bluuebunny/crossref_metadata_2025_split huggingface dataset:
Gouty arthritis in the acquired immunodeficiency syndrome
Authors: Disla Eddys , Stein Scott , Acevedo Mabel , Cuppari Girolamo 
Published: February 2007

AbstractPatients with the acquired immunodeficiency syndrome (AIDS) are characteristically hypouricemic. Therefore, the occurrence of gouty arthritis in association with AIDS would be expected to be a rare phenomenon. We describe a patient with AIDS in whom gouty arthritis developed. Features of both diseases in relation to their coexistence in this patient are discussed.
Every‐other‐week methotrexate in patients with rheumatoid arthritis
Authors: Kremer Joel M. , Davies Joanna M. S. , Rynes Richard I. , Fink Steven , Lawrence David A. , Petrillo Gayle F. , Mullaly Patrick M. 
Published: February 2007

AbstractObjective. To determine if patients with rheumatoid arthritis (RA) that is stable with weekly methotrexate (MTX) therapy could be switched to an every‐other‐week regimen of MTX.Methods. Forty‐seven patients with classic or definite RA who had received MTX for at least 8 months were studied. Clinical measurements consisted of the number of tender and swollen joints, physician and patient global evaluation of disease activity on a 5‐point scale, grip strength, patient evaluation of pain, morning stiffness, and the interval to onset of fatigue from time of awakening. Laboratory measures included the erythrocyte sedimentation rate (ESR), rheumatoid factor, C‐reactive protein (CRP), and baseline serum folate levels. Uptake of MTX was measured with tritiated thymidine from peripheral blood mononuclear cells (PBMC) from patients ex vivo. Serum measures of interleukin‐1β (IL‐1β), IL‐6, and tumor necrosis factor α (TNFα) were performed in sera, and TNFα was also measured on PBMC supernatants.Results. Twelve of the 23 patients receiving every‐other‐week MTX (52%) were able to complete 6 months of this treatment without experiencing a disease flare. Eleven of the 23 patients receiving every‐other‐week MTX (48%) withdrew from the study before completing 6 months of treatment, because of a flare. No significant differences in clinical or laboratory parameters were seen when the 24 patients receiving weekly MTX were compared with the 12 patients in the every‐other‐week MTX group who successfully completed 6 months of the study. None of the changes in serum cytokine levels were significantly different between the patients receiving MTX weekly versus those receiving it every other week, and changes in ESR and CRP did not differ between groups. Age, sex, RA disease duration, MTX weekly dose or duration, baseline joint counts, or serum folate status did not predict a flare. Tritiated MTX uptake did not differ between groups.Conclusion. Some patients with RA that is stable on weekly dosing are able to change to every‐other‐week dosing without experiencing a flare in their disease activity.
Sulfasalazine in the treatment of spondylarthropathy
Authors: Dougados Maxime , Linden Sjef VAN DER , Leirisalo‐Repo Marjatta , Huitfeldt Bernhard , Juhlin Roger , Veys Eric , Zeidler Henning , Kvien Tore K. , Olivieri Ignazio , Dijkmans Ben , Bertouch Jim , Brooks Peter , Edmonds John , Major Gabor , Amor Bernard , Calin Andrei 
Published: February 2007

AbstractObjective. To assess the efficacy and tolerability of sulfasalazine (SSZ) in the treatment of spondyl‐arthropathy.Methods. We conducted a 6‐month randomized, placebo‐controlled, double‐blind, multicenter study of patients with spondylarthropathy whose disease had remained active despite treatment with nonsteroidal antiinflammatory drugs. Patients were treated with SSZ (3 gm/day) or placebo. The primary efficacy variables were the physician's and patient's overall assessments, pain, and morning stiffness. End points were analyzed in the intent‐to‐treat and completer patient populations; the time course of effect was analyzed in the completer patient population.Results. Of the 351 patients enrolled, 263 (75%) completed the 6‐month treatment period. The withdrawal rates were 35 (20%) and 53 (30%) in the placebo and SSZ groups, respectively. In the intent‐to‐treat analysis of end point efficacy, the between‐treatment difference reached statistical significance only for 1 of the 4 primary outcome variables, the patient's overall assessment of disease activity, for which 60% of the patients taking SSZ improved by at least 1 point on a 5‐point scale, in contrast to 44% of the patients taking placebo. Laboratory markers of inflammation also showed statistically significant change in favor of SSZ. In subgroup analysis, the most impressive effects were seen in patients with psoriatic arthritis, both for the 4 primary efficacy variables and for secondary efficacy variables such as the number of inflamed joints. Adverse events were more frequent in the SSZ group than the placebo group, but all were transient or reversible after cessation of treatment.Conclusion. The results of this study show that SSZ had greater efficacy than placebo in the treatment of active spondylarthropathy, notably in patients with psoriatic arthritis.
Monoclonal antibodies that detect biochemical markers of arthritis in humans
Authors: Slater Robert R. , Bayliss Michael T. , Lachiewicz Paul F. , Visco Denise M. , Caterson Bruce 
Published: February 2007

