bluuebunny/crossref_metadata_2025_split huggingface dataset:
Auto antibodies in the cerebrospinal fluid of patients with systemic lupus erythematosus
Authors: Golombek Steven J. , Graus Francesc , Elkon Keith B. 
Published: February 2007

AbstractAutoantibodies may play an important role in the pathogenesis of central nervous system (CNS) disease in systemic lupus erythematosus (SLE). We obtained cerebrospinal fluid (CSF) and, in some cases, sera from 19 SLE patients with CNS lupus and from 12 SLE patients without CNS lupus. Autoantibodies to saline soluble cellular antigens were detected in the CSF of lupus patients and reflected those present in the serum. These antibodies were distinct from the previously described antineuronal antibodies. Analysis of the fine specificities of the anti‐saline soluble cellular antigen antibodies revealed that the antiribosomal P protein antibody was present in 4 of 4 patients with lupus psychosis and was enriched in the CSF of 1 patient. Sera containing antiribosomal P protein showed prominent cytoplasmic staining of human cortical neurons, as well as an epithelial cell substrate. These observations, together with the increase in intrathecal IgG synthesis detected in 71% of patients tested, suggest that several populations of antibodies may contribute to the enhanced immunologic activity in the CSF of CNS lupus patients.
Cryoglobulinemia in autoimmune rheumatic diseases: Evidence of circulating monoclonal cryoglobulins in patients with primary Sjögren's syndrome
Authors: Tzioufas A. G. , Manoussakis M. N. , Costello R. , Silis M. , Papadopoulos N. M. , Moutsopoulos H. M. 
Published: February 2007

AbstractThe incidence and nature of cryoglobulins, as well as their correlation with the clinical and serologic picture of Sjögren's syndrome (SS), were studied in the sera of 30 consecutive primary SS patients. Sera from 29 patients with systemic lupus erythematosus, 58 patients with rheumatoid arthritis, and 125 healthy blood donors were also studied. It was shown that one‐third of the patients with SS had cryoglobulinemia. These cryoglobulins were mixed monoclonal IgM immunoglobulins, whereas those observed in systemic lupus erythematosus and rheumatoid arthritis patients were mixed polyclonal. The nature of the cryoglobulins was demonstrated using high‐resolution electrophoresis combined with immunofixation. The presence of cryoglobulins in the sera of SS patients correlated with extraglandular disease and with antibodies to Ro (SS‐A) and IgM rheumatoid factor. SS patients with cryoglobulins had lower serum C4 levels than did patients without cryoglobulins. These findings suggest that SS expresses, in addition to polyclonal B cell hyperreactivity, a monoclonal process in the absence of lymphoid neoplasia. Further, they show that the extraglandular manifestations of the syndrome may be due to an immune complex‐mediated pathology.
Expression of histocompatibility antigen HLA—DR by salivary gland epithelial cells in Sjögren's syndrome
Authors: Fox Robert I. , Bumol Thomas , Fantozzi Richard , Bone Robert , Schreiber Robert 
Published: February 2007

AbstractRecent studies have suggested that the induction of HLA—DR antigens on epithelial cells plays an important role in the pathogenesis of autoimmune endocrine‐exocrine disorders. We found that salivary gland epithelial cells (i.e., acinar and ductal cells) in salivary gland biopsy specimens from patients with primary Sjögren's syndrome (keratoconjunctivitis sicca) expressed high levels of HLA—DR antigen, which were detected by staining frozen tissue sections with monoclonal antibodies and immunoperoxidase technique. In contrast, salivary gland epithelial cells from normal subjects did not express this antigen. Lymphocytes eluted from the salivary gland biopsy specimens of patients who had Sjögren's syndrome produced a soluble factor that stimulated HLA—DR synthesis by a salivary gland‐derived cell line (Sal‐1). These tissue culture supernatants contained γ‐interferon, and their ability to induce HLA—DR synthesis was blocked by monoclonal anti‐γ‐interferon antibody. These results demonstrate the presence of HLA—DR antigen on salivary gland epithelial cells and suggest that local production of γ‐interferon plays a role in this induction.
Neutral proteases in human osteoarthritic synovium
Authors: Martel‐Pelletier J. , Cloutier J. M. , Pelletier J. P. 
Published: February 2007

