bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cytokine messenger rna expression in the labial salivary glands of patients with Sjögren's syndrome
Authors: Ohyama Yukiko , Nakamura Seiji , Matsuzaki Goro , Shinohara Masanori , Hiroki Akiko , Fujimura Takao , Yamada Akira , Itoh Kyogo , Nomoto Kikuo 
Published: February 2007

AbstractObjective: To characterize the initiation and progress of localized autoimmune damage in Sjögren's syndrome (SS), an autoimmune disease that is also considered to be a lymphoaggressive disorder, by examining the pattern of cytokine production at the site of autoimmune damage.Methods. Using a polymerase chain reaction–based method, cytokine messenger RNA (mRNA) expression in the labial salivary glands of 15 patients with SS was investigated. In addition, the infiltrating lymphocytes in the labial salivary glands were examined immunohistochemically.Results. Messenger RNAs of Th1 cytokines, such as interleukin‐2 (IL‐2) and interferon‐γ, were consistently detected in all patients, while Th2 cytokine mRNAs, such as IL‐4 and IL‐5, were detected in some cases, in association with strong B cell accumulation in the labial salivary glands. Other cytokine mRNAs produced by a variety of cell types, including ILIO, IL‐6, and transforming growth factor β (TGFβ), were also consistently detected in all patients, while IL‐12 mRNA was detected in some of the patients.Conclusion. These results suggest that Th1 cytokines, as well as IL‐10, IL‐6, and TGFβ, are essential in the induction and/or maintenance of SS, while Th2 cytokines are involved in the progression of the disease process, especially local B cell activation.
Juvenile rheumatoid arthritis in rochester, minnesota 1960–1993. Is the epidemiology changing?
Authors: Peterson Lynne S. , Mason Tom , Nelson Audrey M. , O'Fallon W. Michael , Gabriel Sherine E. 
Published: February 2007

AbstractObjective. To examine trends in the incidence and prevalence of juvenile rheumatoid arthritis (JRA) in Rochester, Minnesota, over 33 years.Methods. The diagnostic retrieval system of the Rochester Epidemiology Project was utilized to screen medical records of all Rochester residents with any potential diagnoses of JRA from 1978 to 1993 (based on the American College of Rheumatology 1977 revised criteria). In addition, all cases of JRA from our previously identified cohort from 1960–1979 were verified, and the 2 data sets were combined, resulting in an incidence cohort spanning 33 years (1960–1993).Results. Of the 1,240 medical records screened, we identified 65 cases of JRA diagnosed between 1960 and 1993 (48 females, 17 males). The average followup for cases was 12.7 years (range 0–34 years) for a total of 833 person‐years of observation. A bimodal distribution of age at diagnosis was observed, with peaks between 0 and 4 years and 9 and 15 years. Seventy‐two percent of patients had pauciarticular‐onset, 17% had polyarticular‐onset, and 11% had systemic‐onset disease. Progression of pauciarticular to polyarticular disease occurred in 11% of the cases. The overall age‐ and sex‐adjusted incidence rate was 11.7 per 100,000 population (95% confidence intervals 8.7, 14.8). The incidence rate per 100,000 population was 15.0, 14.1, and 7.8 for the time periods 1960–1969, 1970–1979, and 1980–1993, respectively (P = 0.024). A 3‐year, centered, moving average, which was used to display time trends in incidence, suggested a cyclical pattern, with incidence peaks in 1967, 1975, and 1987.Conclusion. An overall decrease in the incidence rate over the last decade was observed, most marked in the pauciarticular‐ and systemic‐onset subtypes. This decrease, along with the observed cyclical pattern, suggest that environmental factors may influence disease frequency.
Which is the active moiety of sulfasalazine in ankylosing spondylitis? A randomized, controlled study
Authors: Taggart Allister , Gardiner Philip , McEvoy Frances , Hopkins Robbie , Bird Howard 
Published: February 2007

