bluuebunny/crossref_metadata_2025_split huggingface dataset:
Antibody to cytomegalovirus in patients with sjögren's syndrome. As determined by an enzyme‐linked immunosorbent assay
Authors: Shillitoe Edward J. , Daniels Troy E. , Whitcher John P. , Strand C. Vibeke , Talal Norman , Greenspan John S. 
Published: February 2007

AbstractBy use of an enzyme‐lined immunosorbent assay (ELISA), patients with Sjögren's syndrome were found to have levels of serum IgG antibody to cytomegalovirus twice those of matched control subjects, and IgM antibody levels which were three times as high. It may be relevant that features of cytomegalovirus infection are similar to those of Sjögren's syndrome.
Gold inhibition of the production of the second complement component by lymphokine‐stimulated human monocytes
Authors: Littman Bruce H. , Schwartz Pamela 
Published: February 2007

AbstractThe ability of gold sodium thiomalate to inhibit production of the second complement component (C2) by monocytes stimulated by a lymphokine (monocyte complement stimulator) is demonstrated. This gold salt inhibits C2 production irreversibly if monocytes are incubated with it before or during lymphokine stimulation. Thiomalic acid is not inhibitory. Monocytes already stimulated by lymphokine are resistant to inhibition of C2 production by gold sodium thiomalate. Gold salts do not reduce monocyte viability, phagocytic ability (latex beads), accessory cell function (as measured by the ability to present antigen to autologous lymphocytes), or capacity to act as stimulating cells in mixed leukocyte culture. Gold sodium thiomalate's inhibition of monocyte responsiveness to lymphokine may be significant in explaining the therapeutic benefit of gold salts in rheumatoid arthritis.
Stimulation of dna synthesis by ascorbate in cultures of articular chondrocytes
Authors: Krystal Geoffrey , Morris Gregory M. , Sokoloff Leon 
Published: February 2007

AbstractThe addition of 0.2 mM Na L‐ascorbate increased the incorporation of 3H‐thymidine by rabbit articular chondrocytes in cell and organ culture. The stimulatory response of explants to ascorbate was potentiated by pretreatment of the cartilage with 0.2% clostridial collagenase (type 1) or trypsin for 15–30 minutes. In explants there was a latent period of 3 to 4 days before increased labeling of the nuclei could be detected. The effect was transient and declined after 8 days of culture. It was more evident in organ cultures of immature (3‐month‐old) than 2‐ to 3‐year‐old rabbits. Age differences were not detected in cell cultures. Explants of adult human articular cartilage were stimulated by ascorbate when the medium was supplemented with 10% fresh human serum but not by fetal bovine serum. The findings indicated that synthesis of DNA by articular chondrocytes in situ is regulated by responsiveness of the cells proper to compounds such as vitamin C, by properties of the extracellular matrix, and by factors in the serum. Ascorbate was cytotoxic at concentrations >0.2 mM in the presence of certain batches of serum and when added to monolayers before the cells attached to the surface of the flask.
Quantitation of rat liver xanthine oxidase by radioimmunoassay. A mechanism for sex‐specific differences
Authors: Decker Douglas E. , Levinson Dennis J. 
Published: February 2007

AbstractTo further delineate the mechanism responsible for the differences in xanthine oxidase activity in male and female Sprague—Dawley rats, a sensitive and specific radioimmunoassay (RIA) was developed for the measurement of hepatic xanthine oxidase. The RIA could detect as little as 5 ng of liver enzyme. Specificity of the RIA was confirmed by 1) Ouchterlony double immuno‐diffusion in which a single precipitin band exhibited xanthine oxidase activity, when crude liver homogenate and an enzyme‐specific stain were used; 2) parallelism between purified 125I‐labeled xanthine oxidase and serial dilutions of crude liver homogenate; 3) a linear correlation between xanthine oxidase activity and the level of enzyme protein; and 4) a single protein band coincident with purified xanthine oxidase, when an immunoprecipitate prepared from antisera and crude liver homogenate was analyzed on sodium dodecyl sulfate (SDS) polyacrylamide gels. Whether xanthine oxidase activity was assayed in the absence of nicotinamide adenine dinucleotide (NAD+) (oxidase form) or in the presence of NAD+ (dehydrogenase), male values were consistently higher, and both forms of the enzyme correlated significantly with each other. When purified to homogeneity, neither form of the enzyme was appreciably affected by 17β‐estradiol or testosterone propionate. When the RIA was employed, levels of hepatic xanthine oxidase were significantly greater in male than in female rats. We concluded from these data that increased xanthine oxidase activity in the male corresponds to a greater quantitative complement of xanthine oxidase protein. Furthermore, lower xanthine oxidase activity in the female cannot be explained by immunologically cross‐reactive material without enzyme activity nor by a direct sex—steroid enzyme interaction.
Antibodies to and elevations of beta 2 microglobulin in the serum of ankylosing spondylitis patients
Authors: Curry Russell , Thoen Jorn , Shelborne Charles , Gaudernack Gustav , Messner Ronald 
Published: February 2007

