bluuebunny/crossref_metadata_2025_split huggingface dataset:
The geri‐aims. Reliability and validity of the arthritis impact measurement scales adapted for elderly respondents
Authors: Hughes Susan L. , Edelman Perry , Chang Rowland W. , Singer Ruth H. , Schuette Patrick 
Published: February 2007

AbstractWe adapted the Arthritis Impact Measurement Scales (AIMS) for use with frail elderly respondents. The new instrument, called the GERI‐AIMS, generates both generic and arthritis‐specific impairment scores, to control for comorbid conditions that are commonly found in an older population. An analysis of scores obtained on 438 elderly persons (mean age 76) indicated that more than half of the total disability measured by the generic GERI‐AIMS scores is related to arthritis. The GERI‐AIMS scales have standardized‐item alpha levels >0.70 and correlate well with clinical measures of arthritis severity. Information gained by using the GERI‐AIMS has important public policy implications, insofar as information on both generic and diseasespecific functional impairment is needed to establish priorities for basic research, epidemiologic, and intervention studies.
Altered interleukin‐2 secretion in patients with primary fibromyalgia syndrome
Authors: Hader Nader , Rimon David , Kinarty Amalia , Lahat Nitza 
Published: February 2007

AbstractInterleukin‐2 (IL‐2) production was studied in T lymphocytes and isolated CD4+ T lymphocytes from 12 patients with primary fibromyalgia syndrome and 10 healthy volunteers. The dose and time kinetics of IL‐2 production by concanavalin A‐stimulated T cells and CD4+ T cells of fibromyalgia patients differed from findings in controls by 1) a need for a higher concentration of mitogen in order to achieve optimal IL‐2 secretion, and 2) a delay in the peak time of optimal IL‐2 secretion. Unlike normal IL‐2 secretion, which was higher after removal of CD8+ T cells, the pattern and degree of IL‐2 secretion by cells from fibromyalgia patients were not changed following removal of CD8+ T cells. Addition of calcium ionophore in assays using suboptimal concanavalin A concentrations did not correct the reduction in IL‐2 secretion by fibromyalgia patient T cells, but addition of phorbol myristate acetate induced normal secretion of IL‐2. These findings suggest that there is a defect in the IL‐2 pathway, which is related to protein kinase C activation and does not involve impairment of Ca2+ elevation, in patients with fibromyalgia.
Development of a disability measurement tool for juvenile rheumatoid arthritis. The juvenile arthritis functional assessment report for children and their parents
Authors: Howe Steven , Levinson Joseph , Shear Edith , Hartner Sandra , McGirr Gerri , Schulte Marion , Lovell Daniel 
Published: February 2007

AbstractTwo questionnaires were developed for measuring disability due to juvenile rheumatoid arthritis (JRA), one based on patient reports and one on parent reports. These questionnaires were termed the Juvenile Arthritis Functional Assessment Report for Children (JAFAR‐C) and for Parents (JAFAR‐P). The questionnaires were administered to 72 JRA patients ages 7‐18 years and to their parents. Respondents rated the patient's recent ability to perform 23 activities. Patient reports and parent reports were found to correlate highly with each other and with an objective assessment performed by therapists. Questionnaire scores did not correlate significantly with the age of the patient. The JAFAR appears to be a convenient, reliable, and valid measure of disability in patients with JRA.
Ro/SS‐A antigen in human platelets. Different distributions of the isoforms of Ro/SS‐A protein and the Ro/SS‐A–binding RNA
Authors: Itoh Yasuhiko , Reichlin Morris 
Published: February 2007

AbstractRo/SS‐A antigen is present in human platelets at a concentration that is approximately one‐twentieth to one‐thirtieth its concentration in lymphocytes, but the distribution of the Ro/SS‐A isoforms is different from that in lymphocytes or red blood cells. The Ro/SS‐A in platelets is largely the 52‐kd form. Moreover, the 52‐kd isoform in platelets is antigenically different from that in lymphocytes. In addition to the varied isoform distribution, a different distribution of the Ro/SS‐A–binding RNA (hY RNA) is seen in platelets. While there are 4 hY RNA (hY1, hY3, hY4, and hY5) in lymphocytes and other nucleated cells, we have found that platelets contain only 2 hY RNA: hY3 and hY4. This hY RNA distribution is also different from that in red blood cells, which contain only hY1 and hY4. The different distributions of the Ro/SS‐A components in lymphocytes, red blood cells, and platelets suggest different functional roles for the various protein and RNA components, as well as the possibility of different tissue‐specific events related to the Ro/SS‐A–autoanti–Ro/SS‐A system.
Transforming growth factor β1 stimulates inorganic pyrophosphate elaboration by porcine cartilage
Authors: Rosenthal Ann K. , Cheung Herman S. , Ryan Lawrence M. 
Published: February 2007

