bluuebunny/crossref_metadata_2025_split huggingface dataset:
Activation of rat synovium by iron
Authors: Sousa Maria De , Dynesius‐Trentham Roselynn , Mota‐Garcia Fernando , Silva Manuel Teixeira Da , Trentham David E. 
Published: February 2007

AbstractWe observed a consistent sequence of activation changes in rat knee synovia following a single intravenous injection of sterile ferric citrate at a dosage sufficient to cause a transient saturation of transferrin. The initial alteration, appreciated 2 hours postinjection, consisted of an expansion in the lumen of synovial capillaries. At 8 hours, a thickening of the synovial lining and subsynovial tissue due to the hypervascularity and increased cellularity was noted, along with peaks in the mitotic activity of synovial cells (fourfold over baseline) and pinocytosis by endothelial cells. During the period of 8–24 hours, mature collagen appeared in the space between pericyte layers and between pericytes and endothelial cells, and 2–9‐fold increases in ferritin+, W3/13+, W3/25+, Ox8+, and Ox26+ mononuclear cells occurred. In contrast to the action on synovial fibroblasts, iron injection did not affect the mitotic activity of fibroblasts within the serosa of the small intestine. These findings demonstrate that, under experimental conditions, iron can readily induce changes in the synovium that are reminiscent of early events occurring in response to antigen.
Comparison of parotid and minor salivary gland biopsy specimens in the diagnosis of sjögren's syndrome
Authors: Wise Christopher M. , Agudelo Carlos A. , Semble Elliott L. , Stump Thomas E. , Woodruff Ralph D. 
Published: February 2007

AbstractWe conducted a prospective study comparing minor salivary gland and parotid gland biopsy specimens obtained simultaneously from 24 patients who were undergoing evaluation for primary Sjögren's syndrome (SS). Adequate tissue for study was obtained with all minor salivary gland biopsies and 19 of 24 parotid gland biopsies. Parotid inflammation was seen in 6 of 11 patients whose minor salivary gland biopsy results indicated SS, but in none of 8 patients who had normal findings on minor salivary gland biopsy. Patients with parotid inflammation were older and had a higher frequency of dry eyes and mouth, abnormal results on Schirmer's test, serious extraglandular involvement, and serologic abnormalities. We conclude that parotid gland biopsy adds very little to the minor salivary gland biopsy in the diagnosis of primary SS, but that parotid inflammatory changes may reflect disease duration and/or severity.
Immunologic dysfunction in scleroderma: evidence for increased mast cell releasability and hla–dr positivity in the dermis
Authors: Pearson Mark E. , Clark Huff J. , Giorno Ralph C. , Panicheewa Sucheelar , Claman Henry N. , Steigerwald James C. 
Published: February 2007

AbstractTo investigate the role of mast cells and cell‐mediated immunity in the pathogenesis of scleroderma, we studied wheal size after skin testing with compound 48/80, a liberator of mast cell histamine, and demonstrated increased mast cell releasability in skin that appeared normal, adjacent to involved skin. Immunofluorescent staining for HLA–DR showed dermal positivity in 12 of 13 involved‐ and 9 of 13 uninvolved‐skin biopsy specimens from scleroderma patients, compared with only 1 of 10 controls. By immunoperoxidase staining, most of the DR positivity was found in fibroblast‐like cells. These findings further support the notion of immunologic dysfunction in scleroderma.
Neonatal lupus risk to newborns of mothers with systemic lupus erythematosus
Authors: Lockshin Michael D. , Bonfa Eloisa , Elkon Keith , Druzin Maurice L. 
Published: February 2007

AbstractWe prospectively studied 91 infants born to women with systemic lupus erythematosus (SLE) or with SLE‐like disease. Thirty‐eight infants, including 3 sets of twins, were born to women who had anti‐Ro, anti‐La, or anti‐RNP antibodies. Four infants had definite neonatal lupus, and 4 had possible neonatal lupus. No prospectively studied infant had congenital heart block. The presence of neonatal lupus did not correlate with the titer of anti‐Ro antibodies. During the same time period, 2 additional babies with neonatal lupus and congenital heart block were born to mothers not previously known to have SLE. Taken together, these findings confirm the association of anti‐Ro antibody with neonatal lupus, but indicate that life‐threatening neonatal lupus is rare in children born to mothers who are known to have SLE, even when antibodies to Ro, La, or RNP are present. Prophylactic therapy is therefore not indicated for these women. An important proportion of mothers bearing children with neonatal lupus do not have recognized SLE and, currently, cannot be prospectively identified.
Soluble interleukin‐2 receptors in systemic lupus erythematosus
Authors: Wolf Robert E. , Brelsford William G. 
Published: February 2007

