[The effects of the renal pelvic pressure elevation upon local renal blood flow distribution].
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Biomedical subjects
Publications and source records attributed to H Takada.
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Orchitis, epididymitis and prostatitis have been reported in male dogs infected with Brucella canis (B. canis), but the pathogenesis of infertility in male dogs has not been clarified yet. We examined localization of B. canis in the tissue of infected male reproductive organs and production of autoantibody to spermatozoa in male dogs by immunofluorescence and unlabeled antibody peroxidase-antiperoxidase (PAP) methods and electron microscopy. B. canis were found in the cytoplasm of macrophages and epithelial cells in testis, epididymis and prostate. Particularly in the prostate, B. canis multiplied in the cytoplasm of epithelial cells and emerged in the glandular lumen with destroyed epithelial cells. Head-to-head agglutination of spermatozoa was found in the semen, urine and epididymal duct with varying degrees of intensity among the infected dogs. Appearance of the spermagglutination began following the detection of B. canis in urine and semen, suggesting invasion of the organisms in male reproductive organs. In the sera from the dogs orally inoculated with B. canis, (Ig M), Ig G and Ig A anti-spermantibodies were detected in parallel with the appearance of the serum spermagglutinating activity. The heads of agglutinated spermatozoa in the epididymal duct and semen were coated with Ig A antibody, which is considered to be anti-spermautoantibody locally produced. The target of these circulating and local antibodies was acrosome of the dog spermatozoa and spermatids. It seems probable that multiplication of B. canis in epithelial cells is the direct cause of damage to the infected cells, and the damage acts as a trigger of the production of autoantibody to spermatozoa.
The effects of dietary unsaturated and saturated fats on chemically induced colon carcinogenesis were examined in male Donryu rats. The rats were fed two types of semipurified diets consisting of 5% linoleic acid or 4.7% stearic acid plus 0.3% essential fatty acid as dietary fats. The rats were treated with azoxymethane (7.4 mg/kg body weight) s.c. once a week for 11 weeks and sacrificed 15 weeks after the last injection of the carcinogen. The rats fed unsaturated fat diet demonstrated a significantly higher incidence of colon tumors [100%], more tumors per rat [2.68 +/- 1.60 (S.D.)], and greater malignant differentiation histologically than did those fed saturated fat diet [76%, 1.79 +/- 1.59, respectively]. Lipid analysis of colon tumors and colon mucosa showed that unsaturated fat diet altered the phosphatide fatty acyl composition of colon mucosa markedly and increased the content of arachidonic acid in the neutral lipid of colon tumors. The altered lipid composition of the mucosa may increase the sensitivity of the colon to the carcinogen, and the excess of arachidonic acid or its metabolites may be the primary agents of cocarcinogenesis of colon tumors. These findings suggest that dietary unsaturated fats have potent cocarcinogenic effects on colon carcinogenesis.
The immunopharmacological activities of bacterial cell walls and muramyl peptides were collected in table form with a comprehensive literature. The past and present studies emphasizing the host-defense enhancing activities of muramyl peptides for antitumor immunotherapy were surveyed along three possible approaches: 1) the nonspecific enhancement of natural defense ability of host against tumor cells themselves; 2) the enhancement of nonspecific resistance of host to microbial infections which are frequently encountered and difficult to treat in the advanced stage of tumor patients; and 3) the stimulation of immunity against tumor-specific or tumor-associated immunogens. Finally, the prospects of successful antitumor immunotherapy with muramyl peptides and their derivatives was discussed.
The effect of dietary cholesterol on azoxymethane (AOM)-induced colon carcinogenesis was evaluated with two different sets of experiments. Starting at 6 weeks of age, male Donryu rats were divided into four groups, and fed either control chow or one supplemented with 1% cholesterol, and with or without AOM (11 weekly s.c. injections at a dosage of 7.4 mg/kg body weight). The rats were sacrificed at 20 weeks after (first experiment) and at 15 weeks after (second experiment) the last injection of AOM. The AOM-treated groups in both experiments developed tumors in the colon and small intestine, whereas no tumors were seen in the AOM-untreated groups. An interesting observation was that cholesterol feeding significantly increased the number of colon tumors/rat and the number of animals with distant metastases to several organs. Tumor growth and invasiveness were also enhanced, but not significantly. Both bile acids and neutral sterols in the feces were markedly increased in the rats fed the 1% cholesterol supplement (2-3 fold and 5-6 fold, respectively). According to these results, it might be postulated that dietary cholesterol revealed potent promoting effects on AOM-induced colon carcinogenesis through the mechanism of increasing excretion of bile acids and neutral sterols in the gut.
Pertussis toxin isolated from Bordetella pertussis phase I strain Tohama enhanced the migration of human blood monocytes in an assay with a multiwell chemotaxis assembly. The monocyte migration enhancement by pertussis toxin was abolished by heating at 100 degrees C for 30 min, which caused a complete loss of the other biological activities of pertussis toxin. Checkerboard analysis demonstrated that the increased monocyte migration caused by pertussis toxin was directed toward a positive stimulus: chemotaxis.
