Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0271276 (Hudson)
 1,066 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The collagenous components of Ascaris suum intestinal basement membrane were isolated by extraction with 0.1 M Tris-HC1, 0.5 M NaC1, 0.5% 2-mercaptoethanol, pH 8.3, and Sephacryl S-300 gel filtration. Rotary-shadowing electron microscopy showed that the collagenous components occur as monomers and dimers with mean contour lengths of 469 +/- 21 and 918 +/- 24 nm, respectively. The molecules each contain a globular domain, with that of the dimer being slightly larger than that of the monomer. Electrophoresis in sodium dodecyl sulfate-polyacrylamide gels under reducing conditions revealed two polypeptides of Mr = 185,000 and 179,000. A similarity to type IV collagen was indicated by a glycine content of less than 33 mol % and the presence of fucose, mannose, and glucosamine residues. Treatment of the collagen with pepsin resulted in loss of the globular domains but retention of 90% of the length of fibrous collagen segments. Collagenase, however, removed the fibrous regions but left the globular moieties intact. These results extend the previously proposed model (Hung, C.-H., Noelken, M. E., and Hudson, B. G. (1981) J. Biol. Chem. 256, 3822-3826) in which the collagenous domain consists of two monomer-sized triple-helical subunits joined end-to-end by disulfide bonds, with the constituent chains of each subunit being cross-linked by disulfide bonds.
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PMID:Intestinal basement membrane of Ascaris suum. Molecular organization and properties of the collagen molecules. 395 13

Two inhibitors of glycosylation, glucosamine and tunicamycin, were utilized to examine the effect of glycosylation inhibition in mouse neuroblastoma N18 cells on the degradation of membrane glycoproteins synthesized before addition of the inhibitor. Treatment with 10 mM-glucosamine resulted in inhibition of glycosylation after 2h, as measured by [3H]fucose incorporation into acid-insoluble macromolecules, and in a decreased rate of glycoprotein degradation. However, these results were difficult to interpret since glucosamine also significantly inhibited protein synthesis, which in itself could cause the alteration in glycoprotein degradation [Hudson & Johnson (1977) Biochim. Biophys. Acta 497, 567-577]. N18 cells treated with 5 microgram of tunicamycin/ml, a more specific inhibitor of glycosylation, showed a small decrease in protein synthesis relative to its effect on glycosylation, which was inhibited by 85%. Tunicamycin-treated cells also showed a marked decrease in glycoprotein degradation in experiments with intact cells. The inhibition of glycoprotein degradation by tunicamycin was shown to be independent of alterations in cyclic AMP concentration. Polyacrylamide-gel electrophoresis of isolated membranes from N18 cells, double-labelled with [14C]fucose and [3H]fucose, revealed heterogeneous turnover rates for specific plasma-membrane glycoproteins. Comparisons of polyacrylamide gels of isolated plasma membranes from [3H]fucose-labelled control cells and [14C]fucose-labelled tunicamycin-treated cells revealed that both rapidly and slowly metabolized, although not all, membrane glycoproteins became resistant to degradation after glycosylation inhibition.
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PMID:The relationship between glycosylation and glycoprotein metabolism of mouse neuroblastoma N18 cells. 747 93

The goal of this study was to evaluate the effectiveness of an oral joint supplement in working dogs with hip osteoarthritis compared with a positive control group (CG). Fifteen animals were divided in treatment group (TG, n = 10) and CG (n = 5). To TG a commercially available joint supplement, containing glucosamine HCl, chondroitin sulphate, and hyaluronic acid was given for 40 days and a 70-day course of a placebo, to be administered as if it was carprofen. The CG received carprofen for 70 days, and a placebo to be administered as the joint supplement. Response to treatment, measured by the canine brief pain inventory (CBPI) and the Hudson visual analog scale, was evaluated before treatment (T0), after 15 days (T1) and 1 (T2), 2 (T3), 3 (T4), 4 (T5), and 5 (T6) months. With CBPI, no differences were found in pain interference score and pain severity score between TG and CG throughout or when comparing results within groups. Individual results were considered successful in a maximal of three dogs of the TG by T3 (30%) and 1 in CG (25%). With Hudson visual analog scale, improvements where registered with individual results, for 40%-50% of the animals in TG and 60%-80% of cases in CG. The oral joint supplement and carprofen produced some improvements in individual scores but where unable to do so when overall results were considered. Each of these options may not be able, by itself, to fully address the demands of a working dog with joint disease and related pain.
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PMID:Effect of an Oral Joint Supplement When Compared to Carprofen in the Management of Hip Osteoarthritis in Working Dogs. 2952 31