bluuebunny/crossref_metadata_2025_split huggingface dataset:
Substrain heterogeneity in prostaglandin E2 synthesis of human dermal fibroblasts. Differences in prostaglandin E2 synthetic capacity of substrains are not stimulus‐restricted
Authors: Korn Joseph H. 
Published: February 2007

AbstractWe examined prostaglandin E2 (PGE2) biosynthetic heterogeneity in fibroblast substrains and possible mechanisms that might mediate this heterogeneity. PGE2 synthesis of fibroblast substrains, in response to phytohemagglutinin‐stimulated mononuclear cell supernates, ranged from 9.0 ± 1.0 ng/ml to 79.3 ± 7.4 ng/ml (mean ± SD). The phenotypic behavior of individual substrains was stable. Substrains were also heterogeneous in PGE2 response to phorbol myristate acetate, and displayed stability in this phenotype as well. Substrains which were high responders to mononuclear cell supernate also ranked high in response to phorbol myristate acetate. Similar heterogeneity was observed in response to purified interleukin‐1. Arachidonic acid added exogenously did not raise interleukin‐1 responsiveness of low‐producer substrains to that of high producers, suggesting that differences in PGE2 synthesis among substrains did not reflect differences in substrate availability or phospholipase activity. Supernates of high‐ and low‐responder phenotype substrains, when added to cells of the reciprocal strain or to unrelated fibroblasts, did not affect the pattern of PGE2synthesis. The concordance of substrain responsiveness to mononuclear cell supernate and phorbol myristate acetate suggests that heterogeneity among substrains in PGE2 synthesis is related to the ability to produce PGE2 rather than to the ability to respond to a given mediator. In addition, differences in PGE2 synthesis among substrains do not appear to result from release of regulatory autokines.
Kinetics of Extraction of Proteoglycans from Human Cartilage
Authors: Pottenger Lawrence A. , Webb June E. , Lyon Nancy B. 
Published: February 2007

AbstractFifty‐one uniformly sliced human patellar cartilage specimens were extracted with physiologic buffer containing inhibitors. Galactosamine‐rich proteoglycans were more easily extracted than glucosamine‐rich proteoglycans. Extraction occurred in 2 phases. There was a large proteoglycan extraction during the first 30 minutes, followed by a steady loss proportional to the square root of time. The amount of proteoglycans extracted during phase 1 was approximately half that of phase 2. Extraction of proteoglycans varied with age, structural integrity, and cartilage thickness. Intact osteoarthritic cartilage had normal proteoglycan extraction.
Spontaneous in vitro production of anti‐DNA and anti‐RNA by systemic lupus erythematosus and normal peripheral blood mononuclear cells
Authors: Liebling Michael R. , Wong Curtice , Radosevich Jean 
Published: February 2007

AbstractThe spontaneous in vitro production of anti‐DNA and anti‐RNA by peripheral blood mononuclear cells (PBMC) from patients with systemic lupus erythematosus (SLE) and from normal subjects was evaluated employing sensitive solid‐phase assays that are specific for these antibodies. PBMC from SLE patients produced more IgG anti‐DNA and anti‐RNA than did normal PBMC (P < 0.01). In vitro production of IgG anti‐DNA appeared to correlate with serum DNA bindings (r = 0.72, P < 0.005). Similar amounts of IgM anti‐DNA and anti‐RNA were produced by both SLE and normal PBMC. However, IgM anti‐DNA antibodies always appeared to be directed against determinants on denatured DNA. Only PBMC from SLE patients produced IgG antibodies to native DNA.
Relationship between nailfold capillary abnormalities and organ involvement in systemic sclerosis
Authors: Lovy Michael , Mac‐Carter Daryl , Steigerwald James C. 
Published: February 2007

AbstractNailfold capillary abnormalities in 42 consecutive patients with systemic sclerosis were studied by widefield capillary microscopy, and capillary abnormalities were correlated with organ involvement. Twenty‐eight patients had diffuse skin disease, and 14 had the CREST variant of systemic sclerosis (calcinosis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly, telangiectasias) with anticentromere antibodies. Nailfold capillary enlargement and loss were graded from photographs. There was no correlation between the severity of either nailfold capillary loss or enlargement and duration of disease, number of organ systems involved, or acroosteolysis. The presence of telangiectasias correlated with extreme capillary enlargement (P < 0.025). Based on these findings it can be concluded that nailfold capillary changes in individual patients with systemic sclerosis are not useful in predicting organ involvement.
Reduced joint count indices in the evaluation of rheumatoid arthritis
Authors: Egger M. J. , Huth D. A. , Ward J. R. , Reading J. C. , Williams H. J. 
Published: February 2007