AbstractThe activities of neutral collagenolytic enyzmes (CE) and neutral proteoglycan‐degrading enzymes (PE) in the synovial membranes of osteoarthritis (OA) patients were determined. The total neutral metallo‐CE activity showed a significantly higher level of activity when the membranes of OA patients were compared with those of controls. The severely and moderately inflamed synovia had significantly more enzyme activity than did either mildly inflamed or control synovia. Steroids reduced the total metallo‐CE activity. In specimens with severe inflammation, the active form of the neutral metallo‐CE was significantly elevated over that found in controls. The serine‐CE activity was also significantly elevated in OA synovia with severe inflammation and synovial hypertrophy. The total and active neutral metallo‐PE was significantly elevated in synovial membranes of OA patients with severe inflammation. Moreover, the serine‐PE showed much more activity in OA patients than in controls. The enzyme activity remained at a significantly high level in the OA synovium, regardless of the presence or absence of macroscopic synovial hypertrophy or the histologic grading of the synovium (mild, moderate, severe). Our data indicate that, in OA, an increased level of neutral proteases in the synovia could be involved in the local tissue destruction of the periarticular structures. Because of the very high level of serine proteases, their diffusion may render plausible a degradative action on the cartilage surface.
Macrophage activation in rat models of inflammation and arthritis: Systemic activation precedes arthritis induction and progression
Authors: Johnson William J. , Muirhead Katharine A. , Meunier Paul C. , Votta Bart J. , Schmitt Thomas C. , Dimartino Michael J. , Hanna Nabil 
Published: February 2007

AbstractThe association between the induction and progression of adjuvant‐induced arthritis (AA) and the development of synovial and systemic macrophage activation was assessed by studying the temporal development of these parameters in a rat model. Rats with AA developed significant edema of the uninjected hind leg beginning 10 days post‐adjuvant injection, with progressive increases in edema continuing through day 17. Several parameters of macrophage activation, including the enhanced ability to secrete interleukin‐1 and prostaglandin E2, kill tumor cells, accumulate fluorescent cyanine dyes, emigrate into the peritoneal cavity and synovium, and express Ia antigen, as well as the decreased ability to secrete superoxide anion, were associated temporally with the development of the arthritic lesion. In addition to the temporal association between macrophage activation and development of arthritis, a positive correlation between macrophage activation and arthritis induction was seen with the use of synthetic adjuvants at arthritogenic and nonarthritogenic doses. These data taken together suggest that induction and progression of AA in rats is associated with both systemic (blood, spleen, and peritoneal cavity) and local (synovium) macrophage activation.
Detection of native and denatured DNA antibody forming cells by the enzyme‐linked immunospot assay: A clinical study of (New Zealand black × New Zealand white)F1 mice
Authors: Ando Dale G. , Ebling Fanny M. , Hahn Bevra H. 
Published: February 2007

AbstractA new method for measuring DNA antibody forming cells (DNA‐AFC) using the enzyme‐linked immunospot (ELISPOT) assay is described. This method uses enzyme‐linked immunosorbent assay (ELISA) techniques applied to cells cultured on DNA‐coated plates, which allows visual quantitation of spots representing imprints of specific antibodies from DNA‐AFC. Specificity for DNA was confirmed by inhibition studies and lack of reactivity by anti‐lysozyme hybridomas. Isotypes of IgG and IgM can be measured using the appropriate antisera in the assay. A study of 16 female (New Zealand black × New Zealand white)F1 ([NZB × NZW]F1) female mice showed significant correlation between age, rising blood urea nitrogen levels, and increasing proteinuria and increasing numbers of DNA‐AFC. In contrast, the correlation between circulating antibodies to DNA (ELISA method) and clinical parameters of nephritis was not significant. Both the native DNA ELISPOT and the native DNA ELISA had similar significant linear correlations with age. This is the first report of use of the ELISPOT assay for measurement of DNA‐AFC. The DNA‐AFC measured by this method were specific and correlated with the presence of clinical nephritis in (NZB × NZW)F1 mice. This method should allow further study on the regulation of DNA‐AFC in vitro and in vivo, and will be useful in the investigation of DNA‐AFC and cellular mechanisms of autoimmunity.
Eosinophilic synovitis: Clinical observations on A newly recognized subset of patients with dermatographism
Authors: Brown Jacques P. , Rola‐Pleszczynski Marek , Menard Henri‐A. 
Published: February 2007

