bluuebunny/crossref_metadata_2025_split huggingface dataset:
Stress‐induced proteins in chondrocytes from patients with osteoarthritis
Authors: Kubo Toshikazu , Towle Christine A. , Mankin Henry J. , Treadwell Benjamin V. 
Published: February 2007

AbstractRecent studies have shown that a specific set of proteins is produced by a variety of cells after the application of some forms of stress, including heat shock. Human chondrocytes isolated from cartilage with moderate to severe osteoarthritis synthesize at least 1 of these stress proteins (Mr 70, 000) at physiologic temperature (37°C), whereas chondrocytes isolated from non‐pathologic cartilage synthesize this protein only in response to incubation at temperatures above 39°C. The active synthesis of this protein (SP‐70) at 37°C is positively correlated with the severity of osteoarthritis and can be a characteristic indicator of this degenerative disease. We identified the active synthesis of stress proteins after incubating the cartilage tissue in medium containing 35S‐methionine and separating the cell‐associated proteins by sodium dodecyl sulfate–polyacrylamide gel electrophoresis. The radioactive proteins were visualized by autoradiography. Analysis of the longevity of cell‐associated proteins was determined by pulsing the tissue with 35S‐methionine, and after different periods of chase in medium, the proteins were separated by sodium dodecyl sulfate–polyacrylamide gel electrophoresis. Specific protein bands were then excised, and the radioactivity was determined by liquid scintillation counting.
Continuing medical education. Changing behavior and improving outcomes
Authors: Stross Jeoffrey K. , Schumacher H. Ralph , Weisman Michael H. , Spalding David M. 
Published: February 2007

AbstractA study was undertaken to determine if an intensive continuing medical education program in rheumatology could improve patient care. Fifteen primary care practitioners, who fit the description of educationally influential physicians, completed a 2‐week academic medical center–based preceptorship. Improvement in physician knowledge, from a mean score of 65.3% to a mean of 82.9%, was documented using pre‐ and post‐tests. Significant changes in physician behavior were documented using chart audits and patient interviews. The use of diagnostic tests and corticosteroids, and physician–patient interactions were the areas of greatest improvement. Functional outcomes for patients, measured by the Sickness Impact Profile, also improved. These findings suggest that a well‐designed continuing medical education program can effect some changes in physician knowledge and behavior that will result in at least short‐term improvement in patient outcomes.
Lack of correlation between blood gold concentrations and clinical response in patients with definite or classic rheumatoid arthritis receiving auranofin or gold sodium thiomalate
Authors: Dahl Stephen L. , Coleman Miki L. , Williams H. James , Altz‐Smith Mary , Kay Donald R. , Paulus Harold E. , Weinstein Arthur , Kaplan Stanley 
Published: February 2007

AbstractWe investigated the correlation between whole blood gold concentrations and clinical outcomes in 59 auranofin‐treated patients and 51 gold sodium thioma‐late‐treated patients who completed a 21‐week, placebo‐controlled, multicenter parallel trial. Whole blood gold concentrations did not correlate with clinical outcome, as assessed by changes in joint tenderness, joint swelling, or Westergren erythrocyte sedimentation rate. They also did not correlate with toxic reactions necessitating withdrawal from the study.
IgA rheumatoid factor synthesis by dissociated synovial cells. Characterization and relationship to IgM rheumatoid factor synthesis
Authors: Koopman William J. , Schrohenloher Ralph E. , Crago Sylvia S. , Spalding David M. , Mestecky Jiri 
Published: February 2007

AbstractWe examined patterns of IgA rheumatoid factor (RF) and IgM‐RF synthesis by dissociated synovial cells obtained from 27 patients with seropositive rheumatoid arthritis. Synthesis of IgA‐RF was observed in 19 of 34 synovial cell preparations from these patients and constituted a mean of 16% of the total IgA produced. IgA‐RF expression correlated only weakly with IgM‐RF production (r = 0.385) and could be dissociated from production of IgA‐RF (and IgM‐RF) exhibited by simultaneously obtained peripheral blood plasma cells. While wide variations were observed in the ratio of IgA‐RF:IgM‐RF produced by synovial B cells in the patient sample studied, remarkable consistency in the relationship of IgA‐RF to IgM‐RF synthesis was observed overtime in different joints of the same patient. IgA‐RF synthesized by dissociated synovial cells was predominantly of the IgAl subclass and existed in both monomeric and polymeric forms. Our results are compatible with the view that local production of IgA‐RF and IgM‐RF are regulated independently of each other.
Suppression of hyaluronic acid synthesis in synovial organ cultures by corticosteroid suspensions
Authors: Myers Stephen L. 
Published: February 2007

