bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stimulation of the secretion of latent cysteine proteinase activity by tumor necrosis factor α and interleukin‐1
Authors: Huet Guillemette , Flipo René‐Marc , Colin Cécile , Janin Anne , Hemon Brigitte , Collyn‐D'Hooghe Maud , Lafyatis Robert , Duquesnoy Bernard , Degand Pierre 
Published: February 2007

AbstractObjective. Cultured synovial fibroblast‐like cells from 3 patients with rheumatoid arthritis (RA) and 3 patients with osteoarthritis (OA) were evaluated for their potential to secrete cysteine proteinases spontaneously and after stimulation by tumor necrosis factor α (TNFα) or interleukin‐1 (IL‐1).Methods. Culture media and cell lysates were analyzed before and after high performance liquid chromatography (HPLC) using the enzymatic substrate, Z‐Phe‐Arg‐AMC, and by immunoblotting with anti–cathepsin B antiserum. Immunolocalization of cathepsin B was studied on cell monolayers.Results. Latent cysteine proteinase activity was found to be secreted spontaneously by cultured synovial fibroblast‐like cells. This activity was increased after treatment with either TNFα or IL‐1. Stimulated protease activity was eluted by HPLC at a peak coincident with that of purified cathepsin B. By immunoblot, cell supernatants contained a 43‐kd form of cathepsin B, while cell lysates contained a 30‐kd form, consistent, respectively, with cathepsin B before and after cleavage of its propeptide. An intracellular increase in cathepsin B after treatment with TNFα was also seen with immunohistochemical studies.Conclusion. TNFα (in the 6 cases studied) and IL‐1 (in 4 cases) stimulated the secretion of a latent cysteine proteinase activity from synovial fibroblast‐like cells, which appears to represent primarily cathepsin B.
Production of leukemia inhibitory factor by human articular chondrocytes and cartilage in response to interleukin‐1 and tumor necrosis factor α
Authors: Campbell Ian K. , Waring Paul , Novak Ulrike , Hamilton John A. 
Published: February 2007

AbstractObjective. To investigate the production of leukemia inhibitory factor (LIF) by human articular chondrocytes and cartilage.Methods. Chondrocytes and cartilage were cultured with and without added cytokines, and the conditioned media assayed for LIF by a specific radioreceptor competition assay.Results. Interleukin‐1 (IL‐1) and tumor necrosis factor α (TNFα) stimulated LIF production by chondrocyte monolayers and cartilage. LIF was generally not detected in unstimulated cultures. Northern blot analysis showed increased amounts of LIF messenger RNA in IL‐1– and TNFα‐treated chondrocyte cultures.Conclusion. Chondrocytes, stimulated by IL‐1 and/or TNFα, are potential contributors to the elevated levels of LIF observed in the synovial fluids of patients with rheumatoid arthritis and other inflammatory arthritides.
Low‐dose methotrexate with leucovorin (folinic acid) in the management of rheumatoid arthritis. results of a multicenter randomized, double‐blind, placebo‐controlled trial
Authors: Shiroky Jeffrey B. , Neville Carolyn , Esdaile John M. , Choquette Denis , Zummer Michel , Hazeltine Mark , Bykerk Vivian , Kanji Mohamed , St‐Pierre Anne , Robidoux Lise , Bourque Lucienne 
Published: February 2007

AbstractObjective. To determine whether the side effects of methotrexate can be decreased by the concurrent use of leucovorin, without affecting the efficacy of the methotrexate.Methods. We conducted a multicenter randomized, double‐blind, placebo‐controlled trial of leucovorin administration, 2.5–5.0 mg orally, to be given 24 hours after the single, weekly, oral dose of methotrexate. Every 3 weeks for 52 weeks, patients were evaluated for rheumatic disease activity and side effects. Dosage adjustments for both methotrexate and leucovorin were made as needed, according to a defined protocol. The primary outcome evaluated was the frequency of study withdrawals because of side effects and/or inefficacy. Secondary outcomes evaluated included the frequency of side effects and the relative efficacy of methotrexate in the leucovorin and placebo treatment groups.Results. Ninety‐two evaluable patients were analyzed (44 took leucovorin and 48 placebo). Twenty‐two patients withdrew early because of side effects unresponsive to our protocol, and 1 because of inefficacy; 17 had been taking placebo and 6 had been taking leucovorin (35% versus 14%,P < 0.02). The number of visits during which side effects were reported was reduced by almost 50% in the leucovorin treatment group (P < 0.001). There were significant reductions in the frequencies of all common side effects. At 52 weeks, disease activity was similar in both patient groups.Conclusion. The methotrexate–leucovorin protocol used significantly reduces common side effects of methotrexate therapy without significantly altering efficacy.
Differential effects of diclofenac and aspirin on serum glutamic oxaloacetic transaminase elevations in patients with rheumatoid arthritis and osteoarthritis
Authors: Furst Daniel E. , Anderson William 
Published: February 2007

