bluuebunny/crossref_metadata_2025_split huggingface dataset:
Toxicity and serum levels of methotrexate in children with juvenile rheumatoid arthritis
Authors: Wallace Carol A. , Bleyer W. Archie , Sherry David D. , Salmonson Kathy L. , Wedgwood Ralph J. 
Published: February 2007

AbstractTwenty‐three children with destructive polyarticular juvenile rheumatoid arthritis (JRA) were treated for 0.5–4.3 years (median 1.6 years) with weekly doses of methotrexate (MTX) (0.11–0.6 mg/'kg/week). Serum levels of MTX at 1 hour and at 24 hours after drug administration were obtained at each dosage level and every 3 months after a stable dosage was achieved. No patient had serum levels of MTX that were in the toxic range nor evidence of hematologic, skin, mucous membrane, gastrointestinal, or pulmonary abnormalities. Ten patients had transiently elevated serum transaminase levels. Arthritis symptoms improved in 21 of these JRA patients, and the improvement was significantly associated with a mean 1‐hour serum MTX level of ≥5.8 × 10−7 M (P = 0.008)and a dosage of ≥0.3 mg/kg/week (P = 0.004). The 1‐hour serum level of MTX was correlated with the MTX dosage (r = 0.28, P = 0.005). Our observations suggest that with close monitoring, MTX can be used safely at dosages as high as 0.6 mg/kg/week, and improvement in the symptoms of JRA will become evident when the serum levels of MTX 1 hour after administration approach 6.0 × 10−7M.
Association of complement alleles c4aq0 and c4b5 with rheumatoid arthritis in japanese patients
Authors: Takeuchi Fujio , Mimori Akio , Matsuta Kunio , Nakano Keiichiro , Miyamoto Terumasa , Matsuki Kazumasa , Juji Takeo , Maeda Hiroo , Omoto Keiichi , Tokunaga Katsushi 
Published: February 2007

AbstractWe investigated polymorphisms of complement components C2, C4, and factor B (BF) in Japanese patients with rheumatoid arthritis (RA). The frequencies of C4AQ0 (32.1%) and C4B5 (35.9%) among RA patients were significantly higher than among healthy control subjects. C4B5 was strongly associated with HLA–Bw54, Bw59, DR4.1, and DQw4. C4AQ0 showed no association with HLA–Bw54 or Bw59, but there was weak association with HLA–DR4.1 and DQw4. The number of persons with both C4AQ0 and C4B5 was significantly higher in the RA patient group (relative risk 13.5). C2C and BFS were the most common alleles in RA patients, as well as in healthy control subjects. These data support the existence of 2 different putative susceptibility haplotypes (HLA–Bw54 or Bw59;C2C;BFS;C4A3;C4B5;DR4.1;DQw4 and C2C;BFS;C4AQ0;C4B1 or C4B2) in Japanese patients with RA.
Identification of A 2‐Md plasmid from shigella flexneri associated with reactive arthritis
Authors: Stieglitz H. , Fosmire S. , Lipsky P. 
Published: February 2007

AbstractThe development of reactive arthritis, a sterile inflammatory polyarthropathy that primarily affects HLA–B27 positive individuals, has been associated with previous enteric infections caused by various gram‐negative bacteria. The possibility that a common bacterial epitope triggers the disease was investigated by screening a panel of documented arthritogenic Shigella strains as well as 2 epidemic‐associated nonarthritogenic Shigella controls. A 2‐Md plasmid specific to the arthritogenic strains was identified and sequenced. The plasmid encodes a number of small peptides that could be related to the development of reactive arthritis. Within 1 of these is a stretch of 5 consecutive amino acids, inferred from the DNA sequence and contained within an open reading frame, that is homologous to amino acid residues 71–75 of the polymorphic region of the α1 domain of HLA–B27. The data indicate that there is a bacterial plasmid common to arthritogenic Shigella strains that may play a role in triggering reactive arthritis. The finding that this plasmid encodes an epitope shared with HLA–B27 suggests that molecular mimicry may play a role in the induction of this disease.
Increased expression of p150,95 and CR3 leukocyte adhesion molecules by mononuclear phagocytes in rheumatoid synovial membranes. comparison with osteoarthritic and normal synovial membranes
Authors: Allen Catherine A. , Highton John , Palmer David G. 
Published: February 2007

