bluuebunny/crossref_metadata_2025_split huggingface dataset:
Adhesion of peripheral blood mononuclear cells to vascular endothelium in patients with systemic sclerosis (scleroderma)
Authors: Rudnicka Lidia , Majewski Slawomir , Blaszczyk Maria , Skiendzielewska Anna , Makiela Barbara , Skopinska Magdalena , Jablonska Stefania 
Published: February 2007

AbstractObjective. Perivascular infiltrates in skin, subcutaneous tissue, and internal organs are a characteristic feature of early systemic sclerosis (SSc). We studied the first step of migration of peripheral blood mononuclear cells (PBMC) through the vessel wall to the extravascular space, i.e., adhesion of PBMC to endothelial cells (EC), in patients with various forms of SSc (limited scleroderma, diffuse scleroderma, and the transitional form).Methods. Radioisotope‐labeled patient PBMC were coincubated with umbilical cord EC in vitro, and the percentage adhesion was measured.Results. Adhesion of PBMC to EC was markedly decreased, while adhesion of isolated active rosetteforming cells (ARFC) was significantly increased, in SSc patients compared with healthy controls. Decreased adhesion of PBMC to EC was found to correlate with a diminished percentage of ARFC in the peripheral blood. Preincubation of PBMC from healthy donors with interleukin‐2 (IL‐2) enhanced their adhesion to EC, while preincubation of PBMC from SSc patients with this cytokine resulted in a decrease in adhesion in 10 of 14 individuals. IL‐1, interferon‐γ, and transforming growth factor β had no significant effect on adhesion of SSc patient PBMC to EC. Differences in adhesion of PBMC to EC among the SSc subgroups were not significant.Conclusion. Our findings suggest that in SSc, activation of subpopulations of PBMC leads to their enhanced adhesion to vascular endothelium in vivo and to migration of these cells to the extravascular space, resulting in the elimination from the peripheral blood of those PBMC with high ability to adhere to EC.
A Controlled study of the prevalence of cognitive dysfunction in randomly selected patients with systemic lupus erythematosus
Authors: Ginsburg Katherine S. , Wright Elizabeth A. , Larson Martin G. , Fossel Anne H. , Albert Marilyn , Schur Peter H. , Liang Matthew H. 
Published: February 2007

AbstractObjective. To investigate the prevalence of cognitive dysfunction in randomly selected patients with systemic lupus erythematosus (SLE).Methods. Randomly selected, ambulatory patients with SLE (n = 49) or with rheumatoid arthritis (RA) (n = 40) completed neuropsychological tests. These included Associate Learning, Switching Attention, Continuous Performance, Associate Recall, Hand–Eye Coordination, Pattern Comparison, Pattern Memory, the Stroop Color and Word Test, and the Symptoms Checklist–90R. Results were evaluated by multiple linear regression analysis.Results. SLE patients had poorer performance than RA patients on the test of attention (P = 0.002) and tests of visuospatial ability (P = 0.03 and P = 0.04), independent of age, education, or steroid use. The conservative level of statistical significance, adjusting for multiple comparisons, was 0.005. SLE patients reported more symptoms of cognitive difficulty.Conclusion. Cognitive dysfunction is common in ambulatory SLE patients as measured by standardized tests and is a cause of distress and impaired functioning. Self‐reported cognitive difficulty appears to correlate with objective performance.
Recombinant human interleukin‐1 β–induced increase in levels of proteoglycans, stromelysin, and leukocytes in rabbit synovial fluid
Authors: Mcdonnell Joseph , Hoerrner Lori A. , Lark Michael W. , Harper Coral , Dey Tanvi , Lobner Julie , Eiermann George , Kazazis Diana , Singer Irwin I. , Moore Vernon L. 
Published: February 2007