AbstractObjective. To compare the efficacy of sulfasalazine (SSZ) with its two moieties, 5‐aminosalicylic acid (ASA) and sulfapyridine (SP), in patients with active ankylosing spondylitis (AS).Methods. A 26‐week randomized, observer‐blinded, 2‐center, controlled study of treatment with either SSZ, ASA, or SP was conducted in 90 patients with active AS. Patients were evaluated at baseline and at monthly intervals, using several clinical and laboratory measures of disease activity. A global assessment of treatment efficacy was made by both patients and observers at the end of the study period.Results. There were no significant changes in any of the parameters of disease activity in the ASA treatment group. Levels of serum IgG, IgA, and IgM fell significantly during treatment with SP, but none of the other changes reached statistical significance. Plasma viscosity and IgG and IgA levels fell significantly during treatment with SSZ, as did nocturnal spinal pain and overall spinal pain. Patients and observers reported a favorable outcome after treatment with SSZ or SP significantly more often than with ASA treatment.Conclusion. SP appears to be the active moiety in AS, although there was a trend suggesting a better outcome in the SSZ group compared with the SP group, perhaps suggesting the importance of a common sulfonamide structure for efficacy.
Computed tomography of the knee joint as an indicator of intraarticular tophi in gout
Authors: Gerster Jean C. , Landry Michel , Duvoisin Bertrand , Rappoport Georges 
Published: February 2007

AbstractObjective. To evaluate the utility of computed tomography (CT) of the knee joint for detecting intraarticular tophaceous deposits.Methods. A prospective study of 16 patients with gout affecting the knee was conducted. A condition for inclusion in the study was the presence of needle‐shaped crystals with negative birefringence in the knee joint synovial fluid. Conventional radiography and CT were performed in each case.Results. Intraarticular opacities in the capsule and the synovium, consistent with the presence of tophaceous deposits, were found in 5 of the 16 patients (9 knee joints). The mean duration of gout was longer in the patients with intraarticular tophi than in those without tophi, and 2 of the patients with tophi had poor tolerance to antihyperuricemic therapy.Conclusion. Intraarticular opacities considered to represent tophi were observed in approximately one‐third of the patients. The presence of tophi correlated with a longer duration of the disease and a poor tolerance to medication. We therefore suggest that CT of the knees could be useful in the assessment and followup of certain patients with gout.
Antibodies to β2‐glycoprotein I and clinical manifestations in patients with systemic lupus erythematosus
Authors: Tsutsumi Akito , Matsuura Eiji , Ichikawa Kenji , Fujisaku Atsushi , Mukai Masaya , Kobayashi Seiichi , Koike Takao 
Published: February 2007

AbstractObjective. To investigate whether anticardiolipin antibodies (aCL) in patients with systemic lupus erythematosus (SLE) bind to β2‐glycoprotein I (β2GPI), and to search for a relationship between the presence of IgG and/or IgM anti‐β2GPI antibody and clinical manifestations in SLE patients.Methods. IgG and IgM anti‐β2GPI in 308 Japanese SLE patients were measured using phospholipid‐independent enzyme immunoassays. Relationships to clinical histories and to various laboratory data were examined.Results. The values of anti‐β2GPI and aCL, as measured by conventional enzyme immunoassay, showed a strong correlation, but the anti‐β2GPI assay was more useful in distinguishing β2GPI‐dependent aCL from β2GPI‐independent aCL. The presence of IgG anti‐β2GPI was associated with an increased frequency of a history of thrombosis. Comparisons of various laboratory data suggested that the titer of anti‐β2GPI may fluctuate with disease activity.Conclusion. The results suggest that pathogenic aCL is directed against structurally altered β2GPI and that enzyme immunoassay for anti‐β2GPI may prove useful in evaluating the risk of thrombosis and monitoring the clinical course in patients with SLE.
Renal biopsy findings and followup of renal function in rheumatoid arthritis patients treated with cyclosporin A. An update from the international kidney biopsy registry
Authors: Rodríguez F. , Krayenbühl J. C. , Harrison W. B. , Førre Ø. , Dijkmans B. A. C. , Tugwell P. , Miescher P. A. , Mihatsch M. J. 
Published: February 2007

AbstractObjective. To review data from the International Kidney Biopsy Registry, which describes the occurrence of cyclosporin A (CSA)–induced nephropathy, and to discuss the potential risk factors for its development.Methods. The report examines data on a total of 60 first and 14 second renal biopsies performed in rheumatoid arthritis (RA) patients treated with CSA for up to 87 months.Results. Five of the 60 patients with RA included in the Biopsy Registry had findings consistent with CSA‐induced nephropathy at first biopsy. One further patient had such findings at second biopsy. Of the 22 patients who started CSA at dosages < 4 mg/kg/day and subsequently received dosages no higher than 5 mg/kg/day, none developed CSA‐induced nephropathy. Continuous assessment of renal function did not show any evidence of deterioration over time in patients maintained on low‐dose CSA.Conclusion. The data indicate that in RA patients being treated according to current dosing recommendations, the risk of developing CSA‐induced nephropathy is low.
Interrelationship of major histocompatibility complex class II alleles and autoantibodies in four ethnic groups with various forms of myositis
Authors: Arnett Frank C. , Targoff Ira N. , Mimori Tsuneyo , Goldstein Rose , Warner Noranna B. , Reveille John D. 
Published: February 2007