AbstractAntibodies to beta 2 microglobulin are found in systemic lupus erythematosus patients and are important in the lymphocytotoxic reactions of sera from such patients. In this study, beta 2 microglobulin antibodies were measured with the use of an enzyme‐linked immunosorbent assay with purified beta 2 microglobulin antigen and peroxidase‐labeled anti‐human IgG or IgM. IgG antibodies to beta 2 microglobulin were found in 68% of 22 patients with ankylosing spondylitis. This incidence was higher than the 5% in 80 controls (P < 0.01) and similar to the 71% incidence found in 35 patients with systemic lupus erythematosus. Eleven (27%) of 41 patients with rheumatoid arthritis had elevated levels of antibodies to beta 2 microglobulin (P < 0.01). The mean antibody levels expressed in enzyme units were 0.125 for patients with ankylosing spondylitisis, 0.157 for those with systemic lupus erythematosus, 0.101 for those with rheumatoid arthritis, and 0.067 for controls. IgM anti—beta 2 microglobulin was not significantly different from controls. A competitive binding assay with enzyme‐labeled beta 2 microglobulin was used to determine serum beta 2 microglobulin. These values were also found to be elevated in 48% of patients in all 3 disease categories (P < 0.01). Beta 2 microglobulin antibodies and serum beta 2 microglobulin did not correlate with each other, renal diseases or antinuclear antibodies in patients with systemic lupus erythematosus, with rheumatoid factor or severity of articular disease in patients with rheumatoid arthritis, or with peripheral arthritis or iritis in those with ankylosing spondylitis. Although antibodies to beta 2 microglobulin might reflect a general disturbance of immune regulation in patients with systemic lupus erythematosus, their presence in those with ankylosing spondylitis, a disease closely associated with a specific HLA allotype and not usually associated with formation of autoantibody, suggests that they might play a role in the pathogenesis of the latter disease.
Stimulation of the plasminogen activator activity of human synovial fibroblasts by retinoids
Authors: Hamilton John A. 
Published: February 2007

AbstractNonrheumatoid human synovial fibroblasts in culture, while having low basal plasminogen activator levels, were stimulated to produce much more of this protease activity by low concentrations of a series of retinoids. The most potent retinoid tested, all‐trans retinoic acid, was active over the range 10‐11–10–6M. The increased plasminogen activator activity in the presence of 10–6M retinoic acid was first observed within 40 minutes under appropriate experimental conditions, required RNA and protein synthesis, and was reversible after short incubation periods. This stimulation was suppressed by low concentrations of antiinflammatory glucocorticoids such as dexamethasone.
Improving patient cooperation with arthritis treatment regimens
Authors: Jette Alan M. 
Published: February 2007

AbstractThis review of the literature on patient cooperation with arthritis treatment recommendations is categorized into 2 sections—involuntary and voluntary lack of cooperation. Extrapolating primarily from investigations of patients with other chronic diseases, 5 stategies for reducing involuntary patient noncooperation and 4 recommendations for improving voluntary patient cooperation are discussed. Although much remains to be learned about factors that influence patient cooperation with arthritis treatment recommendations, the application of existing knowledge can improve current levels. Determined efforts by health professionals are necessary if the excessive waste resulting from patient noncooperation is to be reduced. Shortcomings of past research and fruitful avenues for future empirical work in this important area are discussed.
Antibodies to collagen in scleroderma
Authors: Mackel Anne M. , Delustro Frank , Harper Frank E. , Roy E. Carwilele 
Published: February 2007

