bluuebunny/crossref_metadata_2025_split huggingface dataset:
Relationship between biochemical markers of bone turnover and bone scintigraphic indices in assessment of Paget's disease activity
Authors: Alvarez Luisa , Peris Pilar , Pons Francisca , Guañabens Nuria , Herranz Ramón , Monegal Ana , Bedini José L. , Deulofeu Ramón , De Osaba M. Jesús Martínez , Munoz‐Gómez José , Ballesta Antonio M. 
Published: February 2007

AbstractObjective. To evaluate the relationship between biochemical markers of bone turnover and bone scan indices of disease activity, as well as to analyze their variations based on skeletal involvement, in Paget's disease.Methods. Serum samples were obtained from 51 patients with Paget's disease to determine the levels of total alkaline phosphatase (total AP), bone alkaline phosphatase (bone AP), propeptide carboxyterminal of type I procollagen (PICP), propeptide aminoterminal of type I procollagen (PINP), osteocalcin, tartrate‐resistant acid phosphatase, and telopeptide carboxyterminal of type I collagen. Urine samples were analyzed for levels of hydroxyproline (HYP), pyridinoline (PYR), deoxypyridinoline (DPYR), C‐terminal telopeptide of type I collagen (CTx), and N‐terminal telopeptide of type I collagen (NTx). In addition, 2 semiquantitative scintigraphic indices, disease activity (AI) and disease extent (EI), were obtained. Pagetic skeletal locations were evaluated individually, with special attention to skull involvement.Results. All biochemical markers correlated with the AI and the EI. Serum PINP, bone AP, and total AP showed the highest proportions of increased values among the bone formation markers (94%, 82%, and 76%, respectively). Among the bone resorption markers, urinary NTx showed the highest proportion of increased values in patients with Paget's disease (96%), compared with PYR (69%), DPYR (71%), CTx (65%), and HYP (64%). In patients with mild disease activity, serum PINP was the marker with the highest proportion of increased values (71%). In contrast, serum PICP and urinary CTx were the most discriminative markers for skull involvement. Except for higher values for most of the biochemical markers of bone turnover in flat bones, no major differences in other skeletal locations were observed.Conclusion. The determination of serum PINP as a marker of bone formation and urinary NTx as a marker of bone resorption provided the best biochemical profile to ascertain the extent and activity of Paget's disease. In patients with skull involvement, serum PICP and urinary CTx were shown to be the most discriminative markers.
Macrophage cathepsin L, a factor in the erosion of subchondral bone in rheumatoid arthritis
Authors: Iwata Yasuo , Mort John S. , Tateishi Hiroomi , Lee Eunice R. 
Published: February 2007

AbstractObjective. To test the hypothesis that the proteinase cathepsin L is involved in the subchondral bone lesions found in chronic rheumatoid arthritis (RA).Methods. The medial tibial plateaus from 4 control cases and 30 patients diagnosed as having end‐stage RA were examined immunochemically for cathepsin L.Results. RA lesions include large groups of mononuclear cells, many of which are rich in cathepsin L. Since these mononuclear cells contained the CD68 glycoprotein and, in the electron microscope, displayed an irregular cell surface, cytoplasmic vacuoles, lysosomes, and phagosomes, they were identified as belonging to the macrophage family. The lesions were classified into 2 main patterns, both displaying these cathepsin L—rich cells, which, in at least 1 of the 2, were closely associated with bone degradation.Conclusion. The cathepsin L—rich macrophages are sufficiently numerous to be considered a major factor in producing the erosion of subchondral bone found in chronic RA lesions.
Chronic meningitis with cranial neuropathies in Wegener's granulomatosis. Case report and review of the literature
Authors: Jinnah H. A. , Dixon Anne , Brat Daniel J. , Hellmann David B. 
Published: February 2007

AbstractWe report the case of a 41‐year‐old man with chronic meningitis and cranial neuropathies in whom leptomeningeal biopsy demonstrated Wegener's granu‐lomatosis. The literature on meningitis in this disease is reviewed. This case illustrates that Wegener's granulo‐matosis can cause chronic meningitis.
Immunogenetic similarities between patients with Felty's syndrome and those with clonal expansions of large granular lymphocytes in rheumatoid arthritis
Authors: Starkebaum Gordon , Loughran Thomas P. , Gaur Lakshmi K. , Davis Paul , Nepom Barbara S. 
Published: February 2007