AbstractThe overproduction of inorganic pyrophosphate (PPi) by cartilage is thought to be a key element in the formation of calcium pyrophosphate dihydrate (CPPD) crystals in joints, and the subsequent development of pseudogout or chondrocalcinosis. We report herein that transforming growth factor β1 (TGFβ1), alone and in synergy with epidermal growth factor (EGF) or TGFα, markedly stimulates PPi elaboration by porcine articular cartilage in organ culture and monolayer culture. This effect is not seen with platelet‐derived growth factor, basic fibroblast growth factor, or insulin‐like growth factor types 1 and 2, substances which also affect chondrocyte metabolism or are mitogenic. TGFβ1 produces only a modest increase in nucleoside triphosphate pyrophosphohydrolase (NTPPPH), a chondrocyte ectoenzyme that produces PPi; this implies the existence of other pathways for PPi elaboration. TGFβ1 is present in joint fluid and cartilage. TGFβ1, TGFα, and EGF are the first known physiologic modifiers of cartilage PPi production. They provide a novel model for the study of CPPD crystal formation in cartilage, as well as new insights into the pathogenesis of this common affliction of aging.
Insufficiency fractures of the distal tibia misdiagnosed as cellulitis in three patients with rheumatoid arthritis
Authors: Straaton Karin V. , López‐Méndez Ada , Alarcón Graciela S. 
Published: February 2007

AbstractWe describe 3 patients with rheumatoid arthritis who presented with diffuse pain, swelling, and erythema of the distal aspect of the lower extremity, suggestive of either cellulitis or thrombophlebitis, but were found to have insufficiency fractures of the distal tibia. The value of technetium‐99m diphosphonate bone scintigraphy in the early recognition of these fractures and a possible explanation for the associated inflammatory symptoms are discussed.
Definition, incidence, and clinical description of flare in systemic lupus erythematosus. A prospective cohort study
Authors: Petri Michelle , Genovese Mark , Engle Eric , Hochberg Marc 
Published: February 2007

AbstractThe course of systemic lupus erythematosus (SLE) is characterized by exacerbations (or flares) and remissions of disease activity. As part of an ongoing prospective cohort study, 3 disease activity indices, the physician's global assessment, the Lupus Activity Index, and the University of Toronto SLE Disease Activity Index, have been recorded, at least quarterly since 1987, on 185 SLE patients. We developed a definition of SLE flare and a description of its clinical epidemiology. Disease flare was defined as a change of ≥1.0 in the physician's global assessment of disease activity (measured on a 0–3 scale) from the previous visit or from a visit within the last 93 days. Of the 185 patients, 98 (53%) had ≥1 flare; the total number of flares was 146. The incidence of flare was 0.65 per patient‐year of followup. The median time from the first study visit to a flare was 12 months. Flares were frequently characterized by constitutional symptoms, musculoskeletal involvement, cutaneous involvement, and decreasing levels of C3 and C4. At the time of flare, the mean University of Toronto SLE Disease Activity Index score increased by 3.0 and the mean Lupus Activity Index score (modified to omit the physician's global assessment) increased by 0.26. Overall, 44.8% of the flares prompted a change in treatment. Patients who experienced flares fulfilled more of the SLE criteria at entry and had been followed up for a longer duration after entry into the study, compared with those who did not have flares. By survival analysis, no specific clinical or laboratory variables present at entry were found to predict the time to first flare. These data show that quantification of flare is possible, flare is frequent in patients with SLE of long duration, and the majority of flares involve the so‐called “minor” organ systems.
Methotrexate versus azathioprine in the treatment of rheumatoid arthritis. A forty‐eight–week randomized, double‐blind trial
Authors: Jeurissen Maurice E. C. , Th. Boerbooms Agnes M. , Van De Putte Levinus B. A. , Doesburg Wim H. , Mulder Jan , Rasker Johannes J. , Kruijsen Marijn W. M. , Haverman Joost F. , Van Beusekom Henk J. , Muller Wim Hissink , Franssen Marcel J. A. M. , De Rooy Dirk‐Jan R. A. M. 
Published: February 2007

