bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increased percentage of cd3+, cd57+ lymphocytes in patients with rheumatoid arthritis. correlation with duration of disease
Authors: D'Angeac Arnaud Dupuy , Monier Serge , Jorgensen Christian , Gao Qinglin , Travaglio‐Encinoza Adolfo , Bologna Christophe , Combe Bernard , Sany Jacques , Reme Thierry 
Published: February 2007

AbstractObjective. To determine whether a small CD3+ lymphocyte population expressing 110‐kd CD57 antigens (HNK1) is expanded in patients with rheumatoid arthritis (RA), as it is in patients who have undergone bone marrow transplantation and patients with the acquired immunodeficiency syndrome, and to investigate whether it is involved in the pathogenesis of RA.Methods. The phenotype of CD3+, CD57+ lymphocytes was analyzed by flow cytometry, and correlations between the percentage of these cells in the blood and various clinical and biologic parameters were investigated.Results. The percentage of CD3+, CD57+ lymphocytes was increased in RA patients compared with controls. These lymphocytes expressed T cell receptor α/β. Eighty percent expressed the CD8 accessory molecule, and 20% expressed the CD4 accessory molecule. The leukocyte common antigen CD45RA isoform was expressed by these CD3+, CD57+ lymphocytes in blood. The HLA–DR antigen was expressed in synovial fluid but not in blood. Finally, the percentage of these lymphocytes in the blood correlated with the duration of RA.Conclusion. The expansion of the CD3+, CD57+ lymphocyte population and their activation in the synovial fluid of RA patients suggest that these cells are involved in the inflammatory process.
The effects of drug therapy on radiographic progression of rheumatoid arthritis. results of a 36‐week randomized trial comparing methotrexate and auranofin
Authors: Weinblatt Michael E. , Polisson Richard , Blotner Steven D. , Leland Sosman J. , Aliabadi Piran , Baker Nancy , Weissman Barbara N. 
Published: February 2007

AbstractObjective. To determine the effects of drug therapy (methotrexate [MTX] versus auranofin [AUR]) on radiographic progression in patients with active rheumatoid arthritis (RA).Methods. We conducted a 9‐month randomized, multicenter, double‐blind trial comparing MTX and AUR. Standardized radiographs of the hands and wrists were obtained at baseline and at completion of the study. Four experienced bone radiologists graded the radiographs for erosions, joint space narrowing, erosion healing, and reparative bone formation.Results. Two hundred eighty‐one patients were enrolled in the study. Radiographs were available on 167 of the 183 who completed the trial. After 9 months of therapy, there was a significantly greater worsening of the erosion score in the AUR group (mean ± SEM change of 1.67 ± 0.4) compared with the change in the MTX group (0.60 ± 0.3) (P = 0.040). There was also a significantly greater worsening of the joint space narrowing score in the AUR group compared with the MTX group (1.36 ± 0.3 versus 0.42 ± 0.2) (P = 0.007). There was no difference demonstrated between groups in healing of erosions or in reparative bone formation.Conclusion. The rate of radiographic progression in patients with RA, as measured by erosion score and joint space narrowing score, was demonstrated to be lower in those treated with MTX, as compared with AUR, over a 36‐week period.
Effects of administration of an anti‐cd5 plus immunoconjugate in rheumatoid arthritis. results of two phase ii studies
Authors: Strand Vibeke , Lipsky Peter E. , Cannon Grant W. , Calabrese Leonard H. , Wiesenhutter Craig , Cohen Stanley B. , Olsen Nancy J. , Lee Martin L. , Lorenz Todd J. , Nelson Betty , Wolfe Frederick , Fleischmann Roy M. , Karr Reynold M. , Krick George H. , Medsger Thomas A. , Rigby William F. C. , Fox David A. , Swartz Timothy J. , Multz Carter V. , Weisman Michael H. 
Published: February 2007

