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 study the biological and immunological properties of influenza virus surface glycoproteins, cDNA copies of the haemagglutinin (HA) and the neuraminidase (NA) genes of A/WSN/33 influenza virus were cloned and expressed in prokaryotic and eukaryotic cells. In Escherichia coli, maximum expression of HA is obtained only as a fusion protein in which the NH2-terminal portion is provided by a bacterial protein (i.e. beta gal or trpLE'). The HA expressed in bacteria (bacterial HA) is recognized by polyclonal anti-WSN antibodies but not by neutralizing monoclonal antibodies. The antibodies made against the bacterial HA bind to the detergent-treated viral HA, intact virus and live influenza infected cells, but fail to show either haemagglutination inhibition (HI) or virus neutralization. These results suggest that the three-dimensional structure as well as the antigenic epitopes of the bacterial HA are different from that of native viral HA. HA, expressed from cDNA in cultured animal cells, is shown to possess the structural features of the native viral HA. It is glycosylated, transported to the apical domain of the plasma membrane of polarized cells, causes haemadsorption and can induce cell to cell fusion at low pH after proteolytic cleavage. An attempt was made to define the structural features of HA required for sorting and directional transport by making chimeras with vesicular stomatitis virus G (VSV G) proteins either by switching the amino terminus or the carboxy terminus of HA with that of VSV G. These chimeric proteins were translocated across the rough endoplasmic reticulum (RER) but were blocked in transport between the RER and cell membrane.(ABSTRACT TRUNCATED AT 250 WORDS)
Vaccine 1985 Sep
PMID:Biological and immunological properties of haemagglutinin and neuraminidase expressed from cloned cDNAs in prokaryotic and eukaryotic cells. 241 36

Intraperitoneal injection of vesicular stomatitis virus, New Jersey serotype (VSV-NJ), into inbred LSH hamsters resulted in an inapparent infection and survival of the majority of the animals. Infectivity titrations of tissues from VSV-NJ-infected hamsters showed that little or no virus was present following infection. The few animals that died from VSV-NJ succumbed to neurological disease. This is in contrast to our previous work where we found that LSH hamsters are exquisitely sensitive to i.p. infection by VSV, Indiana serotype (VSV-IND), and that large amounts of VSV-IND could be detected in tissues. The 50% lethal doses of VSV-NJ and VSV-IND for LSH hamsters are approximately 10(7) pfu and 1 pfu, respectively. When peritoneal cells from LSH hamsters were infected in vitro with both VSV serotypes, the yields of VSV-NJ consistently were lower than yields of VSV-IND. The growth of the two serotypes in fibroblast and epithelial cell lines of hamster origin was similar. VSV-NJ was not more efficient than VSV-IND in inducing interferon in vitro or in vivo, and there appeared to be no difference in the sensitivities of the two serotypes to the antiviral activity of hamster interferon. Thus, i.p. infection with less than 10(7) pfu of VSV-NJ is avirulent for LSH hamsters and this avirulence may be due, in part, to partial intrinsic resistance of peritoneal macrophages to infection by VSV-NJ. When four LSH hamsters that had been immunized with VSV-NJ were challenged with 10(6) LD50 of VSV-IND, three of the four animals survived. Despite the fact that neutralizing antibodies to VSV-NJ did not cross-neutralize VSV-IND, five out of five LSH hamsters were protected by passive transfer of 1 ml of immune hamster anti-VSV-NJ antiserum prior to challenge with VSV-IND. This suggests an important role for non-neutralizing antibodies.
Virus Res 1985 Sep
PMID:Differing responses of hamsters to infection by vesicular stomatitis virus Indiana and New Jersey serotypes. 241 43

The direct introduction with micropipettes of poly(rI).poly(rC) into the cytoplasm of several human cell lines inhibited the multiplication of vesicular stomatitis virus. This antiviral activity was at least partly due to interferon (IFN) production and secretion from the injected cells since it was species-specific, partly neutralized by IFN antibodies and was transmissible to non-adjacent cells. This suggests a mechanism of IFN induction involving the internalization of poly(rI).poly(rC) and its interaction with an intracellular target.
J Gen Virol 1986 Sep
PMID:An antiviral state induced in HeLa cells by microinjected poly(rI).poly(rC). 242 45