AbstractWe conducted a double‐blind, randomized trial comparing azathioprine (AZA) and methotrexate (MTX) in the treatment of patients with rheumatoid arthritis in whom parenteral gold and/or D‐penicillamine treatment had been unsuccessful. Patients were randomly assigned to receive either AZA (100 mg daily) or oral MTX (7.5 mg weekly). After 8 weeks, the dosage was increased depending on the clinical improvement. Sixty‐four patients were followed up for 48 weeks (33 AZA, 31 MTX). Comparison of values at week 24 with baseline values revealed significant improvement in 12 of 13 disease variables in the MTX group and in 6 of 13 in the AZA group. Comparison between the 2 treatment groups at 24 weeks, by area‐under‐the‐curve analysis, showed significantly more improvement in the MTX group in terms of the swollen joint count, pain score, erythrocyte sedimentation rate, C‐reactive protein level, hemoglobin level, thrombocyte level, and disease activity score. A significant overall clinical improvement (disease activity score) was found in 7 of 20 patients treated with AZA and 18 of 30 patients treated with MTX after 24 weeks of therapy, and in 6 of 12 AZA‐treated patients and 19 of 25 MTX‐treated patients after 48 weeks. The number of withdrawals due to side effects was significantly higher in the AZA group. After 48 weeks, only 12 patients from the AZA group (36%), but 25 from the MTX group (81%), were still using the initial drug. These results demonstrate MTX to be superior to AZA in the treatment of rheumatoid arthritis, with a more rapid clinical improvement which is sustained after 1 year, accompanied by a lower rate of serious adverse reactions.
Extravascular fibrin formation and dissolution in synovial tissue of patients with osteoarthritis and rheumatoid arthritis
Authors: Weinberg J. Brice , Pippen ANNE M. M. , Greenberg Charles S. 
Published: February 2007

AbstractFibrin deposition is a prominent finding in the synovium of patients with rheumatoid arthritis (RA). Macrophages are found in increased numbers in RA synovium, and these cells are known to produce a variety of procoagulant and anticoagulant molecules. Using immunohistologic techniques, the content and distribution of several important components of the coagulation system in the synovium of patients with RA, osteoarthritis (OA), or traumatic joint abnormalities requiring surgery were investigated. Samples from 3 patients from each category were examined in detail. RA synovium (compared with that of patients with OA or joint trauma) had increased numbers of macrophages and increased expression/content of fibrinogen, tissue factor, factor XIII, tissue transglutaminase, cross‐linked fibrin (fibrin D dimer), urokinase‐type plasminogen activator, and α2–plasmin inhibitor. Macrophage content in RA synovium was increased in both the lining cell areas and the interstitial cell areas. Fibrinogen was distributed throughout the tissue in all samples and was greater in RA synovium. In trauma and OA synovia, tissue factor was seen only in association with vessels (endothelial cells), but in RA synovium, it was markedly increased throughout the tissues. While fibrin D dimer was seen in small amounts in synovial lining cell areas of trauma and OA synovia, it was present in increased amounts in the lining cell and interstitial cell areas of RA synovium. Factor XIII and tissue transglutaminase were present in scant amounts in trauma and OA synovia, but there were increased amounts of both (especially tissue transglutaminase) in RA synovium in the vessel, lining cell, and interstitial cell areas. Urokinase and α2–plasmin inhibitor were also markedly increased in RA synovium. These results suggest that in inflamed synovium, there is ongoing extravascular tissue fibrin formation and dissolution that correlates with the degree of inflammation and macrophage content. Extravascular coagulation/fibrinolysis in RA represents a potential target for therapeutic intervention in this disease.
Binding of c‐reactive protein to human neutrophils. Inhibition of respiratory burst activity
Authors: Dobrinich Robert , Spagnuolo Philip J. 
Published: February 2007

