bluuebunny/crossref_metadata_2025_split huggingface dataset:
Voiding dysfunction in women with systemic lupus erythematosus
Authors: Yu Hong‐Jeng , Lee Wei‐Chia , Lee Kuang‐Lun , Chen Mao‐Yuan , Chen Cheng‐Yuan , Chen Jun 
Published: January 2004

AbstractObjectiveWe sought to explore bladder dysfunction in a cohort of women with systemic lupus erythematosus (SLE).MethodsWe conducted a prospective study of 152 female patients with SLE during a 15‐month period. The clinical status of SLE was determined according to the SLE Disease Activity Index (SLEDAI), and bladder function was evaluated by lower urinary tract symptoms and urodynamic studies. We adapted the American Urological Association (AUA) index questionnaire to assess lower urinary tract symptoms in patients, which were compared with those in 227 age‐matched healthy women.ResultsThe proportion of individuals reporting urinary frequency, urgency, weak urinary stream, and incomplete emptying, as well as severe lower urinary tract symptoms (AUA index score ≥20), was significantly higher in the SLE group when compared with the control group. The AUA index score showed a modest correlation with the SLEDAI score (r = 0.35, P < 0.001) but not with patient age or disease duration. There was a significant relationship between central nervous system involvement and the AUA index score. The most common urodynamic finding was a small cystometric bladder capacity (<150 ml; n = 7 patients), followed by a subnormal urinary flow rate (<12 ml/second; n = 6 patients). In 3 of 7 patients with small cystometric bladder capacities, imaging studies documented a contracted bladder with marked hydroureteronephrosis.ConclusionPatients with SLE experience an increased prevalence of voiding dysfunction compared with healthy individuals. Voiding dysfunction can be attributable to either direct bladder involvement or other disease‐related factors.
Expression profiling of metalloproteinases and their inhibitors in cartilage
Authors: Kevorkian Lara , Young David A. , Darrah Clare , Donell Simon T. , Shepstone Lee , Porter Sarah , Brockbank Sarah M. V. , Edwards Dylan R. , Parker Andrew E. , Clark Ian M. 
Published: January 2004

AbstractObjectiveTo profile the expression of all known members of the matrix metalloproteinase (MMP), ADAMTS, and tissue inhibitor of metalloproteinases (TIMP) gene families in normal cartilage and cartilage from patients with osteoarthritis (OA).MethodsHuman cartilage was obtained from femoral heads at joint replacement for OA or following fracture to the femoral neck. Total RNA was purified, and gene expression was assayed using quantitative real‐time polymerase chain reaction.ResultsSeveral members of the above gene families were regulated in OA. Genes that showed increased expression in OA were MMP13, MMP28, and ADAMTS16 (all at P < 0.001), MMP9, MMP16, ADAMTS2, and ADAMTS14 (all at P < 0.01), and MMP2, TIMP3, and ADAMTS12 (all at P < 0.05). Genes with decreased expression in OA were MMP1, MMP3, and ADAMTS1 (all at P < 0.001), MMP10, TIMP1, and ADAMTS9 (all at P < 0.01), and TIMP4, ADAMTS5, and ADAMTS15 (all at P < 0.05). Correlation analysis revealed that groups of genes across the gene families were coexpressed in cartilage.ConclusionThis is the first comprehensive expression profile of all known MMP, ADAMTS, and TIMP genes in cartilage. Elucidation of patterns of expression provides a foundation with which to understand mechanisms of gene regulation in OA and potentially to refine the specificity of antiproteolytic therapies.
Ovarian vein thrombosis in the antiphospholipid syndrome
Authors: André Marc , Delèvaux Isabelle , Amoura Zahir , Corbi Pierre , Courthaliac Christophe , Aumaître Olivier , Piette Jean‐Charles 
Published: January 2004

