[A new diagnostic method to evaluate the lower urinary tract function--the synchronous urodynamic and voiding echographic examination].
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Biomedical subjects
Publications and source records attributed to H Takada.
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In this study of the role of microfloral beta-glucuronidase in colonic carcinogenesis, the effect of beta-glucuronidase inhibitor was evaluated. Starting at 5 weeks of age, male Donryu rats were fed either a semisynthetic diet or the same diet containing 0.1% beta-glucuronidase inhibitor as N-cyclohexyl-5-O-acetyl-2,4-O-p-methoxybenzylidene) -D-glucaro-1-amide-6,3-lactone (C-GAL). All animals were given s.c. injections of 7.4 mg azoxymethane (AOM) per kg body weight once a week for 11 weeks and followed for an additional 20 weeks. Most animals receiving the colonic carcinogen developed tumors in the colon, and a few also developed tumors in the small intestine. However, the number of tumors in the large intestine of the rats given C-GAL at the same time as AOM was significantly lower than in the control rats, especially in the proximal half of the colon, but those given C-GAL after AOM treatment had almost the same number of colon tumors as did the controls. It is concluded that, since bacterial beta-glucuronidase activity in the feces of rats given 0.1% C-GAL was significantly inhibited, intestinal microfloral beta-glucuronidase may play an important role in colonic carcinogenesis caused by AOM.
The cytoplasmic membranes and a cytoplasmic fraction of Staphylococcus aureus L-forms increased the incorporation of [3H]thymidine by human lymphocytes in the presence of fetal bovine serum. Both fractions stimulated cord blood lymphocytes as well as adult peripheral lymphocytes, suggesting the possibility that the observed effect was not due to an antigen-specific reaction, but to an immunologically nonspecific action. The membrane mitogen(s) was resistant to trypsin, although it was partially solubilized by trypsin treatment. The mitogen(s) could not be extracted with a chloroform-methanol mixture (2:1, v/v), although the chloroform-methanol soluble fraction was strongly mitogenic to murine splenocytes. Human serum which was added to the assay system in place of fetal bovine serum definitely suppressed the mitogenic effect of both cytoplasmic membranes and the cytoplasmic fraction, especially the latter.
A peptidoglycan layer of Treponema pallidum kazan was isolated by solubilization of whole cells with 1% warm sodium dodecyl sulfate and subsequent digestion of an insoluble residue with proteases. Electron microscopy revealed that the peptidoglycan was isolated as a single-layered sacculus of less than 5 nm in thickness, freed from axial filaments and an envelope sheath. An isolated peptidoglycan fraction was mainly composed of glucosamine, muramic acid, alanine, glutamic acid, ornithine, and glycine in molar ratios of 0.65:0.68:1.63:1.00:0.75:1.03. Amino (N)- and carboxyl (C)-terminal amino acid analyses suggested the involvement of at least a part of the glycine residue in cross-linking between the amino group of ornithine residue at one strand of the stem peptide subunit and the carboxyl group of alanine of the neighboring strand. The treponemal peptidoglycan lacked the immunoadjuvant activity both to stimulate antibody production and to induce delayed-type hypersensitivity against ovalbumin, as well as the properties necessary to stimulate guinea pig and mouse splenocytes and guinea pigs peritoneal macrophages, unlike the cell walls or peptidoglycans (group A type of Schleifer and Kandler's classification, Bacteriol. Rev. 36:407-477, 1972) isolated from many bacterial species parasitic to the mammal. However, the peptidoglycan activated the human complement system through the alternative pathway, as well as the classical one, and caused a liberation of 5-hydroxytryptamine in rabbit blood platelets in a similar manner to the cell wall peptidoglycans of both group A and B types.
