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E Suzuki

Publications and source records attributed to E Suzuki.

At least 451 records · Page 25Linked to original sources

Molecular conformation and packing in collagen fibrils.

New X-ray diffraction data have been collected from specimens of tendon collagen stained with phosphotungstic acid. Measurements of the positions of the Bragg reflections associated with the crystalline lattice provide, for the first time, a complete description of the unit cell. A strong band of intensity in the molecular transform associated with the pitch of the molecular helix can be identified and a detailed analysis of the intensities and positions of the Bragg reflections in this band has been carried out. The principal conclusions are that the portions of the collagen molecule that contribute to these reflections have a common direction; that they have a length very much less than that of a complete molecule; that the paths of the individual portions through the crystal are incompatible with a completely straight molecule, and that the molecule is therefore crimped. No evidence was obtained for a second series of Bragg reflections attributable to a second set of molecular portions linking the first set, and it is concluded that the linking set is more mobile and subject to positional variation from cell to cell. The most plausible explanation of our finding is that the first set corresponds to the portions of the molecules in the overlap zone and the second set to the portions in the gap zone. A detailed analysis of the Bragg reflections in the strong band of intensity associated with the pitch of the molecular helix has provided information about the relative azimuthal orientations and the lateral positions in the unit cell of the five molecular segments in the overlap zone. None of the existing models for fibril structure accounts satisfactorily for all the results obtained in the present studies and alternative models are developed and tested.

Animals↗

Crystallization of phaseolin from Phaseolus vulgaris.

Three different types of crystals were grown from phaseolin, the major storage body protein from French bean. Type I crystals are cubes with space group symmetry P432, a = 67 A. Type II crystals are bipyramids with a rounded basal plane and belong to space group P2(1)2(1)2, a = 128 A, b = 136 A, and c = 162 A. Type III crystals are rhombs grown from phytic acid-free protein. The space group symmetry is P2(1)2(1)2(1), a = 113 A, b = 136 A, and c = 89 A. Both Type II and III crystals are suitable for high resolution x-ray study.

Crystallization↗

Effects of zinc on cadmium-induced alterations in hepatic functions and blood glucose of rats.

The role of zinc (Zn) in preventing cadmium (Cd)-induced alterations of liver function and carbohydrate metabolism was studied in female rats. The animals were divided into four groups. To the diet for Group I was added 200 micrograms Cd/g of diet, to that for Group II was added 200 micrograms Zn/g of diet, and to that for Group III were added 200 micrograms Cd/g and 200 micrograms Zn/g of diet. Group IV was the control group fed normal diet. At the 11th, 26th, and 40th week of exposure, one-third of each group of animals were sacrificed and serum GPT and ALP activities, and glucose and insulin levels were measured. At the 26th and 40th week, serum GPT activity of Group I was significantly higher compared with those of Groups III and IV, and the serum glucose value of Group I was lower than that of Group III. At the 40th week, the serum insulin value of Group I was significantly higher than that of Group III. From these results, it is suggested that orally administered Zn prevents Cd-induced alterations of liver functions and the regulation of blood glucose in rats.

Alanine Transaminase↗

N,N-dibutylnitrosamine metabolism by rat liver S9 fraction and oxidation by chemical model systems.

Oxidative in vitro metabolism of N,N-dibutylnitrosamine (DBN) by 9000g supernatant fraction (S9 fraction) prepared from rat liver and oxidation of DBN by chemical model systems (Udenfriend and Fenton) were investigated. The products retaining the N-nitroso group of DBN were analyzed by gas-liquid chromatography. Incubation of DBN with the S9 fraction gave hydroxy derivatives of DBN at the omega, omega-1, and omega-2 positions, while the chemical reaction of DBN in the Udenfriend and the Fenton model systems afforded compounds with an oxo group at the same positions. In all cases, omega-1 oxidation was predominant, followed by omega and then by omega-2 oxidations, while omega and omega-1 oxidations were the principal metabolic pathways of DBN in vivo in the rat. The differences in the oxidative transformation of DBN among in vitro enzymatic, non-enzymatic and in vivo systems are discussed.

Animals↗

In vitro metabolic activation of N,N-dibutylnitrosamine in mutagenesis.

Enzymatic alpha-hydroxylation is believed to be the initial step in the metabolic activation of mutagenic and carcinogenic nitrosamines. Oxidative in vitro metabolism of N,N-dibutylnitrosamine (DBN) by hepatic microsomal fractions prepared from rats treated with phenobarbital and polychlorinated biphenyl (PCB) was investigated. Following incubation of DBN with the microsomal fractions, N-butyl-N-(3-hydroxybutyl)nitrosamine was identified by gas-liquid chromatography as the principal metabolite with the N-nitroso moiety, and butyraldehyde and/or two isomeric butyl alcohols (n- and sec-) were also identified and determined by gas-liquid chromatography and high-pressure liquid chromatography. The latter compounds originate from the unstable alpha-hydroxylated intermediate, N-butyl-N-(1-hydroxybutyl)nitrosamine, by spontaneous decomposition. An increased production of butyraldehyde with a concomitant enhancement of the mutagenicity of DBN toward Salmonella typhimurium TA1535 was observed when microsomes prepared from phenobarbital- and PCB-treated rats were used. SKF 525-A not only inhibited the mutagenic activation of DBN by microsomes from rats treated with the inducers but also selectively inhibited the formation of butyraldehyde and butyl alcohols from DBN. These results indicate that among the four initial hydroxylations (alpha, omega-2, omega-1, and omega) of the butyl chain demonstrated in the metabolism of DBN, alpha-hydroxylation is primarily involved in the mutagenic activation.