AbstractThe effects of sparingly soluble corticosteroid suspensions prepared for intraarticular therapy, of their vehicles, and of hydrocortisone on synovial hyaluronic acid (HA) synthesis were compared in organ cultures of normal canine villous synovium. Both hydrocortisone and the corticosteroid suspensions suppressed HA synthesis, as did 2 vehicle components, polysorbate 80 and myristyl‐gamma‐picrolinium chloride. Cultures of synovium from joints of dogs which, 1 day previously, had been injected with methylprednisolone acetate suspension synthesized less HA than did control cultures from noninjected joints of the same animals. The results indicate that suppression of HA synthesis is a mechanism by which these drugs can act to reduce joint HA content and promote resolution of synovial effusions.
Effective patient education. A quasi‐experiment comparing an individualized strategy with a routinized strategy
Authors: Lorish Christopher D. , Parker Julia , Brown Sam 
Published: February 2007

AbstractA quasi‐experiment was conducted on 127 hospitalized rheumatoid arthritis patients to determine the relative success of 3 patient teaching strategies—an individualized program, a routinized program, and a no‐planned‐instruction program—on patients' knowledge of their disease and treatment. Data analysis revealed that the individualized program produced a 100% greater learning gain than the routinized program in patients who had low pretest scores. The results suggest that maximum patient learning occurs when the teaching process accommodates important patient differences.
Assessment of radiologic progression in rheumatoid arthritis. A randomized, controlled trial
Authors: Fries James F. , Bloch Daniel A. , Sharp John T. , McShane Dennis J. , Spitz Patricia , Bluhm Gilbert B. , Forrester Deborah , Genant Harry , Gofton Philip , Richman Steven , Weissman Barbara , Wolfe Frederick 
Published: February 2007

AbstractRadiologic assessment of progressive joint destruction in rheumatoid arthritis is generally considered to be the ultimate standard for evaluation of treatment. We compared alternative radiologic techniques by performing a randomized, controlled trial in which hand films of rheumatoid arthritis patients were read by several skilled observers. The number of joints evaluated (34 versus 18) was found to make relatively little difference, but the number of readers and their experience level was critical. Films should be read in pairs. Joint space narrowing and erosion scores were shown to contribute independent information. Use of recommended techniques can reduce the number of patients required and, thus, can reduce the cost of a clinical trial by more than half and can substantially increase the sensitivity and efficiency of a trial. Therefore, critical selection of the method of assessing study endpoint is of great importance.
The allopurinol hypersensitivity syndrome. Unnecessary morbidity and mortality
Authors: Singer Joyce Z. , Wallace Stanley L. 
Published: February 2007

AbstractPatients receiving allopurinol are at risk of developing the allopurinol hypersensitivity syndrome, an immunologic reaction to the drug, characterized by multiple abnormalities such as fever, rash, decreased renal function, hepatocellular injury, leukocytosis, and eosinophilia. The records of 8 patients with the allopurinol hypersensitivity syndrome evaluated at the Downstate Medical Center hospitals and an additional 72 patients described in the literature were reviewed. All were seriously ill. Three of the 8 patients at the Down‐state Medical Center hospitals died as a result of allopurinol hypersensitivity; 19 of the 72 previously described patients also died from consequences of taking the drug. Only 1 of our 8 patients with allopurinol hypersensitivity was given allopurinol for an appropriate reason. Eight of the 59 previously described patients on whom there was adequate information had legitimate indications for allopurinol therapy. Severe, often fatal iatrogenic disease occurred unnecessarily in the others.
Immunofluorescence studies of florid rheumatic Aschoff lesions
Authors: Husby Gunnar , Arora Ramesh , Williams Ralph C. , Khaw Ban An , Haber Edgar , Butler Cooley 
Published: February 2007

AbstractWe studied cardiac tissues of a patient who died of severe rheumatic myocarditis. Multiple Aschoff lesions were present throughout both ventricles and auricles. Immunofluorescence studies showed large monocytoid cells staining with OKM1 and anti‐Leu M‐3 as well as anti‐Ia. Scattered T cells in areas of focal myocarditis stained with OKT3. Parallel staining for cardiac myosin‐heavy chain antigens showed patchy dissolution of cardiac muscle fibers and traces of cardiac myosin within large monocytoid Aschoff cells.
Experimental osteoarthritis induced by selective myectomy and tendotomy
Authors: Arsever Christiane L. , Bole Giles G. 
Published: February 2007

