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)

The growth of Rickettsia prowazekii Madrid E was monitored in mouse L929 cells subcultured for several weeks in the presence of gamma interferon (IFN-gamma) to determine whether the rickettsiae would be eliminated from or would persist in these cultures. R. prowazekii exhibited two distinct patterns in these IFN-gamma-treated cultures. In some cases, IFN-gamma-induced inhibition of rickettsial growth led to elimination of the rickettsiae from the L929 cell cultures; in other cases, the initial inhibition of rickettsial growth was followed by establishment of a persistent rickettsial infection in the IFN-gamma-treated L929 cells. During the first 3 days after infection, the growth rate of the L929 cells was significantly lower and higher percentages of the cells were killed in the IFN-gamma-treated, R. prowazekii-infected cultures than in the untreated, R. prowazekii-infected cultures or the mock-infected cultures, whether treated or untreated. This suppression of cell growth occurred in the infected, IFN-gamma-treated cultures that eventually exhibited the elimination pattern as well as the IFN-gamma-treated cultures that became persistently infected. It was not possible to predict the outcome of a particular infection from the early growth pattern of the culture. It was determined that the L929 cells in the persistently infected, IFN-gamma-treated cultures had not lost the ability to respond to IFN-gamma. These cells, after treatment with an antibiotic to eliminate the persistent rickettsiae, retained the ability to inhibit both the replication of vesicular stomatitis virus and the growth of R. prowazekii Madrid E after treatment with IFN-gamma. In contrast, rickettsiae isolated from two persistently infected, IFN-gamma-treated cultures were less sensitive than R. prowazekii Madrid E to the antirickettsial effects of IFN-gamma in standard L929 cells. The maintenance of the phenotype of these altered rickettsiae during plaque purification and passage in the absence of IFN-gamma suggests an alteration at the genetic level rather than phenotypic adaptation.
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PMID:Isolation of Rickettsia prowazekii with reduced sensitivity to gamma interferon. 249 7

The interferon (IFN) activity of sera from 19 patients with nasopharyngeal carcinoma (NPC) was determined by the plaque-reduction assay with vesicular stomatitis virus (VSV) in HeLa cells and compared to that of sera from matched healthy controls. High titers of interferon were detected in the sera of the NPC patients with a geometric mean titer (GMT) of 43 +/- 25 U/ml. The interferon activity of the patients' sera was acid- and heat-labile (pH = 2 and 56 degrees C for 1 hr) and could be neutralized by a goat antiserum to human IFN-gamma. Interferon titers of the patients, in contrast, to normal controls, were not correlated with natural killer (NK) activity which was abnormally low in the NPC patients. On the other hand, a high percentage of circulating cells co-expressing the LGL marker (HNK-I) and the OKT8 antigen was detected in parallel with high IFN levels in NPC patients.
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PMID:High interferon titer and defective NK-cell activity in the circulation of nasopharyngeal carcinoma patients. 253 26

Phenotypic mixing between Sendai virus and vesicular stomatitis virus (VSV) or the mutant VSV ts045 was studied. Conditions were optimized for double infection, as shown by immunofluorescence microscopy. Virions from double-infected cells were separated by sequential velocity and isopycnic gradient centrifugations. Two types of particles with mixed protein compositions were found. One type was VSV particles with Sendai virus spikes, i.e., phenotypically mixed particles. A second type was Sendai virus-VSV associations, which in plaque assays also behaved as phenotypically mixed particles. The ratio of VSV G protein to Sendai virus glycoproteins on the cell surface was varied, using the VSV mutant ts045 in double infections. Thus, different amounts of the VSV G protein were allowed to reach the cell surface at 32, 38, and 39 degrees C in Sendai virus-infected cells. However, a fixed number of Sendai virus spikes was always found in the ts045 virions. This represented 12 to 16% of the number of G proteins present in normal VSV. Furthermore, the yield of ts045 virions was radically reduced during double infection when the temperature was raised to block G-protein transport to the cell surface, suggesting that the Sendai virus glycoproteins were not able to compensate for G protein in budding. These results emphasize the role of the G protein in VSV assembly.
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PMID:Role of heterologous and homologous glycoproteins in phenotypic mixing between Sendai virus and vesicular stomatitis virus. 255 47

