bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abnormalities of Pulmonary Vascular Dynamics and Inflammation In Early Progressive Systemic Sclerosis
Authors: Furst Daniel E. , Davis James A. , Clements Phillip J. , Chopra Sawtantra K. , Theofilopoulos Argyrios N. , Chia David 
Published: February 2007

AbstractAbnormalities of pulmonary function were studied in 10 patients with progressive systemic sclerosis (PSS) and 3 control subjects. All underwent 81M krypton lung scanning and total body gallium scanning. Immune complexes were measured by Raji cell radio–immunoassay and polyethylene glycol (PEG) assay. Perfusion scans were abnormal in 7 of 9 patients, and 5 of 9 showed a decrease in pulmonary perfusion after cold challenge. Increased gallium uptake was noted in the lungs of 6 of 9 patients. Krypton scans were normal in the control group. Elevated immune complexes were noted in 8 of 10 patients by the Raji assay and in 5 of 10 with the PEG assay. Efforts to separate patients with PSS into subgroups may lead to a better understanding of and advances in therapy for PSS.
Chromosome Breakage and Sister Chromatid Exchange Frequencies in Scleroderma
Authors: Sherer Glenn K. , Jackson Barbara B. , Leroy E. Carwile 
Published: February 2007

AbstractPeripheral lymphocytes from 3 scleroderma patients with systemic disease and from 3 normal controls were examined for frequencies of chromosomal aberration and sister chromatid exchange (SCE). Significant increases in the levels of chromosomal anomaly and SCE were found for all 3 patients. These results are discussed in terms of the diagnostic potential of SCE in scleroderma and the possible etiologic role of cytogenetic instability in this disease.
Identification of Cartilage Wear Fragments in Synovial Fluid from Equine Joints
Authors: Tew William P. , Hackett Richard P. 
Published: February 2007

AbstractSynovial fluids from 72 equine joints were examined for the presence of cartilage debris, and these findings were compared to findings from visual inspection of the articular cartilage surfaces at necropsy. Synovial fluids from 25 joints with visual cartilage damage contained one or more large particles of articular cartilage. Cartilage fragments were not found in synovial fluids from 42 of the 47 apparently normal joints; thus, a correlation may exist between cartilage debris in the synovial fluid and lesions of the articular surfaces.
Proteoglycan Structure and Metabolism in Normal and Osteoarthritic Cartilage of Guinea Pigs
Authors: Schwartz Edith R. , Leveille Cynthia R. , Stevens Jeff W. , Oh Won H. 
Published: February 2007

AbstractSulfated proteoglycan structure and metabolism in osteoarthritic articular cartilage from the hind‐limb joints of guinea pigs in which the disease had been surgically induced were evaluated and compared with those from nonoperated or sham‐operated controls. In these studies, conducted on animals receiving high and low dietary levels of ascorbic acid, the effect of vitamin C on these variables was also examined. Sulfated proteoglycan biosynthesis per unit of DNA as reflected by in vivo uptake of 35S‐sulfate was stimulated both by arthritic development and high dietary vitamin C. Under these conditions, the specific activities, 35S‐cpm/μg uronic acid, of the proteoglycans were elevated. Neither arthritic development nor variation in dietary levels of vitamin C altered the structure of the proteoglycans. Two species of proteoglycans that exhibited the same electrophoretic mobilities in agarose/acrylamide gels, the same elution profiles on high performance liquid chromatography, and the same galactosamine/glucosamine ratios were found in all normal and osteoarthritic cartilage specimens tested. The specific activities of these two species were dissimilar. In all samples, the larger of the two species had a higher specific activity.
An Unusual Morphologic Evolution of Paget's Disease of Bone
Authors: Mallette Lawrence E. 
Published: February 2007

AbstractA patient with early Paget's disease of bone was treated for 12 months with calcitonin and 10 months with etidronate. During this time the cortex of each diseased bone showed a progressive 2‐ to 3‐fold increase in thickness. Lytic areas regressed and the new bone appeared radiographically very compact. No bowing deformity developed in 3 years of observation. This form of morphologic evolution differs markedly from those previously reported during treatment. For this patient, treatment was instituted very early during the course of the disease and moderately high doses of vitamin D were given during part of the treatment course. Observation of a larger number of patients will be needed to determine whether these factors actually modified the treatment outcome.
Pyrophosphate arthropathy in two swedish families
Authors: Bjelle Anders , Edvinsson Ulla , Hagstam ÅSa 
Published: February 2007