AbstractA new model of osteoarthritis has been developed that utilizes an extraarticular surgical technique to alter gait and weight‐bearing capabilities in the hind limbs of experimental animals. Guinea pigs, averaging 650 gm in weight, were subjected to unilateral resection of a segment of the gluteal muscles at the sacral origin, to section of the infrapatellar ligament, or to both procedures. Progressive changes consistent with osteoarthritis developed over 10–24 weeks as judged by gross, radiologic, and microscopic findings. In addition, an increase in mean cartilage water content and 35SO4−2 incorporation into proteoglycans by 10 and 14 weeks, respectively, were consistent with the chemical changes observed in early osteoarthritis. Abnormalities developed not only in the operated hind limb, but in the contralateral, unoperated hind limb at a slightly later time. Thus, this animal model provided the opportunity to evaluate a mild gait abnormality and other biomechanical influences on the evolution of osteoarthritis which is uninfluenced by any intraarticular joint trauma.
Immunomodulatory effects of treatment with naproxen in patients with rheumatic disease
Authors: Ceuppens Jan L. , Robaeys Geert , Verdickt Wilfried , Vertessen Simonne , Deckmyn Hans , Dequeker Jan 
Published: February 2007

AbstractWe evaluated the effects of a nonsteroidal antiinflammatory drug, naproxen, on phytohemagglutinin (PHA)–induced lymphocyte proliferation. When added in vitro to cultures of peripheral blood mononuclear cells, naproxen enhanced the proliferative response toward PHA of lymphocytes from rheumatoid arthritis (RA) patients but not from healthy volunteers, and it reduced prostaglandin E2 (PGE2) synthesis in the cultures. Oral treatment for 7 days with naproxen also resulted in a significant enhancement of the in vitro PHA‐induced proliferation of lymphocytes from RA patients and from age‐matched control patients with noninflammatory rheumatic diseases, but not from young healthy controls. This enhancement of PHA‐induced lymphocyte proliferation after oral intake of naproxen was not accompanied by diminished in vitro PGE2 production in the cultures. It did occur when PGE2‐producing monocytes were removed and when in vitro PGE2 synthesis was blocked with indomethacin. We conclude that oral treatment with naproxen has an immunomodulatory effect and improves in vitro PHA‐induced proliferation of lymphocytes from rheumatic disease patients. This effect is not due to reduced PGE2 synthesis in the in vitro cultures, but reflects a more fundamental in vivo change in immunoregulation.
Low density lipoprotein inhibits the physical interaction of phlogistic crystals and inflammatory cells
Authors: Terkeltaub Robert , Smeltzer Dianne , Curtiss Linda K. , Ginsberg Mark H. 
Published: February 2007

AbstractLow density lipoprotein (LDL) is the major plasma inhibitor of neutrophil oxidative and lytic responses to monosodium urate crystals and may function to modulate acute gouty inflammation. LDL inhibited apparent phagocytosis of urate crystals by human neutrophils, suggesting it may interfere with early events in the crystal‐induced stimulation of neutrophils. The effects were not specific for neutrophils, since human platelet secretory and membranolytic responses to urate crystals were also inhibited by purified LDL in doses as low as 10 μg/ml. As with neutrophils, the inhibitory activity of LDL was stimulus‐specific. Since LDL binds to urate crystals and specifically inhibits a range of cellular responses to them, including phagocytosis, we hypothesized that LDL interferes with the initial crystal‐cell interaction. We measured platelet interaction with urate crystals and found that LDL was a potent inhibitor of crystal‐induced platelet sedimentation and was 10–100‐fold more active than lipoprotein‐depleted plasma or purified high density lipoprotein. In summary, LDL inhibits a broad range of responses of a number of inflammatory cell types to certain inflammatory surfaces, and this effect appears to be due to inhibition of physical association of crystals with cell membranes.
Analysis of interleukin‐2 activity in patients with Behçet's disease. Ability of T cells to produce and respond to interleukin‐2
Authors: Sakane Tsuyoshi , Suzuki Noboru , Ueda Yuji , Takada Shinsuke , Murakawa Yohko , Hoshino Takashi , Niwa Yukie , Tsunematsu Tokugoro 
Published: February 2007