AbstractOvarian vein thrombosis (OVT) is an unusual condition mainly observed during the postpartum period. It has not been reported to date in the antiphospholipid syndrome. Two female patients with definite antiphospholipid syndrome, ages 33 years and 73 years, were diagnosed as having OVT by computed tomography (CT) scan, according to the radiologic criteria described by Zerhouni et al. In 1 of the women, the left vein was affected by OVT, while in the other woman, the right vein was affected. One of the patients had a pulmonary embolism; the diagnosis of OVT was established after she underwent a cesarean section and a right atrium thrombectomy. The other patient had no vascular manifestations. OVT was asymptomatic in both patients. Searches for associated thrombophilic states yielded negative results. With the continuation of anticoagulation therapy, the 2 patients have remained in good condition. Resolution of the OVT was observed in the patient who underwent a CT scan during followup. To our knowledge, this is the first report of OVT occurring in the antiphospholipid syndrome. Given that it may develop in the absence of pelvic clinical manifestations, this complication may be underdiagnosed.
Complex segregation and linkage analysis of familial gout in Taiwanese aborigines
Authors: Wang Wen Hsin , Chang Shun Jen , Wang Tsu Nai , Cheng Li Shu‐Chuan , Feng Yu Ping , Chen Chung Jen , Huang Chun Hsiung , Ko Ying Chin 
Published: January 2004

AbstractObjectiveThe prevalence of gout and hyperuricemia in Taiwanese aborigines is remarkably high. Although previous studies have failed to find evidence of a major gene responsible for gout, the disease is thought to involve genetic predisposition. We sought to determine whether genetic factors for familial gout exist among Taiwanese aborigines, and, if so, their chromosomal location.MethodsWe first performed complex segregation analysis. The study sample comprised 945 relatives distributed in 64 pedigrees; among them, 261 affected members (including probands) were found. In all of the aboriginal probands with gout, the disease was diagnosed and confirmed by rheumatologists. Blood specimens were then collected from 127 individuals living in one community that was used in the segregation analysis (from 25 pedigrees, 36 nuclear families, and 112 full sibpairs), and sibpair linkage analysis and a combined transmission disequilibrium test (TDT) method were used to test the genetic components.ResultsIn segregation analysis, after adjusting for sex and age, an autosomal‐arbitrary major gene model was found to fit the data best, with disease allelic frequency of 0.31 and susceptibility of 0.92. In sibpair analysis, there was a clustering of many flanking markers showing significant linkage, including D1S498 (regression coefficient −0.52), D1S2635 (regression coefficient −0.47), and D1S196 (regression coefficient −0.51), in the 1q21 region of chromosome 1 (all P < 0.005). Results of the combined TDT showed that the marker D1S484 was significantly associated (had linkage) with allele 1 and was transmitted more frequently than other markers to the affected offspring (P < 0.005).ConclusionResults of this study provide evidence of a genetic basis for familial gout in the aboriginal Taiwanese population and suggest that a susceptibility locus may be located in the 1q21 region of chromosome 1.
Prognostic markers of radiographic progression in early rheumatoid arthritis
Authors: Goronzy Jörg J. , Matteson Eric L. , Fulbright James W. , Warrington Kenneth J. , Chang‐Miller April , Hunder Gene G. , Mason Thomas G. , Nelson Audrey M. , Valente Robert M. , Crowson Cynthia S. , Erlich Henry A. , Reynolds Rebecca L. , Swee Ronald G. , O'Fallon W. Michael , Weyand Cornelia M. 
Published: January 2004

AbstractObjectiveTo identify prognostic markers that are predictive of progressive erosive disease in patients with early rheumatoid arthritis (RA).MethodsThe study involved an inception cohort of 111 consecutive patients with RA and a disease duration of <1 year. Patients were treated according to an algorithm designed to avoid overtreatment of mild disease and to accelerate treatment in patients who had continuous disease activity. Patients were evaluated for the presence of clinical and laboratory disease activity markers. We determined the frequency of CD4+,CD28null T cells by flow cytometry, HLA–DRB1 gene polymorphisms by polymerase chain reaction (PCR)/sequencing, and 26 single‐nucleotide polymorphisms in 19 candidate genes by multiplex PCR and hybridization to an immobilized probe array. Data were analyzed using proportional odds models to identify prognostic markers predictive of erosive progression over 2 years on serial hand/wrist radiographs.ResultsAfter 2 years, disease activity in 52% of the cohort was controlled by treatment with hydroxychloroquine and nonsteroidal agents. Forty‐eight percent of the patients did not develop erosions. Older age, presence of erosions at baseline, presence of rheumatoid factor, rheumatoid factor titer, and HLA–DRB1*04 alleles, particularly homozygosity for HLA–DRB1*04, were univariate predictors of radiographic progression. Promising novel markers were the frequency of CD4+,CD28null T cells as an immunosenescence indicator, and a polymorphism in the uteroglobin gene.ConclusionClinical disease activity in patients with early RA can frequently be controlled with nonaggressive treatment, but this is not always sufficient to prevent new erosions. Rheumatoid factor titer, HLA–DRB1 polymorphisms, age, and immunosenescence markers are predictors of poor radiographic outcome. A polymorphism in the uteroglobin gene may identify patients who have a low risk of erosive disease.
Emergence of lyme arthritis after autologous chondrocyte transplantation
Authors: Marlovits Stefan , Khanakah Gelas , Striessnig Gabriele , Vécsei Vilmos , Stanek Gerold 
Published: January 2004

