bluuebunny/crossref_metadata_2025_split huggingface dataset:
Self‐associating igg rheumatoid factors in mrl/1 autoimmune mice
Authors: Nardella Francis A. , Teller David C. , Izui Shozo , Mannik Mart 
Published: February 2007

AbstractPrevious work has shown that the intermediate complexes isolated from the plasma of patients with rheumatoid arthritis are composed of self‐associating IgG rheumatoid factors. Mice of the MRL/1 strain develop spontaneous autoimmune disease with arthritis that is pathologically similar to human rheumatoid arthritis. Also, the sera of MRL/1 mice contain autoantibodies to nuclear antigens as well as IgM and IgG rheumatoid factors. The present studies were done to determine if the IgG rheumatoid factors isolated from these mice undergo self‐association. MRL/1 mouse sera were categorized into groups A and B based on serumserum precipitin interactions. Thirteen of 13 MRL/1 mice sera examined contained intermediate complexes sedimenting between the 6.6S and 19S components of normal serum by sedimentation velocity ultracentrifugation. There were no differences in the level of intermediate complexes between groups A and B. IgG rheumatoid factors were isolated from the sera of 9 other mice. Upon sedimentation equilibrium ultracentrifugation, these rheumatoid factors underwent concentration‐dependent self‐association similar to that described for human self‐associating IgG rheumatoid factors, although the precise stoichiometry of self‐association could not be determined. The IgG rheumatoid factors from group B had higher energies of self‐interaction than those from group A. These studies provide additional evidence that MRL/1 mice may be the best available animal model for the study of human rheumatoid arthritis.
An attempt to predict the response to gold therapy in rheumatoid arthritis
Authors: O'Duffy J. D. , O'Fallon W. M. , Hunder G. G. , Mcduffie F. C. , Moore S. B. 
Published: February 2007

AbstractIn 54 rheumatoid arthritis patients undergoing conventional chrysotherapy, we prospectively sought predictors of response, using strict clinical and laboratory criteria of improvement. Forty‐five patients who completed 6–12 months of therapy were classified into 3 outcome categories: group 0, not significantly improved (18 patients); group 1, improved (18 patients); and group 2, markedly improved (9 patients). Sixty‐two entry variables were tested in univariate and multivariate analysis for predictor function. No continuous variable was predictive. The discrete variables HLA‐A3 positivity and HLA‐DR4 negativity were the best predictors of response to gold. In a multivariate analysis using these 2 univariates (A3 and DR4) plus hemoglobin, we developed a discriminant function that correctly predicted outcome in 21 of 23 patients in groups 0 and 2. We also observed that of 15 DR blank patients (10 of whom were DR4 blank), none entered remission.
Zonal analysis of cytoplasmic components of articular cartilage chondrocytes
Authors: Brighton Carl T. , Kitajima Toshihiro , Hunt Robert M. 
Published: February 2007

AbstractThe cytoplasmic components of chondrocytes in the various zones of articular cartilage of the medial femoral condyle of adult male New Zealand white rabbits were quantitated from electron micrographs. A progressive increase in the content of endoplasmic reticulum, Golgi apparatus, mitochondria, and electrondense bodies (presumed to be lysosomes) from the tangential zone through the top half of the calcified zone was observed. These organelles then showed a decrease in content in the bottom half of the calcified zone. This was associated with an even greater increase in content of holes in the cytoplasm at that level, providing clear evidence of cellular swelling. Based on these quantitative morphologic studies, it is concluded that the chondrocytes in all zones of articular cartilage are metabolically active, but those cells in the calcified zone show signs of degeneration. The ultimate fate of the chondrocytes in the bottom of the calcified zone is not clear from this study.
Low C3B receptor reactivity on erythrocytes from patients with systemic lupus erythematosus detected by immune adherence hemagglutination and radioimmunoassays with monoclonal antibody
Authors: Minota Seiji , Terai Chihiro , Nojima Yoshihisa , Takano Kiyohide , Takai Emiko , Miyakawa Yuzo , Takaku Fumimaro 
Published: February 2007