AbstractWe studied levels of soluble interleukin‐2 receptors (IL‐2R), which are released by activated lymphocytes, in 139 serum samples from 12 patients with systemic lupus erythematosus (SLE). Concentrations of soluble IL‐2R were significantly increased in SLE patients compared with controls (P < 0.001), and they were significantly higher in patients during active SLE defined by low C3 levels (P < 0.001), low C4 levels (P < 0.001), or proteinuria (P < 0.05) than during inactive SLE. Elevated levels of soluble IL‐2R correlated with hypocomplementemia in longitudinal studies (P < 0.001). Measurement of serum concentrations of soluble IL‐2R may provide a sensitive and specific method for monitoring disease activity and immune activation in patients with SLE.
Adjuvant‐induced polyarthritis. synovial cell activation prior to polyarthritis onset
Authors: López‐Bote Juan Pedro , Bernabeu Carmelo , Marquet Alberto , Fernández Jesús M. , Larraga Vicente 
Published: February 2007

AbstractWe studied synoviocytes obtained from rats that had been injected with Freund's complete adjuvant 12 days prior to killing. We found that several activation parameters were affected in these synoviocytes, namely, the concanavalin A protein‐binding pattern, the production of superoxide, and the appearance of the p77 polypeptide, which we have previously shown to be associated with the activation caused by the induction of polyarthritis. Our findings suggest that prior to the establishment of the inflammatory process, synoviocytes are in a state of activation, and may be a component of the molecular mechanism during the early stages of disease.
Synovial fluid lymphocytes in different subtypes of juvenile rheumatoid arthritis
Authors: Bergroth Ville , Konttinen Yrjö T. , Pelkonen Pirkko , Haapala Mervi , Haapasaari Jarkko , Nordström Dan , Kunnamo Ilkka , Friman Claes 
Published: February 2007

AbstractWe studied the subsets of synovial fluid (SF) lymphocytes and their activation states in 4 subtypes of juvenile rheumatoid arthritis. The expression of lymphocyte differentiation antigens and activation markers (Ia and Tac) appeared to be similar in these subgroups. Tac+ DNA‐synthesizing T blasts represented, at most, 5% of all SF mononuclear cells. This finding was in clear contrast to the high proportion of Ia‐positive SF mononuclear cells. There were no differences in Ia and Tac expression or DNA synthesis among the different juvenile rheumatoid arthritis subgroups. This finding suggests that the cell‐mediated immune response may represent secondary features of the disease that are involved as a final common pathogenetic pathway.
Apophyseal arthritis limits lumbar motion in patients with ankylosing spondylitis
Authors: Simkin Peter A. , Downey Daniel J. , Kilcoyne Ray F. 
Published: February 2007

AbstractAnkylosing spondylitis patients who develop progressive spinal flexion may assume this posture to alleviate the pain of apophyseal arthritis. To examine this relationship, we scored injury to L4–L5 and L5–S1 apophyseal joints, as assessed by computed tomography, in 10 men with early ankylosing spondylitis. Both by the modified Schober test and by radiography of the lateral spine, impaired spinal motion correlated highly with evidence of apophyseal injury.
Deficient phytohemagglutinin‐induced interleukin‐2 activity in patients with inactive systemic lupus erythematosus is correctable by the addition of phorbol myristate acetate
Authors: Murakawa Yohko , Sakane Tsuyoshi 
Published: February 2007

AbstractIn systemic lupus erythematosus (SLE) patients, the production of interleukin‐2 (IL‐2) by blood T lymphocytes in response to stimulation with phytohemagglutinin (PHA) either alone or with phorbol myristate acetate (PMA) or ionomycin, a Ca2+ ionophore, was examined. Deficiency in PHA‐stimulated IL‐2 production by cells from SLE patients was repaired by the addition of PMA, but not ionomycin. PMA alone did not stimulate IL‐2 production but, in concert with PHA, induced IL‐2 synthesis. Moreover, PMA was effective in the repair of the deficiency of PHA‐induced IL‐2 production by both T4+ and T8+ subsets. Thus, for effective IL‐2 production, SLE T cells required signals either distinct from or in addition to those supplied by PHA.
Elevated soluble interleukin‐2 receptor levels in the sera and synovial fluids of patients with rheumatoid arthritis
Authors: Keystone E. C. , Snow K. M. , Bombardier C. , Chang Chi‐Hsing , Nelson D. L. , Rubin L. A. 
Published: February 2007