AbstractObjective. To evaluate the effects of intraarticular injection of recombinant human interleukin‐1β (IL‐1β) on levels of proteoglycans, stromelysin, and leukocytes in rabbit synovial fluid (SF), and to determine the effects of leukocyte depletion on SF proteoglycan and stromelysin levels.Methods. Levels of leukocytes and of proteoglycans, stromelysin, and collagenase were evaluated 12 hours after the intraarticular injection of various doses of IL‐1, and over a 24‐hour period after injection at a single dose level. We used a monoclonal antibody (MAb) against leukocyte integrins, which markedly depressed leukocyte accumulation in SF, to evaluate the role of synovial leukocytes on IL‐1–induced increases in SF proteoglycan and stromelysin levels.Results. Levels of both proteoglycans and stromelysin increased in the IL‐1–injected joints between 4 hours and 24 hours after the injection of a single 200‐ng dose of IL‐1. The highest levels of stromelysin and proteoglycans were achieved with IL‐1 doses ≥ 100 ng. Infiltration of polymorphonuclear cells (PMN) into the joint fluid of the IL‐1–injected rabbits also increased, in a dose‐dependent manner. Treatment of rabbits with MAb 1B4 markedly reduced infiltration of PMN into the joint, without affecting either stromelysin or proteoglycan levels.Conclusion. Taken together, the data suggest that there is a coordinate increase in SF stromelysin and proteoglycan levels in rabbits injected with IL‐1, and that leukocytes play a minimal role in the accumulation of proteoglycans and stromelysin in the SF.
Type x collagen synthesis in human osteoarthritic cartilage. indication of chondrocyte hypertrophy
Authors: Von Der Mark K. , Kirsch T. , Nerlich A. , Kuss A. , Weseloh G. , Glückert K. , Stöss H. 
Published: February 2007

AbstractObjective. To investigate the appearance of hypertrophic chondrocytes in osteoarthritic (OA) cartilage, using type X collagen as a specific marker.Methods. The biosynthesis of type X collagen was examined by metabolic labeling of freshly isolated articular chondrocytes with 3H‐proline, immunoprecipitation, and sodium dodecyl sulfate–polyacrylamide gel electrophoresis of the synthesized collagens. Extracellular deposition of types X and II collagen was analyzed immunohistochemically.Results. Immunostaining revealed an irregular distribution of type X collagen, which was localized around chondrocyte clusters in fibrillated OA cartilage, but was absent from the noncalcified region of normal articular cartilage. Freshly isolated OA chondrocytes synthesized predominantly type X collagen, while control chondrocytes synthesized mostly type II collagen.Conclusion. Our findings indicate focal premature chondrocyte differentiation to hypertrophic cells in OA cartilage.
Progressive aortic valve inflammation occurring despite apparent remission of relapsing polychondritis
Authors: Buckley Lenore M. , Ades Philip A. 
Published: February 2007

AbstractWe describe a patient with relapsing polychondritis in whom aortic valve inflammation developed 3 years after diagnosis, when the polychondritis had been in apparent remission for an extended period of time. Infection and cardiac involvement can be significant complications of relapsing polychondritis. Recommendations for monitoring and treatment of patients with this disease are discussed.
Antibodies to glycyl–transfer rna synthetase in patients with myositis and interstitial lung disease
Authors: Targoff Ira N. , Trieu Edward P. , Plotz Paul H. , Miller Frederick W. 
Published: February 2007

AbstractObjective. We have previously described anti‐EJ antibodies, and provided evidence that these antibodies react with glycyl–transfer RNA (gly‐tRNA) synthetase. The aim of the present study was to identify patients with anti‐EJ antibodies and describe the clinical associations of the antibody, in particular, whether it is associated with the syndrome of myositis and interstitial lung disease (ILD) that has been previously associated with autoantibodies to the aminoacyl‐tRNA synthetases for histidine, threonine, and alanine.Methods. Sera from patients with suspected or proven polymyositis or dermatomyositis (DM), sera with anticytoplasmic patterns, and control sera were tested for anti‐EJ antibodies by immunoprecipitation (IPP). Positive sera and controls were tested for the ability to inhibit gly‐tRNA synthetase by preincubation of the enzyme source with the serum.Results. Anti‐EJ antibodies were demonstrated in the sera of 5 patients, by IPP of characteristic tRNAs and protein. Original serum EJ and each of the new sera significantly inhibited the enzymatic activity of gly‐tRNA synthetase but not histidyl‐tRNA synthetase. All 5 of the new patients had inflammatory myopathy, a typical DM rash, and ILD. One, who had an overlap syndrome with systemic lupus erythematosus, had anti‐EJ at least 4 months before the development of clinical myositis. Arthritis and Raynaud's phenomenon, other features associated with antisynthetases, were also seen.Conclusion. Anti‐EJ is associated with the syndrome of myositis and lung disease that is seen in association with other antisynthetases. The finding of specific inhibition of gly‐tRNA synthetase by all anti‐EJ–positive sera strongly supports the identification of EJ antigen as gly‐tRNA synthetase.
Malignant angioendotheliomatosis (intravascular lymphomatosis) clinically simulating primary angiitis of the central nervous system
Authors: Lie J. T. 
Published: February 2007