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Six male dogs orally inoculated with 3.2 X 10(8) Brucella canis and 2 male dogs naturally infected with the organisms were examined weekly for the presence of the organisms in urine and blood as well as for agglutinin titers in serum. Excretion of the organisms into urine started on 1 to 3 weeks after onset of bacteremia, i.e. 4 to 8 weeks after inoculation, and lasted for about 1 to 1.5 years. Non-bacteremic intervals, intermittent or lasting for about 1 to 6 months, followed the initial period of abundant excretion of viable organisms in urine. The highest urinary concentrations of the organisms, 2.5 X 10(4) to 1.5 X 10(6) cells per ml, were obtained in all dogs between the 6th and 14th weeks after the oral inoculation. Serum agglutinin titer rose on the 3rd to 5th weeks after the inoculation and then the titers remained at 1 : 640-1 : 2,560. The titers showed a downward trend over the 40 th to 56th weeks after the inoculation. In one of the spontaneously infected cases, the organisms were demonstrable only from urine for half a year with suspicious serum agglutinin titer of 1 : 160 after the bacteremic phase.
The structure of polygalactosamine purified from the culture fluid of Aspergillus parasiticus AHU 7165 was studied. Partial acid hydrolysis of this polysaccharide, in which 55 to 65% of the monosaccharide residues were N-unsubstituted, gave a series of galactosamine oligosaccharides (dimer to hexamer) in a good yield. From the data on analyses of the polysaccharide and its oligosaccharides by gel filtration, periodate oxidation, methylation, and proton NMR measurement, the polysaccharide was characterized as a linear chain of alpha (1-4)-linked galactosamine residues. The N-unsubstituted galactosamine residues are probably distributed in a random fashion over the polysaccharide chain.
This paper describes a new indication for the latissimus dorsi muscle or musculocutaneous flap, which has been applied to the treatment of congenital, unilateral absence of the pectoralis major muscle for formation of the anterior border of the axilla, by simulation of the pectoralis major muscle using the latissimus dorsi muscle. The results of this operation were satisfactory for both the patients and the surgeon.
The effects of polyclonal B cell activation (PBA) of cell walls and their cell wall fractions obtained from several kinds of gram-positive bacteria were studied using the anti-sheep red blood cell (SRBC) or anti-trinitrophenylated (TNP) SRBC plaque forming cell (PFC) responses of cultured spleen cells from Balb/c, athymic nu/nu, their littermates (nu/+), C3H/He (LPS-responder), C3H/HeJ (LPS-nonresponder), (CBA/N x Balb/c) F1 male with an X-linked defect in B cell function and the F1 female mice. The cell walls of Staphylococcus epidermidis (ATCC 155), Lactobacillus plantarum (ATCC 8014), Micrococcus lysodeikticus (NCTC 2665), Mycobacterium rhodochrous (ATCC 184), Streptomyces gardneri (ATCC 23911) and Nocardia corynebacteriodes (ATCC 14898) had the ability to induce polyclonal B cell responses in the spleen cells of Balb/c, nu/nu, nu/+, C3H/He and C3H/HeJ mice. The cell wall fractions prepared by enzymatic digestion from the cell walls of S. epidermidis, S. gardneri or N. corynebacteriodes were also capable of inducing polyclonal B cell responses. The responses of spleen cells from (CBA/N x Balb/c) F1 male mice to these active preparations, except the cell walls of M. rhodochrous which possess this ability. The PBA-ability of synthetic peptidoglycan, muramyl dipeptide (N-acetylmuramyl-L-alanyl-D-isoglutamine, MDP), was also examined, and a similar activity was observed in MDP.
Cytoplasmic membranes of L-forms of Staphylococcus aureus exerted a strong mitogenic effect on splenocytes of athymic nude mice as well as normal mice, while a cytoplasmic fraction of the same bacteria did not show definite mitogenicity. The mitogenic principle(s) of the membrane fraction was resistant to treatment with trypsin and was heat stable (at 100 C for 10 min). The active principle(s) in the insoluble residue of the membrane fraction digested with trypsin was not extracted with cold acetone, but could be solubilized by extraction with a cold chloroform-methanol mixture (2:1, v/v). The mitogenic principle(s) in the extract was fractionated by silicic acid column chromatography. Among five fractions separated by chromatography, fractions eluted with chloroform-methanol mixtures (1:1 and 1:20, v/v) were found to be strongly mitogenic. The cytoplasmic membranes of the L-forms also exerted a definite mitogenic effect on guinea pig splenocytes, but not on the thymocytes.