AbstractWe investigated the binding of highly purified soluble human C‐reactive protein (CRP) to human neutrophils. Binding of CRP to neutrophils was rapid (50% of maximal binding occurred within 15 seconds), and complete within 5 minutes. Binding was inhibitable by excess unlabeled CRP, and nonspecific binding in the presence of a 200‐fold excess of unlabeled CRP was 10% of total binding. Binding was not affected by other proteins, including albumin, fibroncctin, rabbit IgG, or normal human plasma. Maximal binding required both calcium (0.5 mM) and magnesium (0.24 mM) ions. Calcium phosphorylcholine (10 μg/ml) or sodium citrate (10 μg/ml) completely dissociated bound CRP. Binding was saturable and most consistent with a 2‐site model, demonstrating both a high‐affinity receptor (1.4 × 104 sites/cell Kd 3.7 × 10−8M) and a low‐affinity receptor (4.2 × 105 sites/cell Kd 2.5 × 10−8M). CRP at concentrations of 50 μg/ml inhibited the neutrophil superoxide production induced by phorbol ester. At concentrations of 100 μg/ml or greater, CRP also inhibited superoxide production in a cell‐free xanthine oxidase–acetaldehyde system. These data suggest that CRP can down‐regulate neutrophil oxidative capacity through interaction with receptors on neutrophils as well as by direct antioxidant activity.
Treatment of collagen‐induced arthritis in rats with a monoclonal antibody against the α/β T cell antigen receptor
Authors: Yoshino Shin , Cleland Leslie G. , Mayrhofer Graham 
Published: February 2007

AbstractA monoclonal antibody (MAb) to the α/β T cell receptor (TCRα/β), R73 MAb, completely blocked the induction of collagen‐induced arthritis (CIA) in rats when the MAb was administered at the time of immunization with type II collagen. When administered after CIA had begun, the progression of the arthritis was suppressed significantly by R73 MAb treatment. The preventive and suppressive effects of R73 MAb on CIA were associated with the depletion of peripheral blood α/β‐positive T cells. These results indicate that α/β‐positive T cells play a role in the progression of existing CIA as well as in its induction.
Cerebral vasculopathy associated with collateralization resembling moya moya phenomenon and with anti‐Ro/SS‐A and anti–La/SS‐B antibodies
Authors: Provost Thomas T. , Moses Howard , Morris Edward L. , Altman Jeremy , Harley John B. , Alexander Elaine , Reichlin Morris 
Published: February 2007

AbstractWe describe a 48‐year‐old, previously healthy, anti–Ro/SS‐A and anti–La/SS‐B antibody positive black woman with negative risk factors for atherosclerosis, who developed mental status and personality changes over a 6–12‐month period, and progressive cortical blindness over a 2‐week period. Angiographic and computed axial tomographic studies of the brain demonstrated multiple large areas of infarction correlating with stenosis and occlusions of the internal carotid and posterior cerebral arteries. Moya moya–like findings were prominent radiographically. Results of angiographic, computed tomographic, and magnetic resonance imaging studies were interpreted as being compatible with large, medium, and small vessel disease, most likely a vasculitis.
Expression of Metalloproteinases and Metalloproteinase Inhibitor in Human Arthritic Synovium
Authors: Spence Mccachren S. 
Published: February 2007

AbstractThe expression of messenger RNA encoding neutral metalloproteinases and the tissue inhibitor of metalloproteinases (TIMP) in human arthritic synovium was evaluated in situ, using RNA probes. Interstitial collagenase and stromelysin were expressed by synovial lining cells in patients with active rheumatoid arthritis (RA). Proteinase messenger RNA was found both in cells expressing mononuclear phagocyte antigens and in cells that were negative for the antigens. TIMP was also expressed predominantly along the synovial lining layer. In highly inflammatory RA, TIMP expression appeared less intense than that of the proteases. In osteoarthritic synovium, TIMP was expressed at easily detectable levels, whereas the expression of collagenase and stromelysin was less prominent. The balance between expression of the metalloproteinases and of the metalloproteinase inhibitor in synovium appears to be altered during inflammation. These results are consistent with the notion that synovium plays different roles in the cartilage damage of RA and of osteoarthritis.
Gene Expression (Collagenase, Tissue Inhibitor of Metalloproteinases, Complement, and HLA–DR) in Rheumatoid Arthritis and Osteoarthritis Synovium. Quantitative Analysis and Effect of Intraarticular Corticosteroids
Authors: Firestein Gary S. , Paine Mary M. , Littman Bruce H. 
Published: February 2007