AbstractIn a previous study, we used an enzyme‐linked immunosorbent assay to measure soluble human interleukin‐2 receptors (IL‐2R), and found that when activated lymphocytes produce cell‐associated IL‐2R, they also release a soluble form of IL‐2R into culture supernatants in vitro. Soluble IL‐2R have also been detected circulating in vivo at low levels in the serum of healthy individuals, and at abnormal levels in a variety of diseases, particularly those where immune dysfunction is thought to play an important role. We therefore evaluated serum IL‐2R levels in 77 patients with rheumatoid arthritis (RA), and compared them with levels in 46 age‐matched healthy controls. Nineteen additional RA patients with concurrently obtained sera and synovial fluid (SF) samples were compared with 14 patients with osteoarthritis of the knee or hip. The serum IL‐2R levels were significantly elevated in RA patients, compared with the control groups (P < 0.0001). Serum IL‐2R levels in the RA patients did not correlate with disease activity as determined by a variety of clinical and laboratory parameters. RA SF IL‐2R levels were significantly higher than corresponding RA serum IL‐2R levels (P = 0.0001). No such difference was noted in the osteoarthritis group, where serum and SF IL‐2R levels were comparable with serum levels in healthy controls. These findings support the hypothesis that in vivo lymphocyte activation plays an important role in RA; moreover, soluble IL‐2R measurement in serum and SF may be a very useful way to identify patients at risk for, or manifesting, a chronic immune‐mediated inflammatory arthropathy.
Hybridoma lupus autoantibodies can bind major cytoskeletal filaments in the absence of DNA‐binding activity
Authors: Senécal Jean‐Luc , Rauch Joyce 
Published: February 2007

AbstractA panel of 65 systemic lupus erythematosus (SLE) and 61 normal‐derived human hybridoma auto‐antibodies was studied for cytoskeletal reactivity, using an indirect immunofluorescence method. Reactivity with the cytoskeleton was expressed 3 times more frequently in the SLE‐derived antibody group and included intermediate filaments, microfilaments, microtubules, and centrioles. By immunoblot analysis, the antigenic specificity of intermediate filament—reactive SLE hybridoma antibodies was not restricted to vimentin, but included cytokeratins and desmin. The antibodies were also studied for their DNA‐binding, lupus anticoagulant, and rheumatoid factor activities. These autoantibody activities were expressed 3–5 times more frequently in the SLE‐derived group. The ability to bind DNA was not a prerequisite for reactivity with intermediate filament proteins. Our findings suggest that there are at least 2 subsets of cytoskeletal‐reactive hybridoma antibodies: those that recognize epitopes found only on cytoskeletal proteins, and those that recognize epitopes common to both DNA and certain cytoskeletal proteins. In addition, we hypothesize that there may be a third subset of antibodies that recognize a phosphate‐containing moiety (phospholipid or phosphoprotein) associated with cytoskeletal filaments.
Correlates of a clinical classification schema for the arthritis helplessness subscale
Authors: Stein Mitchell J. , Wallston Kenneth A. , Nicassio Perry M. , Castner Nancy M. 
Published: February 2007

AbstractWe examined the categorization of the helplessness subscale of the Arthritis Helplessness Index (AHI) into clinical ranges analogous to laboratory values, and the predictive validity of these cutoff scores over a 2‐year period. Data were obtained via questionnaires mailed every 6 months over 5 time periods to 368 patients who had been diagnosed as having rheumatoid arthritis. The results demonstrate that patients classified as low helpless were distinct from those classified as normal. In turn, those classified normal were distinct from high helpless patients on numerous measures of beliefs, affect, behavior, and symptom severity. Even after 2 years, the 5‐item helplessness subscale identified distinct clinical courses for these 3 groups.
Radial and spinal bone mineral density in a patient population
Authors: Mazess Richard B. , Barden Howard S. , Ettinger Mark 
Published: February 2007