AbstractWe examined interleukin‐2 (IL‐2) activity in patients with Behçet's disease. T cells from all patients with Behçet's disease were able to produce normal levels of IL‐2 in response to phytohemagglutinin; however, responsiveness to IL‐2 was impaired in their concanavalin A‐activated lymphoblasts. This defect was due to decreased numbers of cells bearing IL‐2 receptors in patients with early active disease; in patients with chronic active or with inactive disease, there was a decrease in density of IL‐2 receptors on T cells bearing these receptors. Unresponsiveness of T cells to IL‐2 may thus contribute to immunologic aberrations in Behçet's disease.
Acute gout presenting in the manubriosternal joint
Authors: Kernodle G. Wallace , Allen Nancy B. 
Published: February 2007

AbstractA 54‐year‐old black man developed acute pain and swelling of the manubriosternal joint. Acute gouty arthritis was diagnosed by arthrocentesis and polarizing microscopy. The histology of the manubriosternal joint and its involvement in other arthritides are briefly discussed.
Alpha1‐antitrypsin phenotypes, including M subtypes, in pulmonary disease associated with rheumatoid arthritis and systemic sclerosis
Authors: Michalski Joseph P. , McCombs Candace C. , Scopelitis Eve , Biundo Joseph J. , Medsger Thomas A. 
Published: February 2007

AbstractAlpha1‐antitrypsin is a glycoprotein that functions as the major protease inhibitor in human serum. Many genetic variants of α1‐antitrypsin can be detected by electrophoretic techniques. We used isoelectric focusing on ultrathin gels to determine the common M subtypes as well as other variants of α‐antitrypsin in 62 white patients with rheumatoid arthritis (RA) and 51 white patients with systemic sclerosis (SSc). We found no increased prevalence of variant phenotypes in either disease group as a whole. In RA, however, the association between pulmonary interstitial fibrosis and α1‐antitrypsin variants was striking. Interstitial fibrosis was seen on chest roentgenogram in only 1 of 30 subjects apparently homozygous for M1 (the “wild type” or “normal” phenotype), compared with 13 of 32 patients with variant phenotypes. Seven of 15 patients with M1M2 (the most common variant phenotype) had pulmonary fibrosis. In contrast, there was no apparent association of variant phenotypes with pulmonary involvement in SSc. Our findings suggest a possible role of α1‐antitrypsin in the pathogenesis of interstitial fibrosis in patients with RA. The absence of such an association in SSc suggests that pulmonary involvement in these 2 rheumatic diseases may have different pathogeneses.
Serum amino‐terminal type III procollagen peptide in rheumatoid arthritis. Relationship to disease activity, treatment, and development of joint erosions
Authors: Hørslev‐Petersen Kim , Bentsen Kirsten D. , Junker Peter , Lorenzen Ib 
Published: February 2007

AbstractUsing 2 radioimmunoassays, increased serum levels of amino‐terminal type III procollagen peptide and its degradation products were demonstrated in rheumatoid arthritis patients. Patients with active disease showed higher serum propeptide levels than did patients with inactive disease. Unlike D‐penicillamine, azathioprine treatment suppressed the propeptide levels in patients with active disease. A 6‐month prospective study showed significantly higher initial serum propeptide levels in patients with erosive progression. The propeptide level reflects disease activity and may be a valuable prognostic marker in rheumatoid arthritis.
Impact of specific therapy upon rheumatoid arthritis
Authors: Fries James F. , Spitz Patricia W. , Mitchell Donald M. , Roth Sanford H. , Wolfe Frederick , Bloch Daniel A. 
Published: February 2007

AbstractWe performed a prospective, parallel, descriptive study of 737 consecutive new uses for 11 drugs prescribed for patients with definite or classic rheumatoid arthritis. The patients were from 5 geographically dispersed sites. Researchers used validated outcome assessment instruments to measure endpoints of disability, pain, patient global assessment, medication costs, laboratory costs, and number of physician visits. Patients were studied by strict prospective protocol at 6‐month intervals for 3 years. Controls included parallel results with other drugs, and before and after values for the individual patient. Beneficial effects were observed with the “disease‐modifying” drugs: intramuscular gold, pencillamine, and methotrexate. Of these, gold had the most apparent effect. An average of 9 months of gold therapy resulted in highly significant reductions in disability (P < 0.005), pain (P < 0.001), and patient global assessment (P < 0.005). However, patients receiving gold and methotrexate had nearly twice as many visits to physicians. In addition, drug costs increased strikingly with gold, and laboratory costs tripled. Relatively minor differences among nonsteroidal antiinflammatory agents were difficult to interpret. The outcome assessment techniques used in the study are sensitive measures, which confirm the results of experimental studies and extend observations to new outcomes, including cost and disability.
Effect of anti‐T cell auto antibodies from systemic lupus erythematosus sera upon T lymphocyte functions
Authors: Goldschmidt Leonard P. , Kresina Thomas F. , Kammer Gary M. 
Published: February 2007

