bluuebunny/crossref_metadata_2025_split huggingface dataset:
Fibronectin synthesis in superficial and deep layers of normal articular cartilage
Authors: Hayashi Takeshi , Abe Etsuko , Jasin Hugo E. 
Published: February 2007

AbstractObjective. To study the distribution and synthesis of fibronectin (FN) in superficial and deep layers of normal articular cartilage.Methods. Superficial and deep bovine and human articular cartilage slices were used to extract and quantitate FN by radioimmunoassay. Chondrocytes were also isolated by collagenase digestion for FN extraction and culture. Superficial and deep cartilage explants were cultured with and without stimulation by cytokines. Quantitation of newly synthesized FN was carried out by incubation with 35S‐methionine. FN was purified on gelatin‐agarose columns and further characterized by polyacrylamide gel electrophoresis. FN messenger RNA (mRNA) was quantitated by Northern blot analysis.Results. Freshly isolated bovine chondrocytes from deep cartilage contained 2.3 ± 0.2 times more FN than was found in superficial cells (P < 0.025). Deep cartilage explants contained 1.2 times more FN than was found in superficial tissue. Explants obtained from deep cartilage synthesized 2.4 times more FN per cell than did superficial tissues (P < 0.01). FN synthesis as a fraction of total protein synthesis was significantly greater in deep explants (P < 0.01) compared with superficial tissues. Isolated deep chondrocytes in culture synthesized 1.89 ± 0.33‐fold more FN than did superficial cells (P < 0.05). Cytokine‐stimulated superficial cartilage explants failed to respond in terms of FN synthesis. FN mRNA quantitation showed no significant differences between superficial and deep populations.Conclusion. Since FN plays a major role in cell adhesion to damaged cartilage surfaces, our results suggest that modulation of FN synthesis near the articular surface of cartilage may be one of the factors that impede pannus invasion following an inflammatory insult to the joint.
Cell‐type specificity of anti‐CD45 autoantibodies in systemic lupus erythematosus
Authors: Czyzyk Jan , Fernsten Philip , Shaw Melody , Winfield John B. 
Published: February 2007

AbstractObjective. To determine the specificity of anti‐CD45 autoantibodies in systemic lupus erythematosus (SLE) for native CD45 and for CD45 expressed by T cells and B cells, and at different stages of cellular activation.Methods. CD45 purified from different types of lymphocytes was examined by immunoblotting with sera from patients with SLE. Indirect immunofluorescence experiments were performed with purified anti‐CD45 autoantibodies.Results. IgM anti‐CD45 autoantibodies in SLE recognize native CD45 expressed on the surface membrane of viable lymphocytes and CD45 purified from activated peripheral T cells and certain T cell lines, but not CD45 purified from B cells or resting peripheral T cells. The presence or absence of reactivity is independent of the individual isoforms expressed.Conclusion. Recognition of CD45 by IgM antilymphocyte autoantibodies in SLE varies with the lineage and state of activation of the lymphocyte target. This pattern of reactivity is consistent with autoantibody specificities involving CD45 glycoforms, rather than CD45 isoforms.
Defective antigen‐presenting cell function in patients with systemic lupus erythematosus: Role of the B7‐1 (CD80) costimulatory molecule
Authors: Tsokos George C. , Kovacs Birgit , Sfikakis Peter P. , Theocharis Stamatis , Vogelgesang Scott , Via Charles S. 
Published: February 2007

AbstractObjective. Patients with systemic lupus erythematosus (SLE) who exhibit defective in vitro responses to recall antigens and normal responses to alloantigens have been shown to have an abnormality in antigenpresenting cell (APC) function. This study was undertaken to further characterize this defect in APC function in lupus patients.Methods. Mononuclear cells (MNC) from the peripheral blood of patients with SLE and from normal individuals were cultured in the presence of either recall antigen tetanus toxoid (TT), anti‐CD3 (OKT3) monoclonal antibody, or alloantigens, and proliferative or interleukin‐2 responses were assessed. Cell surface expression of B7‐1 was assessed by flow cytometry.Results. MNC from all normal individuals and from 7 patients with SLE responded to both TT and alloantigen and were designated +/+. Twelve SLE patients did not respond to TT but did respond to alloantigen stimulation and were designated ‐/+. In both normal subjects and SLE patients, the ability to respond to OKT3 correlated strongly with the ability to respond to recall antigen. A defect in APC costimulatory function was suggested by data demonstrating that interferon‐γ‐induced expression of B7‐1 was significantly reduced in SLE patients compared with controls. Neither controls nor SLE patients expressed detectable amounts of surface B7‐1 molecule on resting APC. Defective recall and anti‐CD3‐stimulated responses could be enhanced in SLE patients in the presence of B7/BB1‐transfected P815 murine mastocytoma cells underscoring an SLE‐associated defect in costimulatory activity. However, nontransfected P815 cells were also able to enhance responses to OKT3 in ‐/+ patients; blocking experiments showed that this was mediated through an IgG Fc receptor‐dependent mechanism.Conclusion. These data indicate that SLE‐associated defects in APC function in vitro can be accounted for by abnormalities in APC surface membrane molecules such as B7, IgG Fc receptors, and possibly others.
A pilot trial of oral type II collagen in the treatment of juvenile rheumatoid arthritis
Authors: Barnett Martha L. , Combitchi Daniel , Trentham David E. 
Published: February 2007