AbstractIn situ hybridization was used to localize and quantify gene expression in rheumatoid arthritis (RA) and osteoarthritis (OA) synovial tissue. Collagenase, tissue inhibitor of metalloproteinases (TIMP), HLA–DR, and complement (C2 and C3) gene expression was studied in synovial tissue from 23 patients with RA, OA, or other inflammatory arthropathies. Gene expression was highly compartmentalized: Collagenase, TIMP, and C2 messenger RNA (mRNA) were localized primarily to the synovial lining layer; HLA–DR mRNA was prominent in the lining and in some sublining lymphoid aggregates; the C3 probe hybridized only to sublining lymphoid aggregates. Relative mRNA levels were quantified using computer‐assisted image analysis. There was significantly more collagenase, C2, C3, and HLA–DR mRNA in RA compared with OA patients. However, TIMP mRNA levels were similar in RA and OA. Expression of collagenase, TIMP, C2, C3, and HLA–DR genes correlated with the degree of synovial inflammation. The effect of intraarticular corticosteroid injection on synovial tissue gene expression was studied using serial percutaneous synovial biopsy samples from the knees of 3 RA patients. Joints were biopsied, injected with triamcinolone, and rebiopsied 1–2 weeks later. Histologic inflammation scores were lower in posttreatment synovia. Collagenase and TIMP mRNA, although abundant in presteroid samples, were nearly undetectable in post‐steroid tissues. HLA–DR mRNA levels also were significantly decreased. C2 and C3 hybridization significantly decreased in 2 of 3 patients and 1 of 3 patients, respectively. Hence, clinical response to intraarticular steroid therapy was accompanied by histologic improvement and decreased expression of genes that play a role in articular destruction. This study demonstrates the power of quantitative in situ hybridization as a tool for studying drug efficacy and mechanism.
Localization of Tumor Necrosis Factor α in Synovial Tissues and at the Cartilage–Pannus Junction in Patients With Rheumatoid Arthritis
Authors: Chu C. Q. , Field M. , Feldmann M. , Maini R. N. 
Published: February 2007

AbstractUsing immunoaffinity‐purified polyclonal anti‐human recombinant tumor necrosis factor α (TNFα) F(ab′)2 fragments and immunohistochemical techniques, the cells that make TNFα were localized in the inflamed synovial tissue of patients with rheumatoid arthritis (RA) and osteoarthritis (OA). Anti‐TNFα antibody–stained cells were demonstrated in 9 of 11 RA and 2 of 4 OA but none of 5 normal synovial membranes examined. In RA, 26–64% of the lining layer cells were positive for TNFα. In the interaggregate area, 10–30% of the cells contained TNFα, often in a perivascular distribution, and up to 19% of the cells in lymphoid aggregates stained for TNFα. Some endothelial cells also stained with these antibodies. In OA tissues, the TNFα‐containing cells were found predominantly in the deeper layer. Cells containing TNFα were also found at the cartilage–pannus junction in all 4 RA specimens examined. Double immunofluorescence analysis demonstrated that most TNFα‐secreting cells in the RA synovial membrane expressed the monocyte/macrophage marker antigens CD11b and CD14, and a few expressed the T cell marker CD3. Our findings provide histologic evidence that TNFα is locally produced in the lining and deeper layers of the synovium by cells of the mónocyte/macrophage lineage, supporting its role in inflammation. Further, our findings demonstrate that TNFα is produced by cells at the cartilage–pannus junction, which could affect chondrocyte metabolism, leading to the cartilage degradation in RA.
Autoantibodies to Human Stress Proteins. A Survey of Various Rheumatic and Other Inflammatory Diseases
Authors: Jarjour Wael N. , Jeffries Brentley D. , Davis John S. , Welch William J. , Mimura Toshihide , Winfield John B. 
Published: February 2007

AbstractUnselected sera from patients with various rheumatic, inflammatory bowel, and autoimmune skin diseases (n = 268) were examined against human cell lysate by immunoblotting procedures, to determine the prevalence of autoantibodies to stress proteins (heat‐shock proteins) hsp60 (homolog of Escherichia coli groEL and mycobacterial 65K antigens), hsp73, and hsp90. Using standard, sensitive and specific assay conditions, IgG and IgM autoantibodies to these stress proteins were not demonstrable, or were detected infrequently, in sera from control subjects (n = 36) and from patients with rheumatoid arthritis, Sjögren's syndrome, ankylosing spondylitis, Reiter's syndrome, systemic lupus erythematosus, and systemic sclerosis. Autoantibodies to hsp60 were relatively more common (≧20% of sera) in patients with mixed connective tissue disease, polymyositis/dermatomyositis, psoriatic arthritis, inflammatory bowel disease, epidermolysis bullosa acquisita, and bullous pemphigoid. Anti‐hsp73 autoantibodies were detected in 20% or more of the sera from patients with Lyme disease and ulcerative colitis. Taken together, these data extend the spectrum of autoimmune and inflammatory diseases in which humoral anti–stress protein autoreactivity develops. However, the paucity of humoral autoreactivity to stress proteins in patients with systemic lupus erythematosus and rheumatoid arthritis argues against a direct role of anti–stress protein autoantibodies in the pathogenesis of these disorders.