bluuebunny/crossref_metadata_2025_split huggingface dataset:
The mutations in the fibronectin gene described in japanese patients with systemic sclerosis are not present in dutch patients
Authors: Verheijen Ron , Oberyé Elna H. , van Venrooij Walther J. , van den Hoogen Frank H. J. 
Published: February 2007

AbstractRecently, a mutant fibronectin gene was identified in skin fibroblasts obtained from sclerotic lesions of 7 Japanese patients with systemic sclerosis (SSc). Two point mutations were found adjacent to the cell‐attachment tetrapeptide DNA sequence in exon 7 of the fibronectin gene. In the present study, we investigated whether these point mutations are present in the fibronectin gene of Dutch patients with SSc. We were unable to demonstrate the point mutations in the Dutch SSc patients studied.
Detection and quantification of human anti‐Sm antibodies using synthetic peptide and recombinant SmB antigens
Authors: Hines John J. , Elkon Keith B. , Danho Waleed 
Published: February 2007

AbstractAnti‐Sm–positive sera from patients with systemic lupus erythematosus (SLE) recognize a major epitope located within the carboxyl‐terminal 27 amino acids of a recombinant SmB fusion protein. To determine whether a synthetic peptide corresponding to this region could be used as an antigen to detect anti‐Sm antibodies, sera were typed as anti‐Sm positive or anti‐Sm negative by counterimmunoelectrophoresis (CIE). Twenty‐three SLE sera that were anti‐Sm positive by CIE, 22 that were anti‐Sm negative by CIE, and 42 sera from patients with other autoimmune diseases were tested for anti‐Sm antibodies by enzyme‐linked immunosorbent assay (ELISA), using either the synthetic peptide (C27) or a recombinant SmB (rSmB) fusion protein as the antigen. More than 90% of the sera that were anti‐Sm positive by CIE were also positive by both the C27 and rSmB ELISAs, and an additional 2 SLE sera originally typed as anti‐Sm negative were found to be positive (1 by the C27 ELISA, 1 by the rSmB ELISA), due to the greater sensitivity of the ELISAs. In the rSmB ELISA, anti‐Sm antibodies were not detected in any of the sera from patients with other autoimmune diseases, whereas 3 patients with anti–U1 RNP antibodies (1 each with polymyositis, scleroderma, and mixed connective tissue disease) had a positive result in the C27 ELISA. These results indicate that both the C27 synthetic peptide and rSmB are excellent antigens for use in ELISAs to quantify anti‐Sm antibodies.
Increased interleukin‐2 production in response to human type I collagen stimulation in patients with systemic sclerosis
Authors: Hawrylko Eugenia , Mele Carol Ann , Spertus Arlene , Oster Neill , Frieri Marianne 
Published: February 2007

AbstractPeripheral blood mononuclear cells (PBMC) from patients with systemic sclerosis (SSc) produced increased amounts of interleukin‐2 (IL‐2), in a dose‐dependent manner, in response to stimulation with human type I collagen, whereas PBMC from normal subjects did not. At a dose of 50 μg human type I collagen/106 PBMC, PBMC from SSc patients (n = 17) produced 8 times as much IL‐2 as did PBMC from 16 normal subjects (P < 0.005) and 3 times as much as did PBMC from a group of 13 rheumatoid arthritis patients (P < 0.05). In contrast, IL‐2 production by PBMC after nonspecific stimulation with the mitogen, phytohemagglutinin, did not differ among the SSc, rheumatoid arthritis, and normal control groups. Cell depletion experiments indicated that the IL‐2‐producing cells in SSc patients are CD4+. Thus, SSc patients have CD4 cells that are specifically sensitized to human type I collagen and can produce increased levels of IL‐2. Measurement of IL‐2 production stimulated by human type I collagen may be useful in evaluating disease activity, and further investigation of this process may contribute to the delineation of the pathogenesis of SSc.
Acute familial myositis with a common autoimmune response
Authors: de la Torre Ignacio García , Ramírez‐Casillas Alberto , Hernández‐Vazquez Lourdes 
Published: February 2007