AbstractUsing the enzyme‐linked immunosorbent assay (ELISA), we detected antibodies to interstitial (type I) and basement membrane (type IV) collagens in the sera of patients with scleroderma (systemic sclerosis). Antibodies against type IV collagen were found in significant levels in these patients and correlated with the presence of abnormal pulmonary diffusion capacity. Levels of antibodies to type I collagens also correlated significantly with pulmonary diffusion capacity. Absorption of sera with type I or type IV collagens before analysis in the ELISA eliminated reactivity in an antigen‐specific pattern, indicating that these antibodies reacted with determinants specific for either type I or type IV collagens. The removal of immune complexes by ultracentrifugation had no effect on serum antibody levels. Autoantibodies to basement membrane and interstitial collagens may participate in the pathogenesis of scleroderma.
Aspirin survival in human blood modulated by the concentration of erythrocytes
Authors: Costello Patrick B. , Green Floyd A. 
Published: February 2007

AbstractIn vitro aspirin hydrolysis rates were measured in fresh human whole blood and in its separate components. The half‐life of aspirin in whole blood was relatively rapid (mean 22.2 ± 3.9 minutes) and exhibited a significant negative correlation with hematocrit (r = −0.96). Hydrolysis of aspirin in buffer that contained only washed red blood cells (40%) was significantly more rapid (mean half‐life 17.5 ± 2.0 minutes) than that in whole blood. When aspirin was incubated in solutions of washed red blood cells that contained human serum albumin in various concentrations, the aspirin half‐life was found to vary directly with the concentration of albumin used; at normal levels of albumin, the hydrolysis rate of aspirin approximated that measured in whole blood. The presence of diisopropyl fluorophosphate in low concentrations (0.02–0.05 mM) markedly inhibited the rate of aspirin hydrolysis in washed red blood cells and whole blood. We conclude that enzyme(s) linked to the erythrocyte, probably membrane‐bound acetylcholinesterase, control the survival of aspirin in blood.
Gonococcal arthritis–dermatitis syndrome. study of serum and synovial fluid immune complex levels
Authors: Manicourt Daniel H. , Orloff Serge 
Published: February 2007

AbstractImmune complexes from serum and synovial fluid were detected by the C1q binding assay in 12 patients with disseminated gonococcal infection. Since immune complexes were regularly higher in synovial fluids than in paired sera and were not detected by the monoclonal rheumatoid factor radioimmunoassay, we suggest that IgM may be present in these complexes and that this represents a primary immune response. In contrast, only 2 of 10 patients with local gonococcal infection were slightly positive both with the C1q assay and the monoclonal rheumatoid factor assay. In patients with disseminated gonococcal infection, immune complexes closely paralleled the disease activity and negatively correlated with complement levels. Synovial fluid immune complexes seem to occur in the early and aseptic phase of polyarthritis and to aid the entrance of circulating gonococcal organisms. From the results of our study, it seems that immunologic processes initiate and/or sustain inflammation in disseminated gonococcal infections that appear, at least in part, as a form of reactive arthritis.
GAMMA‐carboxyglutamate excretion and calcinosis in juvenile dermatomyositis
Authors: Lian Jane B. , Pachman Lauren M. , Gundberg Caren M. , Partridge RAYMOND E. H. , Maryjowski Mona C. 
Published: February 2007

AbstractProteins containing gamma‐carboxyglutamic acid (Gla) are present in subcutaneous calcifications of adults with dermatomyositis or scleroderma. Sixteen children with juvenile dermatomyositis, including 7 with subcutaneous calcifications, were studied to determine if abnormal synthesis or turnover of Gla‐containing proteins occurred. All study children had increased excretion of the amino acid that was greater than that of age‐and sex‐matched controls. Patients who had juvenile dermatomyositis with calcifications had a 3‐fold increase in Gla excretion, and those without calcinosis had a 2‐fold increase. Five other children with various connective tissue disorders and subcutaneous calcification had 2‐fold increased Gla excretion. Decreased excretion of this amino acid was associated with salicylate therapy (80 mg/kg/24 hours). The data suggest an abnormal turnover of Gla‐containing proteins in juvenile dermatomyositis. Metabolism of these proteins may be involved in the pathophysiology of soft‐tissue calcification in children.
Susceptibility to adjuvant arthritis in da and F344 RATS. A dominant trait controlled by an autosomal gene locus linked to the major histocompatibility complex
Authors: Battisto Jack R. , Smith R. N. , Beckman Karla , Sternlicht Mona , Welles Wanda L. 
Published: February 2007