AbstractObjective. To evaluate the potential of using monoclonal antibodies (MAb) 3‐B‐3(–) and 7‐D‐4 to detect biochemical markers of altered cartilage metabolism in human arthritides.Methods. Fifty‐five samples of normal articular cartilage (subjects' age range 18 weeks of gestation to 83 years of age) and 89 samples of arthritic cartilage (patients' age range 20–81 years) were collected, and their proteoglycans were extracted and analyzed for the presence of the epitopes recognized by MAb 3‐B‐3 and 7‐D‐4.Results. Native 3‐B‐3(–) mimotope was expressed at a high incidence in proteoglycans extracted from the cartilage of patients with most of the arthritic diseases examined (osteoarthritis, juvenile rheumatoid arthritis, rheumatoid arthritis, avascular necrosis, and degenerative meniscal tears). Its expression in normal cartilage specimens was very low or absent, occurring mainly in the young, skeletally immature individuals. In contrast, expression of the 7‐D‐4 epitope was more variable in patients with different arthritides and was also frequently found in normal cartilage specimens. Immunohistochemical analyses with both 3‐B‐3(–) and 7‐D‐4 showed strong focal positive staining in superficial areas, where cartilage degeneration, remodeling, and repair were greatest.Conclusion. The biochemical markers recognized by MAb 3‐B‐3(–) and 7‐D‐4 are indicative of altered proteoglycan synthesis and metabolism in human articular cartilage. The data suggest that in human cartilage, the 3‐B‐3(–) epitope might be a better marker of biochemical changes than the 7‐D‐4 epitope.
Large and small proteoglycans of osteoarthritic and rheumatoid articular cartilage
Authors: Cs‐Szabó Gabriella , Roughley Peter J. , Plaas Anna H. K. , Glant Tibor T. 
Published: February 2007

AbstractObjective. To identify characteristic changes in large aggregating (aggrecan) and small proteoglycan (PG) populations in articular cartilages during osteoarthritis (OA) and rheumatoid arthritis (RA).Methods. Aggrecan populations in guanidine extracts of femoral condylar cartilages of 46 OA and 8 RA patients who underwent total knee arthroplasty, as well as of 2 fetuses and 6 normal adults, were separated in agarose‐polyacrylamide composite gels. Small PGs (biglycan, decorin, and fibromodulin) in the same extracts were analyzed in 12% polyacrylamide gels. Gels were stained or electrophoretically transferred and probed with antibodies to aggrecan epitopes and to small PGs. Epitope contents of the samples were also compared by inhibition radioimmunoassay.Results. There were significant differences found among normal and diseased samples in their electrophoretic mobilities, band distributions, and antibody staining. OA and especially RA samples were heavily degraded, lacked certain aggrecan populations, and contained fewer keratan sulfate and chondroitin‐6‐sulfate epitopes compared with normal samples. Levels of chondroitin‐4‐sulfate and “fetal‐type” epitopes were elevated in the OA samples compared with the normal ones. More core proteins of small PGs were found in diseased than in normal cartilages, but they were more heterogeneous in size and glycosaminoglycan substitution.Conclusion. There is extensive degradation of both large and small PGs in diseased cartilages, but a repair process does exist, especially in OA cartilages. Chondrocytes of diseased cartilages are able to synthesize fetal‐type aggrecans. Small PGs are glycosylated differently in diseased cartilages than in normal ones.
Susceptibility to reiter's syndrome is associated with alleles of tap genes
Authors: Barron Karyl S. , Reveille John D. , Carrington Mary , Mann Dean L. , Robinson Mary Ann 
Published: February 2007

