bluuebunny/crossref_metadata_2025_split huggingface dataset:
Synovial tissue response to treatment with campath‐1h
Authors: Ruderman Eric M. , Weinblatt Michael E. , Thurmond Linda M. , Pinkus Geraldine S. , Gravallese Ellen M. 
Published: February 2007

AbstractObjective. Therapeutic trials in rheumatoid arthritis with the monoclonal antibody Campath‐1H have demonstrated recurrent clinical synovitis in some patients, despite profound depletion of circulating lymphocytes. This study was undertaken to examine the cellular infiltrates in synovial tissue at a time of persistent peripheral lymphopenia.Methods. Immunohistochemical staining of synovial tissue and peripheral blood lymphocyte phenotyping.Results. Synovial tissues from 2 patients with recurrent synovitis after Campath‐1H therapy contained significant T lymphocytic infiltrates at a time when circulating T lymphocytes were markedly depleted.Conclusion. These results demonstrate that peripheral blood analysis may not accurately reflect the synovial tissue response to monoclonal antibody therapy.
Pseudoseptic inflammatory knee effusion caused by phagocytosis of sickled erythrocytes after fracture into the knee joint
Authors: Mann Delani , Schumacher H. Ralph 
Published: February 2007

AbstractA 57‐year‐old black man with sickle cell disease was admitted to the hospital because of a painful crisis. After a fall with a fracture into the right knee joint, he developed an acutely painful, swollen knee. Synovial fluid from the right knee showed leukocyte counts of up to 154,000/mm3 and was negative for urate and calcium pyrophosphate dihydrate crystals. Gram stains and cultures were negative. Some sickled red cells were seen by light microscopy; electron microscopy revealed crystal‐like arrays of sickled hemoglobin tactoids in erythrocytes which were enfolded and phagocytized by the cells of the synovial fluid. We suggest that this phagocytosis of sickled red cells is the likely cause for the otherwise unexplained inflammation.
The total costs of drug therapy for rheumatoid arthritis
Authors: Prashker Mark J. , Meenan Robert F. 
Published: February 2007

AbstractObjective. We created a model to estimate the total medication costs of treating patients with rheumatoid arthritis with 6 second‐line agents for the first 6 months of treatment.Methods. Drug costs were obtained from a survey of pharmacies; monitoring costs were calculated from utilization information obtained in a survey of rheumatologists; toxicity costs were obtained using decision trees to represent the evaluation and treatment of potential toxicities. Monitoring and toxicity costs were estimated using costs from the Boston University Medical Center or, for hospitalizations, using appropriate diagnosis‐related group categories. The sum of the 3 components determined the total medication costs.Results. The least expensive medication was penicillamine, at $10.62/week, and the most expensive was injectable gold, at $30.89/week. In terms of monitoring costs, methotrexate had the highest costs associated with necessary laboratory tests and office visits. Hydroxychloroquine had the lowest monitoring costs for office visits, and oral gold had the lowest for laboratory costs. Hematologic toxicities were the largest component of toxicity costs for all 6 medications, and renal toxicities were costly for patients taking oral gold, penicillamine, and injectable gold. Total medication costs revealed oral gold as the least expensive medication and injectable gold as the most expensive. The combination of monitoring and toxicity costs accounted for more than 60% of the total costs for all medications except injectable gold. In all cases, the cost of treating toxicities was the smallest of the 3 components.Conclusion. When calculating the costs of drug therapy, it is important to consider not only the price of the drug, but also the costs of monitoring and treating the toxicities that might occur. Failure to do so will result in underestimating the true costs of treatment with these medications.
The determinants of walking velocity in the elderly
Authors: Chang Rowland W. , Dunlop Dorothy , Gibbs James , Hughes Susan 
Published: February 2007

AbstractObjective. To determine predictors of walking velocity in the elderly.Methods. Five hundred thirty‐two persons from 3 cohorts of elderly persons (retirement community, ambulatory care medical clinic, or chronically homebound population) performed a 10‐foot (for the homebound subjects) or 50‐foot (for all other subjects) walk time test and underwent a standardized interview, chart review, and clinical examination. The 73 independent variables that were evaluated included demographic, musculoskeletal, neurologic, psychologic, and other comorbidity items. Least‐squares and least‐absolute‐deviation regression tree analyses were performed to determine the strongest predictive factors associated with walking velocity.Results. Sampling cohort (homebound versus non‐homebound), quadriceps strength, hip flexion strength, lumbosacral spine impairment, lower joint impairment, and education were found to be associated with walking velocity. Joint pain measures were not associated with walking velocity.Conclusion. Muscle strength variables are better predictors of walking velocity than are joint pain variables. Thus, clinical trials and observational studies using walking velocity as an outcome need to take into consideration the influence of muscle strength on this outcome variable.
Lyme arthritis in european children and adolescents
Authors: Huppertz Hans‐Iko , Karch Helge , Suschke Hans‐Joachim , DÖRing Eva , Ganser Gerd , Thon Angelika , Bentas Wassilios ,   Pediatric Rheumatology Collaborative Group
Published: February 2007

