bluuebunny/crossref_metadata_2025_split huggingface dataset:
Immunohistologic analysis of the distribution of cell adhesion molecules within the inflammatory synovial microenvironment
Authors: Hale Laura P. , Martin Margaret E. , McCollum Donald E. , Nunley James A. , Springer Timothy A. , Singer Kay H. , Haynes Barton F. 
Published: February 2007

AbstractAntigen‐independent binding of T lymphocytes to a variety of cell types has been shown to be mediated by receptor–ligand pairs of adhesion molecules. In forms of inflammatory synovitis (including rheumatoid arthritis), T cells home to synovium, become activated, and participate in the generation of chronic synovitis. Using indirect immunofluorescence assays on synovial frozen tissue sections and on synovial fibroblast cell lines, we studied the distribution of cell adhesion molecules on components of the synovial microenvironment in inflammatory synovitis. We reasoned that analysis of the cell types within synovium that express adhesion molecules might provide clues to lymphocyte–stromal interactions that occur in inflammatory synovitis. We found that antibodies against the lymphocyte function‐associated antigen 3 (LFA‐3) molecule and the intercellular adhesion molecule 1 (ICAM‐1) both reacted with macrophage‐like type A synovial cells and synovial fibroblasts, as well as with tissue macrophages and vessel endothelium. Using flow cytometry, we found that anti‐LFA‐3 and anti–ICAM‐1 (but not antibodies against their ligands CD2 and LFA‐1) reacted with synovial fibroblast cells cultured in vitro. Thus, these data demonstrate that the ligands for lymphocyte LFA‐1 molecules (ICAM‐1) and for T cell CD2 molecules (LFA‐3) are widely distributed among cell types of the synovial microenvironment and provide numerous cell types with which lymphocytes can interact via these 2 adhesion pathways during the course of inflammatory synovitis.
1,25‐Dihydroxyvitamin D3 POtentiates the in vitro inhibitory effects of cyclosporin A on T cells from rheumatoid arthritis patients
Authors: Gepner Patrick , Amor Bernard , Fournier Catherine 
Published: February 2007

AbstractTreatment of rheumatoid arthritis (RA) with cyclosporin A (CsA) has been successful, but the adverse effects of the drug have limited its use. We investigated the capacity of another immunosuppressive agent, 1,25‐dihydroxyvitamin D3 [1,25(OH)2D3], to augment the effect of CsA on in vitro T cell functions. Exposure of CD4+ cells from RA patients or from normal subjects to either molecule alone resulted in a dose‐dependent inhibition of phytohemagglutinin stimulation and interleukin‐2 (IL‐2) production that was more pronounced in cells from RA patients than in cells from normal subjects. Moreover, the action of CsA and 1, 25(OH)2D3 on RA patient T cell functions in vitro was synergistic. Thus, in the presence of the vitamin D3 metabolite, only one‐hundredth the concentration of CsA was required to produce the same effect on IL‐2 production as that produced by CsA alone. IL‐2 receptor expression was also reduced by the addition of both drugs. In contrast, IL‐1 production by RA monocytes was not affected by CsA and 1,25(OH)2D3, either together or alone, and addition of IL‐1 did not restore the ability of CD4+ cells from RA patients to secrete IL‐2. Exogenous IL‐2 reversed a large part of the inhibitory effect induced by both CsA and 1, 25(OH)2D3, indicating that the immunosuppressive properties of these agents are mediated by the inhibition of IL‐2 secretion. This synergy between 2 molecules that are biochemically very different suggests the existence of one or several sites of interaction that take place during the early stages of T cell activation.
Demonstration of a cross‐reactive idiotype (idrq) in rheumatoid factors from patients with rheumatoid arthritis but not in rheumatoid factors from healthy, Aged subjects
Authors: Ruiz‐Arguelles Alejandro , Presno‐Bernal Miguel 
Published: February 2007

AbstractA human monoclonal IgMκ paraprotein with rheumatoid factor (RF) activity was used to elicit anti‐idiotypic antibodies in rabbits. The antiidiotypic anti‐serum thus obtained reacted with samples from 40% of 72 rheumatoid arthritis patients, but not with any of the samples from 22 aged control subjects having serum RF. Our findings suggest that, despite the similarities between RF from rheumatoid arthritis patients and that from healthy individuals, the expression of V region genes may be different in healthy subjects and those with the disease.
A longitudinal study of anticollagen antibodies in patients with rheumatoid arthritis
Authors: Morgan Keith , Clague Roy B. , Collins Ian , Ayad Shirley , Phinn Shirley D. , Holt P. J. Lennox 
Published: February 2007