AbstractObjective. Although HLA–B27 is strongly associated with susceptibility to Reiter's syndrome (RS), recent data suggest that an additional modifying or susceptibility gene(s) acts in concert with HLA–B27 to contribute to disease pathogenesis. The recently described TAP genes (transporters associated with antigen processing) are potential candidates because they are polymorphic and their function is to transport antigenic peptides to be loaded in HLA class I molecules.Methods. TAP1 and TAP2 alleles were determined for 34 patients with RS (28 HLA–B27 positive, 6 HLA–B27 negative), and their frequencies were compared with those observed for 52 HLA–B27 positive and 80 random disease‐free control subjects.Results. The allele frequency of TAP1C was greater in patients with RS (8 of 62, 13%) than in random controls (5 of 160, 3%) (P = 0.009). The frequency of TAP2A was greater in RS patients (51 of 66,77%) than in random controls (88 of 160, 55%) (P = 0.002); likewise, the frequency was greater in HLA–B27 positive RS patients (41 of 54, 76%) than in HLA–B27 positive disease‐free controls (49 of 94, 52%) (P = 0.004). Furthermore, the TAP2A allele was present in all RS patients (100%), whereas TAP2A was present in 79% (63 of 80) of the random controls (P = 0.003).Conclusion. The association observed between TAP alleles and RS is independent of the presence of HLA–B27, and despite the physical proximity of TAP and HLA class II genes, linkage disequilibrium does not account for the observed associations between TAP and RS. Thus, TAP genes are genetically separated but functionally linked to class I genes, and both contribute to susceptibility to RS.
Distinct oligosaccharide content of rheumatoid arthritis‐derived immune complexes
Authors: Bond Angela , Kerr Michael A. , Hay Frank C. 
Published: February 2007

AbstractObective. To investigate the association between glycosylation and immune complex formation in various disease groups.Methods. Immune complexes and IgG were isolated from serum and their carbohydrate content evaluated in a dot‐blot assay using specifically binding lectins.Results. Significantly more N‐acetylglucosamine was detected in complexes from patients with rheumatoid arthritis (RA) than in those from patients with systemic lupus erythematosus, Crohn's disease, or infectious endocarditis, or from normal controls (P < 0.001). The immune complex concentration in the circulation was strongly associated with N‐acetylglucosamine levels (P < 0.001 by chi‐square analysis).Conclusion. The composition of immune complexes from RA patients is distinct in carbohydrate content from those found in other disease groups.
The role of nitric oxide in lipoxin A4‐induced polymorphonuclear neutrophil‐dependent cytotoxicity to human vascular endothelium in vitro
Authors: Bratt Johan , Gyllenhammar Hans 
Published: February 2007

AbstractObjective. To assess the mechanism for the cytotoxicity of human polymorphonuclear neutrophils (PMN) to human umbilical vein endothelial cells (HUVEC) induced by the 5‐ and 15‐lipoxygenase product of arachidonate, lipoxin A4 (LXA4), and the phorbol ester, phorbol myristate acetate (PMA).Methods. HUVEC were grown to confluence and labeled with 51Cr. PMN and stimuli were added, and the release of 51Cr into supernatants was assessed after 4 hours.Results. Both LXA4 and PMA conferred highly significant PMN‐dependent cytolysis. The cytotoxicity activated by LXA4 was inhibited by NG‐monomethyl‐L‐arginine (L‐NMA) and by nitro‐L‐arginine methyl ester, specific inhibitors of the nitric oxide (NO)‐producing enzyme NO synthase. Also, the scavenger of extracellular NO, oxyhemoglobin (HbO2), prevented LXA4‐induced cytolysis in a dose‐dependent manner. In sharp contrast, L‐NMA did not significantly affect the cytolysis induced by PMA. whereas HbO2 showed a modest inhibitory action. In experiments without PMN, addition of the NO donor S‐nitroso‐N‐acetyl‐penicillamine to HUVEC induced marked cytolysis, which was inhibited by HbO2, but not by L‐NMA. Addition of L‐arginine or arginine analogs did not affect superoxide anion production in a cell‐free hypoxanthine/xanthine oxidase system. Both LXA4 and PMA induced the production of superoxide anion from PMN and of NO from HUVEC.Conclusion. NO produced by HUVEC, interacting with PMN which produce superoxide anions, is of marked significance for the endothelial cell damage in this in vitro model of vasculitis. This is probably due to the subsequent formation, via a radical‐radical interaction between NO and ·O2‐, of cytotoxic products, such as peroxynitrite and its metabolites. Furthermore, although LXA4 and PMA induced comparable cytolysis at optimal concentrations, the relative importance of NO compared with other mechanisms mediating cytotoxicity was stimulus dependent, and NO was relatively more important for LXA4‐induced PMN‐dependent endothelial injury.
Autoimmune response to the spliceosome
Authors: Hassfeld Wolfgang , Steiner GÜNter , Studnicka‐Benke Andrea , Skriner Karl , Graninger Winfried , Fischer Inge , Smolen Josef S. 
Published: February 2007