AbstractObjective. To evaluate and describe Lyme arthritis in European children and adolescents.Methods. This was a prospective multicenter study. The diagnosis of Lyme arthritis required the exclusion of other diseases and positive findings on serology for IgG antibodies to Borrelia burgdorferi. Enzyme‐linked immunosorbent assay, immunoblotting, and polymerase chain reaction techniques to identify infection by B burgdorferi were used.Results. Among 62 children and adolescents with Lyme arthritis, only 1 had a preceding erythema migrans. Arthritis was episodic in 62% and was chronic at onset in 18%. The most common manifestation was monarthritis of the knee. Joint involvement in patients with oligoarthritis was predominantly unilateral or symmetric. Arthralgia was very rare. Treatment with 1 or 2 courses of different antibiotics resulted in disappearance of the arthritis in 77% of the patients.Conclusion. The clinical presentation of Lyme arthritis in children is different from that in adults. The calculated incidence of Lyme arthritis in persons under the age of 17 years (4/100,000) exceeds previous estimations.
Epidemiology of polymyalgia rheumatica in olmsted county, minnesota, 1970–1991
Authors: Salvarani Carlo , Gabriel Sherine E. , Michael O'Fallon W. , Hunder Gene G. 
Published: February 2007

AbstractObjective. To determine the incidence, prevalence, and survival of polymyalgia rheumatica (PMR) over a 22‐year period in Olmsted County, Minnesota.Methods. Using the unified record system at the Mayo Clinic for the Olmsted County population, we reviewed all medical records with a diagnosis of PMR from 1970 through 1991.Results. There were 245 (173 female; 72 male) incidence cases of PMR between 1970 and 1991. The average annual age‐ and sex‐adjusted incidence of PMR per 100,000 population ≥ 50 years was 52.5 (95% confidence interval [CI] 45.9–59.2), with a significantly higher incidence in females (61.7; 95% CI 52.3–71.2) than in males (39.9; 95% CI 30.7–49.2). The incidence varied over the period of observation, but no significant trends were found. The prevalence of PMR among persons ≥ 50 years on January 1, 1992 was 6/1,000. There was a small but significantly increased survival rate among male PMR patients compared with the general population.Conclusion. Our data demonstrate that PMR is a common nonfatal disease in the elderly, the incidence and clinical manifestations of which have varied but remained relatively stable over the last 2 decades.
Occurrence of ankylosing spondylitis in a nationwide series of twins
Authors: JÄRvinen Pentti 
Published: February 2007

AbstractObjective. To obtain information on the rate of concordance for ankylosing spondylitis (AS) in a population‐based series of twins.Methods. AS cases were identified by record linkage of the population‐based Finnish Twin Cohort and the nationwide registry for fully reimbursed medications. A clinical examination was performed to establish concordance for AS.Results. There were 6 monozygotic (MZ) pairs and 20 dizygotic (DZ) pairs with at least 1 member affected by AS. Three MZ pairs and 3 DZ pairs were concordant for the disease. All affected subjects were HLA‐B27 positive. The pairwise concordance rate was 50% in MZ twins and 20% in HLA‐B27 positive DZ twins (95% confidence intervals 11.8–88.2% and 4.3%–48.1%, respectively).Conclusion. These results indicate that AS disease expression is largely, but not entirely, genetically based, with a gene or genes other than B27 probably playing a role.
Selective induction of igm rheumatoid factors by cd14+ monocyte‐lineage cells generated from bone marrow of patients with rheumatoid arthritis
Authors: Hirohata Shunsei , Yanagida Tamiko , Koda Michinobu , Koiwa Masahito , Yoshino Shin'Ichi , Ochi Tkahiro 
Published: February 2007