AbstractEosinophilia of synovial fluid is uncommon. Using the identification of Charcot‐Leyden crystals to alert for the presence of eosinophils, we have increased by a factor of 5 the detection rate of synovial fluid eosinophilia. We describe here our clinical and laboratory findings in 7 patients with this feature. We believe they constitute a defined syndrome. Typically, the patients were young (ages 18–51) and had a personal and family history of allergy. They developed an acute, painless monarthritis after a minor trauma, and had no concurrent allergic symptoms. Each episode resolved in 1–2 weeks without therapy, and 3 patients had recurrences. All had pronounced dermatographism. The synovial fluid was mildly inflammatory: 10,850 ± 3,665 white blood cells/mm3, with 41 ± 5% eosinophils (mean ± SEM). The cellularity and chemistry of the peripheral blood was unremarkable, except for a mild elevation of IgE levels (370 ± 104 IU/ml). The exact pathophysiologic mechanism underlying this benign entity is not clear, but we suspect a nonimmunologic triggering event is operant, i.e., synovial trauma which mimics the cutaneous dermatographism.
Intraarticular ferritin‐bound iron in rheumatoid arthritis: A factor that increases oxygen free radical‐induced tissue destruction
Authors: Biemond Pieter , Swaak Antonius J. G. , Van Eijk Henk G. , Koster Johan F. 
Published: February 2007

AbstractIron mobilized from ferritin is able to convert superoxide and hydrogen peroxide, which are produced in large amounts in rheumatoid arthritis (RA), to the extremely toxic hydroxyl radical. We have found that synovial fluid ferritin is increased significantly in RA patients compared with levels in controls. The high synovial fluid:serum ferritin ratio is compatible with the hypothesis that synovial fluid ferritin is derived from the synovial membrane. We found no difference in ferritin concentrations in the synovial membranes of RA patients compared with those of controls. Quantitative data on the amount of iron bound to ferritin showed that the level was 2.9 times higher in RA synovial membranes than in those of controls. Moreover, RA synovial fluid contained considerable amounts of iron bound to ferritin. Calculation of the iron saturation of ferritin revealed that RA synovial membranes contained a mean of 2,210 moles of iron per mole of ferritin: a significant elevation when compared with the mean value of 1,500 moles found in the synovial membranes of the controls. The decreased saturation of ferritin in RA synovial fluid, compared with that in the synovial membrane, could be caused by an uncompensated release of iron from ferritin, which has been induced by superoxide that is produced by stimulated granulocytes. The results demonstrate that in the joints of RA patients, sufficient ferritin loaded with iron is available to stimulate oxygen free radical damage.
Group therapies for rheumatoid arthritis: A controlled study of two approaches
Authors: Strauss Gordon D. , Spiegel Jane Sinden , Daniels Marcia , Spiegel Timothy , Landsverk John , Roy‐Byrne Peter , Edelstein Carole , Ehlhardt Johanna , Falke Roberta , Hindin Lee , Zackler Les 
Published: February 2007

AbstractAn important unanswered question about rheumatoid arthritis (RA) is how the patient's psychological or emotional state relates to disease activity and functional status. No controlled studies of psychothera‐peutic interventions in RA have been reported. To test the hypothesis that a psychosocial intervention would lead to improvement in functional status or disease activity, 57 RA patients were randomly assigned to 1 of 3 groups, which received: 1) conventional group psychotherapy; 2) group assertion/relaxation training; or 3) no treatment (control group). Patient and physician questionnaires collected at baseline, immediately after the interventions, and 12 months after baseline provided outcome data on functional status, social and psychological adaptation, psychological symptoms, and disease activity. There were few outcome measures for which either treatment resulted in significantly higher scores than were seen in controls, though more improvement did occur among patients who received conventional group psychotherapy.
Deficient γ‐interferon production in patients with systemic lupus erythematosus
Authors: Tsokos George C. , Boumpas Dimitri T. , Smith Paula L. , Djeu Julie Y. , Balow James E. , Rook Alain H. 
Published: February 2007