AbstractWe report herein the first known incidence of the emergence of borrelial arthritis following autologous chondrocyte transplantation for repair of a cartilage defect. The patient had no recent manifestation of Lyme borreliosis, but 15 years earlier had had an expanding erythematous lesion after a tick bite. The current infection resulted in massive joint swelling, elevated body temperature, dissemination of the graft, and transplant failure. Results of routine bacteriologic studies were negative. A diagnosis of Lyme arthritis was first considered following the detection of Borrelia‐specific serum antibodies. Additional evidence was provided when borrelial DNA sequences were detected in the synovial fluid through polymerase chain reaction. The diagnosis was confirmed by culture of Borrelia burgdorferi from the synovial fluid. The possibility of a dormant borrelial infection should be considered in patients who undergo repair of cartilage defects with autologous chondrocyte transplantation. We recommend that synovial fluid and joint tissue be screened for the presence of viable Borrelia before transplantation of an autologous graft.
Failure of in vitro–differentiated mesenchymal stem cells from the synovial membrane to form ectopic stable cartilage in vivo
Authors: De Bari Cosimo , Dell'Accio Francesco , Luyten Frank P. 
Published: January 2004

AbstractObjectiveWe previously reported the identification in a nude mouse assay of molecular markers predictive of the capacity of articular cartilage–derived cells (ACDCs) to form ectopic stable cartilage that is resistant to vascular invasion and endochondral ossification. In the present study, we investigated whether in vitro–differentiated mesenchymal stem cells (MSCs) from the synovial membrane (SM) express the stable‐chondrocyte markers and form ectopic stable cartilage in vivo.MethodsChondrogenesis was induced in micromass culture with the addition of transforming growth factor β1 (TGFβ1). After acquisition of the cartilage phenotype, micromasses were implanted subcutaneously into nude mice. Alternatively, cells were released enzymatically and either replated in monolayer or injected intramuscularly into nude mice. Marker analysis was performed by quantitative reverse transcription–polymerase chain reaction. Cell death was detected with TUNEL assay.ResultsCartilage‐like micromasses and released cells expressed the stable‐chondrocyte markers at levels comparable with those expressed by stable ACDCs. The released cells lost chondrocyte marker expression by 24 hours in monolayer and failed to form cartilage when injected intramuscularly into nude mice. Instead, myogenic differentiation was detected. When intact TGFβ1‐treated micromasses were implanted subcutaneously, they partially lost their cartilage phenotype and underwent cell death and neoangiogenesis within 1 week. At later time points (15–40 days), we retrieved neither cartilage nor bone, and human cells were not detectable.ConclusionThe chondrocyte‐like phenotype of human SM MSCs, induced in vitro under specific conditions, appears to be unstable and is not sufficient to obtain ectopic formation of stable cartilage in vivo. Studies in animal models of joint surface defect repair are necessary to evaluate the stability of the SM MSC chondrocyte‐like phenotype within the joint environment.
High insulin levels and increased low‐density lipoprotein oxidizability in pediatric patients with systemic lupus erythematosus
Authors: Posadas‐Romero Carlos , Torres‐Tamayo Margarita , Zamora‐González José , Aguilar‐Herrera Blanca Estela , Posadas‐Sánchez Rosalinda , Cardoso‐Saldaña Guillermo , de Guevara Guadalupe Ladrón , Solis‐Vallejo Eunice , Hafidi Mohammed El 
Published: January 2004

