bluuebunny/crossref_metadata_2025_split huggingface dataset:
Antibodies to type II collagen in early rheumatoid arthritis. Correlation with disease progression
Authors: Cook Andrew D. , Rowley Merrill J. , Mackay Ian R. , Gough Andrew , Emery Paul 
Published: February 2007

AbstractObjective. To establish that frequencies and levels of IgG antibodies to type II collagen are higher in early rheumatoid arthritis (RA), and to correlate these results with disease activity.Methods. Forty‐four patients were characterized as having early RA. Patient sera obtained at initial presentation and at 12 months were tested by enzyme‐linked immunosorbent assay for IgG antibodies to native and denatured type II collagen.Results. IgG antibodies to native and denatured type II collagen were detected at initial presentation in 27% and 82% of patients, respectively, and after 12 months in 14% and 50%, respectively. The presence of antibodies to native collagen was associated with activity of RA and severity of symptoms, and loss of antibodies at 12 months was associated with initially erosive RA and the DRB1 disease susceptibility motif.Conclusion. Levels of serum IgG antibodies to collagen in RA decrease over time and, therefore, are not attributable simply to cartilage destruction. The presence of early positivity for these antibodies, together with the RA susceptibility motif, appears to be predictive of rapidly progressive RA.
Comparison of synovial tissue and synovial fluid as the source of nucleic acids for detection of Chlamydia trachomatis by polymerase chain reaction
Authors: Branigan Patrick J. , Gérard Hervé C. , Hudson Alan P. , Schumacher H. Ralph 
Published: February 2007

AbstractObjective. Difficulties in detecting Chlamydia trachomatis in human joints by polymerase chain reaction (PCR) may be related to whether synovial tissue or synovial fluid (SF) is used as the source of DNA in PCR amplification. In this study, a new PCR assay was developed and used to compare chlamydial DNA in paired samples of SF and synovial tissue from patients with arthritis.Methods. The PCR assay targeted the ribosomal RNA operons, which are present in 2 copies on the C trachomatis chromosome. DNA from several relevant bacteria and chlamydial serovars was used for testing this screening system. The detection of chlamydial DNA in nucleic acid preparations from matched samples of SF and synovial tissue was compared by PCR assay. Samples were obtained from 55 patients, including patients with reactive arthritis, Reiter's syndrome, and other arthropathies.Results. Testing of the PCR screening system confirmed it to be highly specific and sensitive. Use of this assay to screen DNA from SF and synovial tissue samples showed that 29 (53%) of 55 synovial tissue preparations were positive for chlamydial DNA, but only 16 (29%) of the matched SF samples from these 29 patients were similarly positive. Five (9%) of 55 SF samples, but not their tissue counterparts, were positive for chlamydial DNA by PCR.Conclusion. Detection of chlamydial DNA in the joints of patients by PCR gives positive results more often when synovial tissue rather than SF is the source of target nucleic acids. Although synovial tissue is the source of choice for the most reliable determination of chlamydia in the joint, both synovial tissue and SF should be assayed if possible.
Effects of pulse methylprednisolone on cell adhesion molecules in the synovial membrane in rheumatoid arthritis. Reduced E‐selectin and intercellular adhesion molecule 1 expression
Authors: Youssef Peter P. , Triantafillou Sophie , Parker Angela , Coleman Mark , Roberts‐Thomson Peter J. , Ahern Michael J. , Smith Malcolm D. 
Published: February 2007

AbstractObjective. To investigate the effects of a 1,000‐mg intravenous pulse of methylprednisolone succinate (MP) on cell adhesion molecule expression on the synovial vascular endothelium in patients with rheumatoid arthritis (RA).Methods. Sequential arthroscopic biopsy samples were taken before and 24 hours after MP administration (10 patients) and at the time of RA flare (2 patients) and after retreatment with MP (1 patient). Immunoperoxidase staining for E‐selectin (CD62E), P‐selectin (CD62P), intercellular adhesion molecule 1 (ICAM‐1; CD54) and platelet—endothelial cell adhesion molecule (PECAM; CD31) was performed, and the staining was quantified by color video image analysis.Results. MP caused a rapid (within 24 hours) and substantial decrease in the expression of E‐selectin on the synovial vascular endothelium, with a smaller reduction in ICAM‐1 expression on synovial vascular endothelium and the synovial lining. There were no similar effects on synovial membrane P‐selectin or PECAM expression.Conclusion. A potential mechanism by which MP impairs neutrophil trafficking into inflamed RA joints might be by reducing E‐selectin, and possibly, ICAM‐1, expression in the synovial membrane.
Comparison of sulfasalazine and placebo in the treatment of reactive arthritis (Reiter's syndrome). A department of veterans affairs cooperative study
Authors: Clegg Daniel O. , Reda Domenic J. , Weisman Michael H. , Cush John J. , Vasey Frank B. , Schumacher H. Ralph , Budiman‐Mak Elly , Balestra Dominic J. , Blackburn Warren D. , Cannon Grant W. , Inman Robert D. , Alepa F. Paul , Mejias Edwin , Cohen Miriam R. , Makkena Rama , Mahowald Maren L. , Higashida Jean , Silverman Stuart L. , Parhami Nourollah , Buxbaum Joel , Haakenson Clair M. , Ward Richard H. , Manaster B. J. , Anderson Robert J. , Ward John R. , Henderson William G. 
Published: February 2007