AbstractObjective. To examine interrelationships among myositis subsets, autoantibodies, and major histocompatibility complex (MHC) class II alleles across ethnic lines, and to localize genetic susceptibility (presence of HLA–DR versus DQ) to myositis within the MHC class II region.Methods. MHC class II alleles (HLA–DRB1, DQA1, and DQB1, detected by DNA oligotyping) and myositis‐specific autoantibodies (MSA) were determined in 224 patients with various myositis syndromes, including 89 whites, 89 African‐Americans, 25 Mexican‐Americans, and 21 Japanese.Results. Anti–Jo‐1 (histidyl–transfer RNA [tRNA] synthetase) and other MSAs (anti–PL‐12, anti–PL‐7, anti‐OJ, anti‐EJ, anti‐KJ, anti‐tRNA, and anti–signal recognition particle) were equally distributed among the races, but occurred more often in patients with polymyositis (PM) than in those with dermatomyositis (DM) or other myositis syndromes. MSA frequencies were significantly positively associated with anti–Ro (SS‐A) (P = 0.002), and significantly negatively associated with anti–U1 RNP (P = 0.003). Frequencies of the HLA–DRB1*0301 (DR3), DQA1*0501, and DQB1*0201 (DQ2) alleles (and haplotype) were each increased in white patients with myositis, especially those with PM, but most strikingly in those with MSAs. However, in the other ethnic groups, except the Japanese group, only frequencies of HLA–DQA1*0501 and the structurally similar DQA1*0401 alleles were significantly increased. The presence of HLA–DQA1*0501 or *0401 was most significantly associated with anti–Jo‐1, anti–PL‐12, and other MSAs, compared with myositis patients without MSAs (P = 0.0008, Pcorr = 0.01, odds ratio [OR] = 3.7), and with normal, ethnically matched controls (P = 3 × 10−7, Pcorr = 1 × 10−6, OR = 6.5). Among MSA‐positive patients who were negative for HLA–DQA1*0501 and *0401, including Japanese patients, the HLA–DQA1*0101 and *0103 alleles predominated. In addition, there appeared to be a negative association of the HLA–DR2 alleles (DRB1*1501 and *1503) with PM (P = 0.007, Pcorr not significant, OR = 0.39), but not with DM or myositis overall.Conclusion. By transracial gene mapping, genetic susceptibility to anti–Jo‐1 and other MSAs in patients with myositis can be localized within the MHC region to the HLA–DQA1 locus.
Treatment of psoriatic arthritis with extracorporeal photochemotherapy and conventional psoralen–ultraviolet A irradiation
Authors: Vahlquist Carin , Larsson Marianne , Ernerudh Jan , Berlin Gösta , Skogh Thomas , Vahlquist Anders 
Published: February 2007

AbstractObjective. To study the use of combined photopheresis and psoralen–ultraviolet A irradiation (PUVA) in the treatment of psoriatic arthritis.Methods. Eight patients with psoriasis and sero‐negative arthritis received photopheresis for 12 weeks, followed by photopheresis plus PUVA for another 12 weeks. Clinical and laboratory examinations were performed every 3 months for up to 1 year after therapy.Results. Four patients experienced a marked improvement of joint symptoms that lasted for ≥12 months post‐therapy (74% decrease in the Ritchie articular index; P < 0.01). Prior to therapy, these patients had a higher CD4:CD8 ratio than the poor responders. Only minor laboratory changes occurred.Conclusion. A more extensive trial of photopheresis plus PUVA in psoriatic arthritis is warranted.
Chronic arthropathy and musculoskeletal symptoms associated with rubella vaccines. A review of 124 claims submitted to the national vaccine injury compensation program
Authors: Weibel Robert E. , Benor David E. 
Published: February 2007