AbstractAntibodies to native and denatured collagens (types I, II, IX, and XI) were measured in sequential serum samples collected over 1.5–8.7 years (median 4.3) from 15 patients with rheumatoid arthritis. Eleven patients were seropositive and 4 were seronegative. Disease duration ranged from 3 years to 25 years before the first sample was tested. The patients showed a selective and varying response to collagens, even after disease had been present for a long time. Changes in the levels of antibody to one collagen type were not necessarily linked to changes in the levels of antibody to other collagens. Only some patients showed a strong correlation between C‐reactive protein levels (a measure of disease activity) and antibodies to individual collagens. These findings suggest that rheumatoid arthritis patients produce antibodies to a wide variety of epitopes on these collagen molecules, as a result of different antigenic epitopes being exposed by cartilage degradation at different times throughout the disease.
Interleukin‐1 induces interleukin‐1α and interleukin‐1β gene expression in synovial fibroblasts and peripheral blood monocytes
Authors: Dalton Barbara J. , Connor Janice R. , Johnson William J. 
Published: February 2007

AbstractCellular interactions involved in the chronic inflammatory response, characteristic of those found in the joints of rheumatoid arthritis patients, were investigated by examining the effect of interleukin‐1 (IL‐1), tumor necrosis factor α, and γ‐interferon on the regulation of IL‐1 gene expression and production by synovial fibroblasts. Biologically active IL‐1 was detected in lysates of IL‐1–treated rat and human fibroblasts that had been isolated from synovial tissue by collagenase digestion. Northern blot analysis of RNA isolated from these cells revealed the expression of IL‐1α and IL‐1β transcripts. Neither the IL‐1 transcripts nor the biologic activity of IL‐1 was found in untreated synovial fibroblasts. The messenger RNA induction in synovial cells was followed by a time‐ and dose‐dependent expression of intracellular IL‐1 activity. Human monocytes and human skin fibroblasts also responded to IL‐1 treatment by producing IL‐1–specific transcripts. These observations suggest that IL‐1 plays a key role in stimulating immune and inflammatory responses and in sustaining those responses through continued production at sites of inflammation.
Independent effects of interleukin‐1 on proteoglycan breakdown, proteoglycan synthesis, and prostaglandin E2 release from cartilage in organ culture
Authors: Arner Elizabeth C. , Pratta Michael A. 
Published: February 2007

AbstractExposure of bovine nasal cartilage in culture to interleukin‐1 (IL‐1) leads to a time‐ and concentration‐dependent stimulation of proteoglycan breakdown and prostaglandin E2 (PGE2) release, and to inhibition of proteoglycan synthesis. The threshold levels of IL‐1 required for initiating these effects were different, and IL‐1 was 10 times more potent in inhibiting synthesis than in stimulating breakdown of proteoglycan. Kinetic studies indicated that the effects on proteoglycan metabolism occurred earlier (16–24 hours) than those for PGE2 release (48 hours). Selective effects were observed with inhibitors. Nonsteroidal antiinflammatory drugs blocked PGE2 production in response to IL‐1, but had no effect on proteoglycan metabolism, and the antiarthritic drugs that blocked IL‐1–stimulated breakdown augmented the inhibition of proteoglycan synthesis. We suggest that the effects of IL‐1 on proteoglycan breakdown, proteoglycan synthesis, and PGE2 release are mediated by independent post‐receptor mechanisms.
Binding of double‐stranded DNA to glomeruli of rats in vivo
Authors: Horgan Carol , Johnson Richard J. , Gauthier V. Joyce , Mannik Mart , Emlen Woodruff 
Published: February 2007

AbstractIn vivo binding of double‐stranded DNA (dsDNA) to renal glomeruli of rats was examined. 125I‐dsDNA (600 basepairs) was perfused with 131I‐IgG as a blood marker into the right renal artery of normal rats, and blood flow was restored. After 10 minutes, isolated glomeruli showed a specific uptake of DNA, which increased in a saturable fashion with increasing doses of administered DNA. To exclude the possibility that 125I in the glomeruli represented only DNA breakdown products, we extracted the DNA from the glomeruli for analysis by polyacrylamide gel electrophoresis. The extracted DNA was 120–200 bp in size, which is large enough to bind antibodies to DNA. In contrast, the radioactivity of DNA taken up by the liver or renal tissues other than glomeruli was predominantly tri‐chloroacetic acid soluble, i.e., <15 bp. Immunofluorescence studies showed that antibodies to DNA, administered after DNA, were present in glomeruli. Our data indicate that dsDNA binds to glomeruli in vivo in a saturable manner, and remains large enough to be antigenic. Therefore, the binding of DNA to glomeruli, followed by interaction with antibodies to dsDNA may be a mechanism for DNA–anti‐DNA complex formation in glomeruli in patients with systemic lupus erythematosus.
Elevated levels of serum hyaluronate and correlation with disease activity in experimental models of arthritis
Authors: Björk J. , Kleinau S. , Tengblad A. , Smedegård G. 
Published: February 2007