AbstractC3b receptor (CR1) on erythrocytes from 23 patients with systemic lupus erythematosus (SLE) and 124 normal controls was determined by immune adherence hemagglutination (IAHA) and radioimmunoassay. The binding of radiolabeled monoclonal anti‐CR1 to erythrocytes and their lysate was distributed continuously in a wide range. The majority of SLE patients showed low binding by both assays. CR1 sites on erythrocytes were determined also by Scatchard plot analysis and standardized by the number of similarly determined lectin‐binding sites that served as a measure of erythrocyte surface. The numbers of standardized CR1 sites were classified as high, intermediate, and low. Thirty‐six percent of control subjects had high numbers of CR1 sites, 53% had intermediate numbers, and 11% had low numbers. Of SLE patients, the numbers of CR1 sites were high in 0%, medium in 52%, and low in 48%. Negative IAHA was found in 10 controls (8%), all of whom had low numbers of standardized CR1 sites. Among 13 SLE patients with negative IAHA, 11 had low numbers of CR1 sites and the remaining 2 had low intermediate numbers. IAHA, therefore, was particularly efficient in detecting the low numbers of CR1 sites in SLE, which would impair the disposal of circulating immune complexes and accelerate the development of tissue injuries.
Abnormal calcium and magnesium stores in erythrocytes and granulocytes from patients with inflammatory connective tissue diseases. Relationship to inflammatory activity and effect of corticosteroid therapy
Authors: Hällgren Roger , Svenson Karin , Johansson Erland , Lindh Ulf 
Published: February 2007

AbstractThe mass fraction of Ca and Mg in isolated erythrocytes and granulocytes was measured using the nuclear microprobe technique. Conspicuous abnormalities were observed in cells from patients with rheumatoid arthritis and other inflammatory arthritides. Compared with the normal cellular content, total Ca was increased an average of 3 times in erythrocytes and 5 times in granulocytes. Total granulocyte Mg was increased about 3 times, whereas erythrocyte Mg was reduced to as much as 60% of normal. These abnormalities were less prominent or were absent in scleroderma patients, except for levels of granulocyte Ca, which were increased more than 3 times beyond normal in this patient group. A significant positive correlation was found between serum haptoglobin and erythrocyte or granulocyte Ca content among these patients, but not between haptoglobin and erythrocyte or granulocyte Mg values. During corticosteroid treatment, a significant increase in erythrocyte Mg and a significant reduction in erythrocyte Ca were noted, but normalization of these levels was not achieved. Granulocyte Ca was also significantly reduced, while granulocyte Mg remained unaltered. Serum levels of Ca and Mg were within normal ranges and were not influenced by corticosteroid therapy. The results indicate that at least Ca abnormalities in erythrocytes and granulocytes are associated with the intensity of the inflammatory process and that the amounts of Ca and Mg in these cells are influenced by potent antiinflammatory therapy.
Circulating natural killer cells in sjögren's syndrome
Authors: Ichikawa Yukinobu , Yoshida Miyoko , Takaya Masatoshi , Uchiyama Mitsuaki , Shimizu Hiroaki , Arimori Shigeru 
Published: February 2007

AbstractReduced natural killer (NK) cell activity of peripheral blood lymphocytes (PBL) has been reported in a number of diseases including Sjögren's syndrome (SS). In this study, we used 2 monoclonal antibodies directed toward NK cells (anti‐Leu‐7 and anti‐Leu‐11) for determining NK cell activity in 29 patients with SS (9 with primary SS and 20 with secondary SS). The NK activity of PBL was simultaneously determined by the 51Cr release method using K562 as target cells. Contrary to previous reports, we did not find reduced NK activity of PBL in our patients compared with sex‐ and age‐matched healthy controls. Although the percentage of Leu‐7+ cells was significantly higher in the patients than in the controls (P < 0.05), the absolute number of circulating Leu‐7+ cells was not different between the groups. The percentage of Leu‐11+ cells, however, was not significantly different between the patients and the controls, but the number of circulating Leu‐11+ cells was significantly fewer in the patients than in the controls (P < 0.05). Between the primary and secondary SS groups, no significant differences were found in NK cell activity or in the percentage of Leu‐7+ or Leu‐11+ cells. Furthermore, we found a significant correlation of NK activity with the percentage of Leu‐11+ cells (P < 0.05) in the controls as well as the SS patients, although a significant correlation was not identified between NK activity and the percentage of Leu‐7+ cells. These results are compatible with the known specificities of each monoclonal antibody: the anti‐Leu‐11 antibody is more specific for functionally active NK cells than is the anti‐Leu‐7 antibody. The NK activity of PBL, therefore, was proportional to the percentage of NK cells (Leu‐11+ cells) and was not impaired in our patients with SS, although the number of circulating NK cells was fewer in the patients than in the healthy controls.
Effects of long‐term procainamide therapy on immunoglobulin synthesis
Authors: Yu Chia‐Li , Ziff Morris 
Published: February 2007