AbstractA clinical and radiographic survey of 110 members of 2 families with hereditary pyrophosphate arthropathy was performed. The mode of inheritance was autosomal, dominant with a variable penetrance. Twenty‐two percent of the family members had joint involvement related to pyrophosphate arthropathy, 47% of those over 50 years of age had experienced acute attacks of arthritis and/or had joint calcifications. The majority of individuals with both arthritis and joint calcifications suffered from chronic pain that resulted in early retirement. A high frequency of back pain was observed, but no ankylosis or deformity. Surgery was performed for parathyroid hyperplasia on the propositus in 1 family, and several members of her family suffered from symptoms that suggested a disturbance of calcium phosphate metabolism. There were several differences between our patients and 50 cases of sporadic pyrophosphate arthropathy from the same area of Sweden. Familial cases had an earlier onset, a greater number of involved joints, and peripheral joint involvement more often. Back pain was more frequent, and calcifications of intervertebral discs were found only in the hereditary cases.
IgA nephropathy associated with seronegative spondylarthropathies
Authors: Charles Jennette J. , Ferguson Alfred L. , Moore Michael A. , Freeman Douglas G. 
Published: February 2007

AbstractThree patients with a seronegative spondylarthropathy were found to have IgA nephropathy. Two patients had ankylosing spondylitis (one with psoriasis), and one had incomplete Reiter's syndrome. All three had a focal proliferative glomerulonephritis with IgA‐dominant mesangial immune deposits. One patient had a leukocytoclastic vasculitis. This association of IgA nephropathy with seronegative spondylarthropathies raises the possibility of a common or related pathogenesis. There is evidence to suggest that both diseases are mediated by genetically controlled immune responses to mucosal contact with etiologic antigens.
Differential patterns of in vitro IgM rheumatoid factor synthesis in seronegative and seropositive rheumatoid arthritis
Authors: Alarcón Graciela S. , Koopman William J. , Schrohenloher Ralph E. 
Published: February 2007

AbstractThe existence of a subpopulation of patients with rheumatoid arthritis (RA) who lack detectable rheumatoid factor (RF) is well documented. The cellular basis for nonexpression of RF in seronegative RA is not understood. In order to approach this problem, we compared mononuclear leukocytes (MNL) from 20 healthy adult controls, 20 seropositive RA and 22 seronegative RA patients to assess their capacity to synthesize IgM and IgM RF in vitro in the presence and absence of pokeweed mitogen (PWM). MNL from 10 of 20 seropositive RA patients spontaneously elaborated IgM RF (mean = 16.7 ng/106 cells), whereas this was not observed with MNL from either controls or seronegative patients. Small quantities of IgM were spontaneously released by MNL from the seropositive (68.1 ng/106 cells), seronegative (43.1 ng/106 cells), and control (142.3 ng/106 cells) groups. PWM induced IgM RF production by MNL from 10 of 20 controls (18.5 ng/106 cells) and 8 of 22 seronegative RA patients (13.5 ng/106 cells); however, this was significantly less than the production observed with seropositive RA MNL (13 of 20; 37.5 ng/106 cells). In contrast, IgM production in response to PWM was significantly less in both the seronegative (999.7 ng/106 cells) and seropositive RA groups (471.7 ng/106 cells) than in the control group (2,678 ng/106 cells). IgM RF constituted a significantly higher proportion of total IgM synthesized by seropositive RA MNL (10.7%) than either seronegative RA MNL (2.5%) or control MNL (1.2%). Differences in IgM RF production in vitro could not be explained by HLA—DR4 status. Hidden RF was not detected in seronegative MNL supernatants. The results indicate clear differences in the pattern of in vitro release of IgM and IgM RF by MNL from seronegative RA patients as compared to either seropositive RA MNL or control MNL. The similarity of seronegative RA MNL to control MNL with regard to in vitro expression of IgM RF suggests that regulatory mechanisms governing RF synthesis are relatively intact in patients who have seronegative RA.
Superoxide anion generation by human neutrophils exposed to monosodium urate. effect of protein adsorption and complement activation
Authors: Abramson Steven , Hoffstein Sylvia T. , Weissmann Gerald 
Published: February 2007