AbstractObjective. To examine elevations in levels of serum glutamic oxaloacetic transaminase (SGOT) in patients with rheumatoid arthritis (RA) and osteoarthritis (OA) taking placebo, aspirin, or diclofenac, and to seek possible explanations for the occurrence of these elevations.Methods. We conducted a metaanalysis of individual case reports from 3 RA protocols and 5 OA protocols, encompassing 814 diclofenac‐treated patients, 443 aspirin‐treated patients, and 359 placebotreated patients. All of the RA protocols had nearly identical inclusion and exclusion criteria, as well as safety studies and followup; the same was true for the OA protocols. Analysis included correlation analysis and multiple linear and logistic regression, accounting for numerous potential confounding variables, with the SGOT as the dependent variable. F tests were used for hypothesis testing.Results. By several analytic approaches, the principal determinants of SGOT concentrations were found to be baseline SGOT value, the use of aspirin in RA patients, and the use of diclofenac in OA patients. Other significant factors contributing to an increase in SGOT concentrations were duration of therapy and, perhaps, daily dosage (mg/Ib). Hypothesis testing supported these results. Given a statistically average patient, we predicted a 1–2% chance of a mildly elevated SGOT level occurring among placebo‐treated patients, a 6–7% chance among diclofenac‐ or aspirin‐treated patients with RA, a 12% chance among diclofenac‐treated patients with OA, and a 2% chance among aspirin‐treated patients with OA.Conclusion. This study demonstrates a powerful method for performing metaanalysis, using available individual patient data to examine numerous factors that may affect an outcome of interest. In this case, mild elevations of SGOT were examined and found to be related to baseline SGOT levels, diclofenac use (in OA), and aspirin use (in RA). Of numerous other potential factors examined, including age, sex, alcohol use, concomitant medications, and concomitant diagnoses, only duration of therapy and, to a small extent, daily dosage, were also consistent determinants of SGOT elevation. The SGOT elevations were minimal and were not related to the occurrence of clinical hepatitis: No clinical hepatitis occurred.
Association of hla–dr4‐dw15 (drb1*0405) and dr10 with rheumatoid arthritis in a spanish population
Authors: Yelamos José , Raül Garcia‐Lozano J. , Moreno Isabel , Aguilera Isabel , Francisca Gonzalez M. , Garcia Alicia , Nuñez‐Roldan Antonio , Sanchez Berta 
Published: February 2007

AbstractObjective. To analyze the associations of HLA class II antigens with rheumatoid arthritis (RA) in a Spanish population.Methods. We used DNA oligotyping to determine DR types, DQA1 and DQB1 alleles, and DR4 variants in 70 unrelated seropositive RA patients and 189 healthy controls living in Spain.Results. A significantly higher frequency of DR4 was seen in RA patients compared with controls (relative risk [RR] = 2.40). The DR10 specificity correlated most strongly with disease susceptibility (RR = 3.84). A significant decrease in the frequency of DR7 was observed in the RA patients (RR = 0.48). DR4‐Dw15 (DRB1*0405) was found to be the unique DR4 allele associated with RA (RR = 4.27, P < 0.05), whereas Dw4 (DRB1*0401) and Dw14 (DRB1*0404/0408) showed no association, and both D10 (DRB1*0402) and Dw13 (DRB1*0403/0407) were negative risk factors for the disease. Approximately one‐third of the cases of RA could not be explained by the “shared epitope” hypothesis. Investigation of the DQ alleles associated with DR4 showed that the haplotype Dw15‐DQ8 (DRB1*0405‐DQB1*0302) was a susceptibility factor for RA (RR = 6.36, P < 0.05).Conclusion. Our results suggest that HLA class II alleles involved in RA susceptibility can vary among different Caucasian populations.
Association of hla–dr and hla–dq antigens with congenital dislocation and dysplastic osteoarthritis of the hip joints in japanese people
Authors: Torisu Takehiko , Fujikawa Yousuke , Yano Hirokazu , Masumi Shogo 
Published: February 2007