AbstractObjectiveTo examine low‐density lipoprotein (LDL) size, LDL susceptibility to oxidation, and plasma insulin levels in children with systemic lupus erythematosus (SLE).MethodsFifty‐nine SLE patients and 59 healthy, age‐matched control subjects were studied. LDL size was determined by gradient gel electrophoresis. LDL oxidizability was assessed by lag time for conjugated diene formation during copper incubation. Plasma levels of fasting insulin, glucose, lipids, lipoproteins, apolipoproteins B and A‐I, and fatty acids were also measured.ResultsCompared with control subjects, SLE patients showed significantly higher plasma insulin levels and increased susceptibility of LDLs to oxidation. Patients with active disease were more likely than patients with inactive disease or control subjects to have the following lipid characteristics: small, dense LDL subclass, elevated total cholesterol levels, elevated LDL cholesterol levels, elevated triglyceride levels, and low levels of high‐density lipoprotein cholesterol (HDL‐C). Statistically significant direct correlations were observed between disease activity and triglyceride levels and between disease activity and lag time, whereas significant inverse correlations were found between disease activity and HDL‐C levels and between disease activity and LDL size. Prednisone dosage explained only 15.6% of the variance in insulin levels.ConclusionSLE patients have higher plasma insulin levels and increased LDL oxidizability compared with healthy control subjects. These abnormalities may contribute to the accelerated atherosclerosis observed in patients with SLE.
The transcription factors hypoxia‐inducible factor 1α and Ets‐1 colocalize in the hypoxic synovium of inflamed joints in adjuvant‐induced arthritis
Authors: Peters C. L. , Morris C. J. , Mapp P. I. , Blake D. R. , Lewis C. E. , Winrow V. R. 
Published: January 2004

AbstractObjectiveTo determine the relationship between hypoxia and the expression of Ets‐1 and hypoxia‐inducible factor 1α (HIF‐1α) in both normal and inflamed joints. Adjuvant‐induced arthritis (AIA) was used as the model system, since it mirrors many aspects of the pathology of rheumatoid arthritis.MethodsAdjuvant arthritis was induced in a group of 10 female Lewis rats. A second group of 10 uninjected female Lewis rats served as naive controls. When a maximum clinical joint score was achieved in the AIA group, all 20 rats were injected with the specific hypoxic cell marker Hypoxyprobe‐1 and subsequently killed. Hypoxyprobe‐1 adducts, Ets‐1, and HIF‐1α were localized in the joints of the hind feet from these groups using immunohistochemistry.ResultsCompared with the joints from control rats, inflamed joints contained markedly more cells with Hypoxyprobe‐1 adduct immunoreactivity, Ets‐1–immunoreactive nuclei, and nuclear immunoreactivity for both Ets‐1 and HIF‐1α.ConclusionOur results demonstrate the presence of hypoxia in inflamed joints in this experimental model of arthritis. The colocalization of Ets‐1 and HIF‐1α in these hypoxic areas suggests that hypoxia may induce Ets‐1 and HIF‐1α expression during joint inflammation.
A role for chemokines in the induction of chondrocyte phenotype modulation
Authors: Mazzetti Ilaria , Magagnoli Giorgia , Paoletti Samantha , Uguccioni Mariagrazia , Olivotto Eleonora , Vitellozzi Roberta , Cattini Luca , Facchini Andrea , Borzì Rosa Maria 
Published: January 2004

AbstractObjectiveTo extend the study of the chemokine receptor repertoire on human chondrocytes to receptors with reported housekeeping functions (CXCR3, CXCR4, CXCR5, and CCR6) and to evaluate whether ligands of these receptors play a role in chondrocyte phenotype modulation and proliferation.MethodsChemokine receptor expression was determined by flow cytometry. Subcultures of chondrocytes were collected and fixed at confluence or during the exponential phase of growth and analyzed for chemokine receptor modulation. The effects of chemokines on isolated cells as well as chondrocytes cultured within an intact extracellular matrix were investigated. Isolated human chondrocytes were stimulated with 100 nM chemokines (monokine induced by interferon‐γ, stromal cell–derived factor 1α [SDF‐1α], B cell–attracting chemokine 1 [BCA‐1], or macrophage inflammatory protein 3α), and conditioned media were assessed for matrix‐degrading enzyme contents (matrix metalloproteinases [MMPs] 1, 3, and 13, and N‐acetyl‐β‐D‐glucosaminidase [NAG]). Cell proliferation and phenotype modulation were evaluated by bromodeoxyuridine incorporation and cathepsin B production. Induction of cell proliferation was assessed in cartilage explants by immunodetection of the proliferation‐associated antigen S100A4.ResultsCXCR3, CXCR4, CXCR5, and CCR6 were detected on human chondrocytes. CXCR3 and CXCR4 expression was increased in exponentially growing chondrocyte subcultures. Ligands of all receptors enhanced the release of MMPs 1, 3, and 13. Release of NAG and cathepsin B was significantly higher in chemokine‐stimulated cultures than in unstimulated cultures. SDF‐1α and BCA‐1 also induced DNA synthesis and chondrocyte proliferation, as was shown by the up‐regulation of S100A4 in cartilage explants as well.ConclusionOur findings extend the repertoire of functional responses elicited by the activity of chemokines on chondrocytes and open new avenues in our understanding of the control of chondrocyte differentiation status by chemokines and their receptors.
Progression of radiologic damage in patients with rheumatoid arthritis in clinical remission
Authors: Molenaar Esmeralda T. H. , Voskuyl Alexandre E. , Dinant Huib J. , Bezemer P. Dick , Boers Maarten , Dijkmans Ben A. C. 
Published: January 2004