AbstractThe serum hyaluronate (HA) concentration was measured in groups of rats immunized for adjuvant or type II collagen arthritis. Serum HA increased as the arthritic lesions developed, correlating with the severity of the disease. This increase in HA was not related to metabolic impairment, because rats with adjuvant arthritis metabolized intravenously administered tritiated HA at a rate similar to that of normal rats. Serum HA levels may be useful as an indicator of synovitis in experimental and possibly in clinical arthritis. Further, this model could serve as an experimental approach for studies of HA metabolism in chronic joint inflammation.
Suppression of glycosaminoglycan synthesis by articular cartilage, but not of hyaluronic acid synthesis by synovium, after exposure to radiation
Authors: Hugenberg Steven T. , Myers Stephen L. , Brandt Kenneth D. 
Published: February 2007

AbstractWe recently found that injection of 2 mCi of yttrium 90 (90Y; ∼123,000 rads) into normal canine knees stimulated glycosaminoglycan (GAG) synthesis by femoral condylar cartilage. The present investigation was conducted to determine whether radiation affects cartilage metabolism directly. Rates of GAG synthesis and degradation in normal canine articular cartilage were studied following irradiation. Cultured synovium from the same knees was treated similarly, to determine the effects of irradiation on hyaluronic acid synthesis. Twenty‐four hours after exposure to 1,000 rads, 10,000 rads, or 50,000 rads, 35S‐GAG synthesis by the cartilage was 93%, 69%, and 37%, respectively, of that in control, nonirradiated cartilage. The effect was not rapidly reversible: 120 hours after exposure to 50,000 rads, GAG synthesis remained at only 28% of the control level. Autoradiography showed marked suppression of 35S uptake by chondrocytes after irradiation. Cartilage GAG degradation was also increased following irradiation: 4 hours and 8 hours after exposure to 50,000 rads, the cartilage GAG concentration was only 66% and 54%, respectively, of that at time 0, while corresponding values for control, nonirradiated cartilage were 90% and 87%. In contrast to its effects on cartilage GAG metabolism, radiation at these levels had no effect on synovial hyaluronic acid synthesis.
inflammatory myopathy and acquired immunodeficiency syndrome
Authors: Nordstrom David M. , Petropolis Angelo A. , Giorno Ralph , Gates Robert H. , Reddy Vishnu B. 
Published: February 2007

AbstractA 33‐year‐old black woman with advanced acquired immunodeficiency syndrome (AIDS) presented with rapidly progressive muscle weakness and serologic and radiologic evidence of central nervous system Toxoplasma infection. Muscle biopsy revealed an inflammatory infiltrate predominantly composed of macrophages and T suppressor/cytotoxic cells. Human immunodeficiency virus major core protein (p24) was also detected in macrophages and damaged muscle cells around the inflammatory infiltrates. The patient improved clinically with glucocorticoid therapy for polymyositis and pyrimethamine and clindamycin therapy for toxoplasmosis.
Idiotypic characteristics of immunoglobulins associated with systemic lupus erythematosus. Studies of antibodies deposited in glomeruli of humans
Authors: Kalunian Kenneth C. , Panosian‐Sahakian Niver , Ebling Fanny M. , Cohen Arthur H. , Louie James S. , Kaine Jeffrey , Hahn Bevra H. 
Published: February 2007