AbstractObjective. Patients with chronic clonal proliferation of large granular lymphocytes (LGL leukemia) often have splenomegaly, neutropenia, and rheumatoid arthritis (RA), thereby resembling the manifestations observed in patients with Felty's syndrome. The present study sought to determine whether patients with these disorders represent 2 distinct subsets of neutropenic RA.Methods. Prospective cohort study of outpatients attending clinics in university and private hospitals and in offices of private practice physicians. Twenty‐two patients with Felty's syndrome and 22 patients with LGL leukemia, 10 of whom had RA, were studied. HLA genotyping was performed on peripheral blood mononuclear leukocyte genomic DNA.Results. Nineteen of the 22 patients with Felty's syndrome (86%) were DR4 positive. Nine of the 10 patients with LGL leukemia plus RA were also DR4 positive. In contrast, only 4 of the 12 patients with LGL leukemia without RA (33%) were DR4 positive, a frequency that was within the normal range.Conclusion. The finding of an equally high prevalence of DR4 in patients with Felty's syndrome and in those with LGL leukemia plus RA suggests that both disorders have a similar immunogenetic basis and are parts of a single disease process rather than 2 separate disorders.
Past use of oral contraceptives and the risk of developing systemic lupus erythematosus
Authors: Sanchez‐Guerrero Jorge , Karlson Elizabeth W. , Liang Matthew H. , Hunter David J. , Speizer Frank E. , Colditz Graham A. 
Published: February 2007

AbstractObjective. To examine the relationship between past use of oral contraceptives (OCs) and development of systemic lupus erythematosus (SLE).Methods. Prospective cohort study of 121,645 women who were followed up every 2 years between 1976 and 1990 as part of the Nurses' Health Study. Women were classified as never users or past users of OCs based on self‐report. Incidence of SLE was defined by 1) strict American College of Rheumatology (ACR) classification criteria (⩾4 ACR criteria), 2) ⩾4 ACR criteria and any physician's diagnosis, 3) ⩾4 ACR criteria and diagnosis by an ACR‐certified rheumatologist, 4) ⩾3 ACR criteria, or 5) diagnosis by a physician even if the patient did not meet the ACR criteria.Results. Compared with never users of OCs, and after adjusting for age and ever use of postmenopausal hormones, the relative risk (95% confidence interval [95% CI]) for the incidence of SLE in the women who had definite cases of SLE (⩾4 ACR criteria) (n = 99) was 1.4 (0.9–2.1) for past users of OCs. Using the most stringent case definition (ACR criteria plus a diagnosis of SLE by an ACR member) (n = 58), the relative risk for past users compared with never users was 1.9 (95% CI 1.1–3.3). No relationship was observed between duration of OC use or time since first use and the risk of developing SLE.Conclusion. Past use of OCs was associated with a slightly increased risk of developing SLE. The decision to use hormonal contraception must be individualized, but the small absolute risk observed for the development of SLE in white women should not be a dominant factor in the decision.
Decreased T cell response to anti‐CD2 in systemic lupus erythematosus and reversal by anti‐CD28. Evidence for Impaired T Cell‐Accessory Cell Interaction
Authors: Horwitz David A. , Tang Fu Lin , Stimmler Mary M. , Oki Alan , Gray J. Dixon 
Published: February 2007

AbstractObjective. To assess the ability of T cells from patients with systemic lupus erythematosus (SLE) to respond to a mitogenic combination of anti‐CD2 monoclonal antibodies (MAb), and to learn the molecular basis of the documented defect.Methods. Peripheral blood mononuclear cell (PBMC) populations from individuals with SLE and paired controls were stimulated in vitro with anti‐CD2, and the proliferative response was compared with that evoked by stimulation with phytohemagglutinin (PHA) and anti‐CD3. Surface markers on lymphocyte populations were assessed by flow cytometry after staining with specific MAb.Results. The proliferative response to anti‐CD2 was decreased to a greater extent than was the response to anti‐CD3 or PHA in SLE patients. This defect was found in approximately one‐half of the patients examined, was not associated with disease activity, and was maintained upon repeated testing. Since either mono‐cytes or resting B cells can serve as accessory cells for T cells following activation by anti‐CD2, we examined the T cell response after depletion of adherent cells. In approximately two‐thirds of the individuals with a decreased response, depletion of monocytes or substitution of monocytes with allogeneic, resting B cells from normal donors corrected the defect. The addition to PBMC of anti‐CD28, but not of a neutralizing antibody to interleukin‐10, largely reversed the anti‐CD2 proliferative defect. Significantly fewer CD8+ T cells expressed CD28 in SLE, and this defect was also documented, to a lesser extent, in CD4+ cells.Conclusion. This study provides evidence that some functional T cell defects in SLE may be due, at least in part, to decreased CD28‐mediated costimula‐tory activity following the interaction of T cells with conventional accessory cells.
Prevention of murine collagen‐induced arthritis in the knee and ipsilateral paw by local expression of human interleukin‐1 receptor antagonist protein in the knee
Authors: Bakker Andrew C. , Joosten Leo A. B. , Arntz Onno J. , Helsen Monique M. A. , Bendele Alison M. , van de Loo Fons A. J. , van den Berg Wim B. 
Published: February 2007