AbstractObjective. To evaluate the safety and activity of an immunoconjugate of ricin A chain and anti‐CD5 monoclonal antibody (anti‐CD5 IC), with and without concomitant methotrexate and/or azathioprine, in the treatment of rheumatoid arthritis (RA).Methods. Seventy‐nine patients with active RA were enrolled in 2 prospective open‐label protocols.Results. Using composite criteria, response rates were 50–68% at 1 month and 22–25% at 6 months. Transient depletion of CD3/CD5 T cells was observed on days 2 and 5 of treatment, with reconstitution on day 15 or day 29. Treatment‐associated adverse effects were common but resolved rapidly without sequelae.Conclusion. These findings suggest activity of anti‐CD5 IC in active RA and warrant confirmation in a multicenter randomized study (currently underway).
Analysis of immunoglobulin gamma heavy chain expression in synovial tissue of a patient with rheumatoid arthritis
Authors: Louis S. Bridges, , Lee Soo Kon , Koopman William J. , Schroeder Harry W. 
Published: February 2007

AbstractObjective. To gain insight into mechanisms underlying local immune responses in rheumatoid arthritis (RA), we analyzed the utilization of variable‐region heavy chain (VH), diversity (DH), and joining (JH) gene segments expressed in synovial tissue of a patient with RA.Methods. An unrestricted complementary DNA (cDNA) library was generated from unselected cells extracted from synovial tissue obtained at the time of joint replacement. Southern blot analysis for VH, JH, and Cγ subclass utilization was performed on the first 50 Cγ‐ and JH‐positive recombinants for which phage DNA was isolated. Eighteen of the clones were selected at random for sequence analysis. The VH gene segments were compared with an extensive database of germline and cDNA sequences.Results. All transcripts utilized gene segments from the VH1 (28%), VH3 (56%), and VH4 (15%) families. There was a predominance of JH4, JH5, and JH6 gene segment utilization. Fourteen of 18 randomly sequenced clones contained sufficient VH‐region information for analysis. Eight (57%) were most closely related to VH gene segments that are preferentially expressed in human fetal liver or that encode antibodies with self‐reactivity. The variable domains were heavily mutated, and replacement‐to‐silent substitution ratios (R:S ratios) in the antigen‐binding domains (complementarity‐determining regions [CDRs]) were disproportionately high. CDR3 lengths were quite variable, due to extensive N‐region addition and 5′‐exonuclease activity in the VH–DH–JH joins.Conclusion. Plasma cells in this synovial tissue sample appear to express VH gene segments that are preferentially utilized during fetal development or in autoantibodies. The JH repertoire is similar to that seen in adult peripheral blood lymphocytes, but much different from that found during fetal development. The large number of somatic mutations and the high R:S ratios in the CDRs suggest an antigen‐driven response.
Pressure pain threshold in pain‐free subjects, in patients with chronic regional pain syndromes, and in patients with fibromyalgia syndrome
Authors: Granges Gerald , Littlejohn Geoffrey 
Published: February 2007

AbstractObjective. We hypothesized that change in pain threshold to pressure reflects a generalized change in the pain system affecting both tender and control points.Methods. We assessed 18 tender points and 4 control points using an algometer in 60 patients with generalized fibromyalgia/fibrositis syndrome, 60 patients with localized chronic pain syndromes, and in 60 pain‐free subjects.Results. A significant correlation was found between myalgia scores at tender points and control points in these subjects.Conclusion. These results suggest that there is a diffuse change in pain modulation in fibromyalgia, as hypothesized, but the tender point is still clinically useful.
Characteristics of anti‐type ii collagen antibody binding to articular cartilage
Authors: Jasin Hugo E. , Noyori Koji , Takagi Toshitaka , Taurog Joel D. 
Published: February 2007

