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)

Chlorhexidine's structural characteristics give it potent antimicrobial activity, effectiveness at low concentrations, substantivity that prolongs its therapeutic effect in the oral environment, minimal resorption from the gastrointestinal tract, and the ability to reduce plaque. The use of this agent for oral stomatitis in neoplasia patients has recently been studied. Treatment-associated oral soft tissue inflammation and ulceration were significantly reduced by chlorhexidine in patients undergoing intensive chemotherapy. Reductions in total streptococci and yeast counts were also observed. When used in conjunction with systemic antifungal agents, such as nystatin or clotrimazole, a significantly decreased incidence of clinical oral candidiasis and Candida septicemia was observed. In contrast, in two studies in which high-dose head and neck radiation therapy was applied, there was no reduction in stomatitis. Oral gram-negative bacilli have been shown to increase in high-dose chemotherapy patients who are taking chlorhexidine during the treatment period (3 wk to 2 mo). However, no increase in systemic gram-negative infections or other adverse negative medical consequences were observed. This agent appears to be of therapeutic benefit in reduction of dental plaque, gingivitis, and stomatitis in the high-risk chemotherapy population when used in conjunction with other topical and systemic antimicrobial agents as prophylaxis. Although no toxic or serious adverse effects of chlorhexidine rinse have been observed in the short-term studies to date, the effects of longer-term chlorhexidine administration should be evaluated.
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PMID:Oral antimicrobial agents--chlorhexidine. 218 58

Theiler's murine encephalomyelitis virus (TMEV) induces demyelinating disease which is associated with persistent virus infection of the central nervous system. To study the interaction between TMEV and host cells, we infected the G26-20 glioma cell line in vitro, and this resulted in a lytic infection in which most, but not all, cells were killed. Surviving cells divided and formed a viable monolayer in which a small proportion of cells displayed viral cytopathic effects. Levels of virus produced by these cultures over a 6 month period fluctuated between 6 and 8 log10 p.f.u./ml as measured by viral plaque assay. Similarly, the percentage of cells producing both viral antigen and viral RNA, as measured by a simultaneous immunoperoxidase/in situ hybridization technique, varied between 5 and 30%. Although persistently infected cultures were susceptible to challenge by both vesicular stomatitis virus and herpes simplex virus, they were resistant to infection by homologous viruses. Interferon activity was not identified. TMEV isolated from passage 12 produced smaller plaques than wild-type Daniels strain virus (wt-DAV) on L-2 cell monolayers. In contrast to demyelination induced in SJL/J mice after intracerebral inoculation with wt-DAV, mice infected with the small plaque variant virus failed to develop viral persistence or chronic demyelination. However, following immunosuppression by total body irradiation, SJL/J mice infected with the small plaque variant developed viral persistence but no demyelination. Characterization of the biochemical and molecular determinants of the variant will lead to a better understanding of determinants important in viral persistence.
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PMID:Persistent infection of a glioma cell line generates a Theiler's virus variant which fails to induce demyelinating disease in SJL/J mice. 221 94

Alveolar macrophages were isolated by bronchoalveolar lavage from normal subjects to determine whether these cells can be activated to produce interferon. Macrophages were incubated for 24 h, and the supernatants were assayed for interferon using a plaque reduction assay (vesicular stomatitis virus and human amnion cells). The macrophages did not spontaneously release detectable amounts of interferon, but macrophages stimulated with either mitogens or classic inducers did release antiviral activity (titer range, 32 to 962 units/ml). Interferon activity was detectable after 4h incubation. In general, macrophages that responded to one stimulating agent responded to all tested, and concanavalin A (25 micrograms/ml) produced the highest titer (mean, 335 units/ml). Peripheral blood lymphocytes at cell densities (1 X 10(5)/ml) comparable to that present in the macrophage suspension did not produce detectable amounts of interferon using identical culture and assay conditions. There was no difference between monocytes and alveolar macrophages in the amounts of interferon produced after 24 h, and there was also no apparent effect of cigarette smoking on the production of interferon by alveolar macrophages. Alveolar macrophages appeared to release gamma-interferon with mitogen stimulation (Con A) and alpha-interferon with UV-inactivated influenza A virus stimulation. We conclude that stimulated human alveolar macrophages can secrete both alpha- and gamma-interferon. This capacity for interferon production by alveolar macrophages may have important implications for antiviral defenses in the lung and may modulate certain pulmonary inflammatory and immune processes.
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PMID:Stimulated human alveolar macrophages secrete interferon. 240 24

