bluuebunny/crossref_metadata_2025_split huggingface dataset:
Serum and plasma inhibit neutrophil stimulation by hydroxyapatite crystals. evidence that serum αl2‐hs glycoprotein is a potent and specific crystal‐bound inhibitor
Authors: Terkeltaub Robert A. , Santoro Denise A. , Mandel Gretchen , Mandel Neil 
Published: February 2007

AbstractTissue deposits of basic calcium phosphate (BCP) crystals are associated with various clinical manifestations of inflammation. We addressed the possibility that native proteins modify the ability of hydroxyapatite (HA) crystals to stimulate human inflammatory cells. Neutrophil superoxide release and chemiluminescence in response to HA crystals (0.3–4.0 mg/ml) were blunted by serum and plasma. Inhibitory activity was progressively removed from serum by sequential adsorption with HA crystals, suggesting that the inhibitors were crystal‐bound proteins. Thus, we characterized HA crystal‐bound plasma proteins by O'Farrell gels: Fibronectin, transferrin, albumin, α2−HS glycoprotein (AHSG), α1−proteinase inhibitor, α1−acid glycoprotein, Gc globulin, haptoglobin, and high density lipoprotein apolipoproteins were major bound species. Of these, AHSG was the most active inhibitor of HA‐induced neutrophil superoxide release, and this glycoprotein partially (60%) restored inhibitory activity to HA‐adsorbed serum. AHSG also bound in vitro to the related BCP crystal, octacalcium phosphate, but only minimally to calcium pyrophosphate dihydrate crystals and monosodium urate crystals. Suppressive effects on neutrophil stimulation exhibited by AHSG were also specific for BCP crystals. AHSG was present in noninflammatory synovial fluids bound to synthetic HA crystals in vitro, and AHSG could be detected on native synovial fluid HA crystals. We conclude that the binding of AHSG may modulate the inflammatory potential of BCP crystals.
High‐affinity interleukin‐2 receptors on blood lymphocytes are decreased during active rheumatoid arthritis
Authors: Emery Paul , Wood Nigel , Gentry Kay , Stockman Alex , Mackay Ian R. , Bernard Ora 
Published: February 2007

AbstractThe expression of receptors for interleukin‐2 (IL‐2R) was examined in patients with active or inactive rheumatoid arthritis (RA) and in control subjects. Unstimulated blood lymphocytes from patients with active RA had increased levels of total IL‐2R, as measured by Tac‐positive cells, compared with the levels found in the other 2 groups. Mitogen‐stimulated cells from patients with active RA expressed less IL‐2R per cell, but the most striking feature was the failure to express high‐affinity IL‐2R. These changes could reflect persistent antigenic stimulation and explain the defective cell‐mediated immunity in RA patients.
Giant cell inflammation compared with amyloidosis of the internal elastic lamina in temporal arteries
Authors: Muckle Thos. J. 
Published: February 2007

AbstractClose examination of a series of temporal artery biopsy specimens provided histologic and statistical evidence that any association between the occurrence of giant cell arteritis and senile amyloidosis of the temporal artery internal elastic lamina is not direct, but is associated incidentally with old age. Substantial demographic differences between the 2 conditions were found; the prevalence of giant cell arteritis first waxed and then waned with increasing age, while rates for senile amyloidosis of the temporal artery progressed steadily toward 100% in the ninth decade of life.
Temporal patterns of response to d‐penicillamine, hydroxychloroquine, and placebo in juvenile rheumatoid arthritis patients
Authors: Kerckhove Catherine Van , Giannini Edward H. , Lovell Daniel J. 
Published: February 2007

AbstractWe calculated the time required for therapeutic benefit to become apparent following initiation of treatment with D‐penicillamine (DP), hydroxychloroquine (HCQ), or placebo (each administered concomitantly with a nonsteroidal antiinflammatory drug) using data from a double‐blind, randomized 12‐month trial in 162 patients with juvenile rheumatoid arthritis. Using previously published criteria to classify the outcome, we found that 60% of the HCQ group, 46% of the DP group, and 39% of the placebo group responded favorably after 12 months of therapy. Data from examinations between the initial and final assessments were used to determine when the response first occurred. Approximately 50% of all patients who showed improvement at 12 months had already done so by 2 months. After 6 months, 96% of the DP group, 88% of the HCQ group, and 85% of the placebo group responders had met the criteria for response. The average time until response was attained was 105 days for the DP group, 129 days for the HCQ group, and 140 days for the placebo group. Our results indicate that a favorable response to these slow‐acting antirheumatic drugs is unlikely if improvement has not occurred within the first 6 months of therapy.
Low‐dose gold compounds inhibit fibroblast proliferation and do not affect interleukin‐1 secretion by macrophages
Authors: Matsubara Tsukasa , Saegusa Yasuhiro , Hirohata Kazushi 
Published: February 2007

