Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003864 (arthritis)
 69,039 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The macromolecular organization of proteoglycans in morphologically and histochemically normal hip cartilage from aged humans has been studied. In contrast to findings in articular and nonarticular cartilage from other sources, most of the proteoglycans in these tissues did not exist in large aggregates. Treatment with hyaluronic acid beta1 leads to 3 hydrolase failed to diminish the size of proteoglycans prepared under conditions favoring aggregation, a finding suggesting that they were not complexed with hyaluronic acid. Polyacrylamide gel electrophoresis failed to demonstrate the presence of link glycoproteins associated with the proteoglycans. After incubation in vitro with hyaluronic acid, minimal augmentation of hydrodynamic size of the preparation occurred, an indication that hyaluronate-proteoglycan interaction had not taken place. These results suggest that proteoglycan aggregation was diminished because of a defect in the core protein of the proteoglycans resulting in an impaired ability of these molecules to interact with hyaluronic acid.
Arthritis Rheum
PMID:Failure of proteoglycans to form aggregates in morphologically normal aged human hip cartilage. 91 55

The joint tissues from 36 rhesus (age 2-5 years) infected with SIV/Delta were graded into four groups and then correlated with the following systemic immunologic parameters: numbers of CD4+, CD4+ plus CD29+, and CD20+ cells and SIV/Delta antigenemia. Grade I (n = 16) consisted of normal synovial membrane; grade II (n = 8) consisted of synovial hyperplasia; grade III (n = 8) consisted of a mononuclear cell infiltrate, and grade IV (n = 4) consisted of synovial membrane infiltration of syncytial cell and mononuclear type cells. Synovial membranes from 20 uninfected age-matched rhesus were compared with infected animals and were graded 1. Immunostaining of the tissue phase lymphocytes and viral antigen was performed using monoclonal antibodies commercially available and a monoclonal antibody produced against a core protein of the SIV/Delta agent. SIV/Delta infection resulted in a reduction in cells doubly stained for CD4+ and CD29+ and a relative increase in CD8+ stained cells. A significant (ANOVA) difference was not observed in CD4+, CD4+ plus CD29+, CD8+, or CD20+ among the various grades of arthritis. Viral antigen was demonstrated in syncytial cells of the grade IV reaction. This finding suggests that the SIV/Delta arthritis is a primary viral reaction.
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PMID:Arthritis in rhesus monkeys experimentally infected with simian immunodeficiency virus (SIV/DELTA). 175 9

Antibody titers to caprine arthritis-encephalitis virus surface glycoprotein gp135 and core protein p28 in synovial fluid and serum from 35 goats infected for 3 years were compared with the histologic severity of arthritis in these animals. Anti-gp135 antibody titers in synovial fluid and serum directly reflect the severity of carpal arthritis in chronically infected goats.
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PMID:Severity of arthritis is predicted by antibody response to gp135 in chronic infection with caprine arthritis-encephalitis virus. 232 6

Three generations of a nonconsanguineous family with premature onset of primary (idiopathic) osteoarthritis (OA) were studied for clues to the etiopathogenesis of their disorder. Articular symptoms began in their second and third decades of life and involved multiple joints, both typical and atypical for primary OA. Radiographs of the majority of involved peripheral joints showed abnormalities typical of primary OA. Evidence of chondrodysplasia was found in the spines. Pathologic examination of femoral heads obtained at total hip arthroplasty from 3 affected family members showed moderate to severe OA. Articular cartilage proteoglycans from these specimens were evaluated for aggregatability with hyaluronic acid, levels of chondroitin sulfate and keratan sulfate, and core protein structure. The results from each patient's specimen differed from the results of the other specimens. We conclude that this family's disorder, primary OA associated with a mild chondrodysplasia, was a late-onset overlap form of an epiphyseal dysplasia, that a defect common to hyaline articular and physeal cartilage was primary, and that a single structural proteoglycan abnormality was not likely to be the underlying cause.
Arthritis Rheum 1990 May
PMID:Early-onset primary osteoarthritis and mild chondrodysplasia. Radiographic and pathologic studies with an analysis of cartilage proteoglycans. 234 22

In a serological survey, using the immunoblotting technique, we found that substantial numbers of dog sera from both normal and diseased dogs, including dogs with neoplasia, reacted with one or more human immunodeficiency virus (HIV) recombinant proteins. A total of 144 dog sera were tested, and 72 (50%) of them reacted with one or more HIV recombinant structural proteins. Ten dog sera were also tested for reactivity with simian immunodeficiency virus (SIV), feline immunodeficiency virus (FIV), and caprine arthritis encephalitis virus (CAEV). Six dog sera reacted with at least the major core protein of HIV, while one of the dog sera tested reacted with SIV core protein, and there were no reactions with the viral proteins of either FIV or CAEV. Cell extracts from canine peripheral blood lymphocytes cocultivated with human cells and an extract of human cells infected with HIV were immunoblotted against dog sera which previously tested positive or negative on HIV recombinant protein commercially available Western blot strips. Two lymphocyte lysates and the HIV-infected Hut cell lysate reacted with the Western blot strip-positive dog serum; however, no reactions were seen with the Western blot strip-negative dog serum.
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PMID:Studies with canine sera that contain antibodies which recognize human immunodeficiency virus structural proteins. 238 66