AbstractWe studied the capacities of naked and proteincoated monosodium urate (MSU) crystals to stimulate superoxide anion (O2\documentclass{article}\pagestyle{empty}\begin{document}$ \[\bar .\] $\end{document}) release by human polymorphonuclear leukocytes (PMN). Uncoated MSU stimulated significant O2\documentclass{article}\pagestyle{empty}\begin{document}$ \[\bar .\] $\end{document} production by cytochalasin B‐treated PMN. Precoating MSU with IgG caused an increase in mean O2\documentclass{article}\pagestyle{empty}\begin{document}$ \[\bar .\] $\end{document} production, whereas precoating heated MSU with serum or plasma inhibited O2\documentclass{article}\pagestyle{empty}\begin{document}$ \[\bar .\] $\end{document} release. Unheated MSU crystals, which activate complement to a greater extent than heated crystals, also provoked O2\documentclass{article}\pagestyle{empty}\begin{document}$ \[\bar .\] $\end{document} generation, an effect again abrogated by precoating with serum but not with plasma. Coincubation of unheated MSU and plasma resulted in an enhancement of O2\documentclass{article}\pagestyle{empty}\begin{document}$ \[\bar .\] $\end{document} generation. The results of these experiments support the hypothesis that adsorbed proteins modulate the phlogistic potential of MSU and that the surface activation of humoral mediators contributes to the local inflammatory response.
Rheumatoid factor inhibition of in vitro binding of IgG complexes in the human glomerulus
Authors: Bolton W. Kline , Schrock Jon H. , Davis John S. 
Published: February 2007

AbstractWe studied the effects of rheumatoid factor (RF) on binding of immune complexes to activated C3 (C3b) receptors in vitro. IgM fraction of serum containing RF activity (IgM‐RF), IgM isolated from pooled normal human serum and having no RF activity (IgM‐control), bovine serum albumin, and Veronal buffered saline solutions were used in a C3b assay system consisting of aggregated human IgG (AggHuIgG) coupled to sheep erythrocytes (SRBC) with guinea pig and normal human serum complement. The number of glomerular bound AggHuIgG‐SRBC with IgM‐control and bovine serum albumin or Veronal buffered saline was similar, while the number of bound cells with IgM‐RF was reduced significantly. This effect was seen with both guinea pig and normal human serum complements. Supernatant hemolytic complement activity was maintained with IgM‐RF, but reduced with control solutions. The blocking factor was shown to be RF by serial dilutions of IgM‐RF resulting in inverse correlations with latex flocculation and inhibition of SRBC binding, absorption of blocking from IgM‐RF with insolubilized AggHuIgG, and failure of IgM‐control to block binding. IgM‐RF did not directly interfere with activation of complement, but blocked attachment of C3 to AggHuIgG and formation of C3b capable of reacting with glomerular receptors. These results showed that IgM‐RF can inhibit binding of AggHuIgG complexes to human glomeruli. This in vitro phenomenon may represent a possible protective mechanism of RF in vivo in diseases with immune complexes.
Histone antibodies in systemic lupus erythematosus. A possible diagnostic tool
Authors: Gioud M. , Kaci M. Ait , Monier J. C. 
Published: February 2007

AbstractAntibodies to total histones and histone fractions H1, H2a‐H4, H2b, and H3 were measured in serum samples from 61 patients with systemic lupus erythematosus (SLE), 33 with rheumatoid arthritis, 17 with systemic sclerosis, and 20 with various other diseases by use of a sensitive immunoenzymatic assay. Histone antibodies were present in 52.4% of the SLE samples whereas only 1 of the samples from other diseases was positive (systemic sclerosis). The presence of these antibodies in SLE patients was not associated with any specific clinical manifestations, but was correlated with activity of the disease: 87% (20 of 23) of patients with active SLE, in particular 9 of 9 not yet treated, showed histone antibody whereas only 18% (4 of 22) of samples from patients with inactive SLE were positive. We believe that the measurement of histone antibodies would be a useful addition to the present laboratory parameters (antinuclear and double‐stranded DNA antibodies and circulating immune complexes) for the diagnosis and progression of systemic lupus erythematosus, particularly since they seem to appear during or just before the onset of an active phase and tend to be absent during remission.
Natural killer augmentation in systemic lupus erythematosus via a soluble mediator derived from human lymphocytes
Authors: Kaufman Donald B. 
Published: February 2007

AbstractSeventeen patients with diagnosed systemic lupus erythematosus were studied for natural killer activity and the ability of a human soluble immune‐response factor to modify this activity. Defective natural killer activity was found in patients with systemic lupus erythematosus regardless of the stage of disease, medication, or organ system involvement (24.6% versus 47.8% cytotoxicity). After treatment with the immune‐response factor, the natural killer activity increased in all patients, with a mean of 47.3% compared with 24.6% before treatment. This product has other immunologic activities and was shown to be free of interferon. The mechanism of action is not yet known, but such an immune‐response factor has potential use in the treatment of systemic lupus erythematosus.
Chronic arthritis of rabbits induced by mycoplasmas. III. Induction with nonviable mycoplasma arthritidis antigens
Authors: Washburn Leigh Rice , Cole Barry C. , Ward John R. 
Published: February 2007