AbstractThe heritability of adjuvant‐induced arthritis in rats of the DA and Fisher 344 strains was examined. Development of arthritic lesions in response to a single injection of supplemented Freund's complete adjuvant has been found to be controlled by an autosomal, dominant gene locus, Ar. The capacity to respond was present in DA rats and absent in our Fisher rats. Ar has been found to be linked to the major histocompatibility complex genes with which it exhibits a high rate of recombination.
Skin response to intradermal dna and rna in systemic lupus erythematosus
Authors: Konttinen Yrjöt. , Tolvanen Erkki , Johansson Eija , Reitamo Sakari , Wegelius Otto 
Published: February 2007

AbstractThe local response of 18 patients with active systemic lupus erythematosus to 0.1 ml of intradermally injected 0.1% polymerized calf thymus DNA and synthetic double‐stranded polyinosinic‐polycytidylic acid was studied. In 14 patients positive for DNA, 61 ± 8% of the inflammatory cells in the subepidermis at 24 hours were acid alpha‐naphthyl acetate esterase–positive T lymphocytes. A leukocytoclastic vasculitis was observed in the deeper dermis. Rheumatoid arthritis patients and acne patients had negative responses. These results indicated an abnormal cellular and humoral in vivo response by patients with systemic lupus to DNA. It is suggested that the epidermal Langerhans cells were responsible for the topographic dichotomy of the local DNA response. Test results were positive for polyinosinic‐polycytidylic acid in 12 patients, for DNA in 14 patients, and for both in 9 patients. In the 9 patients with positive results for both tests, comparison of responses to each test indicated that the reaction intensity was dependent on the patient and not on the type of polynucleotide acid that was injected.
Prolonged lifespans in female nzb/nzw mice treated with the experimental immunoregulatory drug frentizole
Authors: Walker Sara Ellen , Solsky Marilyn , Schnitzer Bertram 
Published: February 2007

AbstractAutoimmune female New Zealand Black/New Zealand White mice were treated with frentizole, an experimental immunosuppressive drug. Three groups of “young,” 8‐week‐old mice received high‐dose frentizole (80–84 mg/kg/day), low‐dose frentizole (8 mg/kg/day), or no drug (controls); these mice were followed until spontaneous death. Three groups of “old,” 24‐week‐old mice with established lupus‐like disease were treated with high or low doses of frentizole. Old control mice received no drug. After 12 weeks of therapy, surviving old mice were killed. Beneficial therapeutic response was achieved when high‐dose treatment was started at an early age; antiDNA values were suppressed, and longevity was prolonged significantly. Frentizole did not arrest the progression of renal disease in old mice. Glomerulonephritis and vasculitis were the most common causes of death in young and old animals. Twenty‐nine percent of young, high‐dose‐treated mice died with neoplasms. Large glomerular deposits of IgG, IgM, and C3 were present in renal tissue from treated and control mice. Peripheral lymphocyte counts and mitogenic responses of spleen cells were not changed by treatment. The efficacy of frentizole in a murine model of lupus supports its usefulness as an immunoregulatory drug.
Igm and igg anti‐f(ab )2 antibodies in rheumatoid arthritis and systemic lupus erythematosus
Authors: Heimer Ralph , Wolfe Lawrence D. , Abruzzo John L. 
Published: February 2007

AbstractRadioimmunoassays for anti‐F(ab )2 antibodies, which feature the use of goat anti‐human Fc antibody for correcting potentiation of IgM anti‐F(ab )2 antibody titers by endogenous IgM anti‐Fc antibodies (rheumatoid factors), are described. Individuals with classic rheumatoid arthritis had significantly more IgM anti‐F(ab )2 antibody (P < 0.001) and IgG anti‐F(ab )2 antibody (P = 0.05) than did individuals with systemic lupus erythematosus or normal volunteers. There is some similarity in patterns of isotype distribution of anti‐F(ab )2 antibodies and rheumatoid factors.
Cytotoxic activity of sera from scleroderma and other connective tissue diseases. lack of cellular and disease specificity
Authors: Shanahan William R. , Korn Joseph H. 
Published: February 2007