AbstractObjective. To investigate the frequency of HLA‐DR and DQ antigens among patients with congenital dislocation of the hip joint or dysplastic osteoarthritis (OA) and to determine whether tissue typing might contribute to better understanding of these disorders.Methods. HLA–DR and DQ typing was undertaken in 18 patients with congenital dislocation of the hip joints, 65 patients with dysplastic OA of the hip, 42 patients with primary OA of the knee, and 40 normal controls. Typing for HLA–D antigens was performed using the standard microlymphocytotoxicity method.Results. The frequency of HLA–DR4 in patients with congenital dislocation of the hip joint (61.1%) and patients with dysplastic OA of the hip (58.5%) was significantly increased compared with normal controls (27.5%) (Pcorr < 0.05 and P < 0.01, respectively). The relative risk for HLA–DR4 was 4.1428 and 3.7104, respectively, in these 2 disease groups. The frequency of HLA–DR4 in the patients with primary OA of the knee (35.7%) did not differ significantly from that in normal controls.Conclusion. The results strongly indicate that development of congenital dislocation of the hip joint and progression of dysplastic OA of the hip are associated with genes of the HLA–D region.
Serum amyloid p component scintigraphy and turnover studies for diagnosis and quantitative monitoring of aa amyloidosis in juvenile rheumatoid arthritis
Authors: Hawkins P. N. , Richardson S. , Vigushin D. M. , David J. , Kelsey C. R. , Gray R. E. S. , Hall M. A. , Woo P. , Lavender J. P. , Pepys M. B. 
Published: February 2007

AbstractObjective. To evaluate aspects of the natural history of AA amyloidosis complicating juvenile rheumatoid arthritis (JRA), and its response to therapy with chlorambucil.Methods. Scintigraphy and 7‐day turnover studies were performed in JRA patients with histologically proven (n = 35) or clinically suspected (n = 30) AA amyloidosis, following intravenous injection of 123I and 125I–labeled serum amyloid P component (SAP). Prospective monitoring studies were performed over 2–3 years in 20 patients with amyloidosis. All but 2 amyloidosis patients were treated with chlorambucil.Results. Positive scanning results were obtained in all patients in whom imaging was performed within 12 years of positive biopsy findings of amyloid and in 5 patients with clinically suspected amyloidosis. Negative scanning results with normal SAP metabolism, indicating regression of amyloid, were obtained in 4 patients whose amyloidosis had been in full clinical remission for more than 12 years. Prospective monitoring studies in patients whose JRA‐associated inflammatory activity was in remission demonstrated regression of amyloid in 8 patients and no substantial changes in 8 others; however, in 4 further patients with active inflammation, there was accumulation of amyloid. There was a very poor correlation between the amount of amyloid present at a particular site and the resultant organ dysfunction.Conclusion. Radiolabeled SAP scintigraphy and turnover studies are useful complementary tools in the diagnosis, screening, and quantitative monitoring of type AA amyloidosis in JRA. The amyloid deposits may progress and/or regress at different rates in different anatomic sites over short periods.
Hemorrhagic cystitis complicating untreated necrotizing vasculitis
Authors: Block Joel A. 
Published: February 2007

AbstractAlthough the genitourinary system is frequently affected in polyarteritis nodosa, involvement of the wall of the urinary bladder is extremely uncommon; moreover, when reported, it has been merely as an incidental finding late in the disease course. In contrast, hemorrhagic cystitis is a well‐recognized complication of cyclophosphamide therapy for the systemic vasculitides, but has not previously been reported to complicate untreated vasculitis. Herein is described a patient who presented with non–treatment‐related hemorrhagic cystitis which was found to be due to nongranulomatous necrotizing vasculitis of the wall of the urinary bladder. This represents both a novel presentation of polyarteritis and a previously unreported etiology of hemorrhagic cystitis. The differential diagnosis of apparently spontaneous hemorrhagic cystitis should therefore include active necrotizing vasculitis, independent of prior therapy.
Reduced synovial membrane macrophage numbers, elam‐1 expression, and lining layer hyperplasia in psoriatic arthritis as compared with rheumatoid arthritis
Authors: Veale Douglas , Yanni Ghada , Rogers Sarah , Barnes Louise , Bresnihan Barry , Fitzgerald Oliver 
Published: February 2007