AbstractThe expression of leukocyte adhesion molecules CR3 (CD11b) and p150,95 (CD11c) in synovial tissue was evaluated immunohistochemically. Although a significant proportion of synoviocytes in normal and osteoarthritic synovial membranes expressed the leukocyte common antigen and CR3, very few expressed the p150,95 molecule. In contrast, p150,95 was more evident in rheumatoid synovial membranes. Expression of this molecule was strongest in synovial membranes with a prominent macrophage infiltrate and accumulation of mononuclear phagocytes at the joint surface; p150,95 was also present on interdigitating cells in lymphoid collections. The patterns of expression suggest that these leukocyte adhesion molecules may be important in the diapedesis of mononuclear phagocytes into and through inflamed synovial membranes, as well as in cellular interactions within rheumatoid synovial membranes.
Increased expression Of HLA—DQ antigens by interstitial cells and endothelium in the synovial membrane of rheumatoid arthritis patients compared with reactive arthritis patients
Authors: Barkley Diana , Allard Simon , Feldmann Marc , Maini Ravinder N. 
Published: February 2007

AbstractWe investigated cellular phenotypes and expression of class II major histocompatibility complex antigens on endothelium and cellular infiltrates in synovium from patients with rheumatoid arthritis (RA) or reactive arthritis, using an indirect immunoperoxidase technique. The RA specimens showed synovial lining layer hypertrophy and several focal accumulations of lymphocytes, both of which were absent in the reactive arthritis synovium. The percentage of cells expressing monocyte/macrophage markers was significantly higher in RA specimens. The percentages of cells expressing B and T cell markers were similar in both diseases. There was no significant difference in the expression of HLA–DR or DP by endothelium in the 2 diseases, but a marked increase in expression of HLA–DQ by endothelium was observed in the RA synovium versus that from patients with reactive arthritis. This overexpression of HLA–DQ was also seen in the interstitial cells of RA patients compared with reactive arthritis patients. In the reactive arthritis synovium, a significant population of cells (30%) was noted to be HLA–DR positive, and negative for macrophage and lymphocyte markers. Some of these cells had a dendritic morphology. The coexpression of HLA–DQ and HLA–DR may play an important role in antigen presentation and disease chronicity in RA.
Pain control and rational thinking. implications for rheumatoid arthritis
Authors: Parker Jerry C. , Smarr Karen L. , Buescher Keith L. , Phillips Les R. , Frank Robert G. , Beck Neils C. , Anderson Sharon K. , Walker Sara E. 
Published: February 2007

AbstractIn this study, we examined the factor structure of the Coping Strategies Questionnaire and studied the relevance of the coping process to health status in rheumatoid arthritis patients. The 2 factors of the questionnaire that were analyzed were Coping Attempts and Pain Control and Rational Thinking. The Pain Control and Rational Thinking factor was related to pain and psychological status, even after demographic variables and disease severity were statistically controlled. In addition, increases in Pain Control and Rational Thinking scores were related to improvements in pain, psychological status, and health status. Implications for the psychological care of rheumatoid arthritis patients are discussed.
Differential deoxyadenosine toxicity to immature rabbit cartilage in vitro. a model for the chondro‐osseous dysplasia of adenosine deaminase deficiency
Authors: Wortmann Robert L. , Veum Judith A. , Ryan Lawrence M. , Cheung Herman S. 
Published: February 2007

AbstractDeoxyadenosine metabolism was investigated in rabbit growth plate and articular cartilage to elucidate the biochemical basis for the chondro‐osseous dysplasia observed in adenosine deaminase (ADA) deficiency. Models of ADA deficiency, the combination of deoxy‐adenosine and either of 2 ADA inhibitors, were selectively toxic to immature cartilage, supporting the hypothesis that the chondro‐osseous dysplasia of ADA deficiency is the consequence of the enzyme deficiency. Depletion of ATP may play a role in the altered chondrocyte viability and function observed in this model.
Disability and depression in rheumatoid arthritis. A multi‐trait, multi‐method investigation
Authors: Peck Judith R. , Smith Timothy W. , Ward John R. , Milano Roseann 
Published: February 2007