AbstractTwo types of summary measures of joint disease were evaluated in 2 controlled clinical trials in rheumatoid arthritis patients. One measure was based solely on the clinical/biologic judgment approach; the other combined this methodology with statistical approaches using reliability and factor analyses. „Signal joint”︁ indices, summarizing disease activity in 2–5 key joints, were found to be insensitive to deterioriation of nonsignal joints. Therefore, they are not recommended as replacements for the complete articular survey in rheumatoid arthritis. A reduced version of the complete articular survey was found to be desirable based on its validity, reliability, accuracy, precision, and sensitivity to active drugs. Its sensitivity can be slightly higher or lower than that of the full joint survey.
Effectiveness of cyclosporin therapy for Beh¸let's disease
Authors: Nussenblatt Robert B. , Palestine Alan G. , Chan Chi‐Chao , Mochizuki Manabu , Yancey Kim 
Published: February 2007

AbstractBehçet's disease is a clinical entity with mouth and genital ulcers, skin lesions, and both anterior and posterior uveitis as its major criteria. It has been theorized that Behçet's disease is immune complex mediated, and is characterized by multiple attacks which often lead to severe visual handicap. Behçet's disease patients with severe ocular involvement and cytotoxic and/or systemic corticosteroid agent failures were treated with cyclosporin (CsA). CsA therapy effectively abrogated the acute phase of the ocular attack and either totally prevented, or markedly reduced, the recurrences of these attacks. Generally, patients tolerated the medication well; occasionally however, renal toxicity secondary to cyclosporin therapy prevented prescription of a maximally effective therapeutic dose of the drug. CsA levels in plasma were dose‐dependent for each patient, but the dosage per kg of CsA needed to obtain a specific plasma level varied greatly from patient to patient. Circulating immune complex levels were not universally elevated during the acute ocular attack. However, increases in circulating immune complex concentrations were noted after treatment with CsA was begun and the disease became clinically inactive. These data, as well as the effectiveness of CsA, an agent with predominantly anti–T cell effects, raise a question as to whether circulating immune complexes are centrally relevant to the pathogenesis of this disorder, and if T cell mediation of this disease must be contemplated.
Outcomes of self‐help education for patients with arthritis
Authors: Lorig Kate , Lubeck Deborah , Kraines R. Guy , Seleznick Mitchell , Holman Halsted R. 
Published: February 2007

AbstractBehavioral and health status outcomes of an unreinforced, self‐help education program for arthritis patients taught by lay persons were examined in 2 ways: a 4‐month randomized experiment and a 20‐month longitudinal study. At 4 months, experimental subjects significantly exceeded control subjects in knowledge, recommended behaviors, and in lessened pain. These changes remained significant at 20 months. The course was inexpensive and well‐accepted by patients, physicians, and other health professionals.
Utilization of nonsteroidal antiinflammatory drugs
Authors: Baum Carlene , Kennedy Dianne L. , Forbes Mary B. 
Published: February 2007

AbstractInformation derived from pharmaceutical marketing databases on the use of 12 nonsteroidal antiinflammatory drugs in 1983 is presented. Estimates of population exposure, regularity of treatment, average daily dose, age and sex distributions of users, concomitant use of other drugs, associated diagnoses, and trends in use are provided. Utilization patterns were similar for 8 of the nonsteroidal antiinflammatory drugs, with differing patterns seen for mefenamic acid, oxyphenbutazone, phenylbutazone, and zomepirac.
Application, to Japanese patients, of the 1982 American Rheumatism Association revised criteria for the classification of systemic lupus erythematosus
Authors: Yokohari Ryuichi , Tsunematsu Tokugoro 
Published: February 2007

AbstractThe 1982 American Rheumatism Association revised criteria for the classification of systemic lupus erythematosus were tested on Japanese patients. Sensitivity and specificity data were comparable with those presented in the development of the revised criteria by the American Rheumatism Association. Complement determinations were evaluated for their ability to improve the criteria for the diagnosis of early systemic lupus erythematosus.
Influence of the severity and duration of murine antigen‐induced arthritis on cartilage proteoglycan synthesis and chondrocyte death
Authors: Kruijsen Marijn W. M. , van den Berg Wim B. , van de Putte Levinus B. A. 
Published: February 2007