AbstractObjective. To determine whether sulfasalazine (SSZ) at a dosage of 2,000 mg/day is effective in the treatment of reactive arthritis (ReA) that has been unresponsive to nonsteroidal antiinflammatory drug (NSAID) therapy.Methods. One hundred thirty‐four patients with ReA who had failed to respond to NSAIDs were recruited from 19 clinics, randomized (double‐blind) to receive either SSZ or placebo, and followed up for 36 weeks. The definition of treatment response was based on joint pain/tenderness and swelling scores and physician and patient global assessments.Results. Longitudinal analysis revealed improvement in the patients taking SSZ compared with those taking placebo, which appeared at 4 weeks and continued through the trial (P = 0.02). At the end of treatment, response rates were 62.3% for SSZ treatment compared with 47.7% for placebo treatment. The Westergren erythrocyte sedimentation rate declined more with SSZ treatment than with placebo (P < 0.0001). Adverse reactions were fewer than expected and were mainly due to nonspecific gastrointestinal complaints.Conclusion. SSZ at a dosage of 2,000 mg/day is well tolerated and effective in patients with chronically active ReA.
Preliminary experience with low‐dose methotrexate in fibroblastic rheumatism
Authors: Vittecoq Olivier , Mejjad Othmane , Silva Fernando Da , Joly Pascal , Thomine Elizabeth , Lauret Philippe , Thomine Jean Michel , Loët Xavier Le 
Published: February 2007

AbstractFibroblastic rheumatism (FR) is a rare disease characterized by joint manifestations without joint destruction, and associated with cutaneous nodules and sclerodactyly. The diagnosis is usually based on histologic examination of a skin nodule or synovium specimen. In the 11 previously reported cases, corticosteroid treatment, which has been widely used, was shown to have an unpredictable effect on the evolution of FR. We report a case of FR that was treated with methotrexate for 5 years, which led to complete recovery. This drug may be considered an effective treatment for FR. Further cases are needed to confirm this preliminary experience.
Immunohistologic analysis of renal CD40 and CD40L expression in lupus nephritis and other glomerulonephritides
Authors: Yellin Michael J. , D'Agati Vivette , Parkinson Glenn , Han Angelina Soh‐Yung , Szema Anthony , Baum David , Estes Dorothy , Szabolcs Matthias , Chess Leonard 
Published: February 2007

AbstractObjective. To investigate potential mechanisms by which CD40L‐mediated signals may be involved in the pathogenesis of lupus glomerulonephritis (GN).Methods. Renal in situ CD40L and CD40 expression was examined in patient biopsy specimens. Immuno‐histochemical studies were performed on frozen sections utilizing anti‐CD40L monoclonal antibody (MAb), anti‐CD40 MAb, or control MAb. As controls, we analyzed normal kidney specimens and specimens obtained from patients with IgA nephropathy, focal segmental glomerulosclerosis, minimal change disease, idiopathic membranous GN, and antineutrophil cytoplasmic antibody‐positive pauci‐immune GN. Staining distribution was noted and staining intensity scored on a semiquantitative scale of 0 (no staining) to 3+ (intense staining).Results. In normal kidney, CD40 was expressed on parietal epithelial cells, mesangial cells, endothelial cells, and distal tubules but not proximal tubules. Glomerular and tubular CD40 expression was markedly up‐regulated in class III and class IV lupus GN, where there was intense staining of crescents, proximal and distal tubules, and interstitial mononuclear cells. In contrast, CD40 expression in class V lupus GN was similar to that in normal kidney. Interstitial mono‐nuclear cells expressing CD40L were present in class IV lupus GN. However, these findings were not unique to lupus GN: up‐regulation of CD40 and CD40L expression was similarly observed in other inflammatory renal diseases.Conclusion. This study shows that CD40 is expressed on a variety of renal parenchymal and non‐parenchymal cells in normal kidney. Renal CD40 expression is up‐regulated in class III and class IV lupus nephritis, as well as in other inflammatory renal diseases, and is associated with the presence of CD40L+ mononuclear cells.
Suppression of type II collagen‐induced arthritis by the endogenous estrogen metabolite 2‐methoxyestradiol
Authors: Josefsson Elisabet , Tarkowski Andrej 
Published: February 2007

