bluuebunny/crossref_metadata_2025_split huggingface dataset:
Aspiration of the asymptomatic metatarsophalangeal joint in gout patients and hyperuricemic controls
Authors: Rouault Tracey , Caldwell David S. , Holmes Edward W. 
Published: February 2007

AbstractAsymptomatic metatarsophalangeal joints were aspirated in a group of patients with gout, in 2 control groups with hyperuricemia, and in 1 normouricemic control group. Extracellular urate crystals were present in 70% of gout patients, in 1 of 19 patients with asymptomatic hyperuricemia, and in 2 of 9 patients with renal failure and hyperuricemia but no history of joint disease. Crystals were not found in the 10 normouricemic patients who had other types of arthritis. The presence of crystals in the subjects with gout was not correlated with a history of podagra, duration of gout, presence of tophi, or degree of control of hyperuricemia. Though crystals were found on rare occasions in joint fluid of asymptomatic hyperuricemic subjects, the presence of these crystals in asymptomatic joints was more common in subjects with gout.
Variable response to oral angiotensin‐converting‐enzyme blockade in hypertensive scleroderma patients
Authors: Whitman Hendricks H. , Case David B. , Laragh John H. , Christian Charles L. , Botstein Gary , Maricq Hildegard , Leroy E. Carwile 
Published: February 2007

AbstractTwelve scleroderma patients with hypertension, seven of whom had malignant hypertension and renal failure or scleroderma renal crisis, were treated with captopril. The first dose lowered mean pressure in all patients by 21.3 mmHg; in 6 patients it relieved encephalopathy. Blood pressure was controlled in all patients. Two of 7 patients with scleroderma renal crisis had improvement in renal function; the 5 patients who did not have malignant hypertension improved or stabilized. Despite good pressure control, however, renal failure developed in 5 patients with scleroderma renal crisis. The data indicated that captopril is effective antihypertensive therapy in scleroderma and, when given early, may prevent renal failure and death.
Type II collagen—induced auricular chondritis
Authors: Mccune W. Joseph , Schiller Alan L. , Dynesius‐Trentham Roselynn A. , Trentham David E. 
Published: February 2007

AbstractSensitization to type II collagen induced inflammatory destruction of elastic ear cartilage, as well as arthritis, in Sprague—Dawley rats. This auricular lesion morphologically resembled relapsing polychondritis in humans. Moreover, in the experimental model, as has been reported in human disease, extraarticular chondritis occurred in the context of immunologic sensitivity to native type II collagen. These similarities suggest that type II collagen‐induced auricular chondritis may provide insights about the pathogenesis of relapsing polychondritis.
Abnormalities in the content of nucleic acids of peripheral blood mononuclear cells from patients with systemic lupus erythematosus. Relationship to dna antibodies
Authors: Alarcón‐Segovia Donato , Llorente Luis , Fishbein Eugenia , Díaz‐Jouanen Efraín 
Published: February 2007

AbstractWe have completed 59 cytofluorographic studies of DNA/RNA content in acridine orange‐stained peripheral blood mononuclear cells from 44 patients with systemic lupus erythematosus, most of whom received no medications. Most such cells were in resting phases of the cell cycle, particularly those from patients with inactive disease. Nine patients with systemic lupus erythematosus had increased percentages of these cells in the synthesis and postsynthesis phases of the cell cycle; the B lymphocytes had the greatest proportions of activated cells. In 11 patients, we found that cells, particularly T lymphocytes, had increased RNA content without a proportional increase in DNA. This DNA block occurred primarily in patients with serum antibodies to DNA and it could be reproduced in normal mitogen‐stimulated mononuclear cells incubated in heat‐inactivated sera from patients with systemic lupus erythematosus whose own cells showed abnormalities of DNA/RNA content or in purified native DNA antibody. The DNA blocking potential of the DNA antibody was dependent on its Fc portion and on the presence of Fc receptors on T cells. Thus, saturation of Fc receptors by pretreatment with aggregated IgG or incubation with the whole antibody in the cold prevented the DNA block, indicating that it was an active process.
Suppression of the normal autologous mixed leukocyte reaction by sera from patients with systemic lupus erythematosus
Authors: Hahn Bevra H. , Pletscher L. Susan , Muniain Miguel , Macdermott Richard P. 
Published: February 2007