AbstractWe examined the ability of peripheral mononuclear cells (MNC) from patients with systemic lupus erythematosus (SLE) to produce γ‐interferon (γ‐IFN) in vitro. MNC from patients with SLE produced varying amounts of γ‐IFN upon mitogenic stimulation. However, they produced distinctly decreased amounts of γ‐IFN upon in vitro stimulation with interleukin‐2 (IL‐2). Deficient production seemed to be primary, rather than secondary to either excessive monocytic suppresion or failure of IL‐2 to bind to the MNC surface membranes. γ‐IFN‐specific RNA transcription, as determined by slot‐blot analysis, was severely decreased in MNC that had been stimulated with phytohemag‐glutinin or IL‐2. These findings suggest that MNC of patients with SLE have defects in the IL‐2 signal transduction which is required for production of γ‐IFN.
DNA‐daunorubicin complexes specifically suppress in vitro spontaneous anti‐DNA antibody production in lymphocytes of patients with systemic lupus erythematosus
Authors: Takeuchi Tsutomu , Koide Jun , Hosono Osamu , Amano Koichi , Homma Mitsuo , Masuho Yasuhiko , Morimoto Chikao , Takano Makoto , Abe Tohru 
Published: February 2007

AbstractElevated production of anti‐DNA antibody in patients with systemic lupus erythematosus (SLE) is a central problem in the pathogenesis of tissue injury. In the present study, we attempted to manipulate anti‐DNA antibody production through the antigen‐cytotoxic drug conjugates, DNA‐daunorubicin complexes. The effect of DNA‐daunorubicin complexes was determined by examining SLE lymphocytes for spontaneous in vitro production of anti‐DNA antibody. These complexes, at 2 μg/ml, suppressed anti‐DNA antibody production, but not total IgG production, which suggests that specific suppression of anti‐DNA antibody production was achieved at this concentration. We believe that the DNA‐daunorubicin complexes affected mainly B cells, since such suppression was obtained by treating B cells, as well as B plus T cells. Furthermore, the complexes had no effect on the proliferative responses of SLE T cells to DNA, phytohemagglutinin, or concanavalin A. These results indicate that DNA‐daunorubicin complexes may have the potential for selectively suppressing anti‐DNA antibody production in patients with SLE.
Evidence of an immunopathogenic basis for central nervous system disease in primary Sjögren's syndrome
Authors: Alexander Elaine L. , Lijewski Jane E. , Jerdan Myles S. , Alexander Garrett E. 
Published: February 2007

AbstractThe pathogenesis of central nervous system complications in primary Sjögren's syndrome (CNS‐SS) is unknown. In order to determine whether patients with active CNS‐SS have cerebrospinal fluid (CSF) abnormalities indicative of CNS inflammation, CSF analyses from 30 patients with active CNS‐SS (SSA) were contrasted with those from 20 SS patients without CNS involvement (SSI) and 20 patients with systemic lupus erythematosus and active CNS disease (SLEA). Elevations of total protein concentration, IgG concentration, IgG to total protein ratio, and IgG index were observed in patients with SSA, but not in those with SSI. Agarose gel electrophoresis results were abnormal, with 1 or more bands, in 25 of 29 SSA patients (86%), but in only 3 of 18 SSI patients (17%). Similar, but less striking, CSF abnormalities were seen in a minority of SLEA patients. Fifteen SSA patients (50%) had transient, mild‐to‐moderate CSF pleocytosis, while only 1 SSI patient and 2 SLEA patients had similar findings. Cytologic findings were abnormal in 18 SSA patients (60%); these included atypical mononuclear cells, lymphoblastoid cells, and plasma cells. The presence of immuno‐competent cells and evidence for the intrathecal synthesis of IgG within the CSF of SSA, but not SSI, patients provide diagnostic parameters which are indicative of active disease and which can be monitored serially during therapy.
Incidence of arthritis in urban finnish children: A prospective study
Authors: Kunnamo Ilkka , Kallio Pentti , Pelkonen Pirkko 
Published: February 2007

AbstractThe incidence of various types of arthritis in children was estimated by a prospective 1‐year study in the greater Helsinki area (population under 16 years of age: 148,362). Patients were sought from primary care physicians, and 71% of the patients studied were seen within 1 week of the onset of symptoms. All patients received followup care for at least 3 months; patients whose symptoms were prolonged received followup care for a minimum of 2 years. The incidence per 100,000 children under 16 years of age was as follows: 108.5 for all cases of arthritis, 6.7 for septic arthritis, 5.4 for enteropathic arthritis, 51.9 for transient synovitis of the hip, 18.9 for prolonged arthritis (duration >3 months), and 25.8 for acute transient arthritis. The incidence of juvenile rheumatoid arthritis was 19.6. Oligoarticular disease was prevalent (76%) among the juvenile rheumatoid arthritis patients.
Heterogeneity of proteoglycans extracted before and after collagenase treatment of human articular cartilage: I. Physical properties related to age
Authors: Van De Stadt Rob J. , Kuijer Roel , Van Kampen G. P. Jos , De Koning Margret H. M. T. , Van De Voorde‐Vissers Els , Van Der Korst Jan K. 
Published: February 2007