AbstractObjective. To evaluate the antiarthritic properties of 2‐methoxyestradiol, an endogenous metabolite of estradiol, on type II collagen‐induced arthritis (CIA) in DBA/1 mice.Methods. The effects of treatment with 2‐methoxyestradiol on the development of CIA were evaluated clinically and histologically. The in vitro effects of 2‐methoxyestradiol on lymphocyte and endothelial cell proliferation and differentiation were analyzed by standard methods.Results. The development of CIA was significantly suppressed by 2‐methoxyestradiol. Incubation with 2‐methoxyestradiol suppressed the in vitro proliferation of endothelial cells, indicating that this compound down‐regulates angiogenesis. Endothelial cell production of nitric oxide (NO) was also down‐regulated by 2‐methoxyestradiol. In contrast to estradiol, 2‐methoxyestradiol exerted neither detectable feminizing effects on the sex organs nor inhibition of leukocyte development in hematopoietic organs.Conclusion. The development of CIA is suppressed by 2‐methoxyestradiol, possibly via inhibition of angiogenesis. Diminished NO production could be of importance in vivo because it is a potent proinflammatory mediator. Since 2‐methoxyestradiol exerts only mild side effects compared with estradiol, it is an interesting candidate for therapeutic use in inflammatory diseases.
Analysis of the synovial cell infiltrate in early rheumatoid synovial tissue in relation to local disease activity
Authors: Tak Paul P. , Smeets Tom J. M. , Daha Mohamed R. , Kluin Philip M. , Meijers Katharina A. E. , Brand Ronald , Meinders A. Edo , Breedveld Ferdinand C. 
Published: February 2007

AbstractObjective. To define variations in the cellular infiltrate and in the expression of monokines in synovial tissue (ST) from rheumatoid arthritis (RA) patients with different durations of disease and different levels of disease activity.Methods. The immunohistologic features of synovial biopsy specimens from 31 patients with early RA (<1 year) and 35 patients with longstanding RA (>5 years) were compared. The possible associations between these features and local disease activity, as measured by the score for pain in the biopsied knee joint, were also evaluated.Results. The immunohistologic features were not dependent on disease duration. We found a positive correlation between the scores for knee pain and the semiquantitative scores for the number of macrophages, as well as the expression of interleukin‐6 and tumor necrosis factor α, whereas the correlation with the scores for CD4+ T cells was negative. Multivariate analysis showed that these correlations were highly statistically significant (P < 0.003).Conclusion. The results do not support the view that inflammatory mechanisms in the synovial tissues of RA patients differ between early and late stages of the disease. The findings presented here are consistent with the concept that early RA is the result of a synovitis process of longer duration and that macrophage‐derived cytokines play an important role in maintaining the clinical signs of inflammation.
Role of interleukin‐4 and interleukin‐10 in murine collagen‐induced arthritis. Protective effect of interleukin‐4 and interleukin‐10 treatment on cartilage destruction
Authors: Joosten Leo A. B. , Lubberts Erik , Durez Patrick , Helsen Monique M. A. , Jacobs Marike J. M. , Goldman Michel , van den Berg Wim B. 
Published: February 2007