AbstractIn 1986, we diagnosed and treated 4 patients, all members of 1 rural family, who presented simultaneously with a polymyositis‐like syndrome, anticytoplasmic antibodies (on HEp‐2 cells), and precipitating antibodies of anti‐Jo‐1 and anti‐PM‐Scl specificities. Serum samples from these patients reacted by immunodiffusion against serum from a rodent that had been caught in the patients' house. The precipitin line showed complete immunologic identity with anti‐Jo‐1. To study the specificity of this serum‐serum reaction, 2 mice (Mus musculus) and 1 rat (Rattus rattus) from the neighboring areas of the patients' house were caught and killed. Sections of the liver, kidney, spleen, and skeletal muscle were processed for histopathologic examination and for direct and indirect immunofluorescence studies of the patients' sera. The rodents' sera were tested by immunodiffusion against serum samples from 25 patients with systemic lupus erythematosus, 11 with rheumatoid arthritis, 6 with mixed connective tissue disease, and 11 with various other rheumatic diseases, as well as 16 healthy controls. A serum‐serum precipitin reaction was noted between the rodents' sera and sera from 2 of the patients with polymyositis‐like syndrome. A distinct, but weaker, reaction was found with 2 lupus patients' sera (8%), and with 1 healthy control serum (6%). The rodents' sera were antinuclear antibody positive by indirect immunofluorescence on HEp‐2 cells. These results, suggest that some rodents could be carriers of an as‐yet‐unknown transmissible agent that, in susceptible individuals, induces clinical and serologic manifestations similar to those of polymyositis.
A pair of monozygotic twins who are concordant for myasthenia gravis but became discordant for systemic lupus erythematosus post‐thymectomy
Authors: Grinlinton Fiona M. , Lynch Nora M. , Hart Hamish H. 
Published: February 2007

AbstractWe describe a pair of monozygotic twins who are concordant for myasthenia gravis but discordant for systemic lupus erythematosus (SLE). SLE developed in twin 1 18 years post‐thymectomy and has been characterized by recurrent transverse myelitis and optic neuritis. Twin 2 remains well post‐thymectomy, except for a skin rash and persistent leukopenia. Both twins have developed autoimmune thyroid disease. We review genetic and environmental factors of importance in the pathogenesis of SLE and discuss the possible role of thymectomy in the etiology of the disease.
Regression of reactive systemic amyloidosis due to ankylosing spondylitis following the administration of colchicine
Authors: Escalante Agustin , Ehresmann Glenn R. , Quismorio Francisco P. 
Published: February 2007

AbstractWe describe a patient in whom nephrotic syndrome due to renal amyloidosis occurred 4 years into the course of severe ankylosing spondylitis with peripheral joint and extraarticular involvement. Treatment with colchicine was accompanied by reversal of proteinuria, and histologic regression of amyloid deposits was documented from bone marrow obtained from the femoral heads during total hip arthroplasties staged 1 year apart.
Occupation, income, and education as independent covariates of arthritis in four national probability samples
Authors: Leigh J. Paul , Fries James F. 
Published: February 2007

AbstractThe strong associations between education level and prevalence and severity of arthritis have recently been investigated, with some suggestion that the relationships might be causal. Data from 4 national probability samples were analyzed, in which occupation and income were measured currently and prior to the development of arthritis. These data indicate that previous studies overestimated the strength of the association between schooling and arthritis because income and, especially, occupation were not analyzed as separate covariates. The overestimate appears to be especially high for persons currently employed, for men, and for persons employed in dangerous jobs. Health policy strategies directed toward reducing arthritis rates require not simply a focus on education, but the additional socioeconomic status dimensions of income and occupational safety and health.
Phospholipase A2 is a Major Component of the Salt‐Extractable Pool of Matrix Proteins in Adult Human Articular Cartilage
Authors: Recklies Anneliese D. , White Chantal 
Published: February 2007

AbstractAdult human articular cartilage contains a component with an apparent molecular weight of 16 kd, which is extractable with high ionic strength buffers. This protein, which, in addition to lysozyme, is one of the most prominent components in salt extracts of adult cartilage, is not detectable in cartilage from newborns. We performed N‐terminal sequence analysis to identify the protein. The amino acid sequence obtained for the first 20 residues was identical to that reported for phospholipase A2 (PLA2) from human placenta and human synovial cells. The extractable PLA2 was found to be active. The lack of PLA2 in salt extracts from newborn cartilage observed by sodium dodecyl sulfate–polyacrylamide gel electrophoresis analysis was confirmed by the very low levels of PLA2 activity detectable in these preparations. PLA2 was clearly present in cartilage extracts from an 18‐year‐old subject and a 19‐year‐old subject, suggesting that its accumulation begins at some stage during the adolescent growth period. The enzyme does not appear to be released from cartilage matrix under normal physiologic conditions, and it is possible that the accumulation of PLA2 in maturing cartilage is a result of the decreased matrix turnover associated with the termination of skeletal growth. Whether PLA2 is active in the cartilage matrix, its precise localization, and its effects on the resident chondrocytes remain to be determined.
Correlation of Serum Interleukin‐6 Levels with Joint Involvement and Thrombocytosis in Systemic Juvenile Rheumatoid Arthritis
Authors: de Benedetti Fabrizio , Massa Margherita , Robbioni Piera , Ravelli Angelo , Burgio Giuseppe R. , Martini Alberto 
Published: February 2007