AbstractSera from 15 patients with active systemic lupus erythematosus and 7 patients with inactive lupus were added to normal autologous mixed leukocyte reaction (MLR) cultures. Twelve of the 22 sera reduced autologous T cell proliferative responsiveness to B plus null (B+N) cells or macrophages by 50% or more. This inhibition correlated with defective autologous MLR in fresh mononuclear cells from those patients. When normal responding and stimulating cell populations were preincubated with suppressive lupus sera, then added to autologous MLR cultures that contained normal serum, proliferative responses were also reduced; inhibitors are directed against participating mononuclear cell subpopulations. The suppressive serum factors were directed variously against monocyte/macrophage (MΦ), B+N, or T cell populations; MΦ/T interactions were suppressed most frequently. The inhibitors were not removed by high‐speed centrifugation or by depletion of antibodies to DNA, and they did not correlate with the presence of lymphocytotoxic antibodies. The presence of serum inhibitors of normal MΦ/T and B+N/T autologous MLR may be an immunologic abnormality important in the initiation, perpetuation, or exacerbation of systemic lupus erythematosus.
Autologous and allogeneic mixed lymphocyte reactions in progressive systemic sclerosis
Authors: Morse Jane H. , Bodi Betsy S. 
Published: February 2007

AbstractThe autologous and allogeneic mixed lymphocyte reactions (MLR), observed when peripheral blood mononuclear cells from 20 patients with progressive systemic sclerosis were used, were compared with those of age‐, sex‐, and race‐matched normal controls. Such cells were separated by gradient centrifugation of sheep red blood cell (E) rosettes into stimulator (E‐ or non‐T cell) and responder (E+ or T cell) populations. The autologous MLR of both the progressive systemic sclerosis and normal peripheral blood mononuclear cells varied widely but there was no statistical difference between the means of each group. In the allogeneic MLR, proliferation between progressive systemic sclerosis non‐T cells and normal T cells was significantly less than that of normal non‐T cells and progressive systemic sclerosis T cells (P = 0.001). A decreased autologous MLR, while noted with other autoimmune diseases, was lacking in progressive systemic sclerosis. This suggests a different defect. The differences in the allogeneic MLR also suggest that either progressive systemic sclerosis non‐T cells were poor stimulators or T cells associated with this disease were better responders when compared with similarly prepared cell populations from normal individuals. The MLR differences could have also resulted from compositional subset alterations or the sharing of a common antigen. HLA—DR5 was found in 9 of the 17 white patients with progressive systemic sclerosis. Although these individuals were evenly distributed as low, medium, and high responders, this finding showed that some progressive systemic sclerosis non‐T cells shared a common antigen.
Serum interferon levels in patients with systemic lupus erythematosus
Authors: Ytterberg Steven R. , Schnitzer Thomas J. 
Published: February 2007

AbstractLevels of interferon (IFN) were measured in 81 serum samples from 23 patients with systemic lupus erythematosus (SLE) by a plaque‐reduction method and correlated retrospectively with clinical records of disease activity, anti‐DNA binding, and serum complement measurements. IFN titers were found to correlate with both clinical disease activity and anti‐DNA binding, but no relation was found to serum complement. Most (76.6%, 31 of 41) serum samples obtained during periods of active disease contained measureable amounts of IFN, but only 9.1% (2 of 22) of results of tests on samples obtained during periods of disease quiescence were positive (P < 0.005). Of samples with clearly elevated anti‐DNA binding (> 40%), 69.7% (23 of 33) had positive results for IFN, but 57.1% (8 of 14) had negative results when the anti‐DNA binding was normal (< 20%) (P < 0.005). Measurement of serum IFN titers in patients with SLE, therefore, provides another serologic marker of disease activity. Contrary to the findings of previous studies, the IFN found in the present study was characterized as IFN‐α, or Type I IFN, on the basis of acid stability and neutralization by antibody to IFN‐α. Of interest are the questions raised about the origin of IFN in the sera of patients with SLE and what role IFN might have in the pathogenesis of the autoimmune disease in view of the many documented immunomodulating effects of IFN.
Immune functions of human synovial cells. phenotypic and t cell regulatory properties of macrophage‐like cells that express hla–dr
Authors: Klareskog Lars , Forsum Urban , Kabelitz Dieter , Plöen Leif , Sundström Christer , Nilsson Kenneth , Wigren Anders , Wigzell Hans 
Published: February 2007