AbstractObjective. To evaluate the efficacy of oral chicken type II collagen (CCII) in the treatment of juvenile rheumatoid arthritis (JRA).Methods. Ten patients with active JRA were treated with CCII for 12 weeks. Efficacy parameters, which included swollen and tender joint count and score, grip strength, 50‐foot walking time, duration of morning stiffness, and patient and physician global scores of disease severity, were assessed monthly.Results. All patients completed the full course of therapy. Eight patients had reductions in both swollen and tender joint counts after 3 months of CCII. The mean changes from baseline in swollen and tender joint counts for the 8 responders at the end of the study were –61% and –54%, respectively. Mean values for other efficacy parameters also showed improvement from baseline. There were no adverse events that were considered to be treatment related.Conclusion. Oral CCII may be a safe and effective therapy for JRA, and its use in this disease warrants further investigation.
Elevated nitric oxide production in rheumatoid arthritis: Detection using the fasting urinary nitrate:creatinine ratio
Authors: Grabowski Peter S. , England Amanda J. , Dykhuizen Roelf , Copland Mhairi , Benjamin Nigel , Reid David M. , Ralston Stuart H. 
Published: February 2007

AbstractObjective. To develop a simple method for assessing endogenous nitric oxide (NO) production applicable to routine clinical practice in rheumatology.Methods. NO production was assessed in patients with rheumatoid arthritis (RA) as serum nitrate levels and as the urinary nitrate:creatinine ratio in morning samples of urine following an overnight fast. The influence of dietary intake of nitrate on these measurements was investigated in healthy volunteers. The clinical value of the urinary nitrate:creatinine ratio was validated in patients with infectious gastroenteritis, in whom its production is known to be increased.Results. Urinary nitrate:creatinine ratios were significantly elevated in patients with RA (average 3‐fold elevation over controls; P < 0.005) or infectious gastroenteritis (average 10‐fold elevation, P < 0.001). Serum nitrate was significantly elevated only in patients with infectious gastroenteritis (P < 0.001). Dietary intake of nitrate had no significant influence on the fasting morning urinary nitrate:creatinine ratio in the healthy volunteers, showing that this parameter is a useful indicator of endogenous NO production.Conclusion. We have developed a simple procedure for evaluating endogenous NO production that is readily applicable to routine clinical practice. Assessment of NO production will help in our understanding of its role in inflammatory conditions such as RA.
Hair dye use and the risk of developing systemic lupus erythematosus: A cohort study
Authors: Sanchez‐Guerrero Jorge , Karlson Elizabeth W. , Colditz Graham A. , Hunter David J. , Speizer Frank E. , Liang Matthew H. 
Published: February 2007

AbstractObjective. To investigate the role of hair dye use in the etiology of systemic lupus erythematosus (SLE).Methods. Participants included 106,391 women enrolled in the Nurses' Health Study, a prospective cohort study. The subjects were ages 30–55 years in 1976, and were free from SLE and any other connective tissue disease at the time of enrollment. In 1976, 1978, 1980, and 1982, subjects were classified as never‐users or ever‐users of permanent hair dye, based on self‐report. Incidence rates of SLE meeting American College of Rheumatology classification criteria were ascertained and confirmed by chart review.Results. Compared with never‐users of permanent hair dye, the age‐adjusted relative risks (RR) for the development of SLE among ever‐users (n = 85 cases) was 0.96 (95% confidence interval [95% CI] 0.63–1.47). Duration of hair dye use was not related to risk of SLE. Women with 15 or more years of use had no increased risk (RR = 0.92, 95% CI 0.46–1.83). There was no relationship between frequency of use or time since first use and risk of SLE. The results were similar when less stringent criteria for SLE were used.Conclusion. We found no evidence that permanent hair dye use, age at first use, frequency of use, or duration of use is associated with the development of SLE.
Homozygous hereditary C1q deficiency and systemic lupus erythematosus: A new family and the molecular basis of C1q deficiency in three families
Authors: Slingsby Jason H. , Norsworthy Peter , Pearce Glen , Vaishnaw Akshay K. , Issler Helen , Morley Bernard J. , Walport Mark J. 
Published: February 2007

