bluuebunny/crossref_metadata_2025_split huggingface dataset:
The second trimester genetic sonogram
Authors: Breathnach Fionnuala M. , Fleming Ann , Malone Fergal D. 
Published: February 2007

AbstractThe genetic sonogram, a fetal anatomic survey targeted at identifying features associated with aneuploidy, is carried out between 15 and 20 weeks' gestation. It has evolved as an adjunctive screening tool capable of further refining the individualized risk‐calculation for trisomy that is based on maternal age or serum screening markers. The significance of a range of major structural anomalies and so‐called “soft‐markers” for trisomy, detected both in isolation and in combination, has been widely investigated. This review serves to describe the key components of the second trimester genetic sonogram and to illustrate how these markers are integrated into risk assessment for aneuploidy. © 2007 Wiley‐Liss, Inc.
Prenatal diagnosis of structural cardiac defects
Authors: Allan Lindsey 
Published: February 2007

AbstractPrenatal diagnosis of congenital heart defects has been possible now for over 25 years. This ability has extended from a few specialists to being within the scope of any sonographer engaged in routine obstetric evaluation of the low‐risk patient. However, the detection rate is widely varied. The recognition of major structural heart disease in fetal life has important implications for the child's future, so further efforts should be made to improve the success in diagnosis. © 2007 Wiley‐Liss, Inc.
Neuropeptides and inflammation. A somatostatin analog as a selective antagonist of neutrophil activation by substance P
Authors: Kolasinski Sharon L. , Haines Kathleen A. , Siegel Evan L. , Cronstein Bruce N. , Abramson Steven B. 
Published: February 2007

AbstractObjective. Substance P and somatostatin are neuropeptides found in peripheral sensory nerves. In vitro, these have opposing effects on inflammatory cells. We compared the effects of these peptides on the activation of neutrophils.Methods. Neutrophils were isolated from healthy volunteers, and chemotaxis, superoxide anion generation, aggregation, and changes in cytosolic calcium and GTPase activity were measured in the presence of substance P, somatostatin, and the chemoattractant FMLP.Results. Substance P was an effective chemoattractant, 20% as potent as FMLP at equimolar concentrations. Substance P also stimulated GTPase activity in neutrophil plasma membranes. Somatostatin did not activate neutrophils; however, it effectively inhibited neutrophil chemotaxis and GTPase activity provoked substance P, but not by FMLP.Conclusions. These studies demonstrate that substance P can effectively stimulate chemotaxis, possible via effects on a GTP‐binding protein distinct from that triggered by FMLP, and that somatostatin is a selective antagonist of substance P. The biochemical specificities of these peptides on cells may modulate neurogenic inflammation at the local level.
Acute and chronic suppression of leukotriene B4 synthesis EX vivo in neutrophils from patients with rheumatoid arthritis beginning treatment with methotrexate
Authors: Sperling Richard I. , Benincaso Anthony I. , Anderson Ronald J. , Coblyn Jonathan S. , Austen K. Frank , Weinblatt Michael E. 
Published: February 2007

AbstractObjective. To compare the cumulative effects of oral methotrexate (MTX) therapy (after 6–8 weeks) with the acute effects (24 hours after a dose) on arachidonic acid metabolism by the 5‐lipoxygenase (5‐LO) pathway in neutrophils from patients with active rheumatoid arthritis (RA) who were beginning therapy with MTX.Methods. Neutrophils and monocytes were isolated from whole blood from 7 patients with RA, immediately before and 24 hours after their first weekly dose of 7.5 mg of MTX, and again after their dose at 6–8 weeks.Results. Total immunoreactive leukotriene B4 (LTB4) formation in neutrophils activated ex vivo with calcium ionophore A23187 was significantly suppressed (by 33%) before the 6–8‐week dose, compared with the level before the first dose (mean ± SEM 8.29 ± 1.24 ng/106 cells at predose 6–8 weeks versus 12.29 ± 2.13 ng/106 cells at predose 1; P = 0.03). Reductions were also observed after the first dose (27%; P = 0.07) and after the 6–8‐week dose (43%; P = 0.05) compared with the respective predose levels. MTX treatment produced significant reductions in the total generation of 5‐LO pathway products (5‐hydroxyeicosatetraenoic acid + 6‐trans‐LTB4 + LTB4 + ω‐oxidation products of LTB4) by calcium ionophore‐activated neutrophils, as quantitated by integrated optical density after resolution on reverse‐phase high‐performance liquid chromatography. Decreases were observed after the first dose (26%; P = 0.025), immediately before the 6–8‐week dose (23%; P = 0.05), and after the 6–8‐week dose (47%; P = 0.0033) compared with levels before the first dose, and after the 6–8‐week dose compared with the level before it (32%; P = 0.04). The generation of LTB4 by calcium ionophore‐activated monocytes was not significantly affected by MTX therapy.Conclusion. The significant decreases in the formation of ω‐oxidation products of LTB4 and in the total generation of neutrophil 5‐LO pathway products in the absence of a significant change in the release of 3H‐arachidonic acid or the generation of platelet‐activating factor suggest that the activity of the 5‐LO enzyme in neutrophils is inhibited. We conclude that weekly oral MTX therapy in patients with active RA inhibits neutrophil 5‐LO pathway product generation in a pattern consistent with inhibition of the activity of the 5‐LO enzyme; an effect is observed after the first dose. The inhibition of 5‐LO is cell‐selective and cumulative, with a superimposed incremental inhibition observed after the weekly MTX dose.
Synovial fluid analysis of two groups of proteoglycan epitopes distinguishes early and late cartilage lesions
Authors: Saxne Tore , Heinegård Dick 
Published: February 2007

