Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038362 (stomatitis)
 8,852 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To evaluate the "resting" pH and induced pH changes in denture plaque, soft deposits were collected from the fitting surface of the denture, pooled and suspended in water. Plaque pH was determined with microelectrode equipment before and after mouth rinsing with a sucrose solution. A characteristic level in the "resting" pH of denture plaque was found in most of 12 subjects tested. pH values below the baseline level were recorded for more than 2 h after a rinse. The pH depressions were more pronounced in maxillary than in mandibular plaque. Further, the pH minima tended to be lower in subjects with denture stomatitis than in controls. No clear relationship could be established between the "resting" pH and the concentration of Candida hyphae in denture smears or palatal inflammation.
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PMID:Assessment of denture plaque pH in subjects with and without denture stomatitis. 0 Jul 85

The study comprised 30 denture wearers with generalized simple or granular inflammation in the palate and 30 without (controls). )easts, mostly Candida species, were cultivated from the maxillary dentures of all subjects with inflammation and of 23 controls. Hyphae were found in the maxillary denture smears from 28 subjects with inflammation and from 18 controls. Thus it seems unjustified to consider the occurrence of hyphae pathognomonic of denture stomatitis. The pH of whole saliva did not differ in the two groups (inflammation:mean pH 6.5, control:6.6). There was no clear relation between the pH of resting saliva and the amount of fungal cultures. Thirty minutes after a mouthrinse with 10 ml of a 25% sucrose solution, the mean saliva pH had dropped equally in both groups. With regard to the denture plaque, samples taken 40 min after the rinse indicated a more pronounced acid production in the plaque associated with inflammation. The pH of "resting" plaque was also lower in the inflammation than in the control group (mean maxillary pH 5.7 and 6.3 respectively, a=0.002). No association was found between the pH and the occurrence of hyphae in "resting" denture plaque. This supports the view that the pH is of no major importance for filamentation in vivo.
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PMID:Denture stomatitis-yeast occurrence and the pH of saliva and denture plaque. 1 95

The capacity of interferon to inhibit virus production in cells chronically infected with oncornavirus enabled us to develop a simple system for interferon quantitation that was independent of exogenous viral infection. The release of the virus to the culture medium was determined by its reverse transcriptase activity. The inhibitory effect of interferon in this system was linearly proportional to the log of its dilution over a range between 5 and 80% inhibiton. The sensitivity of the system was comparable to that of the vexicular stomatitis virus plaque reduction assay, whereas its reproducibility was found to be even better. This method is very rapid and can be completed within less than 24 h.
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PMID:Rapid quantitation of interferon with chronically oncornavirus-producing cells. 6 Nov 74

A simple and rapid plaque procedure was developed for the assay of hog cholera virus (HCV) of a particular strain, GPE-, based on its intrinsic interference with vesicular stomatitis virus (VSV) on the primary swine testicle cells and on an established swine kidney cell line; the procedure is called the reverse plaque formation (RPF) method. The plaques were produced as colonies of HCV-infected cells which were VSV-sensitive, disintegrated cell sheet. These plaques became visible after 15 to 20 h of superinfection with VSV done 2 days after an initial inoculation of the GPE- strain. The plaque formation was inhibited by a specific antiserum against HCV. All cells within the plaque had HCV antigen detectable by fluorescent-antibody staining. The variations of reverse plaque count were low enough to permit virus titration. The relationship between virus concentration and the number of plaques was essentially linear. The titer measured by the RPF method was a little higher than that of the tube culture interference method.
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PMID:Reverse plaque formation by hog cholera virus of the GPE-strain inducing heterologous interference. 6 Nov 76

Virus plaque-forming cell assay with vesicular stomatitis virus (VSV), which had been originally introduced by Bloom and his colleagues as a tool for the enumeration of activated lymphocytes, was first applied to the immune response of mice to a widely used antigen, i.e. sheep red blood cells (SRBC). When spleen cells taken from mice previously primed with SRBC were cultured in the presence of the antigen, lymphocytes capable of replicating VSV (antigen-induced virus plaque-forming cells, Ag-V-PFC) were generated in the culture. They seemed to appear as early as 1 day of culture, and the peak was attained by the 2nd day. Most of Ag-V-PFC belonged to T-cell population, since 80-90% of Ag-V-PFC was killed by the treatment of cultured cells with anti-thymocyte serum plus complement. In vitro generation of Ag-V-PFC seemed to be highly cross-reactive (about 40%) with a related antigen (horse red blood cells). Ag-V-PFC detected in the present experiment may not represent helper T cells, effector T cells, or their precursors because of the following: (a) The generation of Ag-V-PFC was completely suppressed by the addition of anti-SRBC mouse serum in the culture, though the helper activity was apparently augmented by the same treatment. (b) Development of Ag-V-PFC was almost completely suppressed by the pretreatment of mice with cyclophosphamide 2 days before immunization, by which delayed-type hypersensitivity (DTH) was markedly augmented. (c) After the immunization of mice, Ag-V-PFC began to develop just when the level of DTH declined, at which point helper activity of the spleen cells also diminished. A possible role of Ag-V-PFC in the immune response was discussed.
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PMID:Virus-replicating T cells in the immune response of mice. I. Virus plaque assay of the lymphocytes reactive to sheep erythrocytes. 6 84