AbstractPrimary angiitis of the central nervous system (PACNS) and malignant angioendotheliomatosis (MAE) are two unrelated and lethal diseases that frequently affect the brain. Both are uncommon and both require histologic documentation of their characteristic lesions for a definitive diagnosis. Because brain biopsies are not routinely included in the diagnostic workup of nonneoplastic CNS diseases, a number of unconfirmed nonvasculitic conditions may mimic PACNS. To my knowledge, MAE simulating PACNS clinically and angiographically has not been previously reported, and 3 such cases are described herein.
Effect of gold compounds on the activity of adenylyl cyclase in human lymphocyte membranes
Authors: Lazarevic Milenko B. , Yan Kun , Swedler William I. , Rasenick Mark M. , Skosey John L. 
Published: February 2007

AbstractObjective. To determine the effects of aurothioglucose, aurothiomalate, and auranofin on basal and forskolin‐activated adenylyl cyclase activity in human total lymphocyte membranes, and in membranes of T and B lymphocyte subsets.Methods. Membranes were isolated from human total lymphocytes and T and B cell subsets. The effects of gold compounds on basal and forskolin‐stimulated activity of adenylyl cyclase were measured by radioassay.Results. The gold compounds inhibited adenylyl cyclase activity. This inhibitory effect required the presence of both the sulfhydryl ligands and aurous cation.Conclusion. Regulation of lymphocyte adenylyl cyclase by gold compounds represents a potential mode of action of these drugs in rheumatic diseases.
Analysis of intraarticular fibrinolytic pathways in patients with inflammatory and noninflammatory joint diseases
Authors: Alain J. , Abbink Janna J. , Boer Jan‐Paul De , Roem Dorina , Nieuwenhuys Ed J. , Kamp Angela M. , Swaak Tom J. G. , Erik Hack C. 
Published: February 2007

AbstractObjective. Intraarticular activation of the fibrinolytic system has been suspected to occur in patients with arthritis. We undertook the present study to investigate the relation of this activation to clinical symptoms, and the molecular pathways involved.Methods. We quantitatively assessed levels of plasmin–α2‐antiplasmin (PAP) complexes in synovial fluid (SF) from 25 patients with rheumatoid arthritis (RA), 7 with seronegative spondylarthropathy (SSA), and 10 with osteoarthritis (OA), and conducted an analysis to determine the plasminogen‐activating pathway via which these complexes were generated. In addition, we studied the relationship of intraarticular fibrinolysis to clinical and biochemical parameters.Results. All patients studied had increased SF levels of PAP complexes. Levels in patients with RA and SSA were slightly higher than those in patients with OA. These complexes were probably formed by activation of urokinase‐type plasminogen activator (u‐PA), and not tissue‐type plasminogen activator (t‐PA), since SF levels of both u‐PA antigen and u‐PA–plasminogen activator inhibitor (PAI) complexes were increased in 27 of the 42 patients. Conversely, SF levels of t‐PA were below normal in all but 1 patient. In some patients, activation of factor XII presumably also contributed to plasminogen activation in SF, since levels of factor XIIa–C1 inhibitor in SF were increased in 8 of the 42 patients and correlated, as did u‐PA–PAI levels, with levels of PAP complexes. Several of the parameters of fibrinolysis in SF, particularly u‐PA antigen and u‐PA‐PAI–1 complexes, were found to correlate with clinical and biochemical parameters.Conclusion. Our results suggest that plasminogen is frequently activated in the joints of patients with inflammatory or noninflammatory arthropathy and that this activation mainly occurs via a u‐PA–, and in some cases also via a factor XII–, dependent pathway. The possible relation of this activation process to stimulation of synovial cells by cytokines is discussed.
Autoradiographic localization and analysis of endothelin‐1 binding sites in human synovial tissue
Authors: Wharton John , Rutherford Richard A. D. , Walsh David A. , Mapp Paul I. , Knock Gregory A. , Blake David R. , Polak Julia M. 
Published: February 2007

AbstractObjective. To determine the localization of endothelin binding sites and immunoreactivity in human synovial tissues.Methods. Quantitative in vitro autoradiographic and immunohistochemical techniques were used to localize and characterize 125I‐labeled endothelin‐1 (125I–ET‐1) binding sites and endothelin‐like immunoreactivity in sections of rheumatoid, osteoarthritic, and normal synovium.Results. Specific 125I–ET‐1–binding sites, characteristic of the ETA receptor, were localized to the media of synovial blood vessels in all 3 groups. No difference was found in vascular binding site density in rheumatoid and osteoarthritic synovium. Endothelin‐like immunoreactivity was localized to endothelial cells in blood vessels displaying 125I–ET‐1 binding sites.Conclusion. We conclude that endothelin may act locally, modulating synovial perfusion and exacerbating hypoxia in chronic arthritis.
A rheumatoid factor from a normal individual encoded by VH2 and VkII gene segments
Authors: Stüber Frank , Lee Soo Kon , Bridges S. Louis , Koopman William J. , Schroeder Harry W. , Gaskin Felicia , Fu Shu Man 
Published: February 2007