AbstractPreexposure of rabbits to Mycoplasma arthritidis predisposed them to subsequent development of chronic inflammation in knee joints challenged with nonviable M arthritidis antigens. Rabbits sensitized by hyperimmunization developed a more severe arthritis than those sensitized by infection. Unsensitized rabbits responded minimally to intraarticular injection of nonviable organisms. These results suggested that an immune response to a persisting mycoplasmal antigen might be capable of sustaining chronic inflammation in rabbits with arthritis induced by viable M arthritidis.
Frequencies of epstein‐barr virus—inducible IgM anti‐IgG B lymphocytes in normal children and children with juvenile rheumatoid arthritis
Authors: Fong Sherman , Miller John J. , Moore Terry L. , Tsoukas Constantine D. , Vaughan John H. , Carson Dennis A. 
Published: February 2007

AbstractThe relative frequencies of IgM antilgG autoantibody (rheumatoid factor) producing cells induced by the polyclonal B cell activator Epstein‐Barr virus were measured in peripheral blood lymphocyte cultures of normal children and patients with juvenile rheumatoid arthritis. The frequencies of rheumatoid factor precursor B cells in normal children were lower than adults, but higher than neonates. The frequency increased with the age of the donor. In seronegative children with the systemic‐onset or pauclarticular‐onset types of juvenile rheumatoid arthritis, the number of IgM antiIgG inducible B cells was not significantly different (P>0.05) from age‐matched controls. Patients with seropositive juvenile rheumatoid arthritis or seropositive adult rheumatoid arthritis had significantly higher IgM antiIgG precursor cell frequencies than age‐matched normal subjects (P<0.01 and P<0.02, respectively). In contrast, the patients with seronegative polyarticular‐onset juvenile rheumatoid arthritis had an average precursor frequency significantly lower than normal age‐matched controls (P<0.05), analogous to results previously noted in adult seronegative rheumatoid arthritis. Thus, both children and adults with seronegative polyarticular rheumatoid arthritis had a deficiency in B cells that produce IgM antiIgG and that are induced by Epstein‐Barr virus. This distinguished them from seropositive juvenile rheumatoid arthritis and rheumatoid arthritis patients, normal subjects, and patients with the pauciarticular‐onset and systemic‐onset types of seronegative juvenile rheumatoid arthritis.
Factors influencing articular cartilage wear in vitro
Authors: Radin Eric L. , Swann David A. , Paul Igor L. , Mcgrath Paul J. 
Published: February 2007

AbstractThe in vitro wear of articular cartilage in oscillating and impulsively loaded bovine metatarsophalangeal joints was studied. Articular cartilage scarification had little effect on cartilage wear, but stiffening of the subchondral bone with methyl methacrylate greatly increased the rate of cartilage loss, whether or not it had previously been scarified. Glutaraldehyde treatment of articular cartilage for 30 minutes decreased its wear rate. Guanidinium chloride extraction of the cartilage before wear testing caused it to peel off its subchondral bed. This effect could be spared by prior glutaraldehyde fixation.
Induction of human rheumatoid factor producing cells by aggregated igg
Authors: Pisko Edward J. , Turner Robert A. , Foster Susan L. 
Published: February 2007

AbstractNormal human peripheral blood mononuclear leukocytes were induced to become cells that secrete rheumatoid factor after culture with aggregated IgG, but not monomeric IgG. A plaque‐forming cell assay was used to detect cells that secrete antibodies to IgG. Anti‐haptenated–sheep red cell plaque‐forming cells were also induced by aggregated IgG, suggesting that aggregated IgG may have induced plaque‐forming cells polyclonally. Polyclonal stimulation of mononuclear leukocytes by aggregated IgG may be a mechanism for the in vivo stimulation of cells that produce rheumatoid factor.
Ultrastructure of the esophagus in scleroderma
Authors: Russell M. Lynn , Friesen Dianne , Henderson R. D. , Hanna Wedad M. 
Published: February 2007