AbstractIn a sample of 107 patients with classic or definite rheumatoid arthritis (RA), we examined the convergent and divergent validity of measures of disability and depression. Scores on the self‐report Disability index of the Health Assessment Questionnaire were highly correlated with physical therapist and spouse ratings of disability. Although Health Assessment Questionnaire disability scores were significantly correlated with self‐reported and interviewer‐assessed ratings of depression, these correlations were significantly smaller. Factor analyses of the Beck Depression Inventory (BDI) and rheumatologist ratings of BDI items indicated that this measure is highly contaminated by the inclusion of items reflecting RA disease severity. A dysphoric mood subcomponent of the BDI may be a more valid measure of depression in RA populations. Although depression and disability are clearly positively correlated in RA patients, depression scales that include somatic items are likely to yield an overestimate of the association. Finally, self‐reported pain intensity was more clearly related to disability and reported recent disease activity than to depression.
Combination methotrexate and sulfasalazine in the management of rheumatoid arthritis: case observations
Authors: Shiroky J. B. , Watts C. S. , Neville C. 
Published: February 2007

AbstractFour patients with rheumatoid arthritis received a combination of methotrexate and sulfasalazine for a mean of 24 months (range 20–28 months). All 4 patients experienced clinical improvement, with a reduction in the number of involved joints and in morning stiffness. In all 3 patients who had previously taken methotrexate, we were able to reduce the dosage, and the prednisone dosage was reduced in 2 of 3 patients who had previously taken that drug. No serious toxicity was observed in any patient.
Polymyositis/dermatomyositis associated with dermatitis herpetiformis
Authors: Kalovidouris Apostolos E. , Miller Frederick W. , Lawley Thomas J. 
Published: February 2007

AbstractWe describe 2 patients with dermatitis herpetiformis who developed polymyositis/dermatomyositis. On HLA typing, both patients were found to be HLA–B8, DR3 positive. The concurrence of these two relatively rare diseases, both associated with immunologic abnormalities, further supports the role of autoimmunity in their pathogenesis and indicates a possible common genetic basis. It also suggests that myositis may be more common in patients with dermatitis herpetiformis than in the general population.
Mass spectrometric quantitation of muramic acid, a bacterial cell wall component, in septic synovial fluids
Authors: Christensson Bertil , Gilbart James , Fox Alvin , Morgan Stephen L. 
Published: February 2007

AbstractThis is the first report describing the use of gas chromatography–mass spectrometry for detection of muramic acid in infected synovial fluid (SF). Muramic acid is a ubiquitous component of bacterial cell walls, and it has been proposed that it could serve as a chemical marker for the presence of live bacteria or bacterial debris in rheumatoid joints. Our goal was to determine whether muramic acid was present at detectable levels in septic SF, since this would serve as a positive control for studies of reactive and rheumatoid arthritis. Muramic acid was found to be present at levels of < 250–1, 700 ng/ml in 12 septic SF samples (10 of which were culture positive for Staphylococcus aureus and 1 each for Escherichia coli and Streptococcus pneumoniae). Among these samples, those containing low bacterial colony counts did not contain detectable muramic acid. Muramic acid was also not detected in any SF samples from 20 control patients. We conclude that muramic acid can be used as a marker for the presence of bacterial peptidoglycan in SF. With further lowering of gas chromatography–mass spectrometry detection limits, determination of the quantities of bacterial debris present in joints of patients with rheumatoid or reactive arthritis will be attainable.
Serum keratan sulfate levels in rabbits with experimentally induced osteoarthritis
Authors: Mehraban Fuad , Moskowitz Roland W. 
Published: February 2007

AbstractSerum keratan sulfate (KS) levels were measured with an enzyme‐linked immunosorbent assay using monoclonal antibody (MAb) 5‐D‐4 (anti‐KS) in a rabbit model of osteoarthritis (OA) induced by partial meniscectomy. The partial medial meniscectomy produced pathologic changes of OA in the joints of the rabbits, which were seen when the animals were killed at 3, 6, 9, or 12 weeks postsurgery. Tibial or femoral osteophytes were seen in up to 90% of the operated joints; pitting and ulceration of medial femoral condyles were also frequently noted (77% of cases). Rabbits that underwent sham surgery, back‐skin–operated rabbits, or nonoperated normal rabbits served as controls; the joints of these animals were normal at the time of killing. A rise in the level of serum KS was recorded in 50% of rabbits following partial meniscectomy, but this was matched by similar changes in the control groups. The mean serum KS level of the OA animals at serial intervals (3, 6, 9, or 12 weeks) following surgery was not significantly different from that in the control groups. When measured with a second MAb, 2‐D‐3, KS levels showed similar trends as with MAb 5‐D‐4, although lower assay values were obtained. These findings indicate that experimentally induced OA in rabbits is not associated with a significant rise in serum KS levels. KS levels did not differentiate OA from non‐OA animals, nor did they parallel disease progression.
Lack of association of a restriction fragment length polymorphism for serum amyloid P gene with reactive amyloidosis
Authors: Harats Noam , Kluve‐Beckerman Barbara , Skinner Martha , Passo Murray , Quinn Linda , Benson Merrill D. 
Published: February 2007