AbstractObjective. To investigate whether fragmentation of proteoglycans in arthritis results in domains that have different levels of release from cartilage at different stages of the disease.Methods. Two regions of the proteoglycan, the hyaluronan‐binding region and the glycosaminoglycanrich region of the core protein, were measured, by immunoassay, in knee joint synovial fluids of patients with rheumatoid arthritis or reactive arthritis.Results. Synovial fluid concentrations of the glycosaminoglycan‐rich region were highest in rheumatoid arthritis patients who had little cartilage damage as determined by radiography, whereas release of the hyaluronan‐binding region predominated in patients with advanced cartilage destruction. In reactive arthritis, release of the glycosaminoglycan‐rich region predominated.Conclusion. These findings indicate that the hyaluronan‐binding region is initially retained in the tissue during the development of cartilage destruction. The combined analysis of these markers offers a new avenue for assessment of the degree of cartilage damage in arthritis.
Isolation and culture of synovial microvascular endothelial cells. Characterization and assessment of adhesion molecule expression
Authors: Abbot S. E. , Kaul A. , Stevens C. R. , Blake D. R. 
Published: February 2007

AbstractObjective. In vitro studies investigating the role of the synovial endothelium in the pathogenesis of rheumatoid arthritis (RA) have, until recently, been performed using cultured endothelial cells of nonsynovial macrovascular origin. In an attempt to more correctly model in vivo conditions, a method for the isolation and culture of synovial microvascular endothelial cells (SMEC) has been developed.Methods. SMEC were isolated, primarily, by the use of lectin‐coated (Ulex europaeus agglutinin type I), magnetizable polystyrene beads.Results. Isolated cells exhibit classic endothelial ‘cobblestone’ morphology, express von Willebrand factor, metabolize acetylated low‐density lipoprotein, and exhibit a cytokine (interleukin‐1)–mediated expression of endothelial leukocyte adhesion molecule type 1 (ELAM‐1) and intercellular adhesion molecule type 1 (ICAM‐1). ELAM‐1 levels were significantly elevated in SMEC, compared with human umbilical vein endothelial cells, over a range of interleukin‐1 concentrations.Conclusion. This increased expression of ELAM‐1 by SMEC may be a potentiating step in pathogenesis of RA.
Psychiatric disorder and cognitive impairment in systemic lupus erythematosus
Authors: Hay Elaine M. , Black Dawn , Huddy Alice , Creed Francis , Tomenson Barbara , Bernstein Robert M. , Holt P. J. Lennox 
Published: February 2007

AbstractObjectives. To determine the point prevalence of psychiatric disorder in patients with systemic lupus erythematosus (SLE). To investigate associations between psychiatric disorder and social stress, cognitive impairment, systemic disease activity, and corticosteroid therapy.Methods. A cross‐sectional study of 73 consecutive patients with SLE assessed using standardized psychiatric and clinical research methods.Results. Current psychiatric disorder was present in 15 patients (20.5%) and was significantly associated with social stress, lack of social support, and impairment on 2 tests of cognitive function (Verbal Fluency Test and Benton Visual Retention Test, Part A, number of errors). There was no association with systemic disease activity or corticosteroid therapy. Cognitive impairment on 2 or more tests was found in 26% and was associated with clinical evidence of central nervous system (CNS) disease, but not systemic disease activity or corticosteroid therapy.Conclusions. The point prevalence of psychiatric disorder in this cohort of patients with SLE was found to be similar to that observed in patients with rheumatoid arthritis. It was independently associated with social stress and 2 indicators of cognitive impairment, but not with systemic disease activity or corticosteroid therapy. Marked cognitive impairment was present in a significant percentage of patients even when there was no overt evidence of CNS involvement.
Interferon‐alpha in lupus psychosis
Authors: Shiozawa Shunichi , Kuroki Yasuo , Kim Mitsunori , Hirohata Shunsei , Ogino Tetsuya 
Published: February 2007