AbstractObjective. To describe a new kindred with C1q deficiency and to identify the molecular lesions responsible for complete functional C1q deficiency in this and 2 other previously described kindreds.Methods. The A‐, B‐, and C‐chain genes of C1q were amplified by polymerase chain reaction, cloned, and sequenced. The DNA sequence was checked for mutations.Results. Patient 1 had a homozygous G‐to‐A change at codon 6 of the C chain, causing an amino acid change from Gly to Arg. Patient 2 had a homozygous deletion of a C nucleotide at codon 43 of the C‐chain, causing a frame shift, leading to a premature stop codon at codon 108. Patient 3 had a homozygous C‐to‐T mutation at amino acid position 41 of the C chain, resulting in a premature stop codon.Conclusion. In the homozygous state, the mutations are sufficient to cause complete deficiency of C1q. The mutation in patient 1 has been previously reported in a patient of different ethnic origin. A survey of a series of 158 DNA samples from patients with systemic lupus erythematosus showed no other examples of this mutant allele.
Antiribosomal P antibodies in pediatric patients with systemic lupus erythematosus and psychosis
Authors: Press Joseph , Palayew Karen , Laxer Ronald M. , Elkon Keith , Eddy Allison , Rakoff David , Silverman Earl D. 
Published: February 2007

AbstractObjective. To study antibodies directed against ribosomal P proteins, a sensitive and specific marker of depression and psychosis in systemic lupus erythematosus (SLE), in pediatric patients with SLE.Methods. One hundred six serum samples were obtained from 79 patients with SLE. Sixty age‐ and sex‐matched control sera were obtained, and 12 samples were obtained from children with primary psychosis. Antibodies to recombinant ribosomal P (rRP) protein were detected using a standard enzyme‐linked immunosorbent assay.Results. All 12 children with non–SLE‐associated psychosis had normal levels of anti‐rRP antibodies. Elevated levels of anti‐rRP were found in 11 of 64 pediatric SLE patients without a history of psychosis (17%). In the group of 13 SLE patients with psychosis, 5 (38%) had increased anti‐rRP antibody levels during the time of acute psychosis, and which significantly decreased during remission. In addition, most of the SLE patients without a history of psychosis had a good correlation between anti‐rRP antibody levels and disease activity. The patients with psychosis had significantly less renal involvement than the patients without a history of psychosis. This apparent protection from renal disease was not related to the presence or absence of either antiribosomal P or anti‐DNA antibodies.Conclusion. Elevated serum levels of antibodies to ribosomal P protein can distinguish SLE‐associated psychosis from primary psychosis of childhood. In SLE, elevated antiribosomal P antibody levels were not specific for psychosis. Serial assays were useful for monitoring the disease activity.
Thallium perfusion defects predict subsequent cardiac dysfunction in patients with systemic sclerosis
Authors: Steen Virginia D. , Follansbee William P. , Conte Claudia G. , Medsger Thomas A. 
Published: February 2007

AbstractObjective. To determine the significance of thallium perfusion defects in patients with systemic sclerosis (SSc).Methods. This is a followup study of a series of 48 SSc patients who underwent thallium perfusion scans in the early 1980s. Their cardiac history and survival information over the last 10 years were obtained as part of the Pittsburgh Databank's yearly evaluation. We determined the frequency of subsequent development of arrhythmias requiring treatment or of congestive heart failure through patient and physician information.Results. Patients with larger thallium perfusion defects had a significantly increased risk of developing subsequent cardiac events or death. The size of the initial thallium defect was the best predictor of later adverse events compared with other disease‐related features, in a logistic regression analysis.Conclusion. We conclude that patients with SSc who have significant thallium perfusion defects are at a significantly increased risk of developing subsequent cardiac disease or death.
IgA multiple myeloma presenting as Henoch‐Schönlein purpura/polyarteritis nodosa overlap syndrome
Authors: Birchmore Daniel , Sweeney Christine , Choudhury Devasmita , Konwinski Martin F. , Carnevale Kevin , D'Agati Vivette 
Published: February 2007