The effects of bacterial cell walls, peptidoglycans, and a water-soluble polymer of peptidoglycan subunits on dengue virus type 2 replication in cultured mouse peritoneal macrophages were studied. Pretreatment of macrophage cultures with all of test cell walls isolated from seven bacterial species for 3 days significantly enhanced the virus production in the cultures. Peptidoglycans prepared from four of the above cell walls also exerted the virus production-enhancing effects in a similar manner as the walls. A water-soluble polymer of peptidoglycan subunits which was prepared by treatment of Staphylococcus epidermidis wall peptidoglycan with an interpeptide bridge-splitting enzyme (endopeptidase) also definitely enhanced the virus production in macrophage cultures, although its activity was weaker than that of the original wall and peptidoglycan. Macrophage cultures from athymic nude mice, when treated with cell walls and peptidoglycans of S. epidermidis and Lactobacillus plantarum for 3 days, also showed an increased ability to support dengue virus type 2 replication. The infectious center assay demonstrated that the virus replication enhancement by S. epidermidis cell wall and peptidoglycan was primarily due to an increase in the number of virus-infected cells. This finding did not seem to be in conflict with the observation that macrophages treated with the above cell wall or peptidoglycan phagocytized more latex particles than did untreated macrophages. The conclusions based on the above experiments are that the treatment of mouse peritoneal macrophage cultures with bacterial cell walls and their components increases the take of dengue virus type 2 by macrophages and thus raises the virus production in the macrophage cultures.
Thirteen acylated and phosphorylated derivatives of beta-1,6-linked glucosamine disaccharide (lipid A analogs), which were synthesized after the structural model of Salmonella-type lipid A, and seven similar derivatives of glucosamine monosaccharide (lipid A-related compounds) were studied for their immunobiological activities. These included mitogenicity and polyclonal B cell activation enhancement of migration of monocytes and polymorphonuclear leukocytes derived from human peripheral blood, stimulation of guinea pig peritoneal macrophages, activation of human complement, and stimulation of serum antibody production and induction of delayed-type hypersensitivity against ovalbumin in guinea pigs. Comparisons were made with lipid A, RE-glycolipid, lipopolysaccharide of natural sources, and a well-known synthetic adjuvant, N-acetylmuramyl-L-alanyl-D-isoglutamine. Some of the lipid A analogs were found to manifest the mitogenic, polyclonal B cell-activating macrophage-stimulating, complement-activating, and immunostimulating activities, although the observed activities were generally far less than those of natural products in intensity and efficiency. Other immunobiological effects exhibited by most of the synthetic lipid A analogs were the enhancement of migration of monocytes and polymorphonuclear leukocytes. It is premature to draw definite conclusions on structure-activity relationships, since a few compounds which were active in some assay systems were scarcely active in other assays. However, an indisputable fact was that beta-1,6-glucosamine disaccharide 1 alpha,4'-diphosphate, which carries two amide-bound (R)-3-hydroxytetradecanoyl and three ester-bound tetradecanoyl residues, and thus has the structure most closely resembling natural lipid A among test compounds in this study, was definitely active in all of the present assay systems. However, its potency was generally much less than natural products. Some of glucosamine monosaccharide derivatives, especially N-(R)-3-[(R)-3-hydroxytetradecanoyloxy]tetradecanoyl glucosamine, also exerted all of the in vitro activities described above. This fact suggests that a glucosamine disaccharide structure may not necessarily be a prerequisite as far as the in vitro immunobiological activities tested are concerned.
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Whole cells of a clinical isolate (strain S-3) of the genus Capnocytophaga were divided into cell envelope (CE) and cytoplasm (CP) fractions by mechanical disintegration followed by differential centrifugation, and a part of the CE fraction was further fractionated by sodium dodecyl sulfate (SDS) treatment into the peptidoglycan and SDS-supernatant fractions. The other part of the CE was extracted with butanol-water or hot phenol-water to isolate butanol-lipopolysaccharide and phenol-lipopolysaccharide, respectively. All of the test fractions except CP exhibited multifold immunomodulating activities, namely, the adjuvant activities to cellular as well as humoral immune responses against ovalbumin in guinea pigs, the mitogenicity on splenocytes of guinea pigs and BALB/c mice (but not on their thymocytes), the stimulation of guinea pig peritoneal macrophages (in terms of increased glucosamine uptake), and the activation of the human complement system through alternative as well as classical pathways. In addition, the test fractions other than the CP evoked dermatoxic reactions on rabbit skin with characteristic variations among them. The immunomodulating activities of SDS-supernatant were noteworthy in view of the fact that this fraction was essentially free of muramic acid and diaminopimelic acid and did not cause the gelation of horseshoe crab amoebocyte lysate except when it was used at the very high dose, suggesting that there was practically no contamination by peptidoglycans and lipopolysaccharides in the SDS-supernatant.
A study was made on the activity of various bacterial cell walls and peptidoglycans to liberate serotonin from rabbit blood platelets. All of the test cell walls or peptidoglycans prepared from 27 strains of 21 bacterial species were shown to cause a marked release of serotonin, regardless of differences in types of peptidoglycan and non-peptidoglycan moieties and in some biological properties. The assay made with the water-soluble "digests" of Staphylococcus epidermidis cell wall peptidoglycans, which were prepared by use of appropriate enzymes, revealed that a polymer of peptidoglycan subunits (a disaccharide-stempeptide) was definitely active in the release of serotonin, but a structural unit monomer was inactive. Among a variety of synthetic muramylpeptides and their 6-O-acyl derivatives, only 6-O-(3-hydroxy-2-docosylhexacosanoyl)-N-acetylmuramyl-L-alanyl-D-isoglutaminyl- L-lysyl-D-alanine was found to hold a strong serotonin-liberating activity.
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A new synchronous video urodynamics to evaluate the function of the lower urinary tract is described. The urodynamic study together with the transrectal longitudinal ultrasonotomography of the bladder and urethra can be seen on the colour display monitor through the display controller. An image on the colour display monitor is also stored on the video cassette recorder. This new technique will be indispensable for evaluation of the lower urinary tract dysfunction.