AbstractWe measured interleukin‐6 (IL‐6) levels in 70 serum samples obtained from 25 patients with systemic‐onset juvenile rheumatoid arthritis (JRA), using the hybridoma cell line B9. Patients with systemic‐onset JRA had significantly elevated serum IL‐6 levels during active disease (mean ± SD 92.1 ± 75.1 hybridoma growth factor units/ml; P < 0.00001 versus healthy age‐matched controls), but not during remission. Serum IL‐6 levels correlated with the extent and severity of joint involvement (P < 0.001) and with platelet counts (P < 0.05). Our data suggest that IL‐6 plays a significant role in the pathogenesis of systemic‐onset JRA.
Suppression of Collagen‐Induced Arthritis by Combination Cyclosporin a and Methotrexate Therapy
Authors: Brahn Ernest , Peacock Derek J. , Banquerigo Mona Lisa 
Published: February 2007

AbstractLouvain (LOU) rats were administered either methotrexate (MTX; 0.3 mg/kg/week or 0.8 mg/kg/week intraperitoneally), cyclosporin A (CSA; 4 mg/kg/day or 10 mg/kg/day continuous infusion via osmotic pump), or a combination of both agents. The rats were immunized with native type II collagen (CII) to determine the effects of these agents on collagen‐induced arthritis, an animal model of rheumatoid arthritis. A significant decrease in the incidence (P < 0.01) and severity of arthritis by clinical (P < 0.05) and radiographic assessments (P < 0.05) was found in recipients of combination therapy, compared with controls. Delayed‐type hypersensitivity reactions to CII were measured on day 26, and production of IgG antibody to CII was measured on days 7, 14, and 26. IgG antibody was evident by day 7, and titers were near‐maximal by day 14. Both delayed‐type hypersensitivity and antibodies to CII were reduced in animals that received the higher dosage of CSA. Liver, kidney, and spleen specimens obtained from rats treated with CSA and MTX demonstrated no histologic abnormalities on light microscopy, compared with controls. These studies indicate that CSA and MTX in combination is a safe and effective therapy for collagen‐induced arthritis and may be useful in the treatment of rheumatoid arthritis.
The Anticollagenolytic Potential of Lymecycline in the Long‐Term Treatment of Reactive Arthritis
Authors: Lauhio Anneli , Sorsa Timo , Lindy Otso , Suomalainen Kimmo , Saari Herkko , Golub Lorne M. , Konttinen YrjöT. 
Published: February 2007

AbstractObjective. We sought to determine the antiinflammatory properties of lymecycline in the long‐term treatment of reactive arthritis (ReA).Methods. Quantitative assay of collagenase activity by densitometry after sodium dodecyl sulfatepolyacrylamide gel electrophoresis.Results. Therapeutic levels of lymecycline do not directly inhibit the activity of human neutrophil interstitial collagenase, but can prevent the oxidative activation of latent human neutrophil collagenase.Conclusion. This non‐antimicrobial, anticollagenolytic property of lymecycline may contribute to its therapeutic efficacy in the treatment of patients with ReA.
Bone Marrow Changes in Adjuvant‐Induced and Collagen‐Induced Arthritis
Authors: Hayashida Kenji , Ochi Takahiro , Fujimoto Masahiro , Owaki Hajime , Shimaoka Yasunori , Ono Kero , Matsumoto Keishi 
Published: February 2007