AbstractObjective. To determine the capacity of CD14+ monocyte‐lineage cells induced from bone marrow of rheumatoid arthritis (RA) patients to stimulate the production of IgM rheumatoid factor (IgM‐RF), in order to explore the functional abnormalities of CD14+ cells and gain insight into the mechanism of selective synthesis of IgM‐RF in RA.Methods. CD14+ cells were induced by granulocyte–macrophage colony‐stimulating factor (GM‐CSF) stimulation of CD14– cells purified from bone marrow cells obtained from 6 RA patients and 6 osteoarthritis (OA) patients. The production of IgM and IgM‐RF was induced by stimulating B cells from normal healthy individuals with immobilized anti‐CD3‐activated autologous CD4+ T cells. The effects of CD14+ cells on the proportion of IgM‐RF to total IgM produced by the normal B cells were assessed.Results. CD14+ cells induced by GM‐CSF stimulation of bone marrow CD14– cells from the 6 RA patients significantly enhanced the proportion of IgM‐RF to total IgM produced by anti‐CD3‐activated CD4+ T cell‐stimulated normal B cells (P < 0.05), whereas GM‐CSF–induced CD14+ cells from the bone marrow of the 6 OA patients did not significantly affect IgM‐RF production. CD14+ cells induced by GM‐CSF obtained from different sites in the same RA patient on different occasions consistently enhanced the proportion of IgM‐RF to IgM produced by B cells from different normal subjects.Conclusion. These results indicate that abnormal CD14+ monocytes stimulate RF‐producing B cells to be ready to be activated by the signals delivered through noncognate TßB interactions with anti‐CD3‐activated T helper cells. Moreover, the data suggest that the accelerated generation of such functionally abnormal CD14+ cells from bone marrow precursors might play an important role in the pathogenesis of RA.
The role of the immunoglobulin heavy chain in human anti‐dna antibody binding specificity
Authors: Mahmoudi Ahmoud , Denomme Gregory A. , Edwards Jane Y. , Bell David A. , Cairns Ewa 
Published: February 2007

AbstractObjective. To investigate the structural basis for DNA binding of the natural human IgMλ monoclonal antibody KIM4.6.Methods. An IgMλ, non–DNA‐reactive variant hybridoma was derived during in vitro subcloning of the anti‐DNA antibody KIM4.6. The variable (V)‐region heavy (H) and light (L) chain genes expressed by the variant hybridoma were amplified by polymerase chain reaction, cloned, sequenced, and compared with those of the KIM4.6 parent and other DNA‐binding and non–DNA‐binding antibodies.Results. The VL chain of the variant was identical to that of KIM4.6. In contrast, the VH chain was completely different from the VH chain of the parent but was similar or identical, except in the diversity (D) and joining regions, to the VH chain of the systemic lupus erythematosus (SLE) IgG anti‐DNA antibody T14 and SLE IgM nephritogenic anti‐DNA antibodies NE‐1 and NE‐13.Conclusion. The expression of the KIM4.6 VL chain is not sufficient for DNA specificity. The VH chain and its D region play a key role in conferring DNA binding of the KIM4.6 anti‐DNA antibody.
Major histocompatibility complex class ii gene associations with anti–u1 small nuclear ribonucleoprotein antibody relationship to immunoreactivity with individual constituent proteins
Authors: Kuwana Masataka , Okano Yutaka , Kaburaki Junichi , Tsuji Kimiyoshi , Inoko Hidetoshi 
Published: February 2007

AbstractObjective. To better define immunogenetic associations with the anti–U1 ribonucleoprotein (U1 RNP) autoantibody response.Methods. HLA class II alleles were determined by genotyping in 49 Japanese rheumatic disease patients with anti–U1 RNP antibody and 43 race‐matched healthy controls. Immunoreactivities to U1 RNP constituent proteins (70K, A, B/B′, and C) were detected by immunoblots using purified HeLa cell Sm antigen, and antibody titer was determined by passive hemagglutination assay.Results. DQB1*0302 was significantly more frequent in anti–U1 RNP–positive patients than in controls (43% versus 14%; odds ratio [OR] = 4.6, corrected P = 0.03). All anti–U1 RNP–positive patients had either a DQB1*0601, *0602, *0301, *0302, or *0303 allele, which share tyrosine at position 30, and the amino acid sequence Thr, Arg, Ala, Glu, Leu, Asp, and Thr at positions 71–77 in the DQB1 ß1 domain. In contrast, one of these alleles was found in 81% of the controls (OR = 24, P = 0.002). In addition, anti–U1 RNP antibody was associated with unique DQB*0302; DRB1*0401 haplotype. Anti‐70K reactivity and antibody titer were positively associated with a basic amino acid residue, arginine or histidine, at position 13 (DR2 or DR4) and were negatively associated with the amino acid sequence Ile, Leu, Glu, and Asp at positions 67–70, which was present in some of the DR5‐, DR6‐, and DR8‐associated alleles, in the DRB1 ß1 domain. Anti‐C reactivity was strongly associated with DR2, particularly with DRB1*1502.Conclusion. The several shared epitopes located on HLA–DRB1 and DQB1 genes control the anti–U1 RNP autoantibody response.
E‐selectin expression in salivary endothelial cells and sera from patients with systemic sclerosis
Authors: Hebbar Mohamed , Lassalle Philippe , Janin Anne , Vanhée Dominique , Bisiau Sophie , Hatron Pierre‐Yves , Tonnel André‐Bernard , Gosselin Bernard 
Published: February 2007