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Stimulation of splenocytes from ICR mice by cell walls of 17 species of gram-positive bacteria, and peptidoglycans and water-soluble enzymatic digests prepared from some of them, and by synthetic N-acetylmuramyl-L-alanyl-D-isoglutamine (MDP) was studied in terms of mitogenic activity. All the cell walls tested except those of Micrococcus lysodeikticus, regardless of their mycolic acid content and immunopotentiating activity, had definite stimulatory activity on splenocytes. In general, the cell walls of mycobacteria, nocardia, and stretomyces had stronger mitogenic activity than other cell walls. The mitogenic activity of cell walls was mainly attributable to a peptidoglycan moiety, and the activity was retained even when the peptidoglycan had been degraded into a monomer or a dimer of its subunit, though a polymerized form of the subunits exhibited stronger activity than the monomer or dimer. Definite mitogenicity of synthetic MDP on splenocytes from ICR mice was also confirmed. The origin of the unknown principle(s) that is found in the cell walls of nocardia, mycobacteria and streptomyces and is responsible for their potent mitogenic activity on murine splenocytes was discussed.
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1. An enzyme which hydrolyzes the acetamido groups of N-acetylgalactosamine residues in N-acetylated polygalactosamine was found in the supernatant fraction of Aspergillus parasiticus AHU 7165, a polygalactosamine-producing strain. 2. N-Acetylated polygalactosamine was used as a substrate in the purification and characterization of this enzyme. A 140-fold purification was obtained by means of ammonium sulfate fractionation followed by chromatography on carboxymethylcellulose and DEAE-cellulose. 3. The enzyme releases about 60-70% of the acetyl groups of N-acetylated polygalactosamine, giving a product with free amino groups. Whereas the enzyme also deacetylates oligosaccharides with 14 or more N-acetylgalactosamine units at a rate similar to that of deacetylation of the polymer, it deacetylates shorter oligosaccharides (trimer to hexamer of N-acetylgalactosamine) much more slowly and is virtually inactive toward disaccharide. Deacetylation can not be detected with bacterial cell wall peptidoglycan, N-acetylated heparin, partially O-hydroxyethylated chitin or monomeric N-acetylgalactosamine derivatives as substrates. 4. This enzyme shows double pH optima of 5.3 and 9.3. The Km value for N-acetylated poly-galactosamine is 0.15 g/l (or 0.54 mM with respect to monosaccharide residues). 5. The occurrence of this enzyme may account for the formation of polygalactosamine with free amino groups.
Activation of peritoneal macrophages from guinea pigs by various bacterial cell walls, M-1 endo-N-acetylmuramidase enzymatically digested bacterial cell walls and synthetic muramyl dipeptides was studied in terms of stimulation of [14C] glucosamine incorporation. All test bacterial cell wall preparations significantly increased a [14C]glucosamine uptake by the macrophages. Some of the water-soluble M-1 enzyme digests also exerted stimulating effects on macrophages, although the activity of the digests was found to be weaker than those of original cell walls. Furthermore, an adjuvant-active synthetic MurNAc-L-Ala-D-isoGln (MDP) showed a weak but significant activity, whereas an adjuvant-inactive analog, MurNAc-L-Ala-L-iso-Gln, did not show a significant activity, at least with the dose of 100 microgram. Additional studies with 6-O-acyl derivatives of MDP revealed that 6-O-(2-tetradecylhexadecanoyl)-MDP and 6-O-(3-hydroxy-2-tetradecyl-octadecanoyl)-MDP exhibit stronger macrophage-stimulating effects than MDP. It can be concluded from the above findings that MDP is the essential structure responsible for stimulating the activity of cell walls on guinea pig peritoneal macrophages, but it requires a particle state, which results from an additive character of lipophilicity, to exert the activity fully and effectively.