Animals↗

[Mechanism of bile outflow in cholecystectomized patients].

Intraluminal manometric and cine-cholangiomanometric studies were carried out on the movement of the sphincter of Oddi at the time of excretion of bile into the duodenum in 12 patients after cholecystectomy for gallstone. Two phases were observed in the sphincteric movement; the resting phase without any contraction and active phase with vigorous contraction. On stimulation with CCK-PZ 0.5 u/kg (bolus injection) in a active phase, a prompt transition from the active phase to the resting phase was observed in 4 to 8 minutes. On cine-cholangiomanometric study, the contrast medium injected into the common bile duct did not flow into the duodenum at the resting phase, but in the active phase. In the active phase, the excretion of the contrast medium was observed at the end of each contraction of the sphincter of Oddi. These observations have led a conclusion that bile excretion occurs in the active phase of the sphincter of Oddi in the cholecystectomized patients.

Adult↗

Species variations in the metabolism of N-butyl-N-(4-hydroxybutyl) nitrosamine and related compounds in relation to urinary bladder carcinogenesis.

Species variations in response to urinary bladder carcinogens, N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN), N-ethyl-N-(4-hydroxybutyl)nitrosamine (EHBN), and N,N-dibutylnitrosamine (DBN), were investigated in several animal species from the metabolic point of view. Since N-butyl-N-(3-carboxypropyl) nitrosamine (BCPN) and N-ethyl-N-(3-carboxypropyl) nitrosamine (ECPN) had been found to be the principal urinary metabolites which are responsible for the induction of bladder tumors by BBN or DBN and EHBN, respectively, in rats, acidic urinary metabolites with the N-nitroso moiety were isolated and determined by a colorimetric method after oral administration of these nitrosamines to rats, mice, hamsters, guinea pigs, and dogs. Qualitatively almost no species differences were observed among these animals in regard to the urinary metabolites except in the case of mice, in which the glycine conjugate of BCPN was isolated from the urine and identified as the principal metabolite of BBN and DBN. However, appreciable quantitative differences in the urinary excretion of BCPN or ECPN were found among these animal species, indicating that the differences in the susceptibilities of different animal species to urinary bladder carcinogenesis induced by BBN, DBN and EHBN may be closely related to the different extents of urinary excretion of the active metabolites of these nitrosamines.

Animals↗

Relationship of urinary N-butyl-N-(3-carboxypropyl)nitrosamine to susceptibility of animals to bladder carcinogenesis by N-butyl-N-(4-hydroxybutyl)nitrosamine.

A simple and sensitive procedure is described for the quantitative determination of N-butyl-N-(3-carboxypropyl)nitrosamine (BCPN), the principal metabolite of the bladder carcinogen N-butyl-N-(4-hydroxybutyl)nitrosamine (BHBN-4), in urine. BCPN was analyzed by gas-liquid chromatography as its methyl ester after extraction with ethyl acetate from urine followed by esterification with diazomethane. Species and strain variations in susceptibility to bladder carcinogenesis induced by BHBN-4 are discussed in relation to the urinary excretions of BCPN, determined by the new procedure, after oral administration of the compound to rats (4 strains), mice, hamsters, and guinea pigs at a dose approximately equal to the daily dose used in chronic carcinogenicity assay.

Animals↗

Congenital microangiopathic hemolytic anemia: report of a Japanese girl.

A 4-year-old Japanese girl had hemolytic anemia, thrombocytopenia, distorted and fragmented red cells in the peripheral blood, and megakaryocytosis in the bone marrow from the newborn period. These features were temporarily relieved and prevented by the infusion of fresh frozen plasma from healthy donors. This would indicate a deficiency in the patient's plasma of factor(s) that inhibit platelet aggregation in the blood vessels. An attempt to demonstrate possible in vitro deficiency of the platelet aggregation-prohibiting factor in the patient's plasma was unsuccessful. Laboratory examinations ruled out red cell fragility, abnormalities of red cell enzymes, abnormal hemoglobins, or immune reaction as underlying mechanisms. Our patient, together with three other patients in the literature with similar clinical features, may constitute a clinical entity that could be called "congenital microangiopathic hemolytic anemia".

Anemia, Hemolytic, Congenital↗

Computed tomography of carcinoma of the ampulla of Vater.

CT findings were studied in 14 cases with carcinoma of the ampulla of Vater which were all proved by surgery. At pre-operation period, only 4 cases (29%) were accurately diagnosed and other 10 cases (71%) were misinterpreted on CT. The most concomitant error was a confusion with the pancreatic head carcinoma (57%). Although a mass was retrospectively visualized in 4 cases, indirect signs were rather prominent, such as enlargement of the pancreatic head (57%), dilatation of the pancreatic duct (71%) and that of the common bile duct (79%).

Aged↗

Immunofluorescence for detection of viral antigen in mice infected with Sendai virus.

Sendai virus infection transmitted by contact from cagemates was followed by virus titration and immunofluorescence. The virus grew in the respiratory tract and caused macroscopic lesions in all contact mice. The virus grew to a higher titer in the lung than in the trachea. Tracheal smears, however, were found to be the most suitable for the diagnosis of Sendai virus infection by immunofluorescence, since they contained a large number of cells with intense fluorescence. Diagnosis of Sendai virus infection was made by immunofluorescence within a few hours after autopsy made at early stages of infection.

Animals↗