AbstractObjectiveTo assess whether radiologic progression occurs during clinical remission in patients with rheumatoid arthritis (RA).MethodsOne hundred eighty‐seven patients with RA in clinical remission were followed up clinically and radiologically for 2 years. Clinical remission was defined according to a modification of the American College of Rheumatology criteria (i.e., the criterion of fatigue was omitted, and patients had to fulfill 4 of the 5 remaining criteria). Radiologic joint damage was assessed by the Sharp/van der Heijde method.ResultsAfter 2 years of followup, remission persisted in 52% of patients. The median radiologic score for the total group of patients increased from 21 (interquartile range [IQR] 5, 65) at the time of entry to 25 (IQR 7, 72) after 2 years (P < 0.001). The median score for radiologic progression between baseline and 2 years was 0.5 (IQR 0, 2.5). Among patients with an exacerbation of RA (n = 86), the median score for progression over 2 years was 1.0 (IQR 0, 4.5) (P < 0.001), and in patients with a persistent remission (n = 93) it was 0 (IQR −0.5, 2.0) (P < 0.001). Clinically relevant progression of damage was more frequent in patients with exacerbation (23%) than in those with persistent remission (7%) (P = 0.001). However, in 15% of patients with persistent remission, an erosion developed in a previously unaffected joint. In the logistic regression analysis, the area under the curve of the Disease Activity Score, a continuous measure, was related to the chance of radiologic progression, regardless of the absolute disease activity level. Results were similar when other definitions of remission were used.ConclusionAlthough rare, clinically relevant progression of joint damage does occur in patients with RA in prolonged remission. This suggests the need for markers that predict progression during periods of low disease activity and for drugs that prevent damage that is independent of disease activity.
Longitudinal study of changes in tibial and femoral cartilage in knee osteoarthritis
Authors: Cicuttini F. M. , Wluka A. E. , Wang Y. , Stuckey S. L. 
Published: January 2004

AbstractObjectiveDespite the increasing interest in knee cartilage volume as an outcome measure in studies of osteoarthritis (OA), it is unclear what components of knee cartilage will be most useful as markers of structural change in the tibiofemoral joint. This study was undertaken to longitudinally compare changes in femoral and tibial cartilage volume in patients with OA.MethodsOne hundred seventeen patients with knee OA (58.1% women; mean ± SD age 63.7 ± 10.2 years) were examined. Femoral and tibial cartilage volumes (medial and lateral tibiofemoral joints) were determined from T1‐weighted fat‐saturated magnetic resonance images of the knee from coronal views.ResultsThe study population was followed up for a mean ± SD of 1.9 ± 0.2 years. In the medial tibiofemoral joint, the mean ± SD loss of cartilage was 0.15 ± 0.30 ml/year for femoral cartilage and 0.10 ± 0.25 ml/year for tibial cartilage. In the lateral tibiofemoral joint, the average loss was 0.15 ± 0.22 and 0.12 ± 0.16 ml/year for femoral and tibial cartilage, respectively. There was a significant correlation between the degree of loss of tibial cartilage and the degree of loss of femoral cartilage, in both tibiofemoral joints (r = 0.81, P < 0.001 at the medial tibiofemoral joint; r = 0.71, P < 0.001 at the lateral tibiofemoral joint).ConclusionLongitudinal changes in tibial cartilage and those in femoral cartilage are strongly related to one another. This suggests that in tibiofemoral disease, measuring tibial cartilage alone may be adequate, given the facts that measurements of the total femoral cartilage are less reproducible and there are difficulties inherent in identifying the most appropriate component of femoral cartilage to measure.