AbstractThe ultrastructure of the esophageal wall in progressive systemic sclerosis (scleroderma) was studied in 7 patients and compared with other esophageal diseases. In scleroderma, fibrosis and capillary basement membrane changes were the most characteristic abnormalities. Muscle fibers of patients with scleroderma showed thickened dense bodies and plaques and increased cell organelles in comparison with other disease groups, while neural structures were normal. Our data supported a primary vascular cause, rather than a neurogenic or myopathic process, for esophageal dysfunction in scleroderma.
Experimental hydroxyapatite synovial and articular cartilage calcification. light and electron microscopic studies
Authors: Reginato Antonio J. , Schumacher H. Ralph , Brighton Carl T. 
Published: February 2007

AbstractIntraarticular calciphylaxis with cartilage and synovial calcification was produced in rabbits by oral administration of a single dose of dehydrotachysterol followed by an intraarticular injection of ferrous chloride. Synovial membrane apatite deposits were seen in the interstitium, on collagen fibers, and within cell vacuoles. In contrast, long‐term administration of dehydrotachysterol alone induced only articular cartilage calcification. Such calcification was limited to the mid and deep zone of cartilage. Most calcium deposits were apatite‐like crystals. Acute crystal‐associated inflammation was not demonstrated in these specimens with crystals sequestered in synovial or cartilage tissue. Further studies on these models will examine the relation of apatite to joint disease.
Aspirin aggravates the degeneration of canine joint cartilage caused by immobilization
Authors: Palmoski Marshall J. , Brandt Kenneth D. 
Published: February 2007

AbstractThe effect of aspirin on the degeneration of knee cartilage caused by immobilization was examined. If dogs were fed aspirin daily (serum salicylate = 20–25 mg/dl) for 6 weeks while one hind limb was immobilized in a cast, the decreases in uronic acid content and net proteoglycan synthesis in cartilage from the immobilized knee were significantly greater than the decreases in cartilage from immobilized knees of dogs that had not received aspirin (P<0.01). Furthermore, neither aspirin administration nor immobilization alone affected the extractability of proteoglycans from the cartilage. However, in organ cultures of cartilage from the immobilized knee of dogs fed aspirin, the proportion of the total 35S‐proteoglycans present in the culture medium was nearly twice that from cultures of cartilage of the contralateral knee. Also, more than twice as many of the total tissue proteoglycans (uronic acid) were extractable with 0.4M guanidinium chloride, a nondissociating solvent (P<0.01). Regardless of whether the dogs received aspirin, the in vitro interaction of proteoglycans with hyaluronic acid from cartilage of the immobilized knee was diminished, apparently due to an abnormality in the hyaluronate‐binding region of the core protein. Although these results indicate that aspirin had an adverse effect in vivo on articular cartilage of immobilized joints, aspirin administration did not preclude reversal of all of the above changes if the dog was allowed to walk about in a pen for 3 weeks after cast removal. If, however, the dog was run daily on a treadmill for 3 weeks after cast removal, the decrease in uronic acid content in cartilage from the immobilized knee persisted and was more profound if the animal had received aspirin than if it had not (P<0.01).
Digital sclerosis in children with insulin‐dependent diabetes mellitus
Authors: Seibold James R. 
Published: February 2007

AbstractPalpable thickening and induration of the skin of the fingers were found in 47 (34%) of 137 children with insulin‐dependent diabetes mellitus and in none of 52 normal children. Mild flexion contractures of the interphalangeal joints were seen in 26 (19%), mainly in those children with more extensive and severe skin changes. Such contractures have been linked to microvascular complications of diabetes. The clinical and pathogenic similarities to progressive systemic sclerosis make the digital sclerosis of childhood diabetes a promising model for further rheumatologic study.
Circadian variations of serum myoglobin levels in normal subjects and patients with polymyositis
Authors: Bombardieri Stefano , Clerico Aldo , Riente Lucrezia , Chicca Maria Grazia Del , Vitali Claudio 
Published: February 2007

AbstractCircadian variations in myoglobin levels were determined in 18 normal volunteers and in 10 patients with active polymyositis. In all the controls and in 9 of the 10 patients, serum myoglobin concentrations were highest at 9 AM, fell significantly during the day to reach a nadir between 6 and 12 PM, remained constant until midnight, and then rose again at 3 AM. The percent differences between the highest and lowest values ranged from 21–66%. This pattern was observed in both untreated patients and patients receiving 6‐methyl‐prednisolone, which was given either in a single dose at 8 AM or in divided doses (8 AM and 8 PM). These data demonstrate that the time of sample collection must be taken into account when myoglobin levels are used as a marker of muscle damage.