AbstractObjective. To gain insight into the immunoglobulin variable‐region repertoire of anti‐IgG antibodies (rheumatoid factors [RF]), we characterized the VH and Vk gene segments utilized in an IgM‐RF–secreting lymphoblastoid cell line (SSH23) isolated from a normal individual.Methods. The cell line SSH23 was established by Epstein‐Barr virus transformation of peripheral blood non–T mononuclear cells. First‐strand complementary DNA (cDNA) was generated and used for polymerase chain reaction amplification of the heavy and light chain variable domains. The amplified variable domains were sequenced and compared with an extensive database of germline and cDNA V gene segments.Results. The VH sequence was found to be identical to a previously described fetal VH2 incomplete cDNA and to differ by only 3 nucleotides from a JH proximal germline VH2 gene segment. To our knowledge, this is the first example of a VH2 rheumatoid factor. The Vk2–Jk4 light chain contains an uncommon 10–amino acid third complementarity‐determining region (CDR 3).Conclusion. Utilization of preimmune fetal VH gene segments and unusual light chain junctional diversity appear to be features shared by many physiologic and pathologic rheumatoid factors.
The immunoglobulin kappa light chain repertoire expressed in the synovium of a patient with rheumatoid arthritis
Authors: Lee Soo Kon , Bridges S. Louis , Koopman William J. , Schroeder Harry W. 
Published: February 2007

AbstractObjective. To analyze the nature of the B cell response in the synovial tissue of a patient with rheumatoid arthritis (RA). Specifically, we sought to determine if the pattern of immunoglobulin expression was consistent with polyclonal stimulation of B cells or an antigen‐driven response.Methods. We generated an unrestricted complementary DNA (cDNA) library from the diseased synovium of a rheumatoid factor (RF)–positive patient with an 18‐year history of RA. A random sample of k light chain recombinants was identified, and sequence analysis was performed. The variable domains were compared with an extensive database of germline and cDNA k sequences.Results. We found a light chain repertoire enriched for k transcripts containing 2 Vk gene segments (Humkv325 and Humkv328) that are frequently associated with paraproteins expressing RF activity. Kappa variable domains from synovium contained numerous somatic mutations which resulted in frequent replacement of amino acids that encode the classic antigenbinding site. Unexpectedly, many of these k transcripts contained non–germline‐encoded nucleotides (N regions) at the site of Vk–Jk joining. The combination of N‐region addition and variation in the sites of Vk–Jk splicing generated unusually long complementarity‐determining region 3 regions and charged amino acids near the Vk–Jk splice site.Conclusion. The pattern of somatic mutations found in this patient sample supports the hypothesis that these synovium‐derived plasma cells are the product of immunoglobulin receptor–dependent (i.e., antigen‐driven) selection. The extent of N‐region addition raised the additional possibility that these antibodies derive from an unusual set of B lymphocytes that have escaped normal regulation.
Immunopathology of rheumatoid arthritis
Authors: Kurki Pekka , Aho Kimmo , Palosuo Timo , Heliövaara Markku 
Published: February 2007

AbstractObjective. We sought to determine whether circulating antikeratin antibodies (AKA) precede the onset of rheumatoid arthritis (RA).Methods. By matching the registers of 2 previous population studies with the registry of patients receiving antirheumatic drugs several years later, pre‐illness serum specimens could be obtained from 39 individuals who subsequently developed RA. AKA were assayed with the standard indirect immunofluorescence technique.Results. Ten of 39 serum specimens from individuals who subsequently developed seropositive RA, and 1 of 15 sera from individuals who developed seronegative RA, were positive for IgG‐class AKA by immunofluorescence assay. The AKA‐positive sera were also positive for rheumatoid factors.Conclusion. The findings focus attention on the role of pre‐illness immunologic events in the pathogenesis of RA.
Utility of high‐resolution ultrasound for the diagnosis of dialysis‐related amyloidosis
Authors: Kay Jonathan , Benson Carol B. , Lester Susan , Corson Joseph M. , Pinkus Geraldine S. , Michael Lazarus J. , Owen William F. 
Published: February 2007