AbstractObjective. To report the outcome of 124 claims of chronic arthropathy associated with rubella vaccine submitted to the National Vaccine Injury Compensation Program.Methods. Medical records and testimony were reviewed separately by physicians and Special Masters to determine the clinical diagnosis and eligibility for compensation under the Program.Results. Among the 124 subjects with chronic arthropathy, the onset occurred between 1 week and 6 weeks after the rubella vaccination in 72, and <1 week or >6 weeks after the vaccination in 52. Various conditions developed in the 2 onset groups (1–6 weeks postvaccination, <1 week or >6 weeks postvaccination), including, respectively, unspecified arthritis (n = 29, n = 1), specified arthritis (n = 11, n = 19), arthralgia (n = 24, n = 7), fibromyalgia (n = 4, n = 11), and multiple symptoms with minimal arthralgia or myalgia (n = 4, n = 14). Concordance of medical recommendations by Program physicians and Special Masters' decisions in 56 completed claims was 91%, with awards mainly to patients with chronic unspecified arthritis and arthralgia.Conclusion. The Program and the US Court of Federal Claims have accepted a causal relationship between currently used rubella vaccine in the US and some chronic arthropathy with an onset between 1 week and 6 weeks after vaccine administration.
The spindle kinesin‐like protein HsEg5 is an autoantigen in systemic lupus erythematosus
Authors: Whitehead Clark M. , Winkfein Robert J. , Fritzler Marvin J. , Rattner J. B. 
Published: February 2007

AbstractObjective. Autoantibodies directed against the mitotic spindle apparatus (MSA) have been shown to target an antigen referred to as NuMA (nuclear mitotic apparatus). In this study, we identified a second MSA antigen as the spindle kinesin‐like protein HsEg5. We studied the frequency of antibodies to HsEg5 in human sera that demonstrate the MSA pattern of staining, the frequency of autoantibodies to HsEg5 in patients with systemic lupus erythematosus (SLE), and the clinical features of patients with antibodies to HsEg5.Methods. A prototype serum from an SLE patient was used to isolate a 4.8‐kilobase complementary DNA (cDNA) from a HeLa cDNA library. Western blot, immunoprecipitation, and sequence analysis revealed that the antigen was an ∼130‐kd protein, HsEg5. The frequency of autoantibodies to recombinant HsEg5 in 51 sera that demonstrated an MSA pattern of staining on HEp‐2 and HeLa cells was detected by immunoblotting 2 constructs of the cDNA. The clinical features of patients with antibodies directed against HsEg5 was obtained by retrospective chart review.Results. The antigen responsible for the MSA‐35 pattern was identified as the human kinesin‐like protein HsEg5. Seven of 51 sera (14%) that demonstrated an MSA pattern of staining reacted with recombinant HsEg5. Six of 7 of the HsEg5‐positive patients (86%) had SLE, and 1 had Sjögren's syndrome. The indirect immunofluorescent staining pattern of sera that reacted with HsEg5 could be distinguished from the other sera that reacted with NuMA. In an unselected cohort of 52 SLE patients, 3 (6%) had autoantibodies reactive with the recombinant HsEg5.Conclusion. Autoantibodies to MSA fall into 2 major classes: those reactive with NuMA and those reactive with HsEg5. Autoantibodies to HsEg5 are found in a lower frequency than NuMA in sera that demonstrate the MSA pattern of staining and appear to be specifically associated with SLE. HsEg5 can be distinguished from NuMA by indirect immunofluorescence and Western blotting.
Two major autoantigen—Antibody systems of the mitotic spindle apparatus
Authors: Andrade Luis E. C. , Chan Edward K. L. , Peebles Carol L. , Tan Eng M. 
Published: February 2007

AbstractObjective. To characterize human autoantigen‐antibody systems related to the mitotic poles and spindles.Methods. Thirty‐seven human sera with autoantibodies staining mitotic poles and spindles in indirect immunofluorescence (IIF) studies were further characterized by immunofluorescence on mitotic cells and by immunoblotting and immunoprecipitation. Clinical diagnoses meeting the American College of Rheumatology criteria were based on chart review and interview with the corresponding physicians.Results. Two autoantibody systems reactive with mitotic poles and spindles were defined. Type 1 nuclear mitotic apparatus (NuMA‐1) antibodies were identified in the serum of 30 patients. Interphase cells showed a fine, speckled, nuclear staining, while mitotic cells had bright staining of the rim of the centrosomes and light staining of the spindles proximal to the centrosomes. In telophase, the staining shifted from the centrosomes to the reforming nuclei. On immunoblotting, anti—NuMA‐1 sera reacted with a 210‐kd protein. The reactivity of these sera was identified (with the aid of reference antibodies) as the previously described NuMA antigen—antibody system. Clinical information was available for only 17 of the 30 patients with anti—NuMA‐1; of these, 17 (53%) had clinical and lip biopsy findings that met the criteria for Sjögren's syndrome. NuMA‐2 antibodies were found in the sera of 7 patients. Interphase cells showed no nuclear or cytoplasmic staining, but mitotic cells had brightly stained poles and spindles. At anaphase/telophase, staining shifted to the midbody and the intercellular bridge. Anti—NuMA‐2 sera immunoprecipitated a protein of 116 kd. This group of patients was more heterogeneous and had both systemic and organ‐specific autoimmune diseases.Conclusion. NuMA protein (here called NuMA‐1) and a 116‐kd protein (here called NuMA‐2) are the major targets of the autoimmune response in the mitotic apparatus, since most of the selected sera (based on IIF staining of the mitotic spindles and poles) recognized 1 of these 2 antigens.
Identification of autoantibodies to the I protein of the heterogeneous nuclear ribonucleoprotein complex in patients with systemic sclerosis
Authors: Montecucco Carlomaurizio , Caporali Roberto , Cobianchi Fabio , Biamonti Giuseppe 
Published: February 2007