AbstractObjective. To assess the significance of autoantibodies to RA33, the A2 protein of the heterogeneous nuclear ribonucleoproteins (hnRNP), and to the related hnRNP proteins A1, B1, and B2 in rheumatic diseases.Methods. Using a partially purified preparation of hnRNP‐A and hnRNP‐B proteins, sera from 303 patients with various rheumatic diseases were investigated by immunoblotting. For the analysis of crossreactivities, autoantibodies were affinity purified by blot elution.Results. Anti‐A2/RA33 was found in 35% of rheumatoid arthritis (RA) patients, 38% of mixed connective tissue disease (MCTD) patients, 23% of systemic lupus erythematosus (SLE) patients, and, apart from single exceptions, not in patients with other rheumatic diseases. All anti‐A2/RA33‐positive sera were also reactive with B1 and B2, and anti‐A2/RA33 antibodies cross‐reacted with both proteins. Antibodies to hnRNP‐A1 were found less frequently; moreover, the majority of anti‐A1‐positive sera also contained anti‐A2/RA33 antibodies. In anti‐A1, anti‐A2/RA33 doublepositive sera, cross‐reactivity between the 2 antibodies was generally observed. In SLE patients, the presence of anti‐A2/RA33 was correlated with the presence of anti‐(U1) small nuclear RNP (snRNP) and anti‐Sm (P < 0.0001 and P < 0.005, respectively), but there was no evidence for cross‐reactivity between antibodies to hnRNP and antibodies to snRNP antigens.Conclusion. Since both hnRNPs and snRNPs are essential components of the spliceosome, the data show that the immune systems of patients with RA, SLE, and MCTD react to this functional complex. However, compared with MCTD and SLE patients, RA patients have a more restricted immune response to the spliceosome: they react to hnRNP proteins, particularly to hnRNP‐A2/RA33, but not to snRNPs.
The role of hla antigens as indicators of disease progression in psoriatic arthritis
Authors: Gladman Dafna D. , Farewell Vernon T. 
Published: February 2007

AbstractObjective. To identify HLA markers for the development of severe disease in psoriatic arthritis (PsA).Methods. Patients with PsA who were followed up prospectively over a 14‐year period were included. Clinical and laboratory assessments of both active inflammation and clinical damage were performed at 6‐month intervals according to a standard protocol, which also included serologic HLA typing for class I and II antigens. Progression of damage was defined as transition into higher damage states, defined by the number of damaged joints. Both univariate and multivariate models were developed to identify predictors for progression of damage.Results. Univariate analysis revealed that the HLA antigens B27, B39, and DQw3 were associated with disease progression, while HLA‐DR7 was “protective.” The best multivariate model identified the HLA antigens B27, when DR7 was present, and DQw3, when DR7 was not present, as predicting disease progression across all transitions, while HLA‐B39 was associated with progression in early disease. The addition of these HLA indicators to a model containing clinical variables resulted in a significant improvement in fit.Conclusion. The HLA antigens associated with PsA, B27 and B39, are risk factors for disease progression, as is the HLA class II antigen DQw3. In combination with clinical measures of disease, these HLA variables are the dominant predictors of progression.
Joint space measurement in hand radiographs using computerized image analysis
Authors: James Michael F. , Heald Geoff , Shorter John H. , Turner Robert A. 
Published: February 2007

AbstractObjective. To compare computerized joint space (JS) measurements with conventional joint space narrowing (JSN) scores in patients with mild rheumatoid arthritis.Methods. Serial paired hand and wrist radiographs from 34 patients with classic rheumatoid arthritis were evaluated. Purpose‐written software automatically measured the JS on test images and standard clinical hand radiographs; JSN was scored “blind” by 6 observers.Results. The software proved reliable. JS values differed significantly (men > women; metacarpophalangeal > proximal interphalangeal joints), declining with disease duration more than with age; JSN scores correlated poorly and varied more.Conclusion. Computerization permits sensitive JS measurement and should be of benefit in studies of early joint disease.
Autoantibodies to pyruvate dehydrogenase complex in patients with systemic sclerosis
Authors: Fujimoto Manabu , Sato Shinichi , Ihn Hironobu , Kikuchi Kanako , Tamaki Kunihiko , Takehara Kazuhiko 
Published: February 2007