AbstractNormal and rheumatoid synovial cells have been analyzed in frozen sections and in suspension. HLA–DR‐expressing, macrophage‐like cells are demonstrated in normal synovial intima and in rheumatoid tissue. Suspended normal synoviocytes equaled peripheral blood non–T lymphocytes as stimulators of mixed lymphocyte reactions, whereas adherent rheumatoid synovial cells were extremely efficient as such stimulators and in presenting soluble antigens to autologous T lymphocytes. This HLA–DR‐dependent T lymphocyte regulation might provide a cellular basis for the HLA–D haplotype–arthritis associations.
Seronegative rheumatoid arthritis.
Authors: AlarcóN Graciela S. , Koopman William J. , Acton Ronald T. , Barger Bruce O. 
Published: February 2007

AbstractMeasurement of serum rheumatoid factor (RF) by conventional methods in patients with rheumatoid arthritis (RA) has repeatedly identified a subpopulation of patients without detectable RF. Previous investigators have consistently confirmed the association of HLA–DR4 with seropositive RA, but studies of seronegative RA have been limited and contradictory. We studied 140 randomly selected patients from Alabama, all of whom had either classic or definite RA, and we were able to obtain complete HLA typing for 110 of these individuals. Eighty were consistently seropositive (on at least 2 separate occasions) and 30 were consistently seronegative (on at least 3 separate determinations). There was no statistically significant difference between the seronegative RA patients and 123 control subjects in the distribution of DR antigens. In seropositive RA, there was a significant increase in DR4 (P<0.001; relative risk = 8.02; attributable risk = 49.2%) and a significant decrease in DR3 (P<0.001; relative risk = 0.14) and DR7 (0.01>P>0.001; relative risk = 0.33). The clinical data also distinguished between seropositive RA and seronegative RA; subcutaneous nodules (37.5%) and vasculitis (6.3%) were present only in seropositive RA. DR4 positivity did not correlate with any of the clinical variables measured in the seropositive RA group. In contrast, DR4 in the seronegative RA group was associated with more destructive disease. The data suggest that seronegative RA represents a disease entity clinically and immunogenetically distinct from seropositive RA. Moreover, our results indicate that DR4 may be a previously undisclosed marker for disease severity in seronegative RA.
The role of cell surface proteins in platelet stimulation by monosodium urate crystals
Authors: Jaques Bryon C. , Ginsberg Mark H. 
Published: February 2007

AbstractTo test whether urate crystal‐membrane protein interactions mediate platelet stimulation, platelet membrane proteins were radiolabeled by lactoperoxidase, extracted with 1% Triton X–100, and incubated with urate crystals. The crystal‐associated and supernate fractions were isolated and analyzed by sodium dodecyl sulfate–polyacrylamide gel electrophoresis (SDS–PAGE) and by 2‐dimensional isoelectric focusing followed by SDS‐PAGE. Four of the lactoperoxidaseradiolabeled polypeptides that associated with urate crystals had reduced molecular weights and pIs of Mr = 105,000, pI 4.9; Mr = 123,000, pI = 4.9; Mr = 123,000, pI = 5.3; and Mr = 132,000, pI = 4.8–6.3, respectively. These proteins were characterized with regard to their labeling intensities, apparent isoelectric points, apparent molecular weights (reduced and nonreduced), lectin‐binding properties, carbohydrate‐ and protein‐staining characteristics, and presence or absence in Glanzmann's thrombasthenia. They have been identified as derived from glycoproteins Ib, IIb, and III (Phillips‐Agin nomenclature) and an unidentified membrane protein. To test whether removal of these proteins would result in a diminution of platelet response to urate, intact platelets were digested with chymotrypsin, resulting in cleavage of more than 80% of these proteins and a 5‐fold reduction in secretory responsiveness to urate crystals. Response to a second platelet stimulus, collagen, was unaffected, indicating an intact secretory mechanism. In addition, when platelets were preincubated with F(ab′)2 fragments of an antibody directed against these proteins, platelet secretory response to urate was inhibited by 50%, whereas the responses to collagen and thrombin were unaffected. Thus, membrane proteins appear to mediate platelet stimulation by urate crystals.
Immunosuppression by fractionated total lymphoid irradiation in collagen arthritis
Authors: McCune W. Joseph , Buckley Judith A. , Belli James A. , Trentham David E. 
Published: February 2007