AbstractObjective. To determine the efficacy of local human interleukin‐1 receptor antagonist (HuIL‐1Ra) gene therapy in murine collagen‐induced arthritis (CIA).Methods. DBA/1 mice were immunized against bovine type II collagen. Before the onset of arthritis, NIH/3T3 fibroblasts transfected with pMFG‐IRAP were transplanted into the knee cavity. Normal NIH/3T3 cells served as controls. Paws were evaluated macroscopically for redness, swelling, and deformities during the course of arthritis. Swelling of the knee joints was measured by external gamma counting of 99mtechnetium accumulation in the joint. Paws and knee joints were dissected and processed for histologic studies to evaluate inflammation and cartilage destruction.Results. The NIH/3T3 fibroblasts survived in the joint cavity of DBA mice for at least 7 days. The transduced cells expressed immunoreactive and bioactive HuIL‐1Ra in the knee joint, and produced sufficient amounts to block the effect of 1 ng of recombinant murine IL‐1α on chondrocyte proteoglycan synthesis. The onset of CIA was almost completely prevented in knee joints containing HuIL‐1Ra‐producing cells, whereas joints containing normal cells showed severe inflammation and destruction of cartilage. Moreover, onset of CIA in the draining joints (ipsilateral paws) of the HuIL‐1Ra gene‐bearing knees was also prevented.Conclusion. Local production of HuIL‐1Ra in the knee was able to ameliorate the effects of IL‐1 on cartilage and could prevent the onset of CIA not only in that knee, but also in the “draining” paw. This indicates the feasibility of gene transfer as a therapeutic approach to modulating arthritis.
Acute calcific tendinitis of the hip. Case report with magnetic resonance imaging findings
Authors: Chow Henry Y. , Recht Michael P. , Schils Jean , Calabrese Leonard H. 
Published: February 2007

AbstractThe clinical presentation of acute calcific tendinitis can be quite dramatic. This report describes a patient with this entity who had calcification in an unusual area, accompanied by abnormalities seen on radiography and magnetic resonance imaging. Clinical aspects of acute calcific tendinitis are also reviewed. With recognition of this entity, treatment can be initiated promptly, with dramatic resolution.
Bone morphogenetic protein 2 stimulates articular cartilage proteoglycan synthesis in vivo but does not counteract interleukin‐1α effects on proteoglycan synthesis and content
Authors: Glansbeek Harrie L. , van Beuningen Henk M. , Vitters Elly L. , van der Kraan Peter M. , van den Berg Wim B. , Morris Elisabeth A. 
Published: February 2007

AbstractObjective. To study the effect of bone morphogenetic protein 2 (BMP‐2) on articular cartilage proteoglycan (PG) synthesis in vivo and to investigate whether BMP‐2 is able to counteract the effects of interleukin‐1 (IL‐1) on articular cartilage PG synthesis and content.Methods. BMP‐2 alone or in combination with IL‐1α was injected into murine knee joints. PG synthesis was measured by 35S‐sulfate incorporation using an ex vivo method or autoradiography. Cartilage PG content was analyzed by measuring Safranin O staining intensity on histologic sections.Results. BMP‐2 appeared to be a potent stimulator of articular cartilage PG synthesis in vivo. However, BMP‐2 was not able to counteract the deleterious effects of IL‐1α on articular cartilage PG synthesis and content. In addition, intraarticular injections of BMP‐2 induced chondrophytes.Conclusion. Although BMP‐2 is a very potent stimulator of cartilage PG synthesis in vivo, the therapeutic applications of BMP‐2 are limited due to the inability of BMP‐2 to counteract the effects of IL‐1 and the induction of chondrophytes.
The transcriptional activator Sp1, a novel autoantigen
Authors: Spain Tammy A. , Sun Ren , Gradzka Margaret , Lin Su‐Fang , Craft Joseph , Miller George 
Published: February 2007