A biochemical basis for the pea and lentil lectin resistance of two Chinese hamster ovary (CHO) cell mutants, Lec13 and Lec13A, was investigated. Studies of the G glycopeptides of vesicular stomatitis virus grown in the mutants indicated that Lec13 cells essentially lack the ability to add fucose to complex carbohydrates while Lec13A cells synthesize significant proportions of fucosylated, complex moieties. However, both mutants were known to be reverted to lectin sensitivity by growth in L-fucose, making them similar to the mouse lymphoma mutant, PLR1.3, which is defective in the conversion of GDP-mannose to GPD-fucose [M. L. Reitman, I. S. Trowbridge, and S. Kornfeld (1980) J. Biol. Chem. 255, 9900-9906]. Optimal conditions for the production of GDP-fucose from GDP-mannose by CHO cytosol were found to occur at pH 8 in the presence of 7.5 microM GDP-mannose, 15 mM Mg2+, 0.2 mM NAD+, 0.2 mM NADPH, 10 mM niacinamide, 5 mM ATP, and 50 mM Tris-HCl. Under these conditions, Lec13 cytosol produced no detectable GDP-fucose nor GDP-sugar intermediates while Lec13A cytosol produced significant quantities of both. Mixing experiments with Lec13 cytosol identified the first enzyme of the conversion pathway (GDP-mannose 4,6-dehydratase, EC 4.2.1.47) as the site of the block. In addition to being markedly reduced, the Lec13A 4,6-dehydratase activity was relatively insensitive to changes in pH in comparison to the activity in parental cytosol, suggesting that Lec13A cells might possess a structurally altered GDP-mannose 4,6-dehydratase enzyme.
Arch Biochem Biophys 1986 Sep
PMID:Two Chinese hamster ovary glycosylation mutants affected in the conversion of GDP-mannose to GDP-fucose. 242 10

The human rhabdomyosarcoma cell line RD-114 is partially responsive to interferons (IFNs). In these cells, alpha interferon (IFN-alpha) or gamma interferon (IFN-gamma) inhibits the replication of some viruses but not of others. Similarly, some of the IFN-inducible mRNAs are induced poorly, whereas others are induced well. Here we report the isolation of clonal derivatives of this line which display different spectra of responses to IFNs. Among the eight extensively characterized clonal lines, one, C10, did not respond to IFN-alpha or IFN-gamma at all. Retrovirus production by each of the seven other lines was inhibited by both IFN-alpha and IFN-gamma. Replication of vesicular stomatitis virus was inhibited strongly by IFN-alpha in clone B1 but not in others, whereas it was not appreciably affected by IFN-gamma in any clone. Replication of encephalomyocarditis virus was inhibited strongly by IFN-gamma in clones A1, A2, A3, B3, and B8 and by IFN-alpha in clone A2. Neither IFN inhibited the multiplication of these clones greatly, although their doubling times were slightly increased. Five mRNAs were induced by IFNs to varying degrees in the seven clones. mRNA 2A was most strongly induced by IFN-gamma in clone A3. mRNA 1-8 was strongly induced by IFN-alpha in clone A1 and by either IFN in clones A2 and A3. The highest concentrations of 2',5'-oligoadenylate synthetase mRNA, mRNA 561, and mRNA 6-16 were in IFN-alpha-treated clones A1 and A2. These results demonstrated the existence of clonal heterogeneity in IFN responses in a cell line and strengthened the view that IFN treatment of cells generates multiple signals leading to a variety of IFN-induced phenotypes.
J Virol 1987 Sep
PMID:Clonal derivatives of the RD-114 cell line differ in their antiviral and gene-inducing responses to interferons. 244 Oct 75