AbstractObjective. To investigate the role of bone marrow in arthritis.Methods. Bone marrow changes over time were investigated in rats with adjuvant‐induced and collagen‐induced arthritis, using bioassay techniques and histologic analysis.Results. In both animal models, bone marrow interleukin‐1 and interleukin‐6 activity began to rise before the onset of arthritis and increased in relation to the progression of arthritis. Enhanced myelopoiesis in the bone marrow was noted in conjunction with the increased cytokine activity.Conclusion. Bone marrow changes such as those demonstrated in this study may be common to various models of induced arthritis and may have an important role in the pathogenesis of this disease.
Novel genetic markers of rheumatoid arthritis in chilean patients, by dr serotyping and restriction fragment length polymorphism analysis
Authors: González Alfonso , Nicovani Sandra , Massardo Loreto , Bull Paulina , Rodríguez Luis , Jacobelli Sergio 
Published: February 2007

AbstractObjective. The analysis of genetic markers of rheumatoid arthritis (RA) in a population in which the DR4 serotype is not strongly associated with the disease.Methods. Chilean RA patients (56 seropositive and 22 seronegative) and 141 controls were studied by serotyping. Southern blot analysis of Bam HI restriction fragment length polymorphism (RFLP) was done in genomic DNA from 46 patients with seropositive RA, 17 patients with seronegative RA, and 45 controls, using a complementary DNA probe specific for DRB1 genes.Results. The prevalence of the HLA—DR9 haplotype was strikingly higher in seropositive RA patients (21%) than in controls (3%) (Pcorr < 0.0008, by Fisher's exact test; relative risk [RR] = 9.34). The prevalence of DR4 and DR1 haplotypes, although slightly increased, did not achieve a significant preponderance. The simultaneous presence of two Bam HI fragments (3.6 kb and 4.5 kb) was found with higher prevalence in seropositive patients (83%; RR = 9; Pcorr < 0.00002) than in controls (36%), and seemed higher in seronegative RA patients as well (71%; RR = 4). Furthermore, its prevalence remained increased in comparisons of DR4 positive controls (36%) with DR4 positive seropositive patients (100%; RR = 67; Pcorr < 0.0002) and DR4 positive seronegative patients (100%; RR = 36; Pcorr < 0.006), even after excluding the DR9 positive individuals. A tendency toward higher association with DR1 seropositive RA patients (67%; RR = 12), a group with no DR4 or DR9 positive individuals, than in DR1 positive controls (14%), was also observed.Conclusion. The HLA—DR9 haplotype was definitively consolidated as a very strong genetic marker exclusively for seropositive RA in Chilean patients, as suggested by our previous observations. RFLP analysis showed that the simultaneous presence of 3.6‐kb and 4.5‐kb Bam HI fragments constituted a better RA marker than did any of the heretofore studied haplotypes. These fragments together would be linked to RA independently of the DR1, DR4, and DR9 haplotypes. The overall evidence indicates that Chilean seropositive RA patients display a genetic background that is different from that underlying RA susceptibility in other populations and suggests the existence of common, as well as distinct, genetic elements predisposing to seronegative and seropositive RA.
Impairment of osteophyte formation in hyperglycemic patients with type II diabetes mellitus and knee osteoarthritis
Authors: Horn Claire A. , Bradley John D. , Brandt Kenneth D. , Kreipke Donald L. , Slowman Sally D. , Kalasinski Lorrie A. 
Published: February 2007

AbstractObjective. Since insulin is a potent growth factor for connective tissue, the present study was designed to investigate whether radiographic features of knee osteoarthritis (OA) in patients with poorly controlled, insulin‐resistant type II diabetes mellitus differ from those in nondiabetic controls with knee OA.Methods. Radiographs from 25 female patients with diabetes and knee OA were compared with those from 48 female controls who were similar with respect to age, weight, and duration of OA symptoms.Results. Although the 2 groups were similar with respect to the frequency and severity of joint space narrowing, subchondral sclerosis, and geodes, osteophytes were less common in the patients with diabetes (P = 0.044), and spurring, when present, tended to be ‘marked’ less often in the diabetic patients than in the controls.Conclusion. The data suggest that diminished availability of insulin at the cellular level or diabetic microvascular disease attenuates the chondro‐ and osteogenesis required for osteophyte formation in the joints of patients with OA.
Barriers to return to work among persons unemployed due to arthritis and musculoskeletal disorders
Authors: Straaton Karin V. , Maisiak Richard , Wrigley J. Michael , White Mary B. , Johnson Philip , Fine Philip R. 
Published: February 2007