AbstractObjective. To identify one nuclear autoantigenic protein within a complex of DNA binding proteins that bind to GC‐rich sequences in Epstein‐Barr virus and cellular DNA, and to describe the clinical characteristics of patients whose sera contained autoantibodies to this novel autoantigen.Methods. Antibodies to autoantigen Sp1 were initially measured by an electrophoretic mobility shift assay to detect DNA binding proteins. Nuclear extracts and purified Sp1 protein were used in these assays. Recognition of the autoantigen by autoimmune sera was confirmed by immunoprecipitation and immunoblotting.Results. The autoantigen was identified as Sp1. Anti‐Sp1 was detected in sera from 8 (3%) of 230 patients. These sera contained antinuclear antibodies, but lacked antibodies to double‐stranded DNA or to several extractable nuclear antigens. The patients whose sera contained antibodies to Sp1 were white women with fatigue, arthritis, Raynaud's phenomenon, malar rash, and photosensitivity.Conclusion. Sp1 is the first described example of an RNA polymerase II transcription activator as an autoantigen. The presence of Sp1 autoantibodies is associated with undifferentiated connective tissue disease.
Human cartilage glycoprotein‐39 as a candidate autoantigen in rheumatoid arthritis
Authors: Verheijden Gijs F. M. , Rijnders Antonius W. M. , Bos Ebo , Coenen‐De Roo Christina J. J. , van Staveren Catherina J. , Miltenburg André M. M. , Meijerink Jan H. , Elewaut Dirk , de Keyser Filip , Veys Eric , Boots Annemieke M. H. 
Published: February 2007

AbstractObjective. To identify a cartilage‐derived autoantigen that is relevant to the rheumatoid arthritis (RA) disease process.Methods. A DR4 (DRB1*0401) peptide binding motif was used for the selection of potential self reactive peptides within human cartilage glycoprotein‐39 (HC gp‐39), a protein that is differentially expressed at the site of chronic inflammation. Synthetic peptides accommodating the motif were tested for binding the RA‐associated DR4 (DRB1*0401) molecules. High‐affinity binders were then tested for their capacity to stimulate peripheral blood mononuclear cell responses in RA patients or healthy donors. To assess the arthritogenic nature of native HC gp‐39, the protein was injected into BALB/c mice.Results. HC gp‐39‐derived motif‐based peptides were selectively recognized by peripheral blood T cells from RA patients. Injection of the intact protein into BALB/c mice resulted in immunity to HC gp‐39, which was found to be associated with the development of a chronic, relapsing arthritis. Moreover, inhalation of the protein led to tolerization of antigen‐specific T cells and to suppression of HC gp‐39‐induced arthritis.Conclusion. These data indicate that HC gp‐39 is a target of the immune response in RA. Consequently, HC gp‐39 is a candidate for antigen‐specific immunotherapy.
Mycoplasma infection and rheumatoid arthritis. Analysis of their relationship using immunoblotting and an ultrasensitive polymerase chain reaction detection method
Authors: Hoffman Robert W. , O'Sullivan Frank X. , Schafermeyer Kim R. , Moore Terry L. , Roussell Deborah , Watson‐Mckown Robyn , Kim Mary F. , Wise Kim S. 
Published: February 2007

AbstractObjective. To examine the relationship between infection with Mycoplasma and the development of rheumatoid arthritis (RA) and juvenile rheumatoid arthritis (JRA).Methods. Immunoblotting of patient synovial fluid and sera on detergent‐phase membrane protein extracts of various Mycoplasma species was carried out to learn whether patients exhibited serologic evidence of previous exposure to mycoplasmas. Moreover, an ultrasensitive polymerase chain reaction (PCR) method was developed for assessing whether Mycoplasma DNA could be detected in synovial fluid from patients and controls.Results. Immunoblotting provided serologic evidence of previous Mycoplasma exposure in patients and controls. The genus‐specific PCR detected known human Mycoplasma species and could reliably detect <5 copies of Mycoplasma hominis, Mycoplasma fermentans, or a molecular mimic control in synovial fluid. Repeat testing revealed no evidence of Mycoplasma DNA in patient synovial samples.Conclusion. This study provided serologic evidence suggesting that, while previous exposure to Mycoplasma was common, there was no detectable persistence of Mycoplasma DNA in the synovial fluid or tissue of patients with RA or JRA.
Fibrosing alveolitis in systemic sclerosis. Indices of lung function in relation to extent of disease on computed tomography
Authors: Wells A. U. , Hansell D. M. , Rubens M. B. , King A. D. , Cramer D. , Black C. M. , du Bois R. M. 
Published: February 2007

