bluuebunny/crossref_metadata_2025_split huggingface dataset:
Recombinant human interleukin‐1 receptor type I in the treatment of patients with active rheumatoid arthritis
Authors: Drevlow Barbara E. , Lovis Rosa , Haag Mary Ann , Sinacore James M. , Jacobs Cindy , Blosche Consuelo , Landay Alan , Moreland Larry W. , Pope Richard M. 
Published: February 2007

AbstractObjective. To determine the safety and efficacy of recombinant soluble human interleukin‐1 receptor type I (rHuIL‐1RI) administered subcutaneously in patients with active rheumatoid arthritis (RA).Methods. Twenty‐three patients with active RA (>5 swollen joints) were enrolled into a randomized, double‐blind, 2‐center study. Patients received subcutaneous doses of rHuIL‐1RI or placebo for 28 consecutive days. Patients were treated with 125, 250, 500, or 1,000 μg/m2/day of rHuIL‐1RI. Physical examinations and laboratory assessments were performed at baseline (day 1), and 8, 15, 22, 29, 43, and 57 days after the start of the study. Analysis of peripheral blood by flow cytometry was performed on days 1 and 29 to determine the effects of rHuIL‐1RI on the distribution and phenotypic characteristics of circulating inflammatory cells.Results. Four of 8 patients who received rHuIL‐1RI at 1,000 μg/m2/day demonstrated improvement in at least 1 of 8 individual measures of disease activity; however, only 1 of these 4 patients experienced clinically relevant improvement as defined by predetermined criteria. None of the patients treated with smaller doses of rHuIL‐1RI, and none of the placebo‐treated control patients, experienced any improvement as defined by the predetermined criteria. Monocyte cell surface IL‐1α was significantly reduced following treatemnt with rHuIL‐1RI at each dosage. Administration of rHuIL‐1RI was stopped prematurely because of dose‐limiting rashes in 2 pateints treated with 1,000 μg/m2/day. No other adverse events prevented completion of the study.Conclusion. Only 1 patient, who was treated with the highest concentration of rHuIL‐1RI employed (1,000 μg/m2/day), demostrated clinically relevant improvement in this phase I study on this small group of patients with active RA. Dose‐limiting toxicity was also observed in 2 pateints treated with this highest concentration of rHuIL‐1RI. Treatment with rHuIL‐1RI did result in a reduction of monocyte cell surface IL‐1α, which indicates that the dosages of rHuIL‐1RI employed were functional.
Rheumatoid arthritis in a United States Public Health Service Hospital in Oklahoma. Serologic manifestations in rheumatoid arthritis vary among tribal groups
Authors: Scofield R. Hal , Fogle Mark , Rhoades Everett R. , Harley John B. 
Published: February 2007

AbstractObjective. To study the serologic manifestations of rheumatoid arthritis (RA) at a United States Public Health Service Hospital that serves numerous tribes in Oklahoma.Methods. Forty‐five patients with RA were identified, and serologic studies for antinuclear antibody (ANA), rheumatoid factor, and antibodies to extractable nuclear antigens were performed. Extraarticular manifestions of RA were also evaluated.Results. Twelve of the 45 patients with RA were Kiowa. These patients were significantly more likely to have a positive ANA (75%) than the other patients with RA (28%). In addition, anti‐Ro was significantly more common among Kiowa (33%) than among members of other tribes (3%). There was no difference in the extraarticular manifestions of the Kiowa compared with the other Native American tribes.Conclusion. RA can be distinctly characterized by serology among groups of American Indians living in the same geographic area.
Nonsteroidal antiinflammatory drug–induced enteropathy and severe chronic anemia in a patient with rheumatoid arthritis
Authors: Davies Neal M. , Jamali Fakhreddin , Skeith Kenneth J. 
Published: February 2007

AbstractThis report describes the case of a woman who was admitted to the hospital with severe anemia and refractory rheumatoid arthritis. She had been transfusion dependent for 8 years and was receiving a combination of indomethacin and naproxen. An indium‐111 white blood cell scan revealed small bowel inflammation. Salsalate was substituted for her previous nonsteroidal antiinflammatory drugs (NSAIDs), and metronidazole was initiated. This resulted in maintenance of a normal hemoglobin level for at least 1 year after discharge. Small intestine inflammation and bleeding (enteropathy) due to NSAIDs must be considered in the evaluation of anemia in patients with arthritis.
The effect of progressive resistance training in rheumatoid arthritis. Increased strength without changes in energy balance or body composition
Authors: Rall Laura C. , Meydani Simin Nikbin , Kehayias Joseph J. , Dawson‐Hughes Bess , Roubenoff Ronenn 
Published: February 2007

AbstractObjective. To demonstrate the feasibility of high‐intensity progressive resistance training in rheumatoid arthritis (RA) patients compared with healthy control subjects.Methods. Eight subjects with RA, 8 healthy young subjects, and 8 healthy elderly subjects underwent 12 weeks of high‐intensity progressive resistance training, while 6 elderly subjects performed warm‐up exercises only. Fitness, body composition, energy expenditure, function, disease activity, pain, and fatigue were measured at baseline and followup.Results. All 3 training groups demonstrated similar improvements in strength compared with the change among control subjects (RA group 57% [P < 0.0005], young exercise group 44% [P < 0.01], elderly exercise group 36% [P < 0.05]). Subjects with RA had no change in the number of painful or swollen joints but had significant reductions in self‐reported pain score (21% [P < 0.05]) and fatigue score (38% [P = 0.06]), improved 50‐foot walking times (mean ± SD 10.4 ± 2.2 seconds versus 8.3 ± 1.5 seconds [P < 0.005]), and improved balance and gait scores (48.9 ± 3.8 versus 50.4 ± 2.0 [P = 0.07]).Conclusion. High‐intensity strength training is feasible and safe in selected patients with well‐controlled RA and leads to significant improvements in strength, pain, and fatigue without exacerbating disease activity or joint pain.
Polymyositis, arthritis, and uveitis in a macaque experimentally infected with human T lymphotropic virus type I
Authors: Beilke Mark A. , Traina‐Dorge Vicki , England John D. , Blanchard James L. 
Published: February 2007

AbstractObjective. To establish a simian model of human T lymphotropic virus type I (HTLV‐I) infection and disease.Methods. Irradiated HTLV‐I–producing cells were used to infect two 2‐year‐old rhesus macaque monkeys (Macaca mulatta). One monkey was also simultaneously inoculated with a cell‐free suspension of simian immunodeficiency virus (SIV). Evidence of infection was monitored by serial clinical examinations and by serologic, molecular, and virologic assays.Results. Both HTLV‐I‐inoculated monkeys became persistently infected following inoculation. Clinical disease was observed in the singly inoculated monkey, which developed arthritis (with synovial fluid positive for HTLV‐I by culture and polymerase chain reaction), anterior chamber uveitis, and steroid‐responsive polymyositis confirmed by electrophysiologic studies. The dually inoculated animal remained clinically healthy, despite high levels of SIV and HTLV‐I virus expression and loss of HTLV‐I‐specific antibodies.Conclusion. These results indicate the utility of a nonhuman primate model for studying HTLV‐I disease pathogenesis and the dynamics of SIV‐1/HTLV