AbstractIndirect immunofluorescence with monoclonal antibodies to 6 different idiotypes was used to characterize immunoglobulins deposited in the glomeruli of renal biopsy samples from 32 patients with systemic lupus erythematosus (SLE) and 19 patients with nonlupus immune glomerulonephritis. IdGN2 was present in 75% of the biopsy specimens from SLE patients and in 6% of those from patients with non‐lupus nephritis; IdGN1 occurred in 38% and 6%, respectively. The other idiotypes were not increased in biopsy samples from patients with SLE. Deposition of IdGN2 was associated with a subendothelial location of Ig and proliferative changes in the glomeruli. In studies of glomerular eluates from 4 immunosuppressed SLE patients, an average of 26% of total Ig and 37% of anti‐DNA was composed of IdGN2. Compared with IdGN2– immunoglobulin, IdGN2+ immunoglobulin was enriched in IgG1 in all 4 eluates, and was enriched in high‐avidity anti‐DNA in 2 eluates. IdGN2 is a marker of antibody subsets that are characteristic of SLE and are associated with severe lupus nephritis.
Antibodies to the collagen‐like region of C1q in sera of patients with autoimmune rheumatic diseases
Authors: Wener Mark H. , Uwatoko Shu , Mannik Mart 
Published: February 2007

AbstractAntibodies to the collagen‐like region of C1q have recently been observed in sera of patients with systemic lupus erythematosus (SLE). In this study, we documented that these antibodies were present in 47.3% of SLE patient sera, whereas they were uncommon in sera from patients with rheumatoid arthritis (2.8%) and Sjögren's syndrome (12.8%), as well as in normal sera (6.4%). Markedly elevated antibody levels (>4 SD above the normal mean) were observed almost exclusively in sera of patients with SLE. Levels of antibodies to the collagen‐like region correlated highly with levels of solid‐phase C1q‐binding IgG when analyzed by the C1q solid‐phase assay for immune complexes (r = 0.87). We previously found that, after sucrose density gradient ultracentrifugation, a predominance of the solid‐phase C1q‐binding IgG in SLE sera sediments as monomeric IgG. These findings, together with the present data, indicate that reactivity of SLE patients' sera in the C1q solid‐phase assay reflects primarily the presence of antibodies to the collagen‐like region, and not the presence of immune complexes.
A reexamination of the effectiveness of self‐care education for persons with arthritis
Authors: Goeppinger Jean , Arthur Michael W. , Baglioni Anthony J. , Brunk Susan E. , Brunner Carolyn M. 
Published: February 2007

AbstractWe examined the effectiveness of 2 models of arthritis self‐care intervention, the home study model and the small group model. The effects of disease diagnosis and duration, self‐care behavior, perceived helplessness, social support, treatment choice, and formal education level on outcomes among persons with arthritis who participated in these programs were evaluated. A pretest–posttest control group design was utilized in the initial experimental study; comparison group designs were used in the longitudinal studies. Three hundred seventy‐four subjects completed the interventions and 12 months of research followup. We found that the intervention models had a statistically significant positive impact on arthritis knowledge, selfcare behavior, perceived helplessness, and pain. These findings did not vary when the effects of education level, disease diagnosis and duration, informal social support, and treatment choice were controlled. The small group intervention was more effective in bringing about initial improvements in pain and depression, whereas the home study intervention was more effective in maintaining improvements in perceived helplessness. Changes in perceived helplessness and self‐care behavior appear to explain in part the observed improvement in pain.
Clinical heterogeneity and treatment response in inclusion body myositis
Authors: Cohen Miriam Richter , Sulaiman A. R. , Garancis John C. , Wortmann Robert L. 
Published: February 2007

AbstractInclusion body myositis has been described as an inflammatory myopathy with distinctive clinical and pathologic features that is refractory to treatment. Ten cases of inclusion body myositis, as defined by histopathologic findings, were reviewed to determine whether the clinical characteristics are different in patients whose disease has been defined by light and electron microscopic studies compared with those whose disease has been defined by light microscopic studies alone. The clinical characteristics of both groups of patients were similar, and 2 patients have had excellent responses to treatment. Although inclusion body myositis represents a histologic subset of polymyositis, from a clinical perspective, it must be considered a nonspecific designation. Despite a generally poor prognosis, therapeutic intervention is still warranted.
Age‐ and sex‐related differences in antigen‐induced arthritis in c57bl/10 mice
Authors: van Beuningen Henk M. , van Den Berg Wim B. , Schalkwijk Joost , Arntz Onno J. , van De Putte Levinus B. A. 
Published: February 2007

AbstractThe influence of both age and sex on antigen‐induced arthritis in C57Bl/10 mice was studied. Methylated bovine serum albumin was used to induce arthritis in young adult (3 months) and old (18 months) male and female mice. Arthritis became chronic and led to severe joint damage more often in 18‐month‐old female mice, compared with both young adult female mice and with male mice of both ages. T cell immunity and levels of antibodies against methylated bovine serum albumin were comparable in all groups. Antigen retention in the joint was greater in old compared with young adult mice of both sexes, and could therefore not entirely explain the increased prevalence of persistent arthritis in old females. Our data suggest that female hormones, in combination with age, are important factors in the chronicity and destructive character of this type of arthritis.
Validity of the center for epidemiological studies depression scale in arthritis populations
Authors: Blalock Susan J. , Devellis Robert F. , Brown Gregory K. , Wallston Kenneth A. 
Published: February 2007