Kethoxal bis (thiosemicarbazone) (KTS) inhibited replication of, and plaque formation by, vesicular stomatitis virus (VSV) in chick embryo cells. No other thiosemicarbazones tested were effective. Virus-specific m-RNA and protein synthesis were inhibited by KTS. However, virion RNA-dependent RNA synthesis was not inhibited by the drug. Treatment of VSV virions directly with KTS produced enhancement, rather than inactivation, of plaque formation. KTS inhibited cellular DNA and RNA synthesis by 67 and 25% respectively. Since cellular DNA and RNA synthesis are not required for VSV replication, the inhibition of these processes is probably unrelated to the antivirial activity of KTS. Cellular protein synthesis was inhibited 24% by KTS. Unexpectedly, synthesis of four proteins was induced in KTS-treated uninfected cells.
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PMID:Inhibition of vesicular stomatitis virus by kethoxal bis (thiosemicarbazone). 7 31

It was the purpose of the study to test the efficacy of dissolvent tablets containing mutanase and protease in preventing formation of plaque on the fitting surface of complete dentures. The study group consisted of 60 denture wearers with denture stomatitis who were assigned randomly into an enzyme group, a placebo group, or a Steradent group. After denture treatment was completed the patients were instructed to immerse the new dentures for 15 min once daily for one month in the denture cleanser. The amount of denture plaque, the clinical condition of the palatal mucosa, and the concentration of yeasts in mucosal and denture smears were recorded while the patients used their original dentures and after the experimental period. The study was designed and carried out as a double-blind study. New denture plaque had formed in all patients; however in the enzyme group significantly reduced plaque scores were recorded as compared with the plaque scores recorded on the original dentures. The Steradent tablets or the placebo tablets had no apparent effect.
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PMID:Prevention of denture plaque formation by an enzyme denture cleanser. 12 96

Exposure of vesicular stomatitis (VS) virions to neuraminidase resulted in loss of their ability to agglutinate goose erythrocytes and to attach to L cells concomitant with hydrolysis of sialic acid. These viral adsorptive functions were also destroyed by tryspsinization. Sialyl transferase resialylation in vitro of neuraminidase-treated VS virions restored their hamagglutinating and adsorptive functions almost to original levels. Erythrocyte and L cell receptors for attachment of VS virions were blocked by fully sialylated fetuin and by VS viral sialoglycopeptides. Smaller VS viral glycopeptides generated by extensive trypsinization were less effective inhibitors of hemagglutination than were larger glycopeptides; neuraminic acid and neuraminosyl lactose had no capacity to inhibit hamagglutination or adsorption of virus to L cells. These data suggest that cellular receptors for viral adsorption recognize sialoglycopeptides of a certain size. Neuraminidase desialylation did not significantly alter the isoelectric point of VS virions. Cells exposed to DEAE-dextran, trypsin, or neuraminidase showed significantly increased capacity to attach fully sialylated but not desialylated VS virions. Neuraminidase desialylation of L cells, Chinese hamster ovary cells, and Madin-Darby bovine kidney cells resulted in enhanced susceptibility to plaque formation by VS virus.
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PMID:Cellular adsorption function of the sialoglycoprotein of vesicular stomatitis virus and its neuraminic acid. 16 24

The ability of ascorbic acid, sodium salicylate, and caffeine to alter the circulating serum level of interferon was investigated in mice. The animals were singly injected subcutaneously with one of the compounds, 4-8 h later again singly injected intraperitoneally with poly I:C, and bled 6-8 h afterward. The sera from the mice were assayed for interferon titer by the use of the plaque inhibition method utilizing vesicular stomatitis virus. Ascorbic acid, sodium salicylate, and caffeine increased the serum level of interferon; however, the increase produced by sodium salicylate was dose-dependent, i.e. low doses increased interferon titers, high doses decreased the titers. Caffeine produced minimal increases in the interferon titer. These observations suggest that a potential prophylactic result may occur in virus infections from administration of the three compounds either singly or in combination at the proper concentration.
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PMID:Effect of ascorbic acid, sodium salicylate, and caffeine on the serum interferon level in response to viral infection. 16 98

Mouse serum interferons induced by polyI:C, vesicular stomatitis virus (VSV), reovirus, and Mengo virus were assayed in monolayers of mouse L-929 cells by the plaque-reduction method using both VSV and Mengo as challenge viruses. Titers obtained with Mengo virus as challenge were all lower than with VSV. With the interferons induced by VSV, reovirus, and ployI:C, the reductions were of the order of two- to three-fold. With Mengo virus-induced interferon the reduction was much greater (about 17-fold). This offers an explanation for the observation that, unit for unit (measured by the plaque reduction of VSV), Mengo virus-induced interferon is only about 1/10 as effective as polyI:C-induced interferon in protecting mice against lethal infection with Mengo virus. The data are consistent with the hypothesis that an interferon antagonist is produced in the serum of mice infected with Mengo virus. This antagonist, which is not produced in mice inoculated with polyI:C, or reovirus, effectively blocks the antiviral action of interferon during Mengo virus infections, both in vivo and in vitro.
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PMID:Further studies on the relative antiviral efficacies of interferons induced by poly I:C and Mengo virus. 17 87


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