AbstractObjective. To assess the presence of autoantibodies to the I protein (polypyrimidine‐tract binding protein) of the heterogeneous nuclear RNPs (hnRNP) in different connective tissue diseases. Antibodies to other hnRNP proteins (A1, A2, and B) have been previously found in patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and mixed connective tissue disease (MCTD).Methods. Sera from 101 patients with various connective tissue diseases and 25 normal controls were investigated by enzyme‐linked immunosorbent assay and immunoblotting, for their reactivity to highly purified recombinant hnRNP I. Moreover, reactivity to cellular hnRNP I protein was investigated by immunoblotting using a partially purified preparation of hnRNP proteins (including A1, A2, B, and I), and by indirect immunofluorescence. For the analysis of the fluorescence pattern, affinity‐purified antibodies to hnRNP I, obtained from a selected patient, were tested on HEp‐2 cells.Results. By immunoblotting, antibodies reacting to recombinant hnRNP I were found in 22 of 40 patients with systemic sclerosis (SSc), 3 of 32 with RA, 0 of 23 with SLE, and 0 of 6 with MCTD. Antibodies to recombinant hnRNP I were more frequently found in patients with pre‐SSc or limited SSc (15 of 24) than in those with intermediate or diffuse SSc (7 of 16). In indirect immunofluorescence studies, affinity‐purified anti—hnRNP I autoantibodies gave a diffuse nucleoplasmic staining. Using an hnRNP preparation from nuclear extracts, anti—hnRNP I reactivity was detectable in SSc sera, while it was not detectable in RA, SLE, and MCTD sera reacting with hnRNP A/B proteins.Conclusion. Human autoimmune sera show distinct patterns of anti‐hnRNP reactivity, i.e., anti‐A/B in SLE and RA sera, and anti‐I in SSc sera. This suggests that A/B proteins and the I protein may be involved in different dynamic hnRNP complexes that elicit different autoimmune responses. From a clinical perspective, anti—hnRNP I antibodies are frequently associated with pre‐SSc features, suggesting an early appearance of these antibodies during the course of the disease.
Adherence of synovial cells on EDA‐containing fibronectin
Authors: Hino Kazuo , Maeda Toshinaga , Sekiguchi Kiyotoshi , Shiozawa Kazuko , Hirano Hisanobu , Sakashita Eiji , Shiozawa Shunichi 
Published: February 2007

AbstractObjective. To investigate the role of EDA‐containing fibronectin (EDA+ FN), a splice variant of FN detectable in association with cellular transformation, in the adherence of synovial cells (SC) on rheumatoid cartilage surface.Methods. The number of SC adherent on cartilage slices or on culture plates containing either EDA+ FN or plasma FN (pFN) was enumerated under a phase‐contrast microscope. The portion of the FN molecule responsible for adherence of SC onto EDA+ FN was investigated by inhibition studies using antibodies or peptide fragments.Results. SC adhered more strongly on the surfaces containing EDA+ FN than on those containing pFN (P < 0.01). When monoclonal antibodies against the EDA or the carboxyl‐terminal heparin‐binding (Hep2) domains were used, adhesion of SC onto EDA+ FN was reduced to a level comparable with that onto pFN. FN fragments containing Hep2 or heparan sulfate inhibited the adhesion of SC onto EDA+ FN. Treatment of SC with heparitinase, but not heparinase, reduced the adhesion of SC onto EDA+ FN.Conclusion. EDA+ FN enhances adherence of SC on the matrix via the Hep2 region of EDA+ FN.