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)

We have used cell fusion to address the question of whether macromolecules are rapidly exchanged between lysosomes. Donor cell lysosomes were labeled by the long-term internalization of the fluid-phase pinocytic markers, invertase (sucrase), Lucifer Yellow, FITC-conjugated dextran, or Texas red-conjugated dextran. Recipient cells contained lysosomes swollen by long-term internalization of dilute sucrose or marked by an overnight FITC-dextran uptake. Cells were incubated for 1 or 2 h in marker-free media before cell fusion to clear any marker from an endosomal compartment. Recipient cells were infected with vesicular stomatitis virus as a fusogen. Donor and recipient cells were co-cultured for 1 or 2 h and then fused by a brief exposure to pH 5. In all cases, extensive exchange of content between donor and recipient cell lysosomes was observed at 37 degrees C. Incubation of cell syncytia at 17 degrees C blocked lysosome/lysosome exchange, although a "priming" process(es) appeared to occur at 17 degrees C. The kinetics of lysosome/lysosome exchange in fusions between cells containing invertase-positive lysosomes and sucrose-positive lysosomes indicated that lysosome/lysosome exchange was as rapid, if not more rapid, than endosome/lysosome exchange. These experiments suggest that in vivo the lysosome is a rapidly intermixing organellar compartment.
J Cell Biol 1987 Dec
PMID:Chinese hamster ovary cell lysosomes rapidly exchange contents. 244 96

The growth of vesicular stomatitis virus (VSV) can be inhibited by the antiviral compound tricyclo-decane-9-yl-xanthogenate (D609). On analysing the antiviral mechanism we found no effect on the primary transcription of infecting VSV genomes. In contrast, the processes of replication and transcription during late stages of infection were inhibited. Despite the synthesis of all five virus-coded proteins (41% to 56% of the uninhibited control), as shown by labelling with [35S]methionine, the phosphorylation of the non-structural (NS) protein was reduced in the presence of the xanthate by a factor of at least 17. The pattern of phosphorylation of the bulk of cellular proteins remained unaltered under the same conditions. A relation between a possible loss of biological activity of the NS protein owing to the lack of phosphorylation and the decreased VSV RNA synthesis is suggested.
J Gen Virol 1987 Dec
PMID:Inhibition of the phosphorylation of the regulatory non-structural protein of vesicular stomatitis virus by an antiviral xanthate compound. 244 22

10 patients with diffuse large cell lymphoma were treated with 10 cycles of m-BACOD. 7 patients presented with a pathological stage IV, 2 with a clinical stage III and one with a clinical stage II disease. 8 patients have been in complete remission for 3-21 months (mean 9 months) after completion of therapy. One patient with T-immunoblastic lymphoma and bulky mass died of progressive disease after 6 cycles of m-BACOD. A second patient with T-immunoblastic lymphoma relapsed 24 months after completion of therapy. Treatment-related major complications, especially MTX-related ulcerative stomatitis, did not occur.
Schweiz Med Wochenschr 1987 Dec 12
PMID:[Provisional treatment results of intensive combination chemotherapy (m-BACOD) in non-Hodgkin lymphoma of intermediate and high malignancy]. 244 74

Tumour necrosis factor (TNF) induces antiviral activity in HEp-2 cells. Virus yield reduction assays with vesicular stomatitis virus as challenging virus demonstrated that the antiviral state was more pronounced in confluent cultures under low serum conditions. A significant enhancement of the antiviral state was obtained by combining TNF with low concentrations of either interferon (IFN)-beta 1 or IFN-gamma. The reduction in virus yield was significantly higher than that expected from summation of the independent antiviral activities of either substance alone, i.e. TNF and IFN acted synergistically as antiviral agents. Synergism of TNF with IFN-beta or IFN-gamma appeared to be mediated by different pathways, since different requirements for pretreatment and different effects on oligo-2',5'-adenylate synthetase (2-5AS) induction were observed. Induction of 2-5AS by TNF could be shown to be an indirect event that was sensitive to an antiserum against natural IFN-beta 1.
J Gen Virol 1988 Dec
PMID:Antiviral activity of tumour necrosis factor. Synergism with interferons and induction of oligo-2',5'-adenylate synthetase. 246 15

Dextran sulfate (DS) is a potent inhibitor of the growth of human immunodeficiency virus type 1 (HIV-1) in the H9 cell. Its minimal inhibitory concentration is about 1 microgram/ml. Its therapeutic index is greater than or equal to 200 which is higher than that of 38 for zidovudine. At the ID100 range, DS blocks the synthesis of HIV-1 antigens completely for at least 21 days; zidovudine at the subtoxic concentration of 3 micrograms/ml is incapable of achieving such a complete blockage. DS is still active when added to H9 cell cultures 4 hr after the addition of HIV-1. DS does not inactivate extracellular HIV-1 and is incapable of inducing interferons. It interferes partially with the infection of the H9 cells by the HIV-1. It inhibits the activity of HIV-1 reverse transcriptase. These activities may account, at least in part, for the inhibitory activity of dextran sulfate against the HIV-1. DS has a narrow antiviral spectrum; it is noninhibitory to the herpes simplex, vesicular stomatitis, polio, or adeno viruses. Dextran is not inhibitory to HIV-1. After sulfonation, the sulfonated dextran is highly inhibitory. Therefore, the sulfate group in the DS molecule appears to be essential for its anti-HIV-1 activity. The molecular weights of DS within the range 4000 to 12,000 do not appear to influence its anti-HIV potency.
Proc Soc Exp Biol Med 1988 Dec
PMID:Dextran sulfate as an inhibitor against the human immunodeficiency virus. 246 37