AbstractObjective. Since the level of interferon‐α (IFNα) is increased in the sera of patients with active systemic lupus erythematosus (SLE) and is detectable in the cerebrospinal fluid (CSF) of some SLE patients with neuropsychiatric manifestations, we investigated the contribution of IFNα to the pathogenesis of the neuropsychiatric manifestations of SLE.Methods. IFNα levels were quantitated by radioimmunoassay in CSF and serum samples from 17 SLE patients with neuropsychiatric manifestations and 28 patients with SLE alone or SLE and other neurologic disorders.Results. Levels of IFNα were increased in the CSF of 5 of 6 patients with lupus psychosis, and in 4 of these 5 patients, the levels in CSF were higher than those in serum. IFNα levels decreased when the manifestation of lupus psychosis subsided. In contrast, IFNα levels in CSF samples from patients with seizures alone were not increased. One patient with lupus psychosis died of complications of generalized seizures resulting from the SLE. At autopsy, we investigated whether IFNα protein or messenger RNA was detectable in the subject's brain. IFNα protein was immunohistochemically demonstrated in the neurons and in the microglia (focal accumulation), features not present in the brain tissues of subjects who died of other diseases.Conclusion. These findings support the hypothesis that IFNα, possibly synthesized in the brain, is the cause of the manifestation of psychosis in patients with SLE.
Ureaplasma urealyticum and mycoplasma hominis in women with systemic lupus erythematosus
Authors: Ginsburg Katherine S. , Kundsin Ruth B. , Walter Carl W. , Schur Peter H. 
Published: February 2007

AbstractObjective. To determine the prevalence of genitourinary mycoplasma infection in women with systemic lupus erythematosus (SLE).Methods. Urine specimens from 49 patients with SLE and 22 patients with chronic fatigue syndrome (CFS) were cultured for mycoplasma. Patient records were reviewed for medical history and SLE disease activity.Results. Sixty‐three percent of the SLE patients were culture positive, compared with 4.5% of the CFS patients (P < 0.001). Neither corticosteroid treatment, SLE activity, nor age accounted for this difference.Conclusion. Genitourinary mycoplasma colonization occurs significantly more frequently in SLE than in CFS.
Mycoplasma arthritidis mitogen. Vβ engaged in mice, rats, and humans, and requirement of HLA‐DRα for presentation
Authors: Baccala Roberto , Smith Lawrence R. , Vestberg Mikael , Peterson Per A. , Cole Barry C. , Theofilopoulos Argyrios N. 
Published: February 2007

AbstractObjective. Mycoplasma arthritidis mitogen (MAM) is mitogenic for mouse, rat, and human T cells, and behaves as a superantigen in mice through its capacity to bind to the α chain of I‐E molecules and engage entire sets of T cells expressing specific Vβ. Here, we have attempted to fully characterize the Vβ‐engaging activities of MAM in mice, and define similar activities in rats and humans.Methods. Multiprobe RNase‐protection assays and mice transgenic for human DRα, DRβ, and DRαβ were utilized for this purpose.Results. MAM‐reactive Vβ in the mouse included not only the previously reported Vβ6, Vβ8.1, Vβ8.2, and Vβ8.3, but also Vβ5.1. In the rat, engagement of Vβ5.1, Vβ6, Vβ8.1, and Vβ8.2, but not Vβ8.3, was documented, whereas in humans, the engaged Vβ included primarily Vβ19.1 (alternatively termed Vβ17.1) and, to a lesser extent, Vβ3.1, Vβ11.1, Vβ12.1, and Vβ13.1. In DR transgenic Eα‐Eβ‐ mice, presentation of MAM and engagement of specific Vβ was effected by DRα.Conclusions. Homologous Vβ are engaged by MAM in mice, rats, and humans, presumably through a binding site similar to that proposed previously for other superantigens. MAM presentation primarily via the nonpolymorphic DRα makes it unlikely that there is involvement of such a superantigen in the pathogenesis of autoimmune diseases known to be associated with certain DR haplotypes. The possibility cannot be excluded, however, that superantigen‐activated T cells may lead to disease by cross‐reactions with self‐antigens presented by particular DR haplotypes.
Molecular diagnosis of ureaplasma urealyticum septic arthritis in a patient with hypogammaglobulinemia
Authors: Lee Albert H. , Ramanujam Thaila , Ware Paul , Edelstein Paul H. , Brooks John J. , Freundlich Bruce , Schumacher H. Ralph , Zurier Robert B. , Weiner David B. , Williams William V. 
Published: February 2007