AbstractProteoglycans were isolated from young and mature human articular cartilage 4 different ways: by direct extraction with 4M guanidine hydrochloride (GuHCl); after digestion of the residue from this first extraction with collagenase, by extraction with 4M GuHCl; associatively with 0.5M GuHCl after digestion of the cartilage with collagenase; and dissociatively with 4M GuHCl after digestion of the cartilage with collagenase. The structural properties of these proteoglycans were compared. Proteoglycan aggregates and monomers isolated from second extractions and from young cartilage were of larger hydrodynamic size than proteoglycans isolated from first extractions and mature cartilage, respectively. The same applied to the chondroitin sulfate chain lengths of these proteoglycans. The proteoglycan fraction from second extractions of cartilage contained a larger proportion of monomers than the fraction from first extractions. Associative extraction of mature collagenase‐digested cartilage yielded mainly proteoglycan monomers, whereas an appreciable amount of proteoglycan aggregate was also liberated from young collagenase‐digested cartilage. Our results indicate that, because of their larger size, proteoglycans from second extractions of cartilage are more entrapped in the collagen network. These large proteoglycans can only be liberated from the matrix after extraction of the smaller proteoglycans, followed by digestion of the residue with collagenase. This indicates that proteoglycans overlap and entangle with the collagen and protect it from degradation by collagenase.
Anti‐SS‐A antibodies and fetal outcome in maternal systemic lupus erythematosus
Authors: Ramsey‐Goldman Rosalind , Hom David , Deng Jau‐Shyong , Ziegler Gayle Casterline , Kahl Leslie E. , Steen Virginia D. , Laporte Ronald E. , Medsger THOMAS A. 
Published: February 2007

AbstractIn 155 women with systemic lupus erythematosus, there were no significant differences in the rates of fertility or adverse fetal outcome between the 47 (30%) with serum anti‐SS‐A antibody and the 108 without anti‐SS‐A, except in the frequency of congenital heart block. This complication occurred in 6 of 96 pregnancies in women with anti‐SS‐A and was associated with high‐titer maternal antibody. The overall risk of a woman with lupus having an infant with congenital heart block was estimated to be 1:60, but the risk was considerably higher (1:20) if anti‐SS‐A antibody was present.
Rheumatoid nodulosis: Report of a case with evidence of intraosseous rheumatoid granuloma
Authors: Morales‐Piga Antonio , Elena‐Ibañez Angel , Zea‐Mendoza Antonio C. , Rocamora‐Ripoll Antonio , Beltrán‐Gutiérrez Juan 
Published: February 2007

AbstractWe describe a patient who had multiple subcutaneous rheumatoid nodules associated with episodes of acute intermittent arthritis and subchondral cystic lesions of the small bones of the hands and feet; this condition is termed “rheumatoid nodulosis.” The patient had a cystic lesion in communication with the joint cavity, rheumatoid granulomas, and evidence of a central zone of necrosis opening toward the joint space. His case is compared with 8 previously reported cases, and possible etiologies of the subchondral bone cyst formation in rheumatoid nodulosis are discussed.
Work disability among persons with musculoskeletal conditions
Authors: Yelin Edward H. , Henke Curtis J. , Epstein Wallace V. 
Published: February 2007

AbstractWe examined the question of what distinguishes persons with musculoskeletal disease who continue working after onset of illness from those who do not. We also investigated why persons with musculoskeletal disease have high rates of work disability relative to those with other chronic conditions of comparable activity limitation. Data regarding 3,100 persons with limitations in activities and chronic disease who were respondents to the 1978 Social Security Administration Survey of Disabled and Non‐Disabled Adults were used. Persons with musculoskeletal disease who stopped working had poorer overall health status and physical function, and different work attitudes and working conditions than did those who continued to work. Symptoms of the musculoskeletal condition were poor predictors of whether work disability would result. Persons with musculoskeletal conditions had high rates of work disability, relative to those with other chronic conditions, primarily because of their age, level of comorbidity, and the interaction of the physical limitations imposed by their illness and the requirements of their jobs. They had similar levels of commitment to work and a similar proclivity to seek alternative sources of income as did those with other chronic diseases.