AbstractObjective. To examine the role of endogenous interleukin‐4 (IL‐4) and interleukin‐10 (IL‐10) and the therapeutic effect of the addition of IL‐4 and IL‐10 in early and established murine collagen‐induced arthritis (CIA).Methods. Murine recombinant IL‐4, IL‐10, or the combination was given intraperitoneally twice daily from the day of arthritis onset up to 7–10 days of CIA in DBA/1 mice. Anti‐IL‐4, anti–IL‐10, or both antibodies were given intraperitoneally before or after the onset of CIA. The effect of cytokine or anticytokine treatment was monitored visually by macroscopic scoring. Histology and reverse transcription‐polymerase chain reaction (RT‐PCR) analyses were performed at the end of the treatment period.Results. IL‐4 alone did not provoke any effect, IL‐10 slightly suppressed the arthritis, but a more pronounced amelioration was found with the combination. This cooperative effect was noted after early treatment but also occurred when the start of treatment was delayed until 1 week after onset. Apart from suppression of macroscopic signs of inflammation, combined treatment with IL‐4/IL‐10 also reduced cellular infiltrates in the synovial tissue and caused pronounced protection against cartilage destruction. Moreover, levels of mRNA for tumor necrosis factor α (TNFα) and IL‐1 were highly suppressed both in the synovial tissue and in the articular cartilage. In contrast, levels of IL‐1 receptor antagonist (IL‐1Ra) mRNA remained elevated, which suggests that the mechanism of protection may be related to suppressed production of TNFα and IL‐1, with concomitant up‐regulation of the IL‐1Ra/IL‐1 balance. However, accelerated onset of CIA and increased severity could be achieved with neutralizing anti–IL‐10 antibodies. This expression could be further optimized with a combination of anti–IL‐4 and anti–IL‐10 antibodies, although anti–IL‐4 alone was without effect.Conclusion. Our data are consistent with a dominant role of IL‐10 in the natural suppression of arthritis expression, whereas combined treatment with IL‐4 and IL‐10 appears of potential therapeutic value, not only at the onset, but also in established arthritis.
Growth factor regulation of chondrocyte integrins. Differential effects of insulin‐like growth factor 1 and transforming growth factor β on α1β1 integrin expression and chondrocyte adhesion to type VI collagen
Authors: Loeser Richard F. 
Published: February 2007

AbstractObjective. The ability of growth factors to modulate integrin expression may be important with regard to processes involved in tissue repair and remodeling. This study was undertaken to determine the effect of transforming growth factor β (TGFβ) and insulin‐like growth factor 1 (IGF‐1) on chondrocyte β1 integrin expression and integrin‐mediated adhesion to extracellular matrix proteins.Methods. Chondrocytes obtained from normal bovine articular cartilage were cultured in the presence or absence of 10% fetal bovine serum, 100 pM IGF‐1, or 100 pM TGF β. Integrin expression and function were measured by protein blotting of immunoprecipitated integrins, Northern blot analysis, and cell adhesion assays.Results. Immunoprecipitation with an anti–β1 integrin antibody coprecipitated the α1 integrin subunit and a band representing α3 and α5, as previously reported. Compared with serum‐free cultures, the use of serum resulted in an average 10‐fold increase in the α1 band and a 12‐fold increase in the α3/α5 band. IGF‐1 increased α1 and α3/α5 by an average of 3‐fold and 4‐fold, respectively. TGFβ also increased α3/α5 by >5‐fold but decreased α1 to an average of 24% of that found in serum‐free controls. Northern blot analysis revealed that TGFβ significantly increased α5 integrin subunit RNA levels. IGF‐1 did not have a significant effect on α5 or α1 integrin subunit RNA levels, suggesting that its effects on integrins are posttranscriptional. In cell adhesion assays, TGFβ treatment resulted in a 50% decrease in the adhesion of chondrocytes to type VI collagen, while adhesion to type II collagen and fibronectin was stimulated. IGF‐1 stimulated adhesion to all 3 proteins. An α1 integrin blocking antibody inhibited up to 75% of the adhesion of human chondrocytes to type VI collagen.Conclusion. Both IGF‐1 and TGFβ stimulate chondrocyte cell surface expression of the α3/α5 integrin subunit band and stimulate adhesion of chondrocytes to fibronectin and type II collagen. The 2 growth factors have opposite effects on expression of α1β1, with IGF‐1 increasing and TGFβ decreasing cell surface levels of this integrin. TGFβ‐treated cells also have decreased adhesion to type VI collagen. The opposing effects of IGF‐1 and TGFβ on chondrocyte expression of α1/β1 and on adhesion to type VI collagen suggest that α1β1 mediates chondrocyte adhesion to type VI collagen. This was confirmed by using an antibody to the α1 integrin subunit to block adhesion of chondrocytes to type VI collagen.
Juvenile rheumatoid arthritis. Effects of disease activity and recombinant human growth hormone on insulin‐like growth factor 1, insulin‐like growth factor binding proteins 1 and 3, and osteocalcin
Authors: Davies Ursula M. , Jones Jennifer , Reeve Jonathan , Camacho‐Hubner Cecilia , Charlett André , Ansell Barbara M. , Preece Michael A. , Woo Patricia M. M. 
Published: February 2007