AbstractObjective. Previous studies suggested that it was possible to characterize the intact surface of articular cartilage by probing it with antibodies against matrix macromolecules. The present studies were undertaken to investigate type II collagen (CII) epitope availability on the intact surface of articular cartilage.Methods. Normal bovine, rabbit, and human cartilage specimens were used to measure binding of anti‐CII antibodies to the articular and cut surfaces of cartilage. Antisera were raised against the material obtained after brief extraction of the cartilage surface with 4M guanidine solution.Results. Anti‐CII did not bind to the intact surface of rabbit articular cartilage when compared with control rat sera, but did bind significantly to the cut surface. With normal human articular cartilage, the cut surfaces bound approximately 4 times as much anti‐CII antibody as the intact articular surfaces. These findings suggested that the CII epitopes are normally protected by the superficial cartilage layer. In experiments carried out to characterize this layer, binding of anti‐CII antibodies was unchanged after exhaustive washing of bovine or rabbit cartilage with phosphate buffered saline or 1M NaCl solution, whereas it was significantly increased after brief exposure to 4M guanidine solution or after incubation with neutrophil elastase. No restoration of the protection of CII epitopes in guanidine‐treated cartilage could be achieved by incubation with undiluted normal bovine synovial fluid; however, 8‐day culture of elastase‐treated cartilage explants resulted in partial restoration of protection of the CII epitopes. Rat and rabbit antisera raised against the cartilage surface material extracted with 4M guanidine contained antibodies that bound to the cartilage surface. By Western blotting, rat antibodies identified 50–65‐kd protein bands present in the guanidine extract, but not present either in the material obtained from brief digestion of cartilage with neutrophil elastase or in synovial fluid. The rabbit antisera identified a broad 70–95‐kd band. Exposure of elastase‐treated cartilage to the guanidine‐extracted material resulted in a partial decrease of anti‐CII antibody binding.Conclusion. These results suggest that CII on intact cartilage is protected from antibody binding, and that the protective material is at least partly proteinaceous in nature, is unlikely to be derived from synovial fluid, is noncovalently bound to the underlying intercellular matrix, and is synthesized by resident chondrocytes. Further characterization of the protective material may provide important information on the mechanisms of early cartilage damage in inflammatory arthritis.
Susceptibility to relapsing polychondritis is associated with hla–‐dr4
Authors: Lang Bernhard , Rothenfusser Anna , Lanchbury Jerry S. , Rauh Günter , Breedveld Ferdinand C. , Urlacher Arlette , Albert Ekkehard D. , Peter Hans‐Hartmut , Melchers Inga 
Published: February 2007

AbstractObjective. To determine the frequency of HLA class II antigens in Caucasian central European patients with relapsing polychondritis (RP).Methods. HLA class I, DR, and DQ specificities were identified in 41 patients with RP, and the frequencies were compared with those in 204 healthy, unrelated control subjects. HLA typing was performed using the standard complement‐dependent microcytotoxicity assay. HLA–DR genotyping of 12 DR4‐positive RP patients and 57 controls was performed by allele‐specific oligonucleotide probing after amplification of genomic DNA by polymerase chain reaction.Results. A significant increase in DR4 antigen frequency was found in the patients (56.1%) as compared with that in healthy controls (25.5%) (Pcorr < 0.001). Genotyping of DR4‐positive patients and controls revealed no predominance of any DR4 subtype.Conclusion. There are important clinical similarities and overlaps between RP and rheumatoid arthritis (RA). In RA, the association with DR4 has been well established. Our findings show that although there is a DR4 association with RP, the situation is sufficiently distinct from that of RA to imply considerable differences in pathogenesis of the two conditions.
The polymerase chain reaction for the detection of borrelia burgdorferi in human body fluids
Authors: Liebling Michael R. , Nishio Midori Jane , Rodriguez Annette , Sigal Leonard H. , Jin Tian , Louie James S. 
Published: February 2007

AbstractObjective. To analyze clinical fluids for the presence of Borrelia burgdorferi DNA using the polymerase chain reaction (PCR).Methods. We utilized a modified, nested PCR to detect the presence of Borrelia DNA in 99 samples of serum, urine, cerebrospinal fluid (CSF), or synovial fluid obtained from 44 patients with various stages of Lyme disease and 47 control subjects. Primer specificity was corroborated by examining 2 DNA data banks, testing against DNA from other organisms, and confirming results with a second set of nested primers.Results. Nested PCR was capable of detecting DNA from fewer than 10 organisms in 1 ml of fluid. The specificity of this technique was 96.4%, with a sensitivity of 76.7%. Although the specificity was uniformly high, the sensitivity was dependent upon the body fluid being tested: CSF 100%, urine 100%, synovial fluid 80%, and serum 59%. The rate of false‐positive results was 3.6%.Conclusion. These data demonstrate the potential utility of PCR in confirming the clinical diagnosis of Lyme disease as well as providing insight into the pathogenesis of various stages of this disorder.
Treatment of refractory, systemic lupus erythematosus–associated thrombocytopenia with intermittent low‐dose intravenous cyclophosphamide
Authors: Roach Barbara A. , Hutchinson Gordon J. 
Published: February 2007