AbstractIt has been suggested that serum‐mediated endothelial cell injury in scleroderma might contribute to disease pathogenesis. We compared the effect of serum from 28 scleroderma patients on human umbilical cord vein endothelial cell and human foreskin fibroblast proliferation with sera from 28 healthy controls, 13 patients with isolated Raynaud's disease, 22 patients with systemic lupus erythematosus, 19 patients with rheumatoid arthritis, and 15 patients with other connective tissue diseases. Five sera (2 scleroderma, 1 morphea, 1 rheumatoid arthritis, 1 systemic lupus erythematosus) markedly suppressed 3H‐thymidine incorporation into both endothelial cells and fibroblasts (to > 3 SD below the mean of the control group). These sera were also cytotoxic to endothelial cells and fibroblasts in a 51Cr release assay. Three additional sera (1 Raynaud's, 2 controls) suppressed endothelial cell proliferation moderately (>2 SD but <3 SD from control mean) but did not affect fibroblasts. Mean 3H‐thymidine incorporation by endothelial cells and fibroblasts in scleroderma serum was comparable to that of the other disease and control groups. In contrast to previous studies, we found serum‐mediated endothelial cell cytotoxicity occurred infrequently in scleroderma, occurred also in other connective tissue diseases, and was without target cell specificity. Furthermore, scleroderma serum did not appear to stimulate fibroblast proliferation.
Evidence for pseudomonas antigen in immune complexes in pseudomonas osteomyelitis
Authors: Rahn Daniel W. , Steere Allen C. , Grodzicki Robert L. , Levine Joseph H. , Hardin John A. 
Published: February 2007

AbstractIn infections associated with immune complex disease, microbial antigens have rarely been found in the complexes. Using an enzyme‐linked immunoassay, we studied the immune complexes of a patient who had hematogenous Pseudomonas aeruginosa osteomyelitis associated with palpable purpura, arthritis, and microscopic hematuria. After separation of the complexes into high and low molecular weight fractions, a 6hyphen;fold selective concentration of P aeruginosa antibody was found in the low molecular weight fraction compared with the concentration in the serum. Following disruption of immunoglobulin, the high molecular weight fraction competed with solid‐phase P aeruginosa antigen for P aeruginosa antibody from another source. After successful treatment of the infection, the patient's symptoms resolved, and the complexes disappeared. These findings strongly suggest that immune complexes in this patient contained P aeruginosa antigen and antibody that may have been pathogenetic in his disease.
Immunogenetic factors in inflammatory eye disease. influence of hla–b27 and alpha1‐antitrypsin phenotypes on disease expression
Authors: Wakefield Denis , Breit Samuel N. , Clark Peggy , Penny Ronald 
Published: February 2007

AbstractThe relationship between the nature and severity of inflammatory eye disease was analyzed with respect to HLA antigens and alpha1‐antitrypsin phenotypes. Using standard ophthalmologic criteria, we divided patients with anterior uveitis into acute, chronic (>3‐month duration), bilateral, or recurrent disease. There was a significantly increased incidence of alpha1‐antitrypsin–deficient phenotypes in anterior uveitis, especially in those patients with severe (chronic, bilateral, or recurrent) disease. HLA–B27 acts as an independent predisposing factor: it was present in 22% of patients with their first attack of acute uveitis compared with 51% of patients with recurrent disease. Together, these genetic factors are present in 63% of patients with severe anterior uveitis and represent the most significant predisposing and prognostic factors so far detected.
Quantitation of cells secreting rheumatoid factor of igg, iga, and igm class after elution from rheumatoid synovial tissue
Authors: Egeland Torstein , Lea Tor , Saari George , Mellbye Ove J. , Natvig Jacob B. 
Published: February 2007

AbstractIn an indirect hemolytic plaque assay that used sheep erythrocytes coated with normal rabbit IgG or reduced/alkylated IgG anti–sheep erythrocytes, mononuclear cells eluted from rheumatoid synovial tissue of 7 of 11 patients with seropositive rheumatoid arthritis contained cells that secreted rheumatoid factor of IgG, IgA, and IgM classes. The number of rheumatoid factor–secreting cells varied from <1% to 53% of the total number of eluted immunoglobulin‐secreting cells. In contrast, immunoglobulin‐secreting cells and rheumatoid factor–secreting cells were scanty in blood compared with synovial tissue mononuclear cells.