AbstractDensity of the radius (by single‐photon absorptiometry) and the spine (by dual‐photon absorptiometry) was measured in 281 normal young women and in a large heterogenous group of 1,622 consecutive female patients. Both spinal and radial density were useful measurements when performed on patients with medical indications; spine and radius densities in these patients averaged 10–20% below those of age‐matched controls. However, patients younger than 60 years of age had deficits of spine density that were twice as large as those in the radius, and twice as many of these patients had spinal osteopenia, compared with those with radial osteopenia. After age 70, loss of density in the radius approximated that in the spine and the prevalence of osteopenia was similar at both sites. The poorer sensitivity of the radius measurement reflected the fact that it did not predict spine density. The standard error of the estimate was 0.12 gm/cm2 in normal subjects and 0.15 gm/cm2 in patients. At any given radial density, the spinal density of patients averaged 0.18 gm/cm2 (15–20%) below that in normal subjects. Predictions of spinal density from body weight were as accurate as predictions from radial density. Preferential spinal osteopenia occurring without radial osteopenia precluded radial densitometry as a screening method for individuals with osteoporosis before age 60. However, measurement of the radius was more effective than body weight for defining groups at risk, even though the radius did not reliably predict individual spine density. A radius shaft density < 0.55 gm/cm 2 occurring with a body weight < 55 kg was associated with a high prevalence of spinal osteopenia.
Peripheral lymphocyte depletion in gold sodium thiomalate—treated rheumatoid arthritis patients
Authors: Lundberg Max S. , Cannon Grant W. , Ward John R. 
Published: February 2007

AbstractIt has been reported that gold sodium thiomalate treatment of rheumatoid arthritis reduces the number of peripheral blood lymphocytes. In a prospective, double‐blind, randomized trial comparing gold sodium thiomalate, auranofin, and placebo in the treatment of rheumatoid arthritis, we investigated absolute lymphocyte counts. We found that peripheral lymphocyte counts decreased, but there was no correlation with clinical change in disease activity.
Bromocriptine suppresses postpartum exacerbation of collagen‐induced arthritis
Authors: Whyte A. , Williams R. O. 
Published: February 2007

AbstractWe administered bromocriptine (Parlodel) to arthritic mice immediately postpartum, and found that the drug suppressed the clinical exacerbation of joint involvement that was seen in untreated animals. Approximately 50% reduction in severity of disease was achieved with bromocriptine (P < 0.001). The effect may be due to suppression of the prolactin release that normally occurs postpartum.
Synovial microenvironment‐t cell interactions
Authors: Haynes Barton F. , Grover Betty J. , Whichard Leona P. , Hale Laura P. , Nunley James A. , Mccollum Donald E. , Singer Kay H. 
Published: February 2007

AbstractSynovitis in rheumatoid arthritis is characterized by infiltration of the synovium by T and B lymphocytes and monocytes, as well as by the proliferation of synovial lining cells, fibroblasts, and endothelial cells. To study synovial cell‐T cell interactions in vitro, we established cultures of fibroblast‐like synovial cells, and used these cells in a synovial cell‐T cell binding assay. Using T cells at various stages of differentiation and activation, we found that human thymocytes and mitogen‐activated peripheral blood T cells bound to fibroblast‐like synovial cells, whereas fresh peripheral blood T cells did not. Moreover, activated T cells from inflammatory synovial tissue or from synovial fluid also bound to fibroblast‐like synovial cells cultured in vivo. Antibodies against certain epitopes of the T cell CD2 (35.1) and synovial cell lymphocyte function‐associated antigen‐3 (LFA‐3) (TS2/9) molecules inhibited synovial cell‐thymocyte binding. However, these same anti‐CD2 and anti‐LFA‐3 antibodies only partially inhibited synovial cell binding to activated normal peripheral blood T cells. Moreover, T cells from inflammatory synovium from rheumatoid arthritis and psoriatic arthritis patients also bound to synovial cells in vitro. These findings demonstrate that fibroblast‐like synovial cells are capable of binding to human T cells in vitro, and suggest that during the course of inflammatory synovitis, synovial fibroblast‐T cell interactions may occur in vivo.
Dqβ polymorphism and genetic susceptibility to felty's syndrome
Authors: Alex K. L. SO , Warner Catherine A. , Sansom David , Walport Mark J. 
Published: February 2007

AbstractWe used an oligonucleotide probe specific for a polymorphic sequence in the HLA‐DQβ gene to investigate the role of DQ polymorphism in genetic susceptibility to Felty's syndrome (FS) and rheumatoid arthritis (RA). The sequence of this gene was identified from a complementary DNA library derived from an RA patient's B lymphoblastoid cell line. With this probe, we studied the prevalence of the specific DQβ allele in DR4 positive FS patients, RA patients, and normal control subjects. Significantly more FS patients (17 of 25) showed hybridization with this oligonucleotide probe, compared with the number of DR4 positive non‐FS RA patients (7 of 23) and normal controls (7 of 21). The findings indicate that genes linked to the DQ region are important in determining susceptibility to FS.
Anti‐ige autoantibodies in systemic lupus erythematosus
Authors: Gruber Barry L. , Kaufman Lee D. , Marchese Mary J. , Roth William , Kaplan Allen P. 
Published: February 2007