AbstractThe prevalence of a recently described restriction fragment length polymorphism using Msp I for the serum amyloid P gene was determined in 5 groups of patients. Patients with reactive (secondary) amyloidosis, juvenile rheumatoid arthritis, related inflammatory conditions, or juvenile rheumatoid arthritis with reactive amyloidosis, and healthy control subjects were found to be polymorphic for 8.8‐kb and 5.6‐kb gene fragments; they either had one or the other or both fragments. No significant differences were seen between these groups with relation to this polymorphism, and no correlation with the presence of reactive amyloidosis was observed.
Differences in responses of normal and rheumatoid arthritis peripheral blood t cells to synovial fluid and peripheral blood dendritic cells in allogeneic mixed leukocyte reactions
Authors: Bergroth Ville , Tsai Van , Zvaifler Nathan J. 
Published: February 2007

AbstractWe examined the response of normal T cells to dendritic cells isolated from the synovial fluid (SF) of patients with either rheumatoid arthritis (RA) or seronegative spondylarthropathies (rheumatoid variants) and to dendritic cells from normal and RA peripheral blood (PB) in the allogeneic mixed leukocyte reaction. Despite the differences in the response kinetics, the stimulatory capacity of SF dendritic cells was similar to that of PB dendritic cells in a 7‐day mixed leukocyte reaction. We also tested the responsiveness of normal and RA PB T cells to various allogeneic dendritic cells and found that RA PB T cells responded poorly to both rheumatoid variant SF dendritic cells and normal PB dendritic cells. However, when dendritic cells from RA SF were used as stimulators, the response of RA PB T cells was significantly greater than that of normal PB T cells (P < 0.02). This difference in response was explained in part by a proliferation of the CD8 T cell subset. There was also a shift of low‐intensity CD4+, CDw29+ cells to high‐intensity CD4+, CDw29+ cells seen in RA PB T cells but not in normal PB T cells, by fluorescence‐activated cell sorter analysis.
Increased levels of proteoglycan fragments in knee joint fluid after injury
Authors: Lohmander L. Stefan , Dahlberg Leif , Ryd Leif , Heinegård Dick 
Published: February 2007

AbstractWe measured levels of cartilage proteoglycan (PG) fragments in knee joint synovial fluid obtained from patients with previous trauma of the knee, early gonarthrosis, or pyrophosphate synovitis, and in age‐matched control subjects. During the initial 3–4 weeks after rupture of the anterior cruciate ligament or the meniscus (confirmed by arthroscopy), markedly increased PG fragment levels were found. At later times after trauma (up to 4 years), many of these patients still had significantly elevated levels of cartilage PG fragments in the joint fluid. In a group of older patients with gonarthrosis, these levels were only moderately elevated, while in patients with acute pseudogout, greatly increased levels were observed. Although longitudinal studies are needed to validate the significance, PG fragments in joint fluid may be a marker for early posttraumatic arthrosis.
Rheumatoid arthritis complicated by infection with the human immunodeficiency virus and the development of Sjögren's syndrome
Authors: Calabrese Leonard H. , Wilke William S. , Perkins Alvin D. , Tubbs Raymond R. 
Published: February 2007

AbstractA patient with seropositive rheumatoid arthritis became infected with the human immunodeficiency virus (HIV) through heterosexual transmission. After the primary phase of the HIV infection, persistent lymphadenopathy, leukopenia, and thrombocytopenia developed. Over the ensuing 3 years, the signs and symptoms of inflammatory polyarthritis completely disappeared, and severe Sjögren's syndrome developed. HIV and its associated immune dysfunction may be responsible for these events.
The frequency of complement receptor type 1 (cr1) gene polymorphisms in nine families with multiple cases of systemic lupus erythematosus
Authors: Tebib J. G. , Martinez C. , Schur P. H. , Granados J. , Alarcon‐Segovia D. 
Published: February 2007