AbstractWe describe a patient with systemic lupus erythematosus and severe, treatment‐resistant thrombocytopenia. Prolonged treatment with high‐dose steroids eventually led to reversal of the thrombocytopenia, but the dosage could not be tapered without relapse. Low‐dose intravenous bolus cyclophosphamide was given, producing a response within 1 week. The steroid dosage was tapered, without relapse. Other than reversible alopecia, no toxicity was seen. The use of this treatment should be considered in patients in whom more conventional therapies are not effective or cannot be tolerated.
Cold‐induced potentiation of α2‐adrenergic vasoconstriction in primary raynaud's disease
Authors: Freedman Robert R. , Moten Marriyam , Migaly Peter , Mayes Maureen 
Published: February 2007

AbstractObjective. To determine the effects of local cooling on α‐adrenergic responses in the fingers of patients with idiopathic Raynaud's disease.Methods. Clonidine HCl and phenylephrine HCl were administered through a brachial artery catheter while blood flow was measured by plethysmography in cooled and uncooled fingers.Results. Cooling potentiated α2‐adrenergic vasoconstriction in the patients but depressed this response in the controls. Vasoconstrictive responses to phenylephrine were not significantly affected by cooling but were significantly greater in the patients than in the controls.Conclusion. Cold‐induced sensitization of peripheral vascular α2‐adrenoceptors may be involved in the mechanism by which cooling triggers the vasospastic attacks of Raynaud's disease.
Sarcoidosis accompanied by pulmonary tuberculosis and complicated by sacroiliitis
Authors: Griep Eduard N. , Van Spiegel Paul I. , Van Soesbergen Renée M. 
Published: February 2007

AbstractWe report the unique occurrence of a unilateral sacroiliitis in a patient with active sarcoidosis accompanied by pulmonary tuberculosis. Convincing (clinical) evidence of sarcoidosis as the extremely rare cause of this articular involvement is presented. Discussion is focused on comparison of sarcoidosis and tuberculosis, particularly with respect to their articular involvement, and the literature of previously reported cases of sarcoid sacroiliitis is briefly reviewed.
The American college of rheumatology preliminary core set of disease activity measures for rheumatoid arthritis clinical trials
Authors: Felson David T. , Anderson Jennifer J. , Boers Maarten , Bombardier Claire , Chernoff Miriam , Fried Bruce , Furst Daniel , Goldsmith Charles , Kieszak Stephanie , Lightfoot Robert , Paulus Harold , Tugwell Peter , Weinblatt Michael , Widmark Rudolph , James Williams H. , Wolfe Frederick 
Published: February 2007

AbstractObjective. To develop a set of disease activity measures for use in rheumatoid arthritis (RA) clinical trials, as well as to recommend specific methods for assessing each outcome measure. This is not intended to be a restrictive list, but rather, a core set of measures that should be included in all trials.Methods. We evaluated disease activity measures commonly used in RA trials, to determine which measures best met each of 5 types of validity: construct, face, content, criterion, and discriminant. The evaluation consisted of an initial structured review of the literature on the validity of measures, with an analysis of data obtained from clinical trials to fill in gaps in this literature. A committee of experts in clinical trials, health services research, and biostatistics reviewed the validity data. A nominal group process method was used to reach consensus on a core set of disease activity measures. This set was then reviewed and finalized at an international conference on outcome measures for RA clinical trials. The committee also selected specific ways to assess each outcome.Results. The core set of disease activity measures consists of a tender joint count, swollen joint count, patient's assessment of pain, patient's and physician's global assessments of disease activity, patient's assessment of physical function, and laboratory evaluation of 1 acute‐phase reactant. Together, these measures sample the broad range of improvement in RA (have content validity), and all are at least moderately sensitive to change (have discriminant validity). Many of them predict other important long‐term outcomes in RA, including physical disability, radiographic damage, and death. Other disease activity measures frequently used in clinical trials were not chosen for any one of several reasons, including insensitivity to change or duplication of information provided by one of the core measures (e.g., tender joint score and tender joint count) The committee also proposes specific ways of measuring each outcome.Conclusion. We propose a core set of outcome measures for RA clinical trials. We hope this will decrease the number of outcomes assessed and standardize outcomes assessments. Further, we hope that these measures will be found useful in long‐term studies.
An organizational model for developing multidisciplinary clinical research in the academic medical center
Authors: Charlson Mary E. , Allegrante John P. , Hollenberg James P. , Szatrowski Ted P. , Peterson Margaret G. E. , Robbins Laura , Gordon Karen A. , Ronald Mackenzie C. , Williams‐Russo Pamela , Paget Stephen A. 
Published: February 2007