AbstractWe examined the effect of low concentrations of gold compounds on the proliferation of human fibroblasts. Gold sodium thiomalate (GST) inhibited both basal and interleukin‐1‐induced tritiated thymidine incorporation into fibroblasts in a dose‐ and time‐dependent manner. Significant inhibition was observed at the level of 5 m̈g/ml GST, and >50% inhibition was attained at 10 m̈g/ml. These concentrations are attainable in the serum of treated patients. Similar inhibition was observed when <1 m̈g/ml auranofin, which is also within a serum‐attainable range, was added. Low concentrations of GST (0–10 m̈g/ml) did not affect interleukin‐1 secretion from lipopolysaccharide‐stimulated human mononuclear phagocytes (Mϕ) when assessed by both human fibroblast and C3H/HeJ mouse thymocyte proliferation assays. When Mϕ precultured for 48 hours with GST (0–10 m̈g/ml) were added to the fibroblast culture in the presence or absence of lipopolysaccharide, there was no significant inhibition of Mϕ‐induced DNA synthesis of fibroblasts. In contrast, when fibroblasts were precultured with GST (0–10 m̈g/ml) for 48 hours and freshly separated Mϕ were added, significant inhibition was observed in Mϕ‐induced fibroblast proliferation at 5 m̈g/ml. These results suggest that low concentrations of GST directly cause a reduction of fibroblast proliferation, but do not affect the capability of Mϕ for induction of fibroblast proliferation. Therefore, gold compounds may play a role in the inhibition of the growth of rheumatoid pannus by direct inhibition of fibroblast proliferation.
Stimulation of the hyaluronic acid levels of human synovial fibroblasts by recombinant human tumor necrosis factor α, tumor necrosis factor β (lymphotoxin), interleukin‐1α, and interleukin‐1β
Authors: Butler Debra M. , Vitti Gerard F. , Leizer Tali , Hamilton John A. 
Published: February 2007

AbstractMonocyte/macrophage polypeptides (monokines) alter the properties of synovial cells. This interaction could explain some of the properties of the inflamed synovium in rheumatic disease. Only recently has it been possible to test the action of purified monokines on the target synovial cells. We report here that recombinant human tumor necrosis factor α, tumor necrosis factor β (lymphotoxin), interleukin‐1α, and interleukin‐1β stimulate the hyaluronic acid (HA) levels of human synovial fibroblast‐like cells. The effect of monokines was generally inhibited by indomethacin, suggesting the involvement of an endogenous cyclooxygenase product in the stimulation, and by the glucocorticoid, dexamethasone. In contrast, all‐trans‐retinoic acid stimulated synovial cell plasminogen activator activity but did not increase the HA levels. These findings could help to explain the raised HA levels found in the joint fluids and in the circulation of patients with rheumatic disease.
Serum immunoreactive erythropoietin in rheumatoid arthritis: impaired response to anemia
Authors: Hochberg Marc C. , Arnold Cynthia M. , Hogans Beth B. , Spivak Jerry L. 
Published: February 2007

AbstractSerum immunoreactive erythropoietin (EP) levels were measured in 116 patients with rheumatoid arthritis (RA) and 20 control patients with iron deficiency anemia. Serum EP levels were significantly higher in the 46 anemic RA patients than in the 70 nonanemic RA patients (mean ± 1 SD 31.0 ± 19.8 mU/ml versus 16.8 ± 12.4 mU/ml; P < 0.0001). Furthermore, although a significant inverse correlation between the serum EP level and the hemoglobin value was present in the anemic RA patients (r = −0.57, P < 0.0001), the regression coefficient describing the relationship between serum EP and hemoglobin was significantly lower for the anemic RA patients than for patients with iron deficiency anemia (F = 6.01, P < 0.025).
Effect of inhibitors of eicosanoid metabolism in murine collagen‐induced arthritis
Authors: Griswold Don E. , Hillegass Leonard M. , Meunier Paul C. , Dimartino Michael J. , Hanna Nabil 
Published: February 2007