AbstractRecent studies have shown that joint inflammation can suppress chondrocyte proteoglycan synthesis and can even kill chondrocytes. In the present study, we investigated the influence of the severity and chronicity of murine antigen‐induced arthritis on the degree of these toxic effects on chondrocytes. Joint inflammation, quantitated by measurements of 99mtechnetium pertechnetate uptake, was significantly correlated with the inhibition of proteoglycan synthesis, measured by 35S‐sulfate incorporation. Histologic grading of the extent of chondrocyte death on day 28 after arthritis induction correlated best with the degree of inflammation present on day 14. High scores for chondrocyte death were found only in mice with persistent, severe arthritis. Our data indicate that the severity of joint inflammation is a major determinant of the degree of chondrocyte proteoglycan synthesis inhibition, whereas both the severity and chronicity of the inflammation determine chondrocyte killing and, therefore, irreversible joint destruction.
Impact of diagnosis‐related group‐based reimbursement for treatment of rheumatic diseases in a teaching hospital
Authors: Hartley Robert M. , Liang Matthew H. , Cullen Karen E. 
Published: February 2007

AbstractThe impact of Medicare's diagnosis‐related group (DRG)‐based reimbursement system was examined for care given to 734 rheumatic disease patients discharged from a teaching hospital during a 2‐year period. The analysis accounted for length of stay “outliers” as defined by Medicare and distinguished costs from charges. Excluding outliers, DRG reimbursement would result in net revenues to the hospital of $1,126 per DRG 240 patient and $1, 794 per DRG 241 patient. The difference between DRGs in cost per patient was significant, indicating that DRGs clearly identify 2 groups of rheumatic disease patients. After excluding outliers, the coefficients of variation in costs for DRGs 240 and 241 were 72% and 80%, respectively, which although high, were average for DRGs at our institution. Mean total charge per patient was different for groups defined by their primary rheumatologic diagnosis in DRG 240 but not DRG 241. For rheumatoid arthritis and systemic lupus erythematosus patients, the total charge per patient did not differ, but the types of services did. The cost of treating outliers would create an average loss per outlier of $18,400 and $16,500, respectively, in DRGs 240 and 241. Outliers accounted for 34.5% and 21.8% of the 2 DRGs' total costs, respectively, but only 6.4% and 3.6% of the total number of patients. Under current DRG reimbursement rates, the cost of care for rheumatology patients would be adequately reimbursed in our hospital: losses from outliers would be offset by net revenues from inliers as long as current Medicare adjustments for capital and medical education costs were continued.
The value of complement and immune complex determinations in monitoring disease activity in patients with systemic lupus erythematosus
Authors: Valentijn R. M. , van Overhagen H. , Hazevoet H. M. , Hermans J. , Cats A. , Daha M. R. , van Es L. A. 
Published: February 2007

AbstractSerial serum samples from 33 patients with systemic lupus erythematosus were tested for CH50, C3, C4, and circulating immune complexes. Circulating immune complexes were determined by 5 different assays. Disease activity was determined by a scoring system we devised. On an interpatient analysis, overall disease activity correlated significantly with levels of CH50, C3, and a positive result on C1q binding assay. However, with the exception of depressed C3 levels, the sensitivity, specificity, and predictive values of all the serologic tests were low. An intrapatient analysis revealed a patient‐specific activity parameter in 11 of the 33 patients. We conclude that these serologic tests are not reliable in assessing disease activity in patients with systemic lupus erythematosus, although a small subgroup of patients will exhibit a patient‐specific activity parameter.
A rheumatoid arthritis b cell subset expresses a phenotype similar to that in chronic lymphocytic leukemia
Authors: Plater‐Zyberk C. , Maini R. N. , Lam K. , Kennedy T. D. , Janossy G. 
Published: February 2007