AbstractObjective. Thin‐section computed tomography (CT) provides a sensitive and reproducible method of quantifying the morphologic extent of disease in the clinical management of fibrosing alveolitis associated with systemic sclerosis (FASSc). The aim of this study was to determine which indices of lung function best reflect the extent of disease on CT in FASSc, and to determine the independent influences of smoking history, extent of fibrosing alveolitis, demographic features, and concurrent treatment upon functional impairment in FASSc.Methods. Sixty‐four patients with FASSc were studied using CT and static and exercise lung function testing. Statistical relationships were determined by multiple regression analyses.Results. Five patients with overt pulmonary hypertension were characterized by severe impairment in 3 indices of lung function: diffusing capacity for carbon monoxide (DLCO), DLCO adjusted for alveolar volume (KCO), and arterial partial pressure of oxygen. On multiple regression analysis, the major determinant of functional impairment was the extent of fibrosing alveolitis on CT. A history of smoking was independently associated with preservation of total lung capacity and depression of KCO, but did not otherwise influence functional‐morphologic correlations. The percent predicted DLCO correlated better with extent of disease on CT (r = −0.70) than did oxygen desaturation on exercise (r = 0.55), the physiologic component of the clinical‐radiographic‐physiologic score (CRP index) (r = 0.52), or other indices of lung function. Lung volume measures correlated poorly with disease extent on CT.Conclusion. The percent predicted DLCO best reflects the extent of fibrosing alveolitis in FASSc, and therefore should be measured in routine evaluations. Exercise testing may also have a useful role in staging the severity of pulmonary fibrosis, but the CRP index offers no additional advantage over the DLCO and exercise testing.
Pregnancy in relapsing polychondritis. Twenty‐five pregnancies in eleven patients
Authors: Papo Thomas , Wechsler Bertrand , Bletry Olivier , Piette Anne‐Marie , Godeau Pierre , Piette Jean‐Charles 
Published: February 2007

AbstractObjective. To determine maternal and fetal outcome in pregnant women with relapsing polychondritis (RP).Methods. Retrospective review of 11 records selected from among those of 116 female RP (Michet's criteria) patients.Results. In these 11 women, 25 pregnancies occurred after or concomitantly with the onset of RP. The mean (±SD) age at RP onset was 25 ± 5 years (range 15‐31). Therapeutic abortion was performed in 1 woman because of ongoing cyclophosphamide treatment. Disease flare occurred in 7 of 24 pregnancies, requiring treatment modification in 2 cases. RP was considered stable in 16 and asymptomatic in 1 of the 24. Treatment of RP was with nonsteroidal antiinflammatory drugs (2 of 24), steroids (13 of 24), dapsone (7 of 24), or plasma exchanges (1 of 24); no treatment was given in 8 of the 24 pregnancies. In 14 pregnancies, the course was uneventful. Ten pregnancies were complicated by ectopic nidation (n = 3), spontaneous abortion (n = 3), premature birth (n = 3), and premature rupture of membranes (n = 1). Eighteen normal children were born.Conclusion. Pregnancy does not seem to modify the course of RP. Successful pregnancies may be achieved in women with RP. No RP was observed in the neonates.
The AIMS2‐SF. A short form of the arthritis impact measurement scales 2
Authors: Guillemin Francis , Coste Joel , Pouchot Jacques , Ghézail Marc , Bregeon Christian , Sany Jacques 
Published: February 2007

AbstractObjective. To develop a short form of the Arthritis Impact Measurement Scales 2 (AIMS2) questionnaire, preserving content validity as the priority criterion.Methods. A 2‐step reduction procedure was used: 1) Delphi technique, with 1 panel of patients and 1 panel of experts each selecting 1 set of items independently; and 2) nominal group technique, where members of both panels reached consensus on the final selection of items, using information derived from item analysis. Psychometric properties of the AIMS2‐Short Form (AIMS2‐SF) and AIMS2 were compared using data from a cohort of 127 rheumatoid arthritis patients who completed the AIMS2 twice prior to the initiation of methotrexate (MTX) treatment and 3 months post‐initiation of MTX treatment.Results. The 2 panels reached consensus on a 26‐item AIMS2‐SF (54.4% reduction from the AIMS2). Factor analysis showed preservation of the 5‐component structure. Convergent validity (Physical and Symptom components with clinical variables: r = 0.24‐0.59), test‐retest reproducibility (intraclass correlation coefficient >0.7), and sensitivity to change at 3 months (standardized response mean 0.36‐0.8, except Social Interaction component [0.08]) were very close to the values for the original AIMS2.Conclusion. The AIMS2‐SF is a shorter version of the AIMS2 (i.e., available in 2‐page format) and has psychometric properties similar to those of the AIMS2.