AbstractThe dual inhibitors of arachidonic acid metabolism, Smith Kline & French (SK&F) 86002, SK&F 104351, and phenidone; the corticosteroid, dexamethasone; and the selective cyclooxygenase inhibitors, ibuprofen, indomethacin, naproxen, and piroxicam were evaluated for their antiarthritic potency in the murine, collagen‐induced arthritis model. The ability of these compounds to alter the severity of arthritic lesions and to reduce serum levels of the acute‐phase reactant, serum amyloid P component (SAP) were monitored. Serum concentrations of SAP were found to correlate strongly (r = 0.985) with disease severity at day 35 postimmunization. Treatment with SK&F 86002, SK&F 104351, phenidone, or dexamethasone significantly reduced disease severity, as judged by clinical score (55%, 72%, 41%, and 45% inhibition, respectively) and SAP levels (62%, 94%, 52%, and 94% inhibition, respectively) in arthritic mice. This profile of activity was not shared by the selective cyclooxygenase inhibitors, which did not uniformly inhibit disease activity by both parameters. The results suggest that dual inhibitors of 5‐lipoxygenase and cyclooxygenase may prove more effective than selective cyclooxygenase inhibitors as antiarthritic agents.
Interleukin‐1 stimulation of phospholipase activity in rat synovial fibroblasts
Authors: Godfrey Richard W. , Johnson William J. , Hoffstein Sylvia T. 
Published: February 2007

AbstractTritiated arachidonic acid (3H‐AA)—labeled rat synovial fibroblasts stimulated with human recombinant interleukin‐1β (rIL‐1β) released incorporated radiolabel in a time‐dependent and dose‐dependent manner, with labeled prostaglandins representing 29% of the released radiolabel. Treatment of the cells with dibutyryl cAMP or prostaglandin E2 enhanced both spontaneous and rIL‐1β‐induced 3H‐AA release; treatment with indomethacin or naproxen inhibited the response. The effects of these cyclooxygenase inhibitors on 3H‐AA release were not reversed by the addition of prostaglandin E2. The activities of phospholipase A, phospholipase C, and diglyceride lipase were detected in the homogenates of rat synovial fibroblasts. Pretreatment of synovial cells with rIL‐1β resulted in a threefold stimulation of phospholipase A activity and a slight increase in phospholipase C activity in cell homogenates. These data show that rIL‐1β stimulates phospholipase activities in rat synovial fibroblasts and that at least one of these activities may be regulated by either prostaglandins or cAMP.
Lipid microspherules in synovial fluid of patients with pigmented villonodular synovitis
Authors: Ugai Kazuhiro , Kurosaka Masahiro , Hirohata Kazushi 
Published: February 2007

AbstractWe describe 2 patients with pigmented villonodular synovitis. In both patients, synovial fluids (SF) were characterized by the presence of abundant, strongly birefringent lipid microspherules, which appeared as Maltese crosses and were found both inside foam cells and free in the SF. Histologically, the synovial membranes showed pigmented villonodular synovitis, with aggregation of foam cells containing abundant lipid microspherules in their cytoplasm. Observation of numerous birefringent lipid microspherules and foam cells in SF may be a clue to the diagnosis of pigmented villonodular synovitis.
Evaluation of clinical competence in rheumatology training programs
Authors: Harris Edward D. , Benson John A. , Blank Linda L. 
Published: February 2007

AbstractTo ensure that members of the public and the medical profession can identify physicians who have demonstrated excellence in the field of rheumatology, the American Board of Internal Medicine has called upon directors of rheumatology training programs to establish systems to evaluate, document, and substantiate those components of overall clinical competence that are considered essential for certification. Many of these abilities can be assessed only by repeated, direct observations.
Hepatic ultrastructure after methotrexate therapy for rheumatoid arthritis
Authors: Bjorkman David J. , Hammond Elizabeth H. , Lee Randall G. , Clegg Daniel O. , Tolman Keith G. 
Published: February 2007

AbstractTwenty‐six patients receiving long‐term oral methotrexate (MTX) therapy for rheumatoid arthritis (24 patients) or psoriasis (2 patients) were prospectively evaluated for alterations in liver morphology by light microscopy, electron microscopy, and immunofluorescence microscopy. Although only 4 MTX‐treated patients had light microscopic evidence of mild fibrosis, all had evidence of collagen deposition in the space of Disse near Ito cells and changes in hepatocyte lysosomes on electron microscopy. These findings were absent from control livers. Fibrinogen, fibronectin, and type IV collagen were identified by immunofluorescence in both MTX‐treated patients and controls. We conclude that long‐term MTX therapy for rheumatoid arthritis is associated with alterations in hepatic ultrastructure, including collagen deposition in the space of Disse and changes in hepatocyte lysosomes.
Prostaglandin e2 modulation of rheumatoid factor synthesis
Authors: Alvarellos Alejandro , Lipsky Peter E. , Jasin Hugo E. 
Published: February 2007