To quantify the antiviral effect of interferon (IFN) we applied a mixture of two horseradish peroxidase-labelled monoclonal antibodies, specific for the E1 glycoprotein of Semliki Forest virus, in a direct enzyme immunoassay. This assay is suitable for detection of virus replication in L-cells, seeded as monolayers in 96-well plates. Inhibition of absorbance values caused by IFN was determined in a Flow Titertek Multiskan. Three IFN samples from different sources were titrated simultaneously in the enzyme immunoassay and in the vesicular stomatitis virus plaque reduction test in five consecutive experiments. Titres were calculated as the inverse value of the dilution of IFN causing 25% inhibition of absorbance values and 50% reduction of plaque counts respectively. The results show equality of precision and reproducibility between and within the two assays. However, the enzyme immunoassay is more convenient and objective than the plaque reduction assay.
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PMID:Enzyme immunoassay of interferon with peroxidase-labelled virus-specific monoclonal antibodies. 240 24

CCC/2M, CCC/10Y and CCC/MT-2 cat kidney cells producing Japanese isolates of human T-cell leukemia virus type I (HTLVs) and HOS/PL human osteosarcoma cells producing an American isolate of HTLV were infected with vesicular stomatitis virus (VSV) to prepare VSV pseudotypes bearing envelope antigens of HTLVs. VSV propagated in CCC/2M cells contained plaque-forming fractions that were not neutralized by treatment with anti-VSV serum alone: VSV pseudotypes bearing envelope antigens of HTLV2M and CCC cat endogenous virus were formed by infection of CCC/2M cells with VSV. Japanese HTLV2M, HTLV10Y and HTLVMT-2 and American HTLVPL pseudotypes were neutralized by sera of Japanese, American and British patients with ATL. Each serum, including the serum of the patient from whom HTLV2M or HTLV10Y had been derived, gave similar antibody titers against Japanese and American HTLV pseudotypes. The HTLV pseudotypes were also neutralized by rabbit serum raised against HTLVMT-2. A rabbit antiserum against the C-terminal half of the HTLV env protein produced in E. coli also neutralized Japanese and American HTLV pseudotypes. Thus, VSV pseudotype analyses indicated that envelope antigens of HTLVs represent a single serotype worldwide. The env protein produced in E. coli may be used to raise neutralizing antibody against HTLVs.
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PMID:Human T-cell leukemia virus type I: pseudotype neutralization of Japanese and American isolates with human and rabbit sera. 241 68

The interferon (IFN) assay of the sera from the 26 patients with premalignant lesions such as lichen planus and leukoplakia arising in oral mucosa was performed by the plaque-reduction assay with vesicular stomatitis virus in FL cells derived from human amniotic membrane. When the serum IFN activity was characterized by acid treatment, significant increase of acid-stable IFN in the patients was found as compared with those in the normal controls. The titers of gamma-like IFN defined by anti-HuIFN-alpha and anti-HuIFN-beta in the sera of patients of 50-79 years age group (n = 17, P less than 0.002) showed a highly significant increase as compared with the relevant normal controls (n = 20). All of the 26 patients were treated with topical administration of HuIFN-beta. When the correlation between prognosis of the disease and titers of serum IFN was investigated by measuring gamma-like IFN and acid-stable IFN in the sera of patients, all of 13 patients with good prognosis after the HuIFN-beta therapy showed significantly decreased levels of gamma-like IFN (P less than 0.01), whereas the serum level of acid-stable IFN after HuIFN-beta therapy showed a significant increase compared to that before the therapy (P less than 0.05). These findings indicate that the endogenous IFN system may be associated with the pathophysiology in patients with the oral mucosal lesions.
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PMID:Interferon activity and its characterization in the sera of patients with premalignant lesions arising in oral mucosa. 242 Sep 4