AbstractObjective. To define the immunohistologic features of the synovial membrane (SM) of patients with psoriatic arthritis (PA) and to compare them with those of an age‐ and disease‐duration–matched population of patients with rheumatoid arthritis (RA).Methods. Synovial membrane needle biopsy was performed on 15 PA patients with knee involvement (8 had asymmetric oligoarthritis and 7 had symmetric polyarthritis) and on 15 RA controls. Specimens were stained with monoclonal antibodies against T cells (CD3, CD8, CD4, CD45RO), B cells (CD20), macrophages (Mac387, CD14), and cells bearing class II antigens (DAKO‐DR). Vascular endothelium was examined using a polyclonal antibody to Factor VIII–related antigen, and adhesion molecule expression was examined using antibodies 1.3B6, 6.5B5, and 1.4C3, which identify endothelial leukocyte adhesion molecule 1 (ELAM‐1), intercellular adhesion molecule 1 (ICAM‐1), and vascular cell adhesion molecule 1 (VCAM‐1), respectively.Results. There was significantly less lining layer hyperplasia, fewer macrophages, and a greater number of blood vessels in PA SM than in RA SM. ELAM‐1 expression was less intense in PA than in RA SM, while there was no difference in expression of ICAM‐1 and VCAM‐1. Numbers of B cells, T cells, and T cell subsets (predominantly CD4, CD45RO T cells) were similar in both groups of patients.Conclusion. Our findings demonstrate important differences in the immunohistologic features of PA and RA SM. The PA SM is more vascular, ELAM‐1 expression is less intense, and fewer macrophages invade the stroma and migrate to the lining layer than in RA SM. However, the lymphocytic infiltrate in the SM of both groups is similar.
Increased levels of leukemia inhibitory factor in synovial fluid from patients with rheumatoid arthritis and other inflammatory arthritides
Authors: Waring P. M. , Carroll G. J. , Kandiah D. A. , Buirski G. , Metcalf D. 
Published: February 2007

AbstractObjective. To examine synovial fluid (SF) from patients with arthritis, for the presence of the cytokine leukemia inhibitory factor (LIF).Methods. SF from 152 subjects was examined for LIF, using a radioreceptor competition assay.Results. LIF was present at concentrations of 1–43 ng/ml in the SF of 23% of patients with rheumatoid arthritis (RA) or other inflammatory or infectious arthritides but in only 1 of 29 patients with osteoarthritis (P < 0.01). In the RA patients, the SF LIF concentration correlated significantly with the peripheral blood white blood cell count (WBC) (P < 0.05) and the SF WBC count (P < 0.01), but not with other clinical or radiologic parameters of disease activity or progression.Conclusion. LIF is implicated as a potential mediator of the local or systemic inflammatory response or the joint destruction seen in inflammatory arthritis.
Characterization of gangliosides from normal and osteoarthritic human articular cartilage
Authors: David Marie Jeanne , Portoukalian Jacques , Rebbaa Abdeladi , Vignon Eric , Carret Jean‐Paul , Richard Michel 
Published: February 2007

AbstractObjective. Glycosphingolipids (GSLs) are biologically active molecules in the physiology and pathology of cells. Since changes in GSLs might be associated with the impaired metabolism of articular cartilage in osteoarthritis (OA), we investigated gangliosides from normal and OA human cartilage.Methods. OA and control cartilage was obtained from patients with hip OA and femoral neck fracture, respectively. Gangliosides were extracted and quantified by determining their lipid‐bound sialic acid concentration. Major gangliosides were identified by immunodetection on thin‐layer plates, purified by high performance liquid chromatography, and analyzed for their carbohydrate, fatty acid, and long‐chain base composition.Results. The total ganglioside content of OA cartilage was decreased by 40% (per mg of DNA). Major gangliosides, GM3 and GD3, separated into 3 on thin‐layer chromatography bands. All were decreased except for the lowest migrating band of GM3, which was increased 5‐fold. This ganglioside had the same carbohydrate moiety and fatty acids as the other two, but differed by a long‐chain base composed mainly of C20‐sphingosine.Conclusion. OA cartilage is characterized by a decrease in all gangliosides except GM3, which demonstrates a large increase in the lowest band. These results indicate that there are changes in the biochemical composition of chondrocyte membranes in OA. The causes and roles of these changes remain to be determined.
Autoantibodies to hmg‐17 nucleosomal protein in autoimmune rheumatic diseases
Authors: Tzioufas Athanasios G. , Boumba Vassiliki A. , Seferiadis Konstantin , Tsolas Orestes , Moutsopoulos Haralampos M. 
Published: February 2007