AbstractTreatments with fractionated total lymphoid irradiation (TLI) and cyclophosphamide were evaluated for rats injected with type II collagen. Preadministration of TLI and repeated injections of cyclophosphamide suppressed the severity of arthritis and lowered antibody titers to collagen significantly. TLI initiated at the onset of collagen arthritis decreased humoral and cellular responses to collagen but did not affect the severity of arthritis. These data demonstrate that both TLI and cyclophosphamide are immunosuppressive in an experimentally inducible autoimmune disease.
Clinical responses during gold therapy for rheumatoid arthritis. changes in synovitis, radiologically detectable erosive lesions, serum proteins, and serologic abnormalities
Authors: Sharp John T. , Lidsky Martin D. , Duffy Joseph 
Published: February 2007

AbstractGold therapy given to 73 patients with rheumatoid arthritis was associated with remission of synovitis for 3 months or longer in 27 patients and 50% or greater improvement in 20 patients. New joint deformities did not develop in patients who experienced remission, and progression of radiologically detectable erosive changes was prevented. Serum protein and serologic abnormalities were improved in all groups, but patients who had a good response experienced the greatest improvement. No single clinical or laboratory feature in the pretreatment assessment predicted response, but, as a group, the patients with the best response also ranked best for most prognostic indicators.
Estrogen and glucocorticoid receptors in adult canine articular cartilage
Authors: Young PETER C. M. , Stack Michael T. 
Published: February 2007

AbstractThe cytoplasmic and crude nuclear fractions of adult mongrel dog articular cartilage contained estradiol‐ and dexamethasone‐binding components which had properties of physiologic steroid receptors. The equilibrium dissociation constants averaged 0.37 nM for estradiol and 2.27 nM for dexamethasone. The concentrations of estrogen receptors ranged from below 6 to 101 fmol/mg protein in the cytosols and from below 2.8 to 17.5 fmol/μg DNA in the nuclear fractions. Glucocorticoid receptors were detected in only 4 of 13 cytosols (range: 61.2–132 fmol/mg protein), whereas 10 of 13 nuclear fractions contained 0.8 to 46.8 femtomoles of the receptors for each microgram of DNA. There appeared to be no marked difference between the contents of either steroid receptor in female or male dog cartilage. No receptors were detected for androgen and progesterone.
Prior gold therapy does not influence the adverse effects of D‐penicillamine in rheumatoid arthritis
Authors: Kean Walter F. , Lock Colin J. L. , Howard‐Lock Helen E. , Buchanan W. Watson 
Published: February 2007

AbstractOne hundred fourteen patients with definite or classic rheumatoid arthritis were followed prospectively between January 1976 and April 1981 to monitor their toxicity pattern to D‐penicillamine. The influence of previous sodium aurothiomalate therapy on the toxicity pattern of D‐penicillamine is described. There was no significant difference in overall outcome of the patients treated with D‐penicillamine with respect to adverse effects, whether they had previous gold toxicity, previous gold therapy but no toxicity, or no previous gold therapy. The time from gold toxicity to the start of D‐penicillamine therapy was greater in those who did not develop D‐penicillamine toxicity compared with those who did. This difference just reached statistical significance. Total gold salt received had no effect on eventual outcome of D‐penicillamine treatment, and the toxicity pattern of D‐penicillamine in those patients who had previous gold therapy was similar to those patients who had never received gold therapy.
Ultrastructure of arthritis induced by a caprine retrovirus
Authors: Brassfield Alberta L. , Adams D. Scott , Crawford Timothy B. , Mcguire Travis C. 
Published: February 2007

AbstractThe ultrastructure of early retrovirus‐induced arthritis was studied sequentially in 20 goat kids inoculated with caprine arthritis—encephalitis virus. Synovial lesions began as intercellular edema and collagen fragmentation and continued as progressive mononuclear cell infiltration and lining cell hyperplasia, hypertrophy, and necrosis. At 18 through 45 days after the inoculation, lining cells contained small accumulations of virus‐like particles similar to virus seen in infected tissue culture cells. No virus was seen budding from infected lining cell membranes.
Gas‐liquid chromatographic analysis of synovial fluid. Succinic acid and lactic acid as markers for septic arthritis
Authors: Borenstein David G. , Gibbs Christina A. , Jacobs Robert P. 
Published: February 2007