AbstractObjective. To assess endothelial cell activation in patients with systemic sclerosis (SSc).Methods. Concomitant study of salivary gland biopsy tissues and sera for expression of E‐selectin and its potent activator tumor necrosis factor α (TNFα), using immunostaining and enzyme‐linked immunosorbent essay.Results. E‐selectin was overexpressed in SSc patients, but not in controls. TNFα was detected in mast cells.Conclusion. Mast cell–derived TNFα may contribute to endothelial cell activation in SSc.
Discoordinate gene expression of aggrecan and type ii collagen in experimental osteoarthritis
Authors: Matyas John R. , Adams Mark E. , Huang Dingqiu , Sandell Linda J. 
Published: February 2007

AbstractObjective. To quantify the gene expression of aggrecan core protein and type II collagen in an experimental animal model of osteoarthritis (OA).Methods. Total RNA was extracted from the articular cartilage of unoperated knee joints and from OA joints produced by anterior cruciate ligament transection. The relative amounts of type II collagen and aggrecan core protein messenger RNA (mRNA) were evaluated by Northern blot analysis.Results. Total RNA was elevated 2.5 times, aggrecan mRNA was elevated 2 times, and type II collagen mRNA was elevated 8 times, in OA knees compared to unoperated controls.Conclusion. Chondrocytes are activated metabolically in response to joint injury. Discoordinate gene expression of aggrecan and type II collagen is characteristic of early experimental OA, and we speculate that it may contribute to its pathogenesis.
Polymyositis, pulmonary fibrosis, and hepatitis c
Authors: Weidensaul David , Imam Talha , Holyst Margaret‐Mary , King Paul D. , Mcmurray Robert W. 
Published: February 2007

AbstractPolymyositis has been associated with several viral infections, and a spectrum of immune‐related diseases may occur with hepatitis C virus (HCV) infection. Both polymyositis and HCV infection may be accompanied by interstitial lung disease; however, no association between polymyositis and HCV infection has been reported previously. We report a new association in a patient with HCV infection: anti‐Jo‐1 positive polymyositis and interstitial lung disease.
Apoptosis and functional fas antigen in rheumatoid arthritis synoviocytes
Authors: Nakajima Toshihiro , Aono Hiroyuki , Hasunuma Tomoko , Yamamoto Kazuhiko , Shirai Toshikazu , Hirohata Kazushi , Nishioka Kusuki 
Published: February 2007

AbstractObjective. To determine whether apoptosis occurs in rheumatoid arthritis (RA) synoviocytes, and if this phenomenon is dependent on the Fas/Apo‐1 pathway.Methods. Apoptotic change in vivo was examined in RA synovial cells by several standard methods. The ability of cells to undergo Fas‐induced apoptosis was determined in vitro.Results. Typical apoptotic change was demonstrated in RA synovial cells by each method. Anti‐Fas antibody induced apoptotic synovial cell death in vitro.Conclusion. This is the first reported study to demonstrate apoptosis in RA synovial cells. The findings indicate that rheumatoid synoviocytes undergo Fas‐mediated apoptosis.
Complement components C1q, C1r/C1s, and C1inh in rheumatoid arthritis
Authors: Breitner Susanne , Störkel Stephan , Reichel Wolfgang , Loos Michael 
Published: February 2007