Newborn piglets were treated with various doses of polyinosinic:polycytidylic acid intravenously and their serum interferon responses determined by a plaque reduction assay with vesicular stomatitis virus in Madin-Darby bovine kidney cells. A single dose of 5 mg of polyinosinic:polycytidylic acid was found consistently to induce detectable levels of interferon in serum, while the response to lower doses was inconsistent and higher doses produced clinical signs of toxicity. Piglets receiving 5 mg of polyinosinic:polycytidylic acid had maximum serum interferon titers between four and eight hours after treatment, and interferon was no longer detected at 72 hours after treatment. Following treatment with polyinosinic:polycytidylic acid leukopenia was observed, coincident with peak serum interferon titers. Elevated levels of serum glutamic oxaloacetic transaminase and blood urea, indicative of hepatic and renal dysfunction respectively, were also observed following interferon induction with polyinosinic:polycytidylic acid. Piglets treated with polyinosinic:polycytidylic acid also demonstrated antiviral activity in their intestinal mucosal tissues and intestinal washes, but the antiviral activity in the intestinal wash was not characterizable as interferon. A factor in the intestinal washes from newborn piglets was found to antagonize the antiviral effects of interferon by enhancing the plaque forming ability of vesicular stomatitis virus.
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PMID:Interferon induction with polyinosinic:polycytidylic acid in the newborn piglet. 242 57

The antiviral action of recombinant human tumor necrosis factor (TNF) was studied using assay systems to determine inhibition of viral cytopathic effect (CPE), as well as suppression of virus growth measured by plaque assays. TNF was cloned and prepared by Asahi Chemical Industry, Japan. Antiviral activity against human herpes simplex virus (HSV) types 1 and 2, cytomegalovirus (CMV), varicella-zoster virus (VZ), vesicular stomatitis virus (VSV) and encephalomyocarditis virus (EMC), was demonstrated in human diploid fibroblasts following pretreatment with TNF overnight. The antiviral action was completely neutralized by anti-interferon (IFN)-beta serum, but not by anti-IFN-alpha or -gamma antibodies. This suggested the induction of IFN-beta by TNF. The antiviral action was synergistically enhanced by human IFN-gamma. Several non-human cell lines were tested but 10 of 11 failed to be protected from VSV- and/or EMC-induced CPE following pretreatment by TNF. The anticellular effects of TNF were tested in human and in non-human tumor cell lines. The results indicate that the susceptibility of cells to the two activities of TNF, antiviral and anticellular, was distinct, and that antiviral activity of TNF is more species-specific than its anticellular action.
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PMID:Antiviral effects of recombinant human tumor necrosis factor. 244 53

Monoclonal antibody-resistant mutants have been widely used to estimate virus mutation frequencies. We demonstrate that standard virion neutralization inevitably underestimates monoclonal antibody-resistant mutant genome frequencies of vesicular stomatitis virus, due to phenotypic masking-mixing when wild-type (wt) virions are present in thousandsfold greater numbers. We show that incorporation of antibody into the plaque overlay medium (after virus penetration at 37 degrees C) can provide accurate estimates of genome frequencies of neutral monoclonal antibody-resistant mutant viruses in wt clones. By using this method, we have observed two adjacent G----A base transition frequencies in the I3 epitope to be of the order of 10(-4) in a wt glycine codon. This appears to be slightly lower than the frequencies observed at other sites for total (viable and nonviable) virus genomes when using a direct sequence approach.
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PMID:Virus mutation frequencies can be greatly underestimated by monoclonal antibody neutralization of virions. 247 70

Denture stomatitis is a very frequent complication of the denture wearers. In this study, the relation between denture plaque and denture stomatitis was evaluated by a simplified culture (STOMASTAT). 583 patients wearing dentures (1981-1987) were selected, from 47 to 91 years old. The following results were obtained. 1. Degree of denture plaque in 583 patients was severe, moderate, and no detection: 30, 35 and 35%, respectively. 2. Grade of denture stomatitis in 583 patients was severe, moderate, and no symptom: 24, 36 and 40%, respectively. In this survey, the occurrence of denture stomatitis was about 60%. 3. The good correlation between degree of denture plaque and grade of denture stomatitis was recognized in this study. The present results suggest that denture plaque plays an etiologic role in denture stomatitis and, in daily practice, it is important to instruct denture plaque control for denture wearers.
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PMID:[Clinical survey on denture stomatitis. 1. Relation between denture plaque and denture stomatitis]. 248 96


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