AbstractWe report the unusual case of a man with a 5‐year history of relapsing Henoch‐Schönlein purpura (HSP) and macroscopic polyarteritis nodosa (PAN) as early manifestations of IgAκ multiple myeloma. The glomeruli contained monoclonal IgAκ deposits, without other immunoglobulins or λ light chains. Glomerular deposits lacked the usual electron density but could be demonstrated by immunoelectron microscopy. Multisystem large vessel vasculitis (antineutrophil cytoplasmic antibody negative) produced aneurysms of renal and hepatic arteries, whereas small vessel vasculitis affected the skin and glomeruli, producing a symptom complex of HSP with dermal and glomerular deposits of IgA. We conclude that HSP/overlap syndrome may be the initial manifestation of IgA myeloma and should be considered within the spectrum of monoclonal IgA deposition disease.
Detection of Borrelia burgdorferi by DNA amplification in synovial tissue samples from patients with lyme arthritis
Authors: Jaulhac Benoǐt , Chary‐Valckenaere Isabelle , Sibilia Jean , Javier Rose‐Marie , Piémont Yves , Kuntz Jean‐Louis , Monteil Henri , Pourel Jacques 
Published: February 2007

AbstractObjective. To compare the detection rates of chromosomal flagellin gene from Borrelia burgdorfen in synovial tissue (ST) and synovial fluid (SF) using polymerase chain reaction (PCR) techniques.Methods. B burgdorferi DNA was sought in SF and ST from 12 consecutive patients with Lyme arthritis and from 29 patients with noninfectious diseases (controls).Results. No DNA amplification was observed in samples obtained from the 29 control patients, whereas B burgdorferi DNA was detected in all ST and/or SF samples from the 12 patients with Lyme arthritis. Results from 1 ST sample were not interpretable because of PCR inhibitors. Among the 11 remaining patients, 10 had positive ST samples, whereas only 4 had positive SF samples (P < 0.05).Conclusion. These data suggest that detection of chromosomal B burgdorferi DNA may be more efficient in ST than SF.
Bone mineralization and bone mineral metabolism in children with juvenile rheumatoid arthritis
Authors: Pepmueller Peri Hickman , Cassidy James T. , Allen Susan H. , Hillman Laura S. 
Published: February 2007

AbstractObjective. To identify mechanisms of the osteopenia associated with juvenile rheumatoid arthritis (JRA) by determining parameters of bone mineralization, and bone mineral content and density (BMC and BMD), in children with JRA.Methods. BMC and BMD were measured by dual x‐ray absorptiometry in 41 children with JRA and 62 healthy children. Serum samples were analyzed for concentrations of minerals, vitamin D, parathyroid hormone, osteocalcin, bone‐specific alkaline phosphatase (BAP), procollagen I carboxy‐terminal propeptide, and tartrate‐resistant acid phosphatase (TRAP), and urinary excretion of deoxypyridinoline crosslinks and calcium.Results. BMD was decreased at all sites in JRA patients. BMD, corrected for age, height, weight, and bone area, was decreased at cortical bone sites (1/3 radius, upper and lower extremities, and whole body). Low concentrations of osteocalcin and BAP suggested reduced bone formation, and low TRAP levels suggested decreased resorption. Clinical scales of disease severity were negatively correlated with measures of bone mass. Laboratory markers of disease severity were highly correlated with decreases in markers of bone formation, but not with those of resorption. Although laboratory findings were similar for children with oligoarticular and polyarticular disease, differences in bone mass were greater in children with polyarticular disease.Conclusion. These data suggest an association between decreased bone mineralization in JRA and low bone formation that is related to disease severity. Efforts to stimulate bone formation, therefore, need to be considered clinically in prepubertal children with active JRA.
Anti‐endothelial cell IgG antibodies from patients with Wegener's granulomatosis bind to human endothelial cells in vitro and induce adhesion molecule expression and cytokine secretion
Authors: del Papa Nicoletta , Guidali Luisa , Sironi Marina , Shoenfeld Yehuda , Mantovani Alberto , Tincani Angela , Balestrieri Genesio , Radice Antonella , Sinico R. Alberto , Meroni Pier Luigi 
Published: February 2007