A total of 185 eligible patients with advanced inoperable squamous cell carcinoma of the head and neck were randomized into two groups; the cisplatin, methotrexate, bleomycin, and vincristine (CABO) group received cisplatin (50 mg/m2; day 4), methotrexate (40 mg/m2; days 1, 15), bleomycin (10 mg; days 1, 8, and 15), and vincristine (2 mg; days 1, 8, and 15) and the ABO group received methotrexate, bleomycin and vincristine in the same doses on days 1, 8, and 15. After three courses, patients in both arms received weekly methotrexate as maintenance therapy; those 34 patients with previously untreated locoregional disease went off the study because of subsequent locoregional treatment in form of radiotherapy +/- surgery. The complete response rate was 16% in patients receiving CABO, compared with 5% among patients given ABO. The corresponding overall response rates were 50% and 28%, respectively (P = 0.003). Among patients with recurrent or metastatic disease, progression was delayed in patients receiving CABO (median, 18 weeks) compared to those receiving ABO (median, 14 weeks) (P = 0.07), but there was no difference in survival time. Myelosuppression consisted mostly of leukopenia, which was seen in 67% of the CABO patients versus 47% in the other arm. Myelosuppression-associated infection and hemorrhage led to death in two patients in the CABO treatment group and six patients in the ABO treatment group. Nausea and vomiting, mostly of grades 1 or 2, occurred in 93% of the patients given CABO and 44% of those receiving ABO. Other toxic effects--neuropathy, alopecia, stomatitis, constipation, fever/chills, diarrhea, cutaneous alterations, and renal impairment--occurred equally in the two treatment groups. This study underlines the role of cisplatin in head and neck cancer, although no impact on survival could be demonstrated. It also supports indirectly the superiority of combination chemotherapy over single-agent treatment for this disease.
Cancer 1987 Sep 15
PMID:Combination chemotherapy with methotrexate, bleomycin, and vincristine with or without cisplatin in advanced squamous cell carcinoma of the head and neck. 244 36

We used site-directed mutagenesis to localize serologically defined (s) and CTL (c)-defined alloantigenic determinants to discrete amino acid sequences of a murine MHC class I antigen. Based on the prediction that amino acid position 63-73 of the H-2Dd antigen forms s-allodeterminants, the H-2Ld gene was mutated in a sequential fashion to replace codons for amino acid positions 63, 65, 66, 70, and 73 with those of the H-2Dd amino acids. Epitopes of the mutant antigens expressed in L-cells were examined by the binding of a series of mAbs specific for the H-2Dd antigen. The mutant antigen M66 had substitutions at residues 63, 65, and 66, and resulted in the acquisition of a number of H-2Dd-specific s-epitopes. Mutant M70 had an additional substitution at residue 70, which led to the gain of multiple additional H-2Dd s-epitopes. Together, more than half of all the relevant H-2Dd s-epitopes were mapped into amino acid position 63-70 of the H-2Dd molecule, which was expressed in the mutant H-2Ld gene. The final mutation at residue 73 (M73) caused no new epitope gains, rather, a few Dd s-epitopes acquired by the preceding mutations were lost. All of the H-2Ld-specific s-determinants were retained in the mutant molecules, as were H-2Dd s-determinants specific for the alpha-2 or alpha-3 domains. Changes of these residues affected c-determinants defined by CTL. Anti-H-2Dd CTL cultures and an anti-H-2Dd CTL clone recognized the mutant H-2Ld molecules, M66 and M70. Some CTL clones generated against the Q10d molecule, which has an identical sequence to H-2Dd between residues 61 and 73, failed to recognize native H-2Dd or Ld but did crossreact with mutant Ld. While bulk-cultured anti-H-2Ld CTL cultures reacted strongly against M73, bulk-cultured H-2Ld restricted anti-vesicular stomatitis virus CTL did not. Finally, at the clonal level two of three anti-H-2Ld CTL clones lost reactivity with some or all of these mutant molecules. From these results we conclude that a stretch of amino acids from position 63 to 70 of the alpha-1 domain controls major s- and c-antigenic sites on the H-2Dd antigen and c-sites on H-2Ld antigen.
J Exp Med 1987 Sep 01
PMID:Introduction of H-2Dd determinants into the H-2Ld antigen by site-directed mutagenesis. 244 90