AbstractObjective. To assess the impact of a new organizational model designed to stimulate multidisciplinary clinical research.Methods. We conducted a prospective, 3½‐year follow up of a research training program for residents, fellows, faculty, nurses, and allied health professionals in rheumatology and orthopedic surgery. Program components included a multidisciplinary clinical research conference, a clinical research methods curriculum, consultations, a patient registry, and regular meetings of a Research Methodology Core group. Measures included participation in each program component and the number of new investigators who developed funded clinical research projects.Results. The multidisciplinary clinical research conference was attended by 369 new health professionals; 218 professionals participated in at least one of the courses; and 280 consultations were provided to 108 professionals. Thirteen new investigators developed 17 new grant proposals, of which 14 were externally funded. Investigators who successfully procured funding for new projects demonstrated significantly more participation in program components compared with those who did not (P < 0.001 overall).Conclusion. Participation in the program was significantly correlated with the development of new prospective patient‐based studies. We conclude that our model has the potential to foster such research in other settings.
Quality of life issues in women with vertebral fractures due to osteoporosis
Authors: Cook Deborah J. , Guyatt Gordon H. , Adachi Jonathan D. , Clifton Joanne , Griffith Lauren E. , Epstein Robert S. , Juneper Elizabeth F. 
Published: February 2007

AbstractObjective. To learn about the physical, emotional, and social limitations experienced by postmenopausal women who have back pain due to vertebral fractures resulting from osteoporosis.Methods. We conducted a cross‐sectional survey of female patients with persistent pain due to vertebral fractures.Results. Respondents had a mean (±SD) bone density of 0.87 ± 0.13 gm/cm2 and a mean (±SD) of 2.48 ± 2.18 fractures. Disability was identified in pain, movement, activities of daily living, and emotion. There was a poor correlation between quality of life and findings on radiography or densitometry.Conclusion. To evaluate the effects of osteoporosis on a patient's functional status, direct questioning is required.
Expression of monocyte chemotactic and activating factor in rheumatoid arthritis. regulation of its production in synovial cells by interleukin‐1 and tumor necrosis factor
Authors: Akahoshi Tohru , Wada Chieki , Endo Hirahito , Hirota Kazuhisa , Hosaka Shigeru , Takagishi Kenji , Kondo Hirobumi , Kashiwazaki Sadao , Matsushima Kouji 
Published: February 2007

AbstractObjective. To investigate whether monocyte chemotactic and activating factor (MCAF) contributes to the accumulation of macrophages in the joints of patients with rheumatoid arthritis (RA).Methods. MCAF was measured by radioimmunoassay. MCAF gene expression was determined by Northern blotting and reverse‐transcriptase polymerase chain reaction. Recombinant human MCAF was injected into rabbit joints to evaluate the effect of MCAF on infiltration of macrophages.Results. High levels of MCAF were detected in synovial fluid from patients with RA. Cells freshly isolated from synovial fluid expressed MCAF messenger RNA (mRNA). Fibroblast‐like synoviocytes were found to express MCAF mRNA and to secrete MCAF in response to interleukin‐1 (IL‐1) and tumor necrosis factor in vitro. IL‐1 also promoted MCAF gene expression in rabbit synovial tissue in vivo. MCAF caused marked infiltration of macrophages in rabbit synovial tissue.Conclusion. Our findings suggest that MCAF may contribute to the accumulation of macrophages in inflamed rheumatoid joints.