AbstractObjective. To investigate possible mechanisms of growth impairment in children with juvenile rheumatoid arthritis (JRA).Methods. Eighteen prepubertal children with JRA and growth retardation received recombinant human growth hormone (rHuGH) for 1 year. Growth hormone profiles over 24 hours were obtained before treatment in 12 patients; the levels did not differ from those in “short normal” children. Levels of insulin‐like growth factor 1 (IGF‐1), IGF binding proteins (IGFBPs) 1 and 3, insulin, osteocalcin, and C‐reactive protein (CRP), as well as the erythrocyte sedimentation rate were measured serially. Pretreatment levels were compared with control levels.Results. In JRA patients, IGF‐1, IGFBP‐3, and osteocalcin levels were significantly lower and insulin levels significantly higher than those in controls, but there was no significant difference in the level of IGFBP‐1. With rHuGH treatment, height velocity and mean levels of IGF‐1, osteocalcin, and insulin increased significantly, while mean levels of IGFBP‐1 fell significantly. Levels of IGFBP‐3 correlated with those of IGF‐1. The height velocity correlated positively with IGF‐1 and osteocalcin, and negatively with IGFBP‐1. Levels of IGFBP‐1 were inversely related to those of insulin and IGF‐1. There was a significant negative correlation between the CRP and height velocity, IGF‐1 level, and osteocalcin level.Conclusion. IGF‐1 production is impaired in children with active JRA. Treatment with a therapeutic dose of rHuGH can rectify the IGF‐1 deficiency within 4 days, but its effect is adversely influenced by the acute‐phase response, as reflected by an elevated CRP level.
Reference sera for antinuclear antibodies. II. Further definition of antibody specificities in international antinuclear antibody reference sera by immunofluorescence and western blotting
Authors: Smolen Josef S. , Butcher Brian , Fritzler Marvin J. , Gordon Thomas , Hardin John , Kalden Joachim R. , Lahita Robert , Maini Ravinder N. , Reeves Westley , Reichlin Morris , Rothfield Naomi , Takasaki Yoshinari , van Venrooij Walther J. , Tan Eng M. 
Published: February 2007

AbstractObjective. To define the fine specificity of the 10 reference sera used for determination of antinuclear antibodies (ANA) and ANA subsets which are available from the Arthritis Foundation (AF) and from the Centers for Disease Control and Prevention (CDC).Methods. AF/CDC sera were assessed by experienced laboratory staff, using indirect immunofluorescence and Western blotting.Results. The original assignment of fluorescence patterns to 4 reference sera was confirmed, and the fluorescence intensities were determined using reference fluorescent beads. On Western blots, sera AF/CDC2 (anti—SS‐B/La) and AF/CDC7 (anti—SS‐A/Ro) did not detect Ro antigens, sera AF/CDC9 and AF/CDC10 appeared to be monospecific anti—Scl‐70 and anti—Jo‐1 sera, respectively, serum AF/CDC4 (anti—U1 small nuclear RNP) recognized the 70‐kd band, and serum AF/CDC5 recognized the Sm antigen with its multiple bands. Semiquantitative analyses revealed that AF/CDC5, AF/CDC2, and AF/CDC10 were strongly reactive sera, whereas AF/CDC4 and AF/CDC9 were much weaker and should be used at lower dilutions on Western blots.Conclusion. The AF/CDC ANA reference sera, originally described as reference reagents for indirect immunofluorescence and double immunodiffusion techniques, are also useful for Western blotting. The data presented herein further support the use of these sera for reference purposes.
Breast implants in patients with differentiated and undifferentiated connective tissue disease
Authors: Williams H. James , Weisman Michael H. , Berry Charles C. 
Published: February 2007

AbstractObjective. To assess the frequency of breast implantation and the relationship of the implants to the onset of symptoms in patients with differentiated and undifferentiated connective tissue disease (CTD).Methods. We evaluated an inception cohort of patients with differentiated and undifferentiated CTD and symptoms of < 12 months duration when enrolled in 1983–1987. The risk of having breast implants in those patients with early symptoms of CTD was determined in comparison with that in a non‐concurrent control group.Results. Only 3 of 323 women in the cohort had historical, physical, or chest radiographic evidence of breast implantation. In 1 of the 3 patients, the symptoms of CTD began before the breast implantation. The odds ratio was calculated at 1.15, with a 95% confidence interval ranging from 0.23 to 3.41.Conclusion. This study showed an absence of significant risk for prior breast implantation surgery in patients with well‐defined or undifferentiated CTD.