The coincidence of skin eruption and remission induced by gold has not previously been reported. In 50 out of 247 patients with rheumatoid arthritis treated with gold salts (Solganal) between 1977 and 1987 treatment was stopped owing to adverse reactions. Skin rashes were present in 31 patients, 10 had nephropathy, and nine patients had aphthous stomatitis. All 31 patients who developed skin eruption entered a concomitant clinical and laboratory remission. The remission satisfied the American Rheumatism Association preliminary criteria and was accompanied by a significant decrease of mean erythrocyte sedimentation rate from 43 (SD 13) to 25 (11) mm/h. Disease was exacerbated in 23 patients after three to 60 months. Eight patients are in remission at present, five to 68 months after gold treatment was discontinued. In contrast, no remission was noticed among the 19 patients with nephropathy or stomatitis.
Ann Rheum Dis 1989 Sep
PMID:Association between gold induced skin rash and remission in patients with rheumatoid arthritis. 214 Feb 55

Thirty patients with Stage III non-small cell lung cancer were entered on a trial to evaluate the feasibility of combined radiation and concomitant 5-fluorouracil infusion. Patients had received prior debulking surgery (nine), induction chemotherapy (16), or no therapy (five). Radiation employed standard fractionation (180-200 rad/day) administered to a median cumulative dose of 5500 rad (range, 4500-6200 rad). 5-Fluorouracil was infused 24 hours per day throughout the period of radiation at a dose of 300 mg/m2/day for a median of 42 days (range, 28-56 days). Radiation complications included pneumonitis three of 30 (10%) and esophagitis (27%). Chemotherapy complications included stomatitis, two of 27 (7%), and hand-foot syndrome, three of 30 (10%). Treatment interruptions were necessary in six of 30 (20%) and four of 30 required parenteral nutrition. At a median follow-up of 12 months 26/30 (87%) maintained local control and eight had distant metastases (three of whom presented with Stage IV disease). 5-Fluorouracil delivered continuously throughout standard fractionation radiation to high cumulative doses is feasible and practical. Comparative clinical trials of the various combined radiation and chemotherapy schedules employed are in order. One additional clinical observation was the identification of six of 30 (20%) with brain metastases at presentation or after 12 months, all of whom had adenocarcinoma histologic subtype.
Cancer 1989 Sep 01
PMID:Concomitant 5-fluorouracil infusion and high-dose radiation for stage III non-small cell lung cancer. 254 5

To define the participation of cell-mediated immunity in resistance to amebic infection through the action of soluble mediators or lymphokines (LKs), including gamma interferon (IFN-gamma), we studied their effect on Entamoeba histolytica. Supernatants from cultures of lymphoid cells, which had been stimulated in vitro with concanavalin A and were rich in lymphokines (LRSNs), and recombinant IFN-gamma were used. LRSN and recombinant IFN-gamma inhibited the growth of E. histolytica trophozoites in vitro. These LKs did not show a cytotoxic effect on the ameba, but they did inhibit rather significantly protein and DNA syntheses of the protozoa. Interestingly, LRSN incubated at 4 degrees C in the presence of trophozoites lost the ability to inhibit the replication of vesicular stomatitis virus. IFN-gamma inactivated at pH 2 had no effect on DNA synthesis by the ameba, thus suggesting that IFN-gamma is responsible for the observed inhibition of parasite growth. Furthermore, the IFN-gamma inhibitory effect was abolished by a monoclonal antibody specific for this LK. The results suggest that IFN-gamma may participate in protection against amebiasis infection through the activity of mediators released by lymphocytes during infection.
Infect Immun 1989 Sep
PMID:Effects of gamma interferon on syntheses of DNA and proteins by Entamoeba histolytica. 254 19


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