AbstractAn abnormal subpopulation of B cells expressing the T1 antigen, which is normally restricted to T cells, was demonstrated in the peripheral blood of 16 patients with rheumatoid arthritis. This T1+ B cell population accounted for a mean of 19.6% (upper limit 48%) of the circulating B cells and did not correlate with clinical disease activity, rheumatoid factor, or drug treatment. The highest percentage of T1+ B cells found in the blood of 8 patients with connective tissue diseases, including systemic lupus erythematosus, was 5% of the B cells, and for normal controls, it was was 3% of the B cells. As previously reported, we confirmed that the T1+, Ig+ phenotype was a feature of leukemic cells in B‐type chronic lymphocytic leukemia. The finding of increased numbers of T1+ B cells in patients with rheumatoid arthritis and those with B‐type chronic lymphocytic leukemia raises the possibility that these cells play a role in a spectrum of diseases, including those involving autoimmunity and malignancy.
Total lymphoid irradiation in patients with refractory rheumatoid arthritis
Authors: Nüsslein Hubert G. , Herbst Manfred , Manger Bernhard J. , Gramatzki Martin , Burmester Gerd R. , Fritz Harald , Sauer Rolf , Kalden Joachim R. 
Published: February 2007

AbstractEleven patients with rheumatoid arthritis that had been refractory to conventional drug therapy were treated with total lymphoid irradiation (TLI). Followup continued for 6 months in 9 patients, 12 months in 6 patients, and 24 months in 3 patients. At 6 and 12 months post‐TLI, a significant improvement in clinical disease activity was demonstrated. Side effects noted during TLI included fatigue, nausea, diarrhea, and vomiting. One patient died of cardiorespiratory arrest, 2 patients died of kidney failure secondary to generalized amyloidosis, and 1 patient died of septic shock secondary to a multilocular septic arthritis. One patient experienced 2 episodes of septic arthritis; 2 patients manifested delayed wound healing. Immunologic assessments showed consistent lymphopenia in all patients. T lymphocyte subsets decreased after TLI, and showed a transient increase at 6 months post‐TLI. The suppressed mitogen responsiveness, which was noted 2 months after irradiation, was found to increase almost to the pre‐TLI levels at 12 months. The observed increase in morbidity and mortality after TLI is evidence that discourages the use of this therapeutic technique, at least in its present form.
Ro (SS‐A) antibody and antigen in a patient with congenital complete heart block
Authors: Harley John B. , Kaine Jeffrey L. , Fox Owen F. , Reichlin Morris , Gruber Barry 
Published: February 2007

AbstractCongenital complete heart block is closely associated with the presence of anti‐Ro (SS‐A) autoantibodies. Quantitative solid‐phase assays for Ro (SS‐A) autoantigen and autoantibody have established the presence of Ro (SS‐A) in cardiac tissues and have been used to evaluate an informative pedigree. The propositus we describe here had complete congenital heart block and showed anti–Ro (SS‐A) binding of 13‐fold less than his normal HLA‐identical twin sister. Both had identical titers of antinuclear antibody. These data support the hypothesis that anti–Ro (SS‐A) may be directly involved in the pathogenesis of congenital complete heart block.
Effects of gold sodium thiomalate on functional correlates of human monocyte maturation
Authors: Littman Bruce H. , Hall Robert E. 
Published: February 2007

AbstractThe mechanism of action of gold salts in the treatment of rheumatoid arthritis is unknown. Effects of gold on monocyte‐macrophage function could be due to inhibition of maturation and differentiation. We found that 3 markers of monocyte differentiation, loss of peroxidase activity, spontaneous synthesis of C2, and spontaneous cytotoxicity for chicken erythrocytes, were all inhibited by gold treatment. This was not a general toxic effect since phorbol myristate acetate could still induce gold‐treated monocytes to lyse chicken erythrocytes. Also, phorbol myristate acetate‐stimulated superoxide production, a monocyte function not requiring further differentiation, was not inhibited by incubation with gold. Lymphokine‐stimulated cytotoxicity for nucleated target cells, another function of monocytes, was inhibited only partially for certain target cells and not at all for others. These data suggest that gold has the capacity to selectively inhibit some monocyte functions which are associated with macrophage differentiation.
Persistence of scleroderma‐like phenotype in normal fibroblasts after prolonged exposure to soluble mediators from mononuclear cells
Authors: Worrall Jennifer G. , Whiteside Theresa L. , Prince Robert K. , Buckingham Robert B. , Stachura Irene , Rodnan Gerald P. 
Published: February 2007

