IS SENSITIVE TO INHIBITIOn by DRB but that 20-30% is resistant. This analysis of the methyl-labeled caps provides evidence that DRB causes early termination of a large fraction (approximately 70-80%) of hnRNA precursor chains. In contrast to the finding of continued synthesis and accumulation of short m7GpppN1mpN2p-capped chains in the presence of DRB, the synthesis of m2,2,7GpppN1mpN2mp-capped small nuclear RNAs was inhibited by approximately 70% by DRB.
Muscle transplantation was used to evaluate the ability of normal and dystrophic chickens to support regeneration of both normal and dystrophic muscle fragments. Pectoralis muscles were grafted into the site of the biceps muscle of host chickens. Identification of dystrophic characteristics of intact and regenerating muscle fibers was made by cytochemical analysis of mitochondrial succinic dehydrogenase (SDH) and by fiber size. In the biceps muscle of dystrophic chicks at 40 days ex ovo, the mean size of muscle fibers with low activity of SDH and fibers with high SDH activity was 29.0 +/- 5.9 micrometers and 42.0 +/- 10.4 micrometers, respectively. The mean size of normal muscle fibers was notably smaller than in dystrophic muscle and was 17.8 + 3.1 micrometers. The hypertrophy of fibers coupled with elevation of SDH activity tended to increase with age. Transplants were examined at 56 days postoperatively. The results of cross-transplantation between normal and dystrophic genotypes were similar to unoperated muscles in the correlation between SDH activity and fiber size. Donor muscles determined the type of myofibers regenerated in transplants regardless of whether the host was normal or dystrophic. In addition, combined transplantation was attempted to produce a single hybrid myofiber in which normal and dystrophic pectoralis muscle were mixed in equal volume. The mixtures were then allowed to regenerate in host chicks. A number of mosaic myofibers appeared in transplants and had regional differences in SDH activity along their length. It was concluded that: (1) The characteristics of high SDH activity and fiber hypertrophy are an expression of dystrophic nuclei, (2) combined transplantation of both normal and dystrophic muscle fragments can produce mosaic myofibers in SDH reaction; and (3) the local control of SDH activity and fiber size within nuclear territories in mosaic myofibers seems likely to be due to phenotypic expression of either normal or dystrophic genomes.
The stereochemical course of dehydrogenation catalyzed by acyl-CoA oxidase was investigated using the enzymes from rat liver peroxisomes and Candida lipolytica. Stearoyl-CoA and nonanoyl-CoA, stereospecifically labeled with deuterium at either C-2 or C-3, were incubated with the enzyme, the products were converted to methyl esters and their deuterium contents were measured by gas chromatography-mass spectrometry. The results suggested that acyl-CoA oxidase-catalyzed dehydrogenation occurred by anti-elimination of the pro 2R and pro-3R hydrogens of acyl-CoA.
An investigation was made of the differences between colorectal cancer and adenoma using HLA markers. Subjects included 60 cases of colorectal cancer, 43 of colorectal adenoma and 120 healthy Japanese controls. In comparison with the controls, Bw40 was increased (p < 0.02) and B5 was decreased (p < 0.005) in the colorectal adenoma cases, whereas in the colorectal cancer cases, Bw35 was increased (p < 0.005). B5 was significantly less frequent in the adenoma cases than in the cancer cases (p < 0.05). It is suggested that the susceptibility of BW35 to the causal factors of colorectal cancer is under genetic control.
HLA antigens were studied in 60 patients with ulcerative colitis, 10 with Crohn's disease and 120 healthy Japanese controls. HLA typing was performed by the microdroplet lymphocyte cytotoxicity test.B5 was recognized in 62% of the patients with ulcerative colitis, whereas in 40% of controls (p smaller than 0.01). Furthermore, in these patients B7 was decreased in incidence (p smaller than 0.05) and there was the highest relative risk value for A3 (R.R = 6.3). When the patients were classified into 2 groups according to the extent of the lesions, left-sided or total colitis group and proctitis group, B5 was recognized in 65% of the patients with left-sided colitis or total colitis; and this increase was statistically significant. However, no significant difference in the incidence of B5 was recognized between the patients with proctitis and controls, probably because the number of patients studied was too small for evaluation. In the patients with Crohn's disease, B27 was recognized in one patient, showing an increase in incidence (p smaller than 0.001), although the number of patients studied was very small.
To study association between juvenile onset diabetes (JOD) and major histocompatibility gene complex, 40 patients with childhood onset diabetes and 120 healthy subjects were typed for HLA. Bw54 was present in 33 percent of the patients with JOD, while it appeared in 8 percent of the controls. Expressed as a relative risk, the antigen Bw54 confers a susceptibility to the development of JOD which is 5.3 times that in the controls. JOD shows a little high degree of association with A9 (78%). However, the A9-antigen is common in the Japanese and appears in 58 percent. Though less striking, the decreased frequency of B12 was 3 percent of JOD, less than 15 percent of the controls (p less than 0.05). There was no association between Bw54 and JOD with family history of diabetes.