The effect of cimetidine on survival was investigated in mice infected with herpes simplex virus type 2 (HSV-2), murine encephalomyelitis virus (GD-VII), and vesicular stomatitis virus (VSV). BALB/c mice, 5 weeks of age, were injected intraperitoneally (i.p.) with 5.5 x 10(5) plaque-forming units (PFU) of virus/0.5 ml, and cimetidine (1 mg/0.5 ml) was administered simultaneously. The survival rates of 80% and 85% in the cimetidine groups were significantly greater than the 10% and 23% for the control groups. The GD-VII- and VSV-infected control mice were dead at 3 days after virus inoculation. However, more cimetidine-treated mice survived than control mice. When anti-mouse T-cell serum or cyclosporine, which is a helper T-cell suppressor, was administered to BALB/c mice; the effect of cimetidine against the HSV-2 infection could be observed. When injected with anti-asialo GM1, BALB/c mice or beige mice with low natural killer (NK) cell activity were not affected by cimetidine. Lastly, cimetidine was shown to activate the cytotoxic action on NK cells. The above results indicate that the antiviral effects of cimetidine depend on NK cell activation.
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PMID:The effect of cimetidine on survival of mice infected with herpes simplex virus type 2, murine encephalomyelitis virus and vesicular stomatitis virus infections. 256 3

The chicken embryo cell line LSCC-H32 was tested for the propagation and titration of several animal viruses of the families Toga-, Reo-, Rhabdo-, Herpeto-, Orthomyxo-, Paramyxo-, and Poxviridae and compared with secondary chicken embryo cells. The LSCC-H32 cells were demonstrated to be as susceptible for most of the tested viruses as were secondary chicken embryo cells. Both produced comparably sized virus plaques. The titers of Sindbis and Semliki Forest viruses in LSCC-H32 cells were 5- to 40-fold higher than in secondary chicken embryo cells or BHK-21 cells, respectively. Furthermore, exogenous chicken standard interferon was titrated in the LSCC-H32 cells, and a 50% plaque titer reduction of the challenging vesicular stomatitis virus was achieved by 0.12 IU of a standard chicken interferon preparation. Endogenous chicken interferon could not be induced by treatment of the cells with polyinosinic acid-polycytidylic acid. Due to its high plating efficiency and metabolic activities, the LSCC-H32 cell line provides a useful cell system for the titration and large-scale production of the tested animal viruses and for the titration of exogenous chicken interferon.
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PMID:Use of chicken cell line LSCC-H32 for titration of animal viruses and exogenous chicken interferon. 258 11

The present article discusses the rationale for daily use of the combination of amphotericin B (4 lozenges) intraorally and chlorhexidine denture disinfection (15 min) extraorally vs separate use of polyene antimycotics or chlorhexidine in the treatment of infectious denture stomatitis, frequently considered as the most common form of oral candidiasis. The amphotericin B/chlorhexidine combination has been standard treatment of infectious denture stomatitis in Scandinavia for more than 15 years. It was found to be the best among several regimens tested in 100 patients after a series of subjective and objective parameters had been used to record treatment efficacy in controlled clinical and microbiological studies. The fact that there was a significant (5% level) higher reduction of yeasts cultured from the palatal mucosa with this drug regimen than with the other modalities tested, including chlorhexidine lozenges/chlorhexidine denture disinfection, suggested that no drug interaction of clinical importance took place in vivo with this combination. Therefore, care should be taken when extrapolating findings on drug interaction in vitro (12) to the in vivo situation, and guidelines for treatment of oral candidiasis should preferably be based on controlled clinical and microbiological trials with patients. In order to prevent relapse of oral candidiasis after treatment, local and general predisposing factors should be eliminated, in particular reestablishment of plaque on the fitting side of the denture should be prevented.
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PMID:[Few aspects with regard to diagnosis and treatment of oral candidiasis]. 262 22