AbstractUsing data from 3 studies of patients with rheumatoid arthritis, we examined the extent to which responses to items in the Center for Epidemiological Studies Depression Scale (CES‐D) are influenced by aspects of the disease process other than depression. Our findings suggested that 4 CES‐D items (i.e., “I felt that everything I did was an effort,” “I felt hopeful about the future,” “My sleep was restless,” and “I could not get going”) may be influenced by aspects of the disease process and, thus, are not necessarily indicative of depression among persons with arthritis. The impact that these items have on the interpretation of CES‐D scores was assessed in relation to 2 research issues: estimation of the prevalence and severity of depression in arthritis populations and identification of the determinants of depression among individuals with arthritis. Our results suggest that the original CES‐D may overestimate the prevalence and severity of depression among patients with arthritis. The magnitude of this bias is modest, however. The results also suggest that in studies designed to identify the determinants of depression among individuals with arthritis, inclusion of the 4 items identified is unlikely to have any effect on study findings.
Serum IgG antibodies to C1q in hypocomplementemic urticarial vasculitis syndrome
Authors: Wisnieski Jeffrey J. , Naff George B. 
Published: February 2007

AbstractUrticaria, angioedema, and arthritis are cardinal features of hypocomplementemic urticarial vasculitis syndrome (HUVS). Considered to be an immune complex–mediated disorder, HUVS has been differentiated from systemic lupus erythematosus (SLE), based on its clinical manifestations and the C1q precipitin (C1q‐p) reaction, which is manifested as gel precipitation of C1q by a small percentage of HUVS IgG molecules. This phenomenon has been attributed to an Fc region abnormality, and the responsible IgG molecules are said to possess C1q‐p activity. We purified IgG from 4 HUVS patients and confirmed that HUVS IgG contains C1q binding activity. F(ab')2 fragments from these patients also bound to C1q, as measured by 2 different C1q binding methods at physiologic ionic strength; HUVS IgG Fc fragments did not bind to C1q. Preincubation of HUVS F(ab')2 fragments with antibody to human F(ab')2 prevented subsequent binding to C1q. We conclude that IgG antibodies to C1q are present in HUVS serum, and it is likely that these antibodies are C1q‐p. Because the clinical manifestations of HUVS and the presence of anti‐C1q antibodies have been described in patients with SLE, our findings support the concept that HUVS is an autoimmune syndrome related to SLE.
Septic acromioclavicular arthritis and osteomyelitis in a patient with acquired immunodeficiency syndrome
Authors: Iii Bernard Zimmermann , Erickson Allan D. , Mikolich Dennis J. 
Published: February 2007

AbstractWe describe a patient with acquired immunodeficiency syndrome who developed Staphylococcus aureus septic arthritis and osteomyelitis of the acromioclavicular joint. The case is unusual because of the rarity of reported bone and joint infections in patients with acquired immunodeficiency syndrome and because of the indolent nature of the infection.
Levels of chondroitin‐6‐sulfate and nonaggregating proteoglycans at articular cartilage contact sites in the knees of young dogs subjected to moderate running exercise
Authors: Säämänen Anna‐Marja , Tammi Markku , Kiviranta Ilkka , Jurvelin Jukka , Helminen Heikki J. 
Published: February 2007

AbstractThe levels and types of proteoglycans in articular cartilage of the knees of young beagle dogs were studied after 15 weeks of running exercise, at 4 km/day. Running increased the levels of proteoglycans in the cartilage of the patella, the superior patellofemoral groove, and the summit of the medial condyle of the femur, all of which are considered contact sites subject to enhanced loading caused by running. The elevated content of uronic acid at the femoral sites proved to be due to proteoglycans that were unable to aggregate with hyaluronic acid. There was no change in the content of aggregating proteoglycans. Analysis of chondroitinase AC–derived disaccharides at the same sites showed an increase in chondroitin‐6‐sulfate content as compared with chondroitin‐4‐sulfate levels. We believe that this modulation of the proteoglycan matrix reflects enhanced tissue maturation and physiologic adjustment to higher local contact pressures.