AbstractProcainamide is a potent inducer of autoantibodies. In order to evaluate the immunologic effects of this drug in vivo, 23 cardiac disease patients who had received procainamide for at least 6 months and an equal number of matched cardiac disease control subjects were studied, and percentage of circulating T cell subsets, concanavalin A‐induced suppressor cell activity, and pokeweed mitogen‐stimulated generation of immunoglobulin‐secreting cells was quantitated. There was no significant difference between patient and control groups in the percentage of T cell subsets defined by OKT4 and OKT8 monoclonal antibodies or in concanavalin A‐induced suppressor cell activity. The numbers of pokeweed mitogen‐induced immunoglobulinsecreting cells were markedly decreased in the patient group, as measured by the protein A‐augmented reverse hemolytic plaque assay (3,000 ± 644, mean ± SEM in patients versus 10,826 ± 1,529, mean ± SEM in control subjects, P < 0.005). Removal of the adherent cell fraction did not improve the hyporesponsiveness. When B and T cell fractions of 6 patients were mixed with normal T and B cell fractions, all of the patients demonstrated diminished B cell responses, and one‐half also had diminished T cell responses. Addition of patient adherent cells to a co‐culture of normal B cells with deficient patient T cells restored plaque formation to normal levels, suggesting that the T cell defect was correctable by a macrophage‐derived factor. The data obtained suggest that procainamide exerts an immunosuppressive action on both B and T cell function in patients receiving this drug.
Serum c‐reactive protein in polymyalgia rheumatica. A prospective serial study
Authors: Mallya R. K. , Hind C. R. K. , Berry H. , Pepys M. B. 
Published: February 2007

AbstractA prospective serial study of 13 well‐documented, previously untreated cases of polymyalgia rheumatica was undertaken in order to assess the behavior of the nonspecific indices of disease activity, erythrocyte sedimentation rate and serum C‐reactive protein (CRP) concentration, during induction of disease remission by prednisolone therapy. The clinical manifestations of all patients responded rapidly and completely to steroids, and the serum CRP value, which was raised in all patients at presentation, fell to normal at a rate which precisely reflected the clinical improvement. The erythrocyte sedimentation rate also fell, but did so much more slowly than the CRP concentration and, in half the patients, was still not normal after 14 days. These results indicate that assay of serum CRP provides a precise means of objectively assessing the course of polymyalgia rheumatica during initial therapy with steroids, and suggest that routine measurements of CRP may make a useful contribution to the management of the disease.
Phagocytosis and intracellular killing by polymorphonuclear cells from patients with rheumatoid arthritis and felty's syndrome
Authors: Breedveld Ferdinand C. , Van den Barselaar Maria T. , Leijh Peter C. J. , Cats Arnold , van Furth Ralph 
Published: February 2007

AbstractThe present in vitro study concerned the phagocytosis and intracellular killing by polymorphonuclear cells (PMN) of 5 patients with rheumatoid arthritis (RA) and 12 patients with Felty's syndrome (FS). PMN phagocytosis was assessed by microbiologic and morphologic methods, and intracellular killing was measured independently of continuous phagocytosis of viable bacteria (Staphylococcus aureus). PMN from patients with RA or FS ingested S aureus opsonized with immunoglobulins and complement as effectively as did PMN from healthy donors. However, the capacity of patient PMN to ingest S aureus opsonized with sera lacking complement activity, e.g., heat‐inactivated donor serum and the sera of 2 patients with FS, was lower than that of healthy donor PMN. This decreased ingestion is associated with diminished expression of Fc receptors on the membrane of PMN from patients who have RA or FS. As with sera lacking complement activity, decreased capacity to ingest S aureus was observed after preloading donor PMN with immune aggregates, which also decreased the expression of Fc receptors. PMN from patients with RA or FS were found to be as active in killing S aureus as cells from healthy donors.
Human rheumatoid arthritic cartilage and its neutral proteoglycan‐degrading proteases. The effects of antirheumatic drugs
Authors: Martel‐Pelletier Johanne , Cloutier Jean‐Marie , Howell David S. , Pelletier Jean‐Pierre 
Published: February 2007