AbstractObjective. To elucidate the role of antiendothelial cell antibodies (AECA) in vascular inflammation in patients with Wegener's granulomatosis (WG).Methods. IgG fractions from 3 AECA‐positive WG patients, IgG from 3 AECA‐negative WG patients, and IgG from healthy donors were tested for their ability to: a) bind to endothelial cells and to display complement‐dependent or antibody‐dependent cellular cytotoxicity, b) modulate cell membrane expression of adhesion molecules, as evaluated by cytofluorometry and by immunoenzymatic assay, and c) induce the secretion of interleukin‐1β (IL‐1β), IL‐6, IL‐8, and monocyte chemotactic protein 1 (MCP‐1).Results. We found that AECA IgG from WG patients do not display any significant cytotoxicity but are able to up‐regulate the expression of E‐selectin, intercellular adhesion molecule 1 and vascular cell adhesion molecule 1 and to induce the secretion of IL‐1β, IL‐6, IL‐8, and MCP‐1.Conclusion. AECA in patients with WG could play a potential pathogenetic role by activating endothelial cells, and thus facilitating leukocyte recruitment and adhesion to endothelial surfaces, rather than by displaying a cytotoxic activity.
Aberrant expression pattern of the SS‐B/La antigen in the labial salivary glands of patients with Sjögren's syndrome
Authors: de Wilde P. C. M. , Kater L. , Bodeutsch C. , van den Hoogen F. H. J. , van de Putte L. B. A. , van Venrooij W. J. 
Published: February 2007

AbstractObjective. Salivary glands of patients with Sjögren's syndrome (SS) have been shown to be a site of anti‐SS‐B/La antibody production. The present study investigated differences in the localization of the SS‐B/La antigen in labial salivary gland (LSG) tissue between SS and non‐SS patients, which may explain the local antigen‐driven anti–SS‐B/La response.Methods. Distribution of SS‐B/La was studied immunohistologically in the LSG biopsy samples of 9 SS patients, 10 non‐SS patients, and in normal tissues obtained at autopsy within 2 hours after death, using a mouse monoclonal antibody directed to SS‐B/La. In 3 SS and 3 non‐SS patients, LSGs were also studied with affinity‐purified biotinylated human antibodies directed against SS‐B/La.Results. In the non‐SS patients, SS‐B/La was primarily observed in the nucleoli of acinic cells of the LSGs. Patients with either primary SS or secondary SS showed an accumulation of SS‐B/La in the nucleoplasm of acinic cells. In the SS patients, SS‐B/La was also detected in the cytoplasm as a diffuse or perinuclear staining. Sometimes, SS‐B/La was found along the membrane of acinic cells as well. This aberrant nuclear and cytoplasmic distribution of SS‐B/La in SS patients correlated well with abnormalities in the composition of the plasma cell population in the LSGs, but not with a lymphocytic focus score > 1.Conclusion. The accumulation and redistribution of SS‐B/La in the LSGs may play an important role in the local antigen‐driven anti–SS‐B/La response in SS, and can also be used to improve the diagnostic possibilities of the LSG biopsy.
Elevated serum level of soluble HLA class I antigens in patients with systemic lupus erythematosus
Authors: Tsuchiya Naoyuki , Shiota Michiko , Yamaguchi Akihiro , Ito Koji 
Published: February 2007

AbstractObjective. To examine the clinical significance of serum soluble HLA class I antigens (sHLA class I) in patients with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA).Methods. Serum levels of sHLA class I were measured by enzyme‐linked immunosorbent assay, using a monoclonal antibody against monomorphic determinant of HLA class I (W6/32) and an enzyme‐labeled polyclonal antibody to human β2‐microglobulin.Results. The serum sHLA class I concentration was 1.85 ± 1.15 μg/ml (mean ± SD) in 27 patients with SLE (P < 0.0001 versus normal controls, P = 0.0001 versus RA), 0.61 ± 0.34 μg/ml in 16 patients with RA (P = 0.02 versus normal controls), and 0.41 ± 0.20 μg/ml in normal controls. The HLA class I levels were significantly correlated with the SLE Disease Activity Index (r = 0.62, P = 0.0004) and with a reduction of CH50 levels (r = −0.60, P = 0.0007). A longitudinal analysis of patients with SLE indicated that serum sHLA class I levels fluctuated in conjunction with other disease activity markers.Conclusion. Serum sHLA class I may be useful as a disease activity marker of SLE. The mechanism of secretion and the physiologic role of sHLA class I require further study.