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.
J Virol 1989 Dec
PMID:Virus mutation frequencies can be greatly underestimated by monoclonal antibody neutralization of virions. 247 70

Twenty-two patients with locally advanced or metastatic head and neck tumors received a total of 84 courses of a combination of cisplatin, bleomycin, and Methotrexate (PBM) for a median of four courses per patient (range, 1-7). Among these 22 patients there were four patients (18%) who achieved complete remission (CR) and 13 patients (60%) who had a partial remission (PR). The overall remission rate (CR + PR) thus reached 78%; five patients (22%) progressed while on therapy. The mean duration of objective response (CR + PR) was 8 months; CR lasted a median of 18 months (range, 2-48). Survival was not influenced by tumor histology or by previous surgery. The presence of locoregional disease did adversely affect survival from the onset of chemotherapy (P = 0.1). The rate of survival was also affected by primary tumor site; patients with nasopharyngeal primaries survived longer than all other patients (22 vs. 11 months, P = 0.06). Toxicity to chemotherapy consisted mainly of nausea and vomiting and stomatitis. Three patients developed fever while leukopenic. One patient experienced irreversible renal damage, and another suffered from bleomycin-induced pulmonary fibrosis. The high response rate obtained in our group of patients did not have a substantial impact on overall survival. Aggressive, multimodality approaches should be considered in the treatment of these patients when possible.
J Surg Oncol 1989 Dec
PMID:Cisplatin, bleomycin, and methotrexate (PBM) chemotherapy in locally advanced and metastatic head and neck cancer. 248 Apr 93

Forty-six patients with Stage III-IV previously untreated squamous cell carcinoma of the head and neck were treated with neoadjuvant chemotherapy with cisplatin, methotrexate, bleomycin and vincristine. The overall response rate was 70%, with a 9% complete response rate. The most frequent side effects were myelosuppression, nausea and vomiting, alopecia, neurotoxicity and stomatitis. Definitive local therapy consisted of surgery alone in 13 cases, surgery plus radiation in another 13, and radiotherapy alone in 14. Six patients, four of whom died, received no definitive local therapy and two were lost to follow-up. The median disease-free survival time was 10.5 months, and the most frequent cause of failure was local regional relapse (85%). Median survival time was 13 months and there were eight long-term survivals (median 48 months). Response to chemotherapy was independent of all analysed prognostic factors. Disease-free survival and survival were significantly influenced by the presence or absence of lymph nodes. Our results do not support the routine use of neoadjuvant chemotherapy with cisplatin, methotrexate, bleomycin, and vincristine in patients with advanced cell carcinoma of the head and neck.
Eur J Surg Oncol 1989 Dec
PMID:Neoadjuvant chemotherapy with cisplatin, methotrexate, bleomycin and vincristine (CABO) in patients with stage III and IV squamous cell carcinoma of the head and neck. 248 Sep 22

Responsiveness to granulocyte-macrophage colony-stimulating factor (GM-CSF) and macrophage CSF (M-CSF) of bone marrow cells derived from different mouse strains was investigated. There were great variations in proliferation between different strains of inbred mice. Bone marrow cells from mouse strains with a high rate of proliferation in response to GM-CSF also had a high proliferating capacity to M-CSF. The response to either CSF did not correlate with a certain H-2 haplotype. GM-CSF induced consistently higher proliferation than M-CSF. Proliferation in response to M-CSF, but not to GM-CSF, could be enhanced by the addition of antibodies against interferon (IFN). IFN is the only known inducer of (2'-5') oligoadenylate (oligo (A] synthetase. This enzyme was induced in macrophages grown in the presence of M-CSF, but not in GM-CSF promoted cells. Enzyme induction was completely abrogated by simultaneous treatment with anti-IFN alpha/beta. Infection of macrophages with herpes simplex virus type 1 (HSV) and vesicular stomatitis virus (VSV) revealed that GM-CSF-promoted cells were highly susceptible to lytic infection by these viruses. In contrast, virus titres in M-CSF-cultured cells were 100-fold lower. We conclude that, contrary to M-CSF, GM-CSF does not induce autocrine IFN during haematopoiesis. As judged from data with BALB/c mice, the sensitivity to the anti-proliferative effect of the autocrine IFN may be a factor which influences M-CSF-promoted proliferation.
Scand J Immunol 1989 Dec
PMID:In vitro development of bone-marrow-derived macrophages. Influence of mouse genotype on response to colony-stimulating factors and autocrine interferon induction. 248 39

Persistent influenza C virus infection was readily initiated in Madin-Darby canine kidney (MDCK) cells at low m.o.i. and has been maintained for over 1 year. The persistently infected (p.i.) cultures were characterized by the following properties: virus infection was limited to a minority of cells, small amounts of infectious virus were produced together with low levels of interferon (IFN) and the cultures were resistant to superinfection by homologous virus and vesicular stomatitis virus, but not by influenza A and B viruses. These properties fluctuated cyclically with passage of the p.i. culture. When p.i. cultures were cured by cultivation in the presence of antiserum, the cultures lost their IFN-producing activity and became as susceptible to homologous virus as normal MDCK cell culture. The results suggest that persistent influenza C virus infection may be regulated by endogenously produced IFN. Under the condition of high m.o.i. a persistent influenza C virus infection could not be initiated in MDCK cells due to the development of cytopathic effects.
J Gen Virol 1989 Dec
PMID:Persistent infection of MDCK cells by influenza C virus: initiation and characterization. 248 13


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