AbstractObjective. To evaluate the utility of real‐time, high‐resolution ultrasound of the shoulder in the diagnosis of dialysis‐related amyloidosis.Methods. We performed a case series study of 2 groups of patients seen at a referral‐based clinic in a tertiary care hospital. The shoulders of 13 patients with normal renal function and of 38 patients receiving long‐term hemodialysis were studied by real‐time, high‐resolution ultrasound. All hemodialysis patients were evaluated clinically for the presence of dialysis‐related amyloidosis. Surgical specimens of joints were available for all 13 patients with normal renal function and for 17 of the 38 hemodialysis patients. These specimens were evaluated for the presence of β2‐microglobulin (β2m) amyloid by Congo red and immunohistochemical staining.Results. Two ultrasonographic findings were selectively observed in the dialysis patients with clinical and histologic evidence of β2m amyloid in comparison with patients with normal renal function and no evidence of amyloid: rotator cuffs >8 mm in thickness and echogenic pads between muscle groups of the rotator cuff. The presence of at least 1 of these 2 findings corresponded to the presence of clinically and histologically evident β2m amyloid with a sensitivity of 79% and a specificity of 100%. When additional patients without surgical specimens for histologic confirmation of amyloidosis were included, the sensitivity of these 2 sonographic findings was 72% and the specificity was 97%.Conclusion. Real‐time, high‐resolution ultrasound is a relatively sensitive and highly specific noninvasive adjunct to the clinical diagnosis of β2m amyloidosis in patients receiving long‐term hemodialysis.
Anti–interleukin‐6 autoantibodies in rheumatic diseases
Authors: Takemura Hiroyuki , Suzuki Hiroshi , Yoshizaki Kazuyuki , Ogata Atsushi , Yuhara Takamichi , Akama Takao , Yamane Kazuhide , Kashiwagi Heihachiro 
Published: February 2007

AbstractObjective. To investigate the presence and the roles of anti–interleukin‐6 (anti–IL‐6) autoantibodies in rheumatic diseases, and to further elucidate clinical and pathophysiologic significance of anticytokine autoantibodies.Methods. Anti–IL‐6 IgG autoantibodies were measured by the 125I–IL‐6 binding activity of IgG, which was isolated from serum by protein A–Sepharose.Results. Nine of 52 sera (17.3%) from patients with systemic sclerosis (SSc) contained anti–IL‐6 antibodies, whereas only 1.9% of sera from normal subjects and 0–5% of sera from patients with other rheumatic diseases were positive for the antibodies. Moreover, anti–IL‐6 autoantibodies were found predominantly among patients with the limited form of SSc (42.9%), compared with those with the diffuse form (7.9%).Conclusion. Anti–IL‐6 IgG autoantibodies were detected in patients with SSc, particularly those with the limited form of the disease, at a significantly increased frequency compared with normal subjects and patients with other rheumatic diseases. These results suggest that the development of anti–IL‐6 autoantibodies and IL‐6 may have a role in the pathophysiology of SSc.
Anti–Ro/SS‐A and Anti–La/SS‐B autoantibody levels in relation to systemic lupus erythematosus disease activity and congenital heart block
Authors: Derksen Ronald H. W. M. , Meilof Jan F. 
Published: February 2007

AbstractObjective. To analyze the anti–Ro/SS‐A and anti–La/SS‐B autoantibody responses, both quantitatively and qualitatively, in relation to the occurrence of congenital heart block (CHB) and disease activity in a patient with systemic lupus erythematosus.Methods. The patient's course was carefully documented for a period of 80 months. Specific enzyme‐linked immunosorbent assays, a HeLa cell immunoblotting test, and an RNA precipitation assay were used to determine autoantibody levels and fine specificities.Results. Anti–Ro/SS‐A and anti–La/SS‐B antibody did not disappear. Levels of anti–Ro/SS‐A appeared to fluctuate more frequently than levels of anti–La/SS‐B. Fluctuations were unrelated to disease activity or immunosuppressive treatment. There was no characteristic relationship between levels of these antibodies and the occurrence of CHB.Conclusion. The occurrence of CHB cannot be predicted by frequent measurement of anti–Ro/SS‐A and anti–La/SS‐B levels. The immunoregulatory control of anti–Ro/SS‐A and anti–La/SS‐B antibodies differs from that of anti‐DNA and anti–tetanus toxoid antibodies.