AbstractSupernatants of mononuclear cells (MNC‐SN) were shown to increase synthesis of glycosaminoglycan (GAG) by cultured normal dermal fibroblasts. Fibro‐blasts from the skin of patients with progressive systemic sclerosis (PSS, scleroderma) were hyporesponsive. We exposed fibroblasts outgrowing from explants of normal adult skin to MNC‐SN for up to 30 generations in culture. MNC‐SN were obtained by incubating normal MNC with concanavalin A. Four experimental, 4 normal control, and 3 PSS control lines were passaged by trypsinizing and splitting the cultures 1:2 every 7 days. At the third and fifth passages, portions of the experimental fibroblasts were removed from MNC‐SN, then passaged in medium alone. Cell counts, assays for GAG, and electron microscopy were performed and increases in GAG after brief reexposure to MNC‐SN were determined at the third, fifth, and eighth passages. In normal dermal fibroblasts, baseline GAG production, measured by 3H‐glucosamine uptake, was low and increased as much as 15 times after reexposure to MNC‐SN. In contrast, production was high in both experimental and PSS lines, and increases after reexposure to MNC‐SN were consistently small. This PSS‐like behavior persisted in experimental fibroblasts removed from MNC‐SN at the third and fifth passages. Growth of experimental and scleroderma fibroblasts was slower than that of control fibroblasts. Ultra‐structurally, both scleroderma and experimental dermal fibroblasts differed from normal fibroblasts by their oval cellular shape, indentations in nuclear membrane, numerous organelles and bundles of microfilaments, prominent Golgi, and intranuclear inclusions. These experiments indicate that normal adult dermal fibroblasts subjected to MNC‐SN in vitro acquire a scleroderma‐like phenotype that persists for many generations.
Hereditary joint disorder in progressive ankylosis (ank/ank) mice. II. Effect of high‐dose hydrocortisone treatment on inflammation and intraarticular calcium hydroxyapatite deposits
Authors: Hakim Frances T. , Brown Kenneth S. , Oppenheim Joost J. 
Published: February 2007

AbstractMice homozygous for the progressive ankylosis trait develop an inflammatory joint disorder associated with the intraarticular deposition of calcium hydroxyapatite. When affected (ank/ank) mice were treated with high doses of hydrocortisone, synovitis receded, development of cartilaginous and bony osteophytes halted, and calcium hydroxyapatite accumulated in and distended the synovial spaces. No changes, however, occurred in the joint morphology of hydrocortisonetreated normal (ank/+) mice. Since inhibition of inflammation by hydrocortisone treatment did not block apatite accumulation, intraarticular deposition of hydroxyapatite occurs independent of inflammation in progressive ankylosis.
Histamine stimulates prostaglandin E production by rheumatoid synovial cells and human articular chondrocytes in culture
Authors: Taylor David J. , Yoffe Joan R. , Brown Diane M. , Woolley David E. 
Published: February 2007

AbstractHistamine stimulates prostaglandin E (PGE) production by cultures of adherent rheumatoid synovial cells and human articular chondrocytes. When subcultured synovial fibroblasts or human articular chondrocytes were “primed” by preincubation with conditioned media from primary adherent rheumatoid synovial cell cultures (synovial factor), each produced even higher PGE levels upon histamine exposure. This histamine stimulation was prevented by histamine H1, but not H2, antagonists and was more marked if serum was absent from the culture media. Thus, histamine‐induced PGE production by these cells is mediated via H1 receptor activation and subsequent arachidonic acid liberation.
Phagocytosis and intracellular killing of Staphylococcus aureus by polymorphonuclear cells from synovial fluid of patients with rheumatoid arthritis
Authors: Breedveld Ferdinand C. , Lafeber Geertruida J. M. , van den Barselaar Maria T. , van Dissel Jaap T. , Leijh Peter C. J. 
Published: February 2007

AbstractThe phagocytosis and intracellular killing by synovial fluid (SF) polymorphonuclear cells (PMN) of 10 patients with rheumatoid arthritis was studied. PMN phagocytosis was assessed by morphologic and microbiologic methods and intracellular killing was measured independently of continuous phagocytosis of Staphylococcus aureus. Phagocytosis of S aureus by SF PMN or peripheral blood (PB) PMN was as effective in the presence of synovial fluid as in the presence of serum. On average, SF PMN ingested S aureus opsonized with synovial fluid and serum more efficiently than patient or donor PB PMN did. Enhanced ingestion of S aureus was associated with increased expression of C3 receptors on the membrane of SF PMN. In the presence of heat‐inactivated synovial fluid, the capacity of SF PMN to ingest S aureus was greater than that of patient or donor PB PMN. Under these conditions, phagocytic activity was correlated with Fc receptor expression. SF PMN was found to be as active in killing S aureus as PB PMN from healthy donors.