Antibodies were used in radioimmunoassays with gel chromatography to detect the hyaluronic acid-binding region, core protein, and keratan sulfate of human cartilage proteoglycan in the synovial fluids of patients with rheumatoid arthritis, juvenile rheumatoid arthritis, and osteoarthritis. All fluids contained proteoglycan that was mainly included on Sepharose CL-4B; this result indicates cleavage of proteoglycan (which is normally excluded). The hyaluronic acid-binding region was the smallest and most commonly detected fragment. It was relatively free of keratan sulfate and core protein, and it could sometimes bind to hyaluronic acid. Other larger fragments containing core protein and/or keratan sulfate were detected in every fluid.
Arthritis Rheum 1987 May
PMID:The immunologic detection and characterization of cartilage proteoglycan degradation products in synovial fluids of patients with arthritis. 243 90

A 33-year-old black woman with advanced acquired immunodeficiency syndrome (AIDS) presented with rapidly progressive muscle weakness and serologic and radiologic evidence of central nervous system Toxoplasma infection. Muscle biopsy revealed an inflammatory infiltrate predominantly composed of macrophages and T suppressor/cytotoxic cells. Human immunodeficiency virus major core protein (p24) was also detected in macrophages and damaged muscle cells around the inflammatory infiltrates. The patient improved clinically with glucocorticoid therapy for polymyositis and pyrimethamine and clindamycin therapy for toxoplasmosis.
Arthritis Rheum 1989 Apr
PMID:Inflammatory myopathy and acquired immunodeficiency syndrome. 246 39

Feline immunodeficiency virus (FIV) is a T-lymphotropic retrovirus associated with immunodeficiency and opportunistic infections in cats. The discovery of FIV provides an opportunity for the development of a small animal model for AIDS. To initiate the molecular and biological characterization of FIV, cDNA clones were synthesized and used to isolate a proviral clone of FIV. Molecular cross-hybridization analysis of FIV with five lentiviruses revealed that nucleotide-sequence similarities exist between FIV and these lentiviruses in the gag-pol genes. However, nucleotide-sequence similarities were not seen upon comparison of the FIV long terminal repeat sequence with known viral sequences. Common antigenic determinants appeared to be shared by FIV, caprine arthritis encephalitis virus, and visna virus as shown by serological cross-reactivity of rabbit antibodies to caprine arthritis encephalitis virus and visna virus with the putative FIV core protein p28. These studies demonstrated that FIV is a member of the lentivirus subfamily and is distantly related to the AIDS lentiviruses of primates. Importantly, progeny virions of our molecular clone were infectious for experimentally inoculated cats. The availability of an infectious molecular clone will make possible a detailed dissection of the molecular pathogenesis of FIV, which may facilitate the development of vaccine and therapeutic strategies for AIDS.
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PMID:Molecular cloning of feline immunodeficiency virus. 292 41

The proteins of an isolate of caprine arthritis-encephalitis virus (CAEV) were analysed by SDS-PAGE and Western blotting. Monoclonal antibodies (MAbs) produced to the main core protein p24 and the small structural protein p14 also recognized two major polypeptides of Mr 41K and 55K in infected cell material, consistent with a precursor role for these gag polypeptides. In addition, the p24 MAbs detected a 33K polypeptide in extracellular virus preparations, while the p14 MAbs reacted strongly with a polypeptide of 18K (corresponding to structural protein p18) and weakly with another of 21K. The use of these MAbs in an indirect fluorescent antibody method revealed an intracytoplasmic location of these viral antigens in both mononucleated and multinucleated (syncytial) infected cells. Cross-reactivity with several other isolates indicated that these MAbs may be useful for diagnosis of CAEV infection.
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PMID:Virus-specific polypeptides of caprine arthritis-encephalitis virus recognized by monoclonal antibodies to virion proteins p24 and p14. 337 82

Cartilage degradation is a characteristic feature of various types of human arthritis, notably rheumatoid arthritis and osteoarthritis. The influence of glucocorticoid and other steroid hormones on cartilage proteoglycan breakdown was examined in a model system in which breakdown is readily quantified by the release of proteoglycan from cultured bovine nasal cartilage discs. Endotoxin (bacterial lipopolysaccharides) treatment enhanced the depletion of cartilage proteoglycan by 2-3 fold. This was inhibited in a concentration-dependent manner by hydrocortisone (10(-9) to 10(-5) M) or other glucocorticoid hormones (dexamethasone, prednisolone, cortisone). Inhibition required the continued presence of the steroid. Removal of hydrocortisone (3 x 10(-7) M) after 4 days from endotoxin-treated cultures resulted in the rapid restoration of an endotoxin response, so that proteoglycan release approached maximum levels during a second 4-day culture period. Other C-21 steroid hormones (progesterone, aldosterone) were also inhibitory at 10(-5) M, but testosterone and beta-estradiol showed little influence on endotoxin action. Proteoglycan products of smaller average mol wt (Sepharose CL-2B chromatography), consistent with core protein cleavages, were released from endotoxin-treated cartilage. Cleavage was unaffected by beta-estradiol, partially blocked by aldosterone and largely prevented by hydrocortisone administration.
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PMID:Effect of steroid hormones on endotoxin-mediated cartilage degradation. 337 77


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