AbstractLow levels of complement receptor type 1 (CR1) on the erythrocytes of patients with systemic lupus erythematosus (SLE) may be acquired or genetically determined. Nine families with multiple cases of SLE were studied using a CR1 probe and restriction fragment length polymorphism analysis, to address this question. The absence of a significant increase in the frequency of a 6.9‐kb band (previously shown to be associated with low‐level CR1 on erythrocytes) suggests that this genetic marker does not play a major role in determining SLE, either in these families or in SLE patients in general.
Demonstration of a new antinuclear antibody (ANTI‐RA33) that is highly specific for rheumatoid arthritis
Authors: Hassfeld Wolfgang , Steiner Günter , Hartmuth Klaus , Kolarz Gernot , Scherak Othmar , Graninger Winfried , Thumb Norbert , Smolen Josef S. 
Published: February 2007

AbstractUsing immunoblot analysis with soluble nuclear extracts from HeLa cells, we identified autoantibodies to an antigen with a molecular weight of ∼33,000 in 36% of 95 sera from rheumatoid arthritis patients, but in only 1 of 170 controls. The antigen, termed RA33, was resistant to DNase and RNase digestion but sensitive to proteinase K treatment. There was no discernible relation to other autoantibodies. Thus, this newly described autoantibody appears to be highly specific for rheumatoid arthritis.
Regulation of human synovial fibroblast collagenase messenger RNA by interleukin‐1
Authors: McCachren S. Spence , Greer Paula K. , Niedel James E. 
Published: February 2007

AbstractInterleukin‐1 (IL‐1) may contribute to tissue destruction in rheumatoid arthritis, in part, by inducing messenger RNA (mRNA) that encodes interstitial collagenase. In human synovial fibroblasts in vitro, IL‐1 induced collagenase mRNA accumulation 6 hours after being added to the cells. High levels of mRNA remained present for at least 48 hours after treatment. The rate of transcription of collagenase in isolated nuclei peaked after approximately 6 hours of treatment with IL‐1 and declined thereafter, becoming nearly undetectable by 24 hours. The persistence of mRNA, in view of the transient peak of transcription, suggested that collagenase mRNA was stable in synovial fibroblasts. The half‐life of collagenase mRNA after the synoviocytes were treated with actinomycin D was approximately 27 hours, both in the presence and in the absence of IL‐1. It has been noted that induction of the expression of collagenase by phorbol esters requires fos protein synthesis and is mediated through a tetradecanoyl phorbol acetate response element in the 5′‐flanking region of the gene. However, we found that cycloheximide, when added to synovial fibroblast cultures up to 6 hours after treatment with IL‐1, inhibited the expression of collagenase mRNA. These results suggest that fos alone is unlikely to be sufficient for collagenase expression, and that additional factors, or alternative pathways, are involved in the induction of collagenase by IL‐1.
Arthritis in nursing home residents. A validation of its prevalence and examination of its impact on institutionalization and functional status
Authors: Guccione Andrew A. , Meenan Robert F. , Anderson Jennifer J. 
Published: February 2007

AbstractWe studied nursing home residents to validate the method used in national surveys for estimating the prevalence of arthritis, and to examine the impact of arthritis on institutionalization and on the physical function of residents. Five homes were studied using a 3‐phase approach. Directors of nursing in each home classified residents (n = 629) with respect to the presence of arthritis and senile dementia. The presence of osteoarthritis or rheumatoid arthritis and their impacts on a resident's initial placement were separately assessed by a physician through a chart review of a stratified subsample. The physician also rated a resident's likelihood of returning to community living. Finally, the functional impact of arthritis was assessed by a physical therapist. The nurses' estimate of the prevalence of arthritis in this population was 23.33%, while the physician estimate was 23.03%. These results are consistent with the 24.6% prevalence found in a 1977 national survey. Arthritis itself was a major cause of nursing home placement in 15% of all residents without dementia. Among those without dementia who also had arthritis, arthritis was a major cause of institutionalization in 31%. None of the residents without dementia showed substantial potential for reintegration into the community. Controlling for age, residents with arthritis had more pain, were more likely to require assistance in functional tasks, and were more likely to use a wheelchair daily than were their fellow residents. Nevertheless, our results suggest that arthritis, despite its impact on function, in and of itself is not a major cause of nursing home placement or ongoing institutionalization.