AbstractObjective. We report a hypogammaglobulinemic patient with a destructive oligoarticular arthritis, whose synovial fluid cultures were repeatedly sterile.Methods and Results. We identified a Ureaplasma urealyticum infection in his affected joints, using a polymerase chain reaction (PCR) assay.Conclusion. The PCR technique promises to be extremely valuable in the rapid and specific diagnosis of infectious arthritis.
Autoantibodies to small nuclear and cytoplasmic ribonucleoproteins in japanese patients with inflammatory muscle disease
Authors: Hirakata Michito , Mimori Tsuneyo , Akizuki Masashi , Craft Joe , Hardin John A. , Homma Mitsuo 
Published: February 2007

AbstractObjective. To elucidate the profile and clinical significance of autoantibodies to small nuclear and small cytoplasmic ribonucleoproteins in Japanese patients with polymyositis and dermatomyositis (PM/DM).Methods. Radioimmunoprecipitation assays were performed with sera from 91 patients with various inflammatory muscle diseases and from 254 control patients with other rheumatic diseases. Patients with PM/DM were categorized according to autoantibody specificities, and clinical comparisons were made.Results. Antibodies to aminoacyl transfer RNA (tRNA) synthetases and the signal recognition particle (SRP) were found to be specific for PM/DM. PM/DM patients with antibodies to 3 aminoacyl‐tRNA synthetases (histidyl, threonyl, and glycyl) appeared to form a distinct clinical subset, associated with chronic interstitial lung disease, polyarthritis, and myositis, while 3 patients with antibodies that bound the SRP had severe myositis that was resistant to corticosteroid therapy. In general, the frequency and clinical correlations of anti—aminoacyl‐tRNA synthetase antibodies in Japanese patients were similar to those in North American populations. In contrast, among this Japanese cohort, the occurrence of anti‐PM/ScI appeared to be reduced in frequency, whereas anti‐Ku and anti—U2 RNP antibodies were accentuated in patients with overlap syndromes.Conclusion. We conclude that racial groups differ somewhat in their characteristic autoimmune responses to individual autoantigens. These differences could reflect variation in immunogenetic background or different etiologic mechanisms which might occur at different geographic locations.
Serologic studies of monozygotic twins with systemic lupus erythematosus
Authors: Reichlin Morris , Harley John B. , Lockshin Michael D. 
Published: February 2007

AbstractObjective. The goal of these studies was to assess the role of genetic factors and disease expression in the pattern and titer of autoantibodies to several RNA protein antigens in patients with systemic lupus erythematosus (SLE) by studying identical twins concordant and discordant for disease expression.Methods. Autoantibodies to Ro/SS‐A, La/SS‐B, U1 RNP, and Sm were measured by quantitative enzyme‐linked immunosorbent assay using affinity‐purified antigens.Results. Detailed serologic studies were performed in 7 pairs of identical twins, 3 of whom were concordant and 4 of whom were discordant for disease expression. Autoantibody titers were higher in affected than in unaffected twins from discordant pairs, but in 3 of 4 pairs, the profile of anti—RNA proteins (e.g., Ro/SS‐A, La/SS‐B, U1 RNP, and Sm) was virtually identical. In the SLE pairs concordant for disease expression, the autoantibody titers were very similar, as were the anti—RNA protein profiles. When the identical twins were matched by sex, race, and age to pairs of nontwin SLE patients, the 6 white twins shared an average of 2.5 (± 1.05 SD) anti—RNA proteins, while the control SLE pairs shared only 0.33 (± 0.82), P < 0.01 (t = 4.0, P < 0.01). In addition, in the white SLE twins, all had elevated levels of anti—U1 RNP while in white nontwin SLE patients, the frequency of anti—U1 RNP was 30%.Conclusion. These data point to a dominant role for genetic factors in the determination of specific autoantibody profiles.
Differences in t cell receptor restriction fragment length polymorphisms in patients with rheumatoid arthritis
Authors: Funkhouser Sheana Whelan , Concannon Patrick , Charmley Patrick , Vredevoe Donna L. , Hood Leroy 
Published: February 2007