AbstractWe examined the influence of prostaglandin E2 (PGE2) on the in vitro synthesis of rheumatoid factor (RF) by purified human B and T lymphocytes stimulated with Staphylococcus aureus Cowan 1 or pokeweed mitogen (PWM). Supernatants were assayed for total IgM and RF. PGE2 at concentrations of 10−7M to 10−9M significantly inhibited RF and IgM secretion stimulated by S aureus Cowan 1, a cross‐linker of B cell surface Ig. The magnitude of inhibition of RF production was significantly greater than that of total IgM at low PGE2 concentrations (P &lt; 0.05). In contrast, PWM‐stimulated cultures were only minimally inhibited by PGE2 at all concentrations tested. Since cross‐linking of surface Ig renders B cells more susceptible to inhibition by PGE2, heat‐aggregated IgG (HAIgG) was added to the PWM‐stimulated cultures in an attempt to increase the sensitivity of precursors of RF‐secreting cells to the inhibitory effects of PGE2. Addition of HAIgG markedly increased PGE2‐mediated inhibition of RF synthesis without significantly affecting IgM production. Inhibition could not be overcome by the addition of soluble T helper cell factors, indicating that PGE2‐mediated suppression was not the result of an inhibitory action of T helper cells. When lymphocytes from patients with rheumatoid arthritis were examined, HAIgG was found to be unable to induce sensitivity to PGE2‐mediated inhibition of responsiveness. These results suggest that down‐regulation of RF synthesis requires both cross‐linking of surface Ig and the influence of PGE2. Abnormalities in this immunoregulatory mechanism may explain the ongoing production of RF in patients with rheumatoid arthritis.
Structure of t cell antigen receptor β chain in synovial fluid cells from patients with rheumatoid arthritis
Authors: Keystone E. C. , Minden M. , Klock R. , Poplonski L. , Zalcberg J. , Takadera T. , Mak T. W. 
Published: February 2007

AbstractWe attempted to identify a clonal proliferation of T cells from synovial fluid samples from patients with rheumatoid arthritis, using techniques of restriction fragment length polymorphism. We used probes for the β chain of the T cell receptor to analyze restriction fragments prepared from the genomic DNA of synovial fluid mononuclear cells from 10 patients and synovial fluid T cell preparations from 5 additional patients. The results demonstrated unarranged (germline) T cell receptor gene fragments of DNA in all cell preparations, indicating the lack of clonality of rheumatoid arthritis synovial fluid T cells.
Arthritogenicity of minor cartilage collagens (types IX and XI) in mice
Authors: Boissier Marie‐Christophe , Chiocchia Gilles , Ronziere Marie‐Claire , Herbage Daniel , Fournier Catherine 
Published: February 2007

AbstractNative type II collagen, the major cartilage collagen, is immunogenic and arthritogenic in rodents. To investigate whether minor cartilage collagens are arthritogenic, we immunized DBA/1 mice with the pepsin‐soluble fractions of type IX or type XI collagen emulsified in Freund's complete adjuvant. Both collagens were arthritogenic in DBA/1 mice after only 1 injection. However, the incidence of the polyarthritis was lower and the severity was lesser than with that induced by bovine type II collagen, even when a booster injection was administered. All mice developed a humoral response to the immunizing antigen, without any relationship to the arthritic status. Interestingly, competition experiments showed that antibodies raised against type XI collagen also bound with high avidity to type II collagen. In contrast, sera from type IX collagen‐immunized mice did not react with either type II or type XI collagen. We conclude that types IX and XI minor cartilage collagens are both arthritogenic and immunogenic in DBA/1 mice. Whether the recognition of epitopes common to different collagens is relevant to the articular pathology remains to be elucidated.
Correlation of serologic indicators of inflammation with effectiveness of nonsteroidal antiinflammatory drug therapy in rheumatoid arthritis
Authors: Cush John J. , Lipsky Peter E. , Postlethwaite Arnold E. , Schrohenloher Ralph E. , Saway Anthony , Koopman William J. 
Published: February 2007