AbstractNonvolatile short‐chain fatty acids from 80 synovial fluids were quantified by gas‐liquid chromatography. Succinic acid was detectable in all 23 septic synovial fluids infected with either gram‐positive or gramnegative organisms and in only 5 of 57 nonseptic synovial fluids. Lactic acid was present in all of the effusions but was correlated with septic arthritis only when present in concentrations greater than 250 mg%. Neither short‐chain fatty acid was more sensitive than high white blood cell counts (>50,000 mm3) or depressed glucose concentration (<40 mg/dl) in diagnosing septic arthritis before antibiotic therapy; however, the detection of succinic acid was helpful in identifying patients with septic arthritis who had been given antibiotic treatment before arthrocentesis. Thus, gas‐liquid chromatography, a rapid and sensitive method for the detection of short‐chain fatty acids, may complement the currently available methods used to diagnose septic arthritis.
Nailfold capillary abnormalities and clinical outcome in childhood dermatomyositis
Authors: Spencer‐Green George , Crowe William E. , Levinson Joseph E. 
Published: February 2007

AbstractThe nailfold capillary pattern was observed in a population of patients with childhood dermatomyositis. Distinctive nailfold capillary loop abnormalities were found in 11 of 19 childhood dermatomyositis patients and in none of 2 control populations (P < 0.001). By a retrospective analysis of the childhood dermatomyositis patients, we found that the presence of nailfold capillary abnormalities correlates with more severe forms of the disease (ulcerative and chronic types), as opposed to limited type of disease. These changes occurred independently of disease activity or of cutaneous abnormalities.
Interrelationships of HLA‐DR, MB, AND MT phenotypes, autoantibody expression, and clinical features in systemic lupus erythematosus
Authors: Ahearn Joseph M. , Provost Thomas T. , Dorsch Carole A. , Stevens Mary Betty , Bias Wilma B. , Arnett Frank C. 
Published: February 2007

AbstractThe interrelationships of serologic and clinical features and the HLA–DR, MB, and MT specificities were examined in 70 white patients with systemic lupus erythematosus. HLA–DR2 and MB1 were significantly increased when compared with controls from the Eighth International Histocompatibility Testing Workshop but not with local controls. DR2 and DR3 correlated with increased seroreactivity (anti‐Ro, antiDNA, rheumatoid factor, and hyperglobulinemia), and anti‐Ro with clinically overt sicca complex. Thus, DR2 and DR3 may be markers of a major histocompatibility complex–mediated immune hyperresponsiveness that affects expression of systemic lupus erythematosus.
Serum pepsinogen i in rheumatic diseases. reduced levels in sjögren's syndrome
Authors: Maury C. Peter J. , Räsänen VESA , Teppo Anna‐Maija , Helve Tapani , Wegelius Otto 
Published: February 2007

AbstractGroup I pepsinogens were measured by radioimmunoassay in the sera of 93 patients with rheumatic diseases and 99 controls. Patients with rheumatoid arthritis and systemic lupus erythematosus had levels of pepsinogen I similar to controls, whereas patients with Sjögren's syndrome had levels significantly lower than either controls (P<0.001) or patients with rheumatic diseases not associated with sicca syndrome (P<0.001). The concentrations of serum pepsinogen I were lower in patients with sicca syndrome alone than in those with sicca syndrome associated with some other connective tissue disease (P<0.05). In patients with Sjögren's syndrome, a negative correlation was found between serum concentrations of β2‐microglobulin and pepsinogen I (r = −0.46, P<0.05).
STRAIN and sex variation in the susceptibility to streptococcal CELL WALL–INDUCED POLYARTHRITIS IN THE RAT
Authors: Wilder Ronald L. , Calandra Gary B. , Garvin A. Julian , Wright Karen D. , Hansen Carl T. 
Published: February 2007

AbstractSixteen inbred rat strains were examined for susceptibility and resistance to group A streptococcal cell wall–induced polyarthritis. The findings indicated that 2 or more genetic loci, as well as sex‐related factors, played a major role in determining susceptibility to arthritis in this model. Breeding studies demonstrated that susceptibility was a dominant or codominant trait. A positive association between the severity of arthritis and the development of chronic inflammation in multiple tissues was also observed. In strains that were relatively resistant to arthritis, chronic inflammation was generally limited to the spleen. Since translocation of the poorly degradable and phlogogenic streptococcal cell walls to the synovium and other tissues appears to initiate inflammation, these studies suggested that susceptibility might be the result of a defect in host mechanisms limiting cell wall dissemination.