AbstractMeasurements were made of the neutral proteoglycan–digesting protease activity in the cartilage matrix breakdown observed in the rheumatoid arthritic process. Normal knee (tibial plateau) cartilage specimens were obtained from 7 fresh cadavers and 29 cartilage specimens were obtained from 23 patients diagnosed as having rheumatoid arthritis (RA). The total neutral metalloproteoglycan–degrading enzyme (NMPE) activity in RA cartilages exhibited roughly an eightfold elevation over that of control subjects. The active form of the NMPE for diseased cartilage was higher than that observed for normal cartilage, but was not statistically different. A very low level of activity was detected for serine proteases and no variation was observed between normal and diseased cartilages. Data obtained from RA cartilages were also analyzed with respect to the relationship between enzyme activities and the patients' medications. Four groups of patients were then selected according to their drug treatments: S + G patients received steroid and gold therapy; S patients received steroids only; NS + NG patients did not receive steroid or gold therapy; G patients received gold therapy alone. The total NMPE activity for each of these groups remained at a very high level. The active enzyme activity measured in S + G and S patients was decreased to a level not different from that of normal controls. Specimens from NS + NG patients presented a significantly higher level of the active form of the enzyme (P < 0.05) when compared with either normal controls, S + G, or S patients. No significant difference was noted in the level of serine protease activity between the RA cartilage and normal cartilage. These data strongly support the role of NMPE in the destruction of RA cartilage. Steroids, whether alone or associated with gold compounds, are able to suppress the activity of the active form of the NMPE.
Antibodies to human T cell leukemia virus are absent in patients with systemic lupus erythematosus
Authors: Koike Takao , Takabayashi Katsuhiko , Maruyama Naoki , Tomioka Hisao , Yoshida Sho 
Published: February 2007

AbstractIt has been anticipated that type C oncornaviruses, which participate in the pathogenesis of murine systemic lupus erythematosus (SLE), would be found to have a role in the development of SLE in humans. In studies of tissues from SLE patients, type C–related proteins have been identified. Using information obtained on the recent isolation of the human T cell leukemia virus (HTLV), together with that from studies of murine SLE, we attempted to clarify the role of antibodies to HTLV in the pathogenesis of human SLE. Using a solid‐phase enzyme‐linked immunosorbent assay and sodium dodecyl sulfate–polyacrylamide gel electrophoretic techniques, we were unable to find evidence of the participation of antibodies to HTLV proteins in the development of human SLE.
Nifedipine and esophageal dysfunction in progressive systemic sclerosis. A controlled manometric study
Authors: Kahan André , Bour Bruno , Couturier Daniel , Amor Bernard , Menkes Charles J. 
Published: February 2007

AbstractWe evaluated the effect of the calcium channel blocking agent, nifedipine, on esophageal dysfunction in 15 patients with progressive systemic sclerosis, using a double‐blind, randomized, crossover, placebo‐controlled manometric study. Nifedipine significantly decreased lower esophageal sphincter pressure in these patients; this reduced lower esophageal sphincter pressure may cause gastroesophageal reflux. Thus, nifedipine may have detrimental effects on progressive systemic sclerosis patients.
Selective inhibition of excessive scleroderma fibroblast collagen production by lymphokines from normal human mononuclear cells
Authors: Jimenez Sergio A. , McArthur William M. , Bashey Reza I. , Rosenbloom Joel 
Published: February 2007

AbstractWe studied the effects of lymphokines from mitogen‐stimulated normal human mononuclear cells on collagen production by confluent monolayer cultures of scleroderma dermal fibroblasts. We examined 10 cell lines obtained from patients with early onset, rapidly progressive disease. All cell lines exhibited increased collagen production, compared with cell lines from ageand sex‐matched normal individuals. We found that supernatants from phytohemagglutinin‐stimulated mononuclear cells caused >45% inhibition of collagen production by the cultured scleroderma fibroblasts; the degree of inhibition was concentration‐dependent. Partially purified lymphokine preparations produced 84–94% inhibition of collagen production by scleroderma cells. The lymphokine effects were shown to be selective for collagen, since the synthesis of noncollagenous proteins was not significantly affected. The results suggest that lymphokines from normal mononuclear cells can modulate the excessive collagen biosynthesis that is characteristic of scleroderma fibroblasts, and these lymphokines may have a place as possible therapeutic agents for this incurable disease.
Impaired killer cell generation in the autologous mixed leukocyte reaction by rheumatoid arthritis lymphocytes
Authors: Goto Makoto , Zvaifler Nathan J. 
Published: February 2007