AbstractObjective. Previous studies have shown that serum from patients with systemic lupus erythematosus (SLE) contains antibodies directed against HMG‐17, a nucleosomal nonhistone high mobility group (HMG) protein found in chromatin. The aim of the present study was to investigate any associations between the presence of antibodies to HMG‐17 and clinical and serologic features of SLE.Methods. Using porcine thymus as a source, HMG‐17 was purified by Sephacryl S‐200 chromatography followed by high performance liquid chromatography. An enzyme‐linked immunosorbent assay utilizing the purified HMG‐17 as antigen was developed and was used to evaluate sera from patients with autoimmune rheumatic diseases, for the presence of autoantibodies.Results. Anti–HMG‐17 antibodies were found in the serum of 34.8% of the patients with SLE, compared with 11.5% of patients with primary Sjögren's syndrome, 4.4% of patients with rheumatoid arthritis, and 4.1% of normal blood donors. Analysis of the clinical features of SLE using 2 different lupus activity indices revealed that anti‐HMG‐17 antibodies were more frequently found in patients with active disease. A positive correlation was also observed between anti–HMG‐17 and anti‐dsDNA levels, and levels of both of these autoantibodies demonstrated a negative correlation with C4. Analysis of sequentially obtained serum samples from 4 SLE patients revealed that, in 2 patients, anti‐HMG‐17 levels fluctuated in parallel with both disease activity and anti‐dsDNA levels, and in the remaining 2, anti–HMG‐17 levels fluctuated in parallel with disease activity.Conclusion. Antibodies to HMG‐17 are found in patients with many different autoimmune rheumatic diseases, although they are more frequently observed in those with SLE. Their presence appears to be associated with lupus disease activity as well as with anti‐dsDNA and C4 levels.
Antibodies to vesicular stomatitis virus proteins in patients with systemic lupus erythematosus and in normal subjects
Authors: Hardgrave Kathy L. , Neas Barbara R. , Scofield R. Hal , Harley John B. 
Published: February 2007

AbstractObjective. To determine the presence of antibodies that bind vesicular stomatitis virus (VSV) proteins in systemic lupus erythematosus (SLE) patient sera, as well as to examine any relationship between antibodies binding the viral nucleocapsid (N) protein and anti‐Ro autoantibodies.Methods. Eighty SLE patient sera, 80 normal control sera, 47 rheumatic disease patient control sera, and 9 sera from Panamanian subjects (6 of whom were infected with VSV) were evaluated by immunoblot of purified VSV proteins.Results. Findings on immunoblots of the Panamanian subjects' sera were consistent with histories of endemic exposure to VSV, as determined by virus neutralization assays. Significantly different binding to viral proteins was seen in the group of 80 SLE patients compared with the normal control group and with the rheumatic disease control group, by a variety of measures. For example, most of the reactivity in the SLE patient sera included binding to the internal viral matrix (M) and N proteins, while the reactivity in the normal control sera was mostly against the surface viral glycoprotein (G) protein alone or the N protein alone. Within this SLE patient cohort, associations were found between binding to N protein and anti‐Ro precipitins and between binding to M protein and anti–nuclear RNP autoantibody precipitins.Conclusion. The data are consistent with the original specific hypotheses of a relationship between 60‐kd Ro autoantigenicity and VSV, as well as with the suggestion that a rhabdovirus may be important in SLE. They do not, however, make possible any conclusions concerning the role of rhabdoviruses in the development of SLE or of anti‐Ro autoimmunity.
Acetylation phenotypes and environmental chemical exposure of people with idiopathic systemic lupus erythematosus
Authors: Reidenberg Marcus M. , Drayer Dennis E. , Lorenzo Beverly , Strom Brian L. , West Suzanne L. , Snyder Ellen S. , Freundlich Bruce , Stolley Paul D. 
Published: February 2007

AbstractObjective. To test the hypotheses that there is an excess percentage of slow acetylators among patients with idiopathic systemic lupus erythematosus (SLE) and that these patients had excessive exposure to environmental amines and hydrazines before the onset of illness.Methods. Case–control study with structured interview and acetylation phenotyping.Results. No excess proportion of slow acetylators or environmental amine exposure was found.Conclusion. Slow acetylation phenotype and exposure to environmental amines are not principal causes of idiopathic SLE.
The synthetic retinoid (4‐hydroxyphenyl)retinamide decreases collagen expression in vitro and in the tight‐skin mouse
Authors: Delany Anne M. , Brinckerhoff Constance E. 
Published: February 2007

AbstractObjective. We documented the effect of the retinoid (4‐hydroxyphenyl)retinamide on collagen expression in a tissue culture and in an animal model of scleroderma.Methods. We used RNA analysis, chloramphenicol acetyltransferase assays, organ culture, and histologic evaluation.Results. We showed that (4‐hydroxyphenyl)retinamide decreases αl(I) collagen messenger RNA and transcription in cultured cells, and decreases collagen levels in the dermis of tight‐skin mice.Conclusion. These results provide a basis for further experiments to address the efficacy of (4‐hydroxyphenyl)retinamide in the treatment of scleroderma.