AbstractIgG and IgM autoantibodies directed against IgE were determined in 95 serum samples from 67 patients with systemic lupus erythematosus, by an enzyme‐linked immunosorbent assay. IgM anti‐IgE autoantibodies were found in 18 patients (27%) and IgG anti‐IgE autoantibodies were detected in 23 patients (34%). The specificity of the immunoassay was confirmed by the ability to inhibit binding with IgE myeloma, but not other immunoglobulin isotypes and the demonstration that the reactivity was directed to the Fc ε fragment of IgE. The IgG fraction of certain sera with anti‐IgE activity was capable of inducing histamine release from control basophils and cutaneous mast cells. Clinical associations with the presence of anti‐IgE activity were sought by retrospective chart analysis of 61 patients. Significant correlation was found with articular involvement, lymphadenopathy, and anti‐DNA antibodies (P < 0.05). Anti‐IgE autoantibodies are observed in a significant number of patients with systemic lupus erythematosus and may contribute to the pathogenesis of the vascular and articular lesions characteristic of this disease.
Distribution of chondroitin 4–sulfate and chondroitin 6–sulfate in human articular and growth cartilage
Authors: Mourão Paulo A. S. 
Published: February 2007

AbstractThe relative concentrations of chondroitin 4– and chondroitin 6–sulfate in different normal human cartilages are reported. Articular cartilages contained higher concentrations of chondroitin 6‐sulfate, whereas growth cartilages contained nearly equal amounts of chondroitin 4– and chondroitin 6–sulfate. Adult cartilages, in which the calcification process is already complete, contained only chondroitin 6–sulfate. The results suggest that chondroitin 6–sulfate is related to the integrity of the articular surfaces, whereas chondroitin 4–sulfate seems to be an important factor in the calcification process. The pathogenesis of the bone and cartilage alterations that occur in patients affected by heritable disorders of the sulfation of chondroitin sulfate are discussed in view of these findings.
Detection of tumor necrosis factor α but not tumor necrosis factor β in rheumatoid arthritis synovial fluid and serum
Authors: Saxne T. , Palladino M. A. , Heinegãrd D. , Talal N. , Wollheim F. A. 
Published: February 2007

AbstractSynovial fluids from 6 of 12 patients with rheumatoid arthritis (RA) and from 3 of 11 patients with reactive arthritis contained measurable levels of tumor necrosis factor α (TNFα). Seven of 12 sera from RA patients contained TNFα, while only 1 of those from reactive arthritis patients was positive. Gamma‐inter‐feron was detected in the synovial fluids and sera of only the RA patients. Tumor necrosis factor β was not detected in any sera or synovial fluids. RA patients with detectable TNFα had higher erythrocyte sedimentation rates and synovial fluid leukocyte counts.
Studies of a common idiotype pr4 in autoimmune rheumatic disease
Authors: Williams W. , Zumla A. , Behrens R. , Locniskar M. , Voller A. , Mcadam K. P. W. J. , Isenberg D. A. 
Published: February 2007

AbstractA new common idiotype, designated PR4, is described. This idiotype was originally identified on a human hybridoma‐derived monoclonal antibody from a patient with leprosy, which binds the major Mycobacterium leprae‐derived antigen, phenolic glycolipid‐1, poly(ADP)‐ribose, DNA, and poly(dT). The PR4 idiotype was found in patients with systemic lupus erythematosus (SLE) (70%), rheumatoid arthritis (40%), and Sjögren's syndrome (15%). It was not, however, found in the spouses of the SLE patients or (unlike other lupus idiotypes) in their healthy first‐degree relatives. Although no correlation between PR4 idiotype levels and disease activity in SLE was found, a subset of rheumatoid arthritis patients with high levels of the idiotype was identified.
Lupus retinopathy
Authors: Stafford‐Brady Frances J. , Urowitz Murray B. , Gladman Dafna D. , Easterbrook Michael 
Published: February 2007

AbstractIn a prospective study of 550 patients with systemic lupus erythematosus (SLE), 41 were found to have retinopathy. Lupus retinopathy in the majority of cases consisted of a microangiopathy, with an excellent prognosis for vision. Five patients developed other complications that resulted in loss of visual acuity. Lupus retinopathy was associated with active SLE in 88% of patients and with lupus cerebritis in 73% of cases. Retinopathy in SLE was a marker of poor prognosis for survival.