AbstractObjective. To analyze the synovial site and the cell types expressing C1q, C1r/C1s, and C1–esterase inhibitor (C1INH) and to characterize newly synthesized C1q in patients with rheumatoid arthritis (RA).Methods. Tissue and primary cell cultures of synovium from RA patients were analyzed for C1q, C1r/C1s, and C1INH by Northern blotting, in situ hybridization, and pulse‐chase experiments for C1q.Results. The de novo synthesis of C1q, C1r/C1s, and C1INH in synovium and primary cell cultures was proven by Northern blot and by antigenic and functional analysis. In in situ hybridization experiments, the synovial lining cell layer was identified as the site of C1q, C1r, and C1INH expression. In contrast, immunohistologic analysis showed that C1q, C1s, and C1INH proteins were present in a thin film covering the synovial lining cells. In situ hybridization performed on primary cell cultures provided evidence that only macrophages were able to express C1q, whereas fibroblasts and stellate cells synthesized C1r.Conclusion. The synovium is important for the synthesis and secretion of C1q and C1r/C1s, as well as the control protein C1INH, which supports the idea of a locally occurring inflammatory process in RA patients.
Use of immunohistologic and in situ hybridization techniques in the examination of sacroiliac joint biopsy specimens from patients with ankylosing spondylitis
Authors: Braun JÜRgen , Bollow Matthias , Neure Lucia , Seipelt Eva , Seyrekbasan Fikret , Herbst Hermann , Eggens Ulrich , Distler Armin , Sieper Jochen 
Published: February 2007

AbstractObjective. To investigate mechanisms involved in inflammation and new bone formation in the sacroiliac (SI) joints of patients with ankylosing spondylitis (AS).Patients and methods. Computed tomography–assisted biopsy of the SI joint was performed in 5 patients with AS with a mean disease duration of 4.5 years and radiographic stage 2–3 disease. Immuno‐histologic studies were performed with the alkaline phosphatase–anti–alkaline phosphatase technique, and cytokine messenger RNA (mRNA) was detected by in situ hybridization.Results. Dense cellular infiltrates with varying amounts of CD3+ cells (mean ± SD 53.3 ± 24.1%), CD4+ cells (29.7 ± 17.6%), CD8+ cells (15.8 ± 11.4%), CD14+ cells (23.6 ± 16.9%), CD45RO+ cells (48.4 ± 23.6%), and CD45RA+ cells (4.5 ± 2.9%) were found in the synovial portion of the SI joints of all 5 patients. In these infiltrates a high amount of tumor necrosis factor α (TNFα) mRNA and, near the site of new bone formation, a lower amount of transforming growth factor β (TGF β) mRNA, were detected, while no message for interleukin‐1 was found in the 3 patients examined by this technique.Conclusion. The presence of T cells and macrophages was demonstrated in cellular infiltrates in the SI joints of 5 patients with active AS. The finding of abundant TNFα message in these joints could have implications regarding potential immunotherapeutic approaches to this disease. TGFβ might be involved in new bone formation in AS.
Increased proteoglycan synthesis in cartilage in experimental canine osteoarthritis does not reflect a permanent change in chondrocyte phenotype
Authors: Venn G. , Billingham M. E. J. , Hardingham T. E. 
Published: February 2007

AbstractObjective. To determine whether chondrocytes in early experimental osteoarthritic (OA) cartilage continue to show increased synthesis and turnover of proteoglycans (PGs) during explant culture. A comparison was also made between the responsiveness of experimental OA and control cartilage to interleukin‐1β (IL‐1β) and tumor necrosis factor α (TNFα) after 1 day and 3 days in culture.Methods. OA was induced in mature animals by sectioning of the anterior cruciate ligament followed by 3 months of normal exercise. PG synthesis in the articular cartilage was determined by measuring 35S‐sulfate incorporation during explant culture over 1–3 days. Inhibition of PG synthesis was also determined with various concentrations of IL‐1β and TNFα after 1 and 3 days in culture. PGs extracted from the articular cartilage over 1–3 days in culture were examined by agarose–polyacrylamide gel electrophoresis.Results. Up to 24 hours after excision from the joint, PG synthesis was higher in experimental OA cartilage than in control cartilage. It was also less sensitive to inhibition by TNFα. These differences were no longer detected after 48–72 hours in culture. There were no changes in the relative proportions of aggrecan and decorin/biglycan extracted from and synthesized by control and experimental OA cartilage over the 3 days in culture.Conclusion. Previous results indicated that PG synthesis and turnover in articular cartilage was increased for many months after induction of experimental OA. Our present results show that the enhanced rate of PG synthesis and turnover were evident in freshly explanted tissue, but the differences were lost over 3 days in culture. A decreased responsiveness to TNFα was also lost. The hypermetabolic activity of experimental OA chondrocytes was thus reversible and not a permanent change in chondrocyte phenotype.