Infection of the oral mucous membrane is frequent in patients with removable prostheses, either totally of partially, and particularly when the prostheses is palatal. The principal etiological factor causing the infection is accepted to be "Candidas" aided by the presence of plaque bacteria (in patients with poor oral hygiene care), and a poor fit of the prostheses to the soft tissues. Treatment of the infection must proceed in the following order: a) use of effective medication against oral fungus such as Nystatin or Ketoconazole. b) Meticulous oral hygiene care in the mucous membrane as well as in the prostheses, but using the prostheses as little as possible during the treatment period. c) A total cure of the infection (denture stomatitis) before proceeding to the next phase of the treatment. d) Determination of the adjustment and occlusion of the prostheses in order to determine those areas of the prostheses which need to be refilled because of maladjustment of the prostheses to the soft tissues of the patient.
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PMID:[Stomatitis from dentures: etiopathological and therapeutic considerations]. 263 9

Two doses of a formalin-killed, cell culture-derived vesicular stomatitis virus (vsv)-New Jersey serotype vaccine were administered intramuscularly, 30 days apart, to all lactating and nonlactating cows in a 350-cow dairy herd. Serum specimens were obtained serially from 96 cows before vaccination and at 30, 52 and 80 days after vaccination and from 24 of these cows 175 days after vaccination. Serum neutralizing antibody titers to vsv-New Jersey serotype were determined from serum-dilution, plaque-reduction tests. Serum neutralizing antibody titers also were determined during the same period for 67 nonvaccinated heifers in the herd. Peak group geometric mean serum neutralizing antibody titers of 1:530.46 +/- 1.14 (group geometric mean titer log10, 2.725 +/- 0.055) developed 21 days after the second vaccination, but decreased to a low value of 1:65.36 +/- 1.38 (group geometric mean titer log10, 1.815 +/- 0.142) by 175 days after vaccination. The nonvaccinated group had no detectable antibody titer to vsv-New Jersey serotype throughout the study. All serum specimens from the vaccinates and controls were negative for heterologous reactivity to vsv-Indiana serotype.
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PMID:Serum neutralizing antibody titers in dairy cattle administered an inactivated vesicular stomatitis virus vaccine. 282 13

More than 10(4) plaque-forming units (pfu)/ml of HIV are inactivated during the alcohol fractionation step from plasma to fraction (Fr)-II+III, greater than 10(4) pfu/ml is inactivated from Fr-II+III to Fr-II and greater than 10(4) pfu/ml is inactivated during the polyethylene glycol (PEG) fractionation process from Fr-II+III to intravenous IgG (IVIG). The total inactivation rate from plasma to IVIG via Fr-II+III or Fr-II was calculated to be greater than 10(8) or 10(12), respectively. The PEG fractionation method produces an intact and unmodified IVIG. In addition, the PEG fractionation method at a low ionic strength was found to be effective for the elimination of greater than 10(5) units of other viruses, including hepatitis B, vesicular stomatitis and Sindbis viruses.
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PMID:Elimination of viruses (human immunodeficiency, hepatitis B, vesicular stomatitis and Sindbis viruses) from an intravenous immunoglobulin preparation. 282 31

A double-blind trial was carried out to study the effect of oral administration of fluconazole in the treatment of Candida-associated denture stomatitis. The study group consisted of 38 denture stomatitis patients who harbored yeasts, predominantly Candida spp., in significant numbers as determined by culture from the lesions. Half of the patients received 50 mg of fluconazole per day orally for 14 days, and the other half received placebo capsules. The following parameters were studied: degree of palatal erythema, presence of yeast cells (by plate count and microscopy of smears), identification to the species level of dominant yeast organisms, biotyping of Candida albicans, and treatment-related side effects. A significant reduction of erythema was seen after treatment with fluconazole, but the inflammation showed partial relapse 2 to 4 weeks after treatment was terminated. Reduced soreness of the oral mucosa was reported by six of the patients in the fluconazole group. No significant clinical or yeast flora changes were observed in the placebo group. Extensive changes in the yeast flora were observed in the fluconazole group, both in quantity and in composition of yeast species and C. albicans strains (biotypes), which perhaps indicated differences in pathogenicity and fluconazole susceptibility among various yeast species and C. albicans strains. Fluconazole did not produce any changes in the results of blood and urine analyses. The results indicate that fluconazole is a safe and well-tolerated antimycotic drug. The transient clinical and antimycotic effect may have been due in part to the possibility that therapeutic concentrations of the drug were not reached beneath the fitting denture surface and within the denture plaque.
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PMID:Fluconazole in the treatment of Candida-associated denture stomatitis. 285 55


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