AbstractForty‐seven patients with rheumatoid arthritis (mean duration 5.7 years) who were receiving neither disease‐modifying drugs nor corticosteroids were enrolled in a 12‐week, multicenter study of the relationship between clinical and serologic measures of disease activity in patients taking nonsteroidal antiinflammatory drugs. After a 2‐week drug washout period, patients received flurbiprofen (200 mg/day) or sustained‐release ibuprofen (2,400 mg/day) for a 10‐week trial. Clinical response was assessed biweekly using standard clinical parameters, including 50‐foot walk time, tender joint score, duration of morning stiffness, and global assessment of disease activity and pain (by both the patient and the physician). Patients were classified as responders if there was ⩾30% improvement in at least 3 of the 4 clinical measures of disease activity. Thirty patients completed at least 8 weeks of therapy; there were 12 responders and 18 nonresponders. Of the laboratory parameters examined, the responders, but not the nonresponders, demonstrated significant reductions (from postwashout values) in levels of IgM rheumatoid factor and C‐reactive protein (CRP), along with significant increases in the number of circulating lymphocytes and decreases in the number of circulating granulocytes (P ⩽ 0.05). In contrast, the nonresponders demonstrated either no change or worsening of the laboratory correlates of disease activity. The responders also appeared to have more aggressive disease at baseline, with significantly more painful joints, greater 50‐foot walk times, elevated CRP values, and elevated erythrocyte sedimentation rates (P ⩽ 0.05). These data suggest that there is a subset of rheumatoid arthritis patients in whom clinical improvement with nonsteroidal antiinflammatory drug therapy is associated with significant reductions in IgM rheumatoid factor and CRP levels.
Abnormal t suppressor cell function in juvenile rheumatoid arthritis
Authors: Silverman Earl D. , Somma Catherine , Khan Manzoor M. , Melmon Kenneth L. , Engleman Edgar G. 
Published: February 2007

AbstractThe purpose of this study was to analyze T suppressor cell function in juvenile rheumatoid arthritis (JRA). JRA is a chronic inflammatory childhood disease of unknown etiology that is characterized by arthritis and immunoregulatory abnormalities. T suppressor cell precursors (CD8+, CD28−) were purified from the peripheral blood of 24 JRA patients, using a combination of monoclonal antibodies. These cells were treated with histamine or concanavalin A, agents that are known to induce suppressor activity. They were also tested for their ability to inhibit the proliferative response of autologous T cells to phytohemagglutinin. In some experiments, the accumulation of intracellular cAMP following histamine treatment was also measured. Twelve of 13 patients with clinically active JRA showed abnormal histamine‐inducible T suppressor cell function, characterized by the failure of CD8+, CD28− T cells to mediate any detectable suppression. The failure of these cells to accumulate intracellular cAMP after histamine treatment was observed in 5 of 5 patients tested who had active disease. In contrast, 11 of 11 patients with clinically inactive JRA, 5 of 5 patients with cystic fibrosis, and 9 of 9 pediatric control subjects had normal histamine‐and concanavalin A‐inducible T suppressor cell function, and a normal cAMP response to histamine. These results suggest that patients with clinically active JRA have a reversible defect in T suppressor cell function that is associated with a failure of T suppressor cell precursors to accumulate intracellular cAMP following their exposure to selected immune stimuli.
Subsequent behavior of users of an arthritis information telephone service
Authors: Maisiak Richard , Koplon Sandra , Heck Louis W. 
Published: February 2007

AbstractFollowup telephone interviews were conducted with a stratified random sample of 305 users of a prototype telephone information service for arthritis 2–4 months after their initial contact with the service. The percentage of respondents who reported taking at least 1 positive action for their arthritis because of service usage was 79%. The most frequently reported actions of users were asking their doctor more questions and greater compliance with their doctor's orders. About one‐half of the respondents felt more in control of their arthritis because of service usage. Both the taking of at least 1 action and the taking of certain specific actions were significantly correlated with feeling more in control of the arthritis (P > 0.01). Respondents who were less than 60 years old, black, or symptomatic were significantly more likely to take an action and took significantly more actions (P > 0.01). This minimal intervention may stimulate positive behaviors for individuals with arthritis.
Accuracy of creatinine clearance in measuring glomerular filtration rate in patients with systemic lupus erythematosus without clinical evidence of renal disease
Authors: Ratain Jill S. , Petri Michelle , Hochberg Marc C. , Hellmann David B. 
Published: February 2007

AbstractWe sought to determine whether creatinine clearance (Ccr) gives an accurate measurement of the glomerular filtration rate in patients with systemic lupus erythematosus (SLE) with no clinical evidence of renal disease. Eighteen such SLE patients underwent measurement of Ccr and 99mtechnetium‐DTPA clearance (CDTPA). The mean ± SD Ccr:CDTPA ratio was 1.12 ± 0.15 (95% confidence interval 1.04–1.20). These results indicate that Ccr gives an accurate measurement of the glomerular filtration rate in the majority of SLE patients who do not have clinical evidence of renal disease.