AbstractThis study was undertaken to establish whether IgM and IgG anti‐T cell autoantibodies obtained from sera of patients with active systemic lupus erythematosus, impair normal T lymphocyte functions. Two in vitro models of T cell function were examined: (a) the capacity of cells to cap, endocytose, and regenerate the T3, T4, and T8 surface antigens; and (b) the adenosine‐induced T4 → T8 phenotype switch. The results demonstrated that autoantibody neither impaired the capping process, nor impeded the phenotypic switch. Thus, bound anti‐T cell autoantibodies do not appear to interfere with these specific T lymphocyte functions and cannot directly account for either the impaired T cell capping mechanism or the block in adenosine‐induced phenotype switch observed during active systemic lupus erythematosus.
Pulmonary amyloidosis associated with systemic lupus erythematosus
Authors: Nomura Shigeo , Kumagai Naoki , Kanoh Tadashi , Uchino Haruto , Kurihara Jiro 
Published: February 2007

AbstractThe association between amyloid and systemic lupus erythematosus is rarely reported. Our patient, a 26‐year‐old woman with systemic lupus erythematosus, developed steroid‐resistant exertional dyspnea and pulmonary fibrosis, without proteinuria or the nephrotic syndrome. Our studies showed that she had pulmonary amyloidosis.
Complement activation in rheumatoid arthritis evaluated by C3dg and the terminal complement complex
Authors: Mollnes Tom E. , Lea Tor , Mellbye Ove J. , Pahle Jan , Grand Øyvind , Harboe Morten 
Published: February 2007

AbstractComplement activation was evaluated in plasma and synovial fluid from patients with rheumatoid arthritis. The activation fragment C3dg and the fluid‐phase terminal complement complex were used as indicators of initial and terminal activation, respectively. Considerable activation of the whole complement cascade was demonstrated in most synovial fluid samples and in one‐third of the plasma samples. No correlation was found between the level of activation products in synovial fluid and the level in plasma. Therefore, both compartments must be examined in order to evaluate local and systemic complement activation in rheumatoid arthritis.
Decreased expression of the C3b/C4b receptor (CR1) and the C3d receptor (CR2) on B lymphocytes and of CR1 on neutrophils of patients with systemic lupus erythematosus
Authors: Wilson James G. , Ratnoff William D. , Schur Peter H. , Fearon Douglas T. 
Published: February 2007

AbstractDecreased numbers of complement receptor type 1 (CR1) have been observed on erythrocytes of patients with systemic lupus erythematosus (SLE) and on glomerular podocytes of patients having proliferative nephritis of SLE. In the present study, the analysis of the cellular expression of CR1 has been extended to include leukocytes. In addition, expression by B lymphocytes of the C3d receptor (CR2), which also serves as the receptor for the Epstein‐Barr virus, was assessed. Receptor expression was measured by 2‐color fluorescent flow cytometry of peripheral blood B cells, identified by the presence of the B1 antigen, that had also been stained with anti‐CR1 or anti‐CR2. B cells from 17 patients with SLE exhibited a mean relative fluorescence for CR1 that was 61% of that found in 17 normal individuals (P < 0.001). The expression of CR2 by the patients' B cells (n = 14) was 62% of that of the B cells from normal subjects (n = 17) (P < 0.001). The expression of CR1 correlated with that of CR2 among patients (r = 0.63; P < 0.01) but not with the expression of CR2 among normal individuals (r = 0.36; P > 0.1). The mean CR1 content of the patients' neutrophils was only 59% of the normal mean (P < 0.001). Thus, abnormalities of complement receptor expression occur on the leukocytes of patients with SLE. These deficiencies may be secondary to interaction of the cells with the products of complement activation, or, in some individuals, the deficiencies may be familial.