AbstractNatural killer‐like cells are generated along with interleukin‐2 (IL‐2) in the autologous mixed leukocyte reaction (AMLR). Patients with active rheumatoid arthritis (RA), but not those whose disease is in remission, are poor producers of AMLR killer cells. This defect cannot be explained by age, medications, or serum factors. The impaired generation of natural killer‐like cells was not influenced by γ‐interferon but could be partially restored by addition of indomethacin to the AMLR culture, or by culturing RA T cells with exogenous IL‐2. However, the response of RA T cells to IL‐2 was significantly less than that of controls. These results suggest that the defect in the generation of AMLR killer cells in patients with active RA may be due in part to defective production of IL‐2 and a lesser sensitivity of RA T cells to IL‐2.
Salicylate‐induced depletion of endogenous inorganic sulfate. Potential role in the suppression of sulfated glycosaminoglycan synthesis in murine articular cartilage
Authors: De Vries Bernard J. , van den Berg Wim B. , van de Putte Levinus B. A. 
Published: February 2007

AbstractSodium salicylate has been shown to suppress glycosaminoglycan (GAG) synthesis by articular hyaline cartilage in vitro. We investigated the in vivo effect of sodium salicylate on murine patellar cartilage, using incorporation of intraperitoneally administered 35S‐sulfate as a measure of sulfated GAG synthesis. Our results indicated that a single dose of sodium salicylate (200 mg/kg) inhibited in vivo sulfated GAG synthesis by 56%, compared with controls, and had no effect on sulfated GAG breakdown. A striking finding was that sodium sulfate treatment reduced the serum concentration of inorganic sulfate from 1.1 mM to approximately 0.3 mM, and that this serum reduction was associated with a twofold increase in urinary excretion of sulfate. Using anatomically intact patellar cartilage, in vitro studies clearly showed that, in concentrations reached in vivo (⩾1 mM), salicylate suppressed murine chondrocyte GAG synthesis. However, in the presence of serum, the effects of 1 mM salicylate were abolished. We also found that sulfated GAG synthesis was clearly inhibited at low concentrations of sulfate (<0.5 mM). Our data indicate that sodium salicylate can suppress articular chondrocyte sulfated GAG synthesis in vivo, and that this effect may particularly be due to a drug‐induced reduction of endogenous sulfate.
No demonstrable relationship between IgM and IgG antinuclear antibody levels and acetylator phenotype in patients with systemic lupus erythematosus
Authors: Portanova Joseph P. , Small Calvin J. , Kohler Peter F. 
Published: February 2007

AbstractTo ascertain the possible influence of acetylator phenotype on antinuclear antibodies in systemic lupus erythematosus (SLE), we assayed sera from 11 rapid acetylators and 10 slow acetylators for IgM and IgG antibodies to chromatin, histones, denatured DNA, and native DNA. Whereas the majority of SLE patients of both acetylator phenotypes had elevated levels of antibodies to all 4 antigens compared with normal controls, there was no difference in antibody activities between slow acetylator patients versus rapid acetylator patients for these antigens. We conclude that levels of antibody to chromatin, histones, and DNA in SLE patients are similar irrespective of acetylator phenotype, and that if a protective effect of slow acetylation on spontaneous development of antinuclear antibodies does occur, a prospective study of presymptomatic individuals at high risk for lupus may be required to reveal this effect.
MOrphologic and cytochemical changes in maturing and osteoarthritic articular cartilage in the temporomandibular joint of mice
Authors: Livne Erella , von der Mark Klaus , Silbermann Michael 
Published: February 2007

AbstractWe studied the light microscopic, ultrastructural, and cytochemical characteristics of the temporomandibular joints of male ICR mice, from early neonatal life until they reached senescence, when spontaneous osteoarthritis is a common phenomenon. Aging of mandibular condylar cartilage was accompanied by decreasing total proteoglycan content and by an unmasking of collagen fibers, with no shift in collagen type. Fibronectin was also commonly present on the articular surface of specimens from old animals. Chondrocytes of aged mice contained an increased number of lysosomes, and their adjacent matrix vesicles reacted positively for acid phosphatase and arylsulfatase, but not for alkaline phosphatase. Such vesicles were also found to be devoid of calcium complexes and, thus, did not appear to be involved in the mineralization process. Similar age‐related changes have been described in human mandibular condyles; hence, the male ICR mouse could serve as a useful model for studies of spontaneous osteoarthritis in the human mandibular joint.