AbstractObjective. The purpose of this study was to determine whether a T cell receptor (TCR) polymorphism, either by itself or in combination with particular HLA polymorphism, leads to susceptibility to rheumatoid arthritis (RA).Methods. Eight restriction fragment length polymorphisms (RFLPs) detected with TCR gene segments were investigated in 46 individuals with RA and were compared with data from normal control subjects.Results. A statistically significant difference in the genotype frequencies of a Taq I RFLP detected with the TCRα constant region (Cα) gene was noted. In addition, when the DR4+ subpopulations were examined, the allelic frequency of a 2‐kb Bam HI fragment detected with a Vβ8 gene was increased in the samples from RA patients (P < 0.0086).Conclusion. The results of this study suggest that germline differences in the TCR repertoire may be associated with RA, and that there is a contributory effect of DR4+ haplotypes with certain TCR haplotypes in susceptibility to RA.
Autoantibodies to the chromosomal protein HMG‐17 in juvenile rheumatoid arthritis
Authors: Neuer Gunter , Bustin Michael , Michels Hartmut , Truckenbrodt Hans , Bautz Friedlinde A. 
Published: February 2007

AbstractObjective. To determine the antibody profiles in sera from patients with juvenile rheumatoid arthritis (JRA).Methods. Immunoblotting using nuclear extracts and recombinant high‐mobility group (HMG) nonhistone chromosomal proteins.Results. Antibodies directed against HMG‐17 were found in 47% of antinuclear antibody (ANA)–positive patients with pauciarticular‐onset JRA and in 16% of ANA‐positive patients with polyarticular‐onset JRA. HMG‐17 values of 6% and 8%, respectively, were detected in ANA‐negative patients with JRA and in those with nonrheumatic diseases.Conclusion. There is evidence for a high prevalence of anti—HMG‐17 antibodies in sera of patients with pauciarticular‐onset JRA.
Magnetic resonance imaging detection of aortic and pulmonary artery wall thickening in the acute stage of takayasu arteritis. Improvement of clinical and radiologic findings after steroid therapy
Authors: Tanigawa Ken , Eguchi Katsumi , Kitamura Yoshio , Kawakami Atsushi , Ida Hiroaki , Yamashita Shunichi , Matsunaga Naofumi , Hayashi Kuniaki , Nagataki Shigenobu 
Published: February 2007

AbstractObjective. Early diagnosis of Takayasu arteritis in the acute stage (prepulseless stage) is extremely difficult. Identification of a useful approach to detecting the initial changes of arteritis is therefore desirable.Methods. Careful clinical examination of a young woman with persistent fever and dry cough revealed faintly audible bruits at the cervical, supraclavicular, and abdominal regions. Aortographic features suggested thickening of the wall of the descending thoracic aorta. Magnetic resonance imaging (MRI) of this area was diagnostic.Results. MRI demonstrated involvement of the ascending aorta and right main pulmonary artery. Steroid therapy (prednisolone 60 mg/day) induced dramatic clinical and radiologic improvement in 2 months.Conclusion. This is the first report of MRI‐documented reduction in the thickness of the walls of both the aorta and the pulmonary artery following steroid therapy.
Effect of food on the bioavailability of low‐dose methotrexate in patients with rheumatoid arthritis
Authors: Oguey D. , Kölliker F. , Gerber N. J. , Reichen J. 
Published: February 2007

AbstractObjective. To evaluate the influence of food on the bioavailability of an oral dose of methotrexate in patients with rheumatoid arthritis.Methods. Methotrexate (15 mg) was given intravenously and orally, with or without a meal, to 10 patients. Blood samples were drawn at specific intervals to evaluate drug levels.Results. Food reduced the peak concentration, from a mean of 0.71 μmoles/liter to 0.49 μmoles/liter (P < 0.02), and slightly increased the time to peak concentration, from a mean of 1.3 hours to 2.0 hours. Bioavailability was highly variable (range 28–94%) but was not affected by food intake.Conclusion. Bioavailability of oral methotrexate shows marked interindividual variation but is not affected by the presence of food.