AbstractObjective. To determine the prevalence and clinical significance of anti‐pyruvate dehydrogenase complex (anti‐PDC) antibodies in systemic sclerosis (SSc).Methods. Serum samples from patients with limited cutaneous SSc (n = 81) or diffuse cutaneous SSc (n = 63) were examined for anti‐PDC antibodies by enzyme‐linked immunosorbent assay (ELISA) and immunoblotting.Results. IgG‐ and/or IgM‐isotype anti‐PDC antibodies were demonstrated by ELISA in 26 of 144 patients with SSc (18%). By immunoblotting, 19 patients had IgG anti‐PDC antibodies. Among these patients with IgG anti‐PDC antibodies, antibody to the E1α subunit was significantly associated with the presence of laboratory abnormalities typical of primary biliary cirrhosis (PBC).Conclusion. Antibody to the E1α subunit of PDC may be a serologic indicator for the development of PBC in patients with SSc.
Identification of col2a1 gene mutations in patients with chondrodysplasias and familial osteoarthritis
Authors: Ritvaniemi Pertti , Körkkö Jarmo , Bonaventure Jacky , Vikkula Miikka , Hyland James , Paassilta Petteri , Kaitila Ilkka , Kääriäinen Helena , Sokolov Boris P. , Hakala Markku , Mannismäki Pertti , Meerson Elena M. , Klemola Tero , Williams Charlene , Peltonen Leena , Kivirikko Kari I. , Prockop Darwin J. , Ala‐kokko Leena 
Published: February 2007

AbstractObjective. To use a recently developed procedure for analysis of blood leukocyte DNA to detect mutations in the gene for type II procollagen (COL2A1) in patients with cartilage diseases ranging from early‐onset familial osteoarthritis (OA) to lethal chondrodysplasias.Methods. The technique of denaturing gradient gel electrophoresis was used to scan polymerase chain reaction (PCR) products from 45 exons and exonflanking sequences of the COL2A1 gene in more than 70 patients with cartilage diseases whose severity ranged from mild to lethal. PCR products with abnormal migrations were then sequenced.Results. Among the 3 patients with lethal hypochondrogenesis who were analyzed, all 3 were found to have a mutation in the COL2A1 gene. Among 17 patients with spondyloepiphyseal or spondyloepimetaphyseal dysplasia, 2 well‐defined and 2 probable mutations were found. Among 15 patients with the Wagner‐Stickler syndrome, 2 well‐defined and 2 probable mutations were found. Among 45 patients with early‐onset familial OA, 1 probable mutation was found.Conclusion. Using the procedure developed for analysis of the COL2A1 gene, mutations were detected in >20% of patients with chondrodysplasias and up to 2% of patients with early‐onset familial OA. However, these percentages are only minimal estimates because all possible mutations in the gene cannot be detected with this procedure.
Increased susceptibility to oxidation of low‐density lipoproteins isolated from patients with systemic sclerosis
Authors: Bruckdorfer K. Richard , Hillary Janet B. , Bunce Tim , Vancheeswaran Rama , Black Carol M. 
Published: February 2007

AbstractObjective. To examine the resistance to oxidation of low‐density lipoproteins (LDL) from patients with systemic sclerosis (SSc) and primary Raynaud's phenomenon (RP) compared with healthy controls.Methods. Plasma LDL were isolated from patients with diffuse cutaneous and limited cutaneous SSc (dcSSc and lcSSc, respectively), patients with primary RP, and healthy control subjects. The lipoproteins were assessed for their resistance to oxidation in the presence of cupric ions, using spectrophotometric assays.Results. LDL from patients with dcSSc and lcSSc were more susceptible to oxidation than were those from healthy control subjects or patients with RP.Conclusion. Our findings suggest that free radicals may play a role in the pathology of SSc.
A human monoclonal antiphospholipid antibody that is representative of serum antibodies and is germline encoded
Authors: Harmer Ian J. , Loizou Sozos , Thompson Keith M. , So Alex K. L. , Walport Mark J. , Mackworth‐Young Charles 
Published: February 2007

AbstractObjective. To investigate the origins of antiphospholipid antibodies associated with thrombosis and other disorders that are found in patients with systemic lupus erythematosus and primary antiphospholipid syndrome (APS).Methods. Characterization, idiotypic study, and nucleotide sequencing of a human monoclonal antiphospholipid antibody generated from a patient with primary APS. Identification of the germline genes from which the antibody is derived.Results. A human monoclonal antibody, BH1, was generated. This antibody has ligand‐binding properties that closely resemble those of the serum antiphospholipid antibodies found in our patient and in other individuals with APS: it recognizes negatively charged phospholipids, and has lupus anticoagulant activity; it does not bind to neutral phospholipids, or to singlestranded or double‐stranded DNA. The relevance of BH1 to the patient's serum antibodies is supported by our idiotypic studies. BH1 is encoded by a new germline VH gene, and by a λ light chain gene that displays >99% homology with the VλIII.1 germline gene.Conclusion. Serum antiphospholipid antibodies associated with thrombosis may be encoded by either germline or only slightly mutated variable‐region genes.