AbstractObjective. To identify barriers to return to work (RTW) among persons likely to be seen in a clinician's practice who are unemployed due to arthritis and musculoskeletal disorders.Methods. Two hundred eighteen persons unemployed due to arthritis and musculoskeletal disorders were interviewed at baseline and followed up for 1 year, at which time their work status was ascertained. Backward stepwise logistic regression was used to determine the association of baseline clinical, sociodemographic, and work‐related factors to their work status at 1 year of followup.Results. Fifty‐one (24%) of 216 initially unemployed subjects had returned to permanent paid employment of ≥20 hours/week after 1 year. Having rheumatoid arthritis, Social Security Disability Insurance (SSDI) status, a high pain level, older age, and lower education were barriers to reemployment.Conclusion. This study establishes the importance of chronic pain and having rheumatoid arthritis as factors independently associated with failure to RTW among persons unemployed due to arthritis and musculoskeletal disorders. The importance of SSDI beneficiary status, age, and education level in RTW is further confirmed. Duration of unemployment or previous work factors were not predictors of RTW in this group.
Responsiveness of human T lymphocytes to bacterial superantigens presented by cultured rheumatoid arthritis synoviocytes
Authors: Tsai Carlene , Diaz Luis A. , Singer Nora G. , Li Lan Lan , Kirsch Anita H. , Mitra Raj , Nickoloff Brian J. , Crofford Leslie J. , Fox David A. 
Published: February 2007

AbstractObjective. Type B fibroblastic synoviocytes are abundant in inflamed joints of patients with rheumatoid arthritis (RA), and can secrete cytokines and other mediators of inflammation. The aim of this study was to determine whether cell lines derived from RA type B synoviocytes could also serve as accessory cells for T lymphocyte activation.Methods. Cells from RA synoviocyte lines, with or without preculture in interferon‐γ (IFNγ), were cultured with purified peripheral blood T cells, in the presence or absence of superantigens or other accessory cell–dependent T cell mitogens. T cell proliferation was measured by thymidine incorporation, and synoviocyte surface markers were analyzed by flow cytometry.Results. RA type B synoviocyte lines were potent accessory cells for T cell responses to bacterial superantigens or lectins, and direct cell‐cell contact was required. Preculture in IFNγ augmented synoviocyte expression of major histocompatibility complex (MHC) class II molecules and of ligands for some T cell costimulatory receptors, but synoviocyte accessory cell function was evident even in the absence of IFNγ. Blocking studies using monoclonal antibodies supported the notion of a role for CD2, CD11a/CD18 and MHC class II molecules in synoviocyte‐dependent T cell activation. Monoclonal antibodies against IFNγ, interleukin‐1β (IL‐1β), IL‐6, IL‐8, and tumor necrosis factor α failed to block the T cell proliferative responses, but anti–IL‐2 was strongly inhibitory.Conclusion. Cultured RA type B synoviocytes can perform some of the functions of professional antigen‐presenting cells. If such cells have similar properties in vivo, they may be important participants in activation of immune responses, in addition to their previously described synthetic and proinflammatory roles. If RA synovial tissue T cells, like normal peripheral blood T cells, can respond to superantigens presented by synoviocytes, this interaction could be important in the pathogenesis of RA.
Activation of transcription factor NF‐κB in human synovial cells in response to tumor necrosis factor α
Authors: Fujisawa Koushi , Aono Hiroyuki , Hasunuma Tomoko , Yamamoto Kazuhiko , Mita Shiro , Nishioka Kusuki 
Published: February 2007

AbstractObjective. To examine whether nuclear factor κB (NF‐κB) is activated in cultured synovial cells in response to tumor necrosis factor α (TNFα) and to investigate the correlation between NF‐κB activation and synovial cell proliferation.Methods. Activation of NF‐κB was detected by electrophoretic mobility shift assay. The transcription of several NF‐κB–dependent genes was evaluated by reverse transcriptase polymerase chain reaction and transient expression assay using human immunodeficiency virus–long terminal repeat chloramphenicol acetyltransferase. Proliferative activity was determined by measurement of 3H‐thymidine incorporation.Results. Stimulation of synovial cells with TNFα activated NF‐κB and subsequent transcription of several genes. Treatment of synovial cells with N‐acetyl‐L‐cysteine (NAC), an antioxidant agent, inhibited TNFα‐induced NF‐κB activation and transcription. Moreover, NAC also inhibited synovial cell proliferation induced by TNFα.Conclusion. Our results suggest that NF‐κB plays a pivotal role in synovial cell activation by TNFα. Thus, suppression of NF‐κB could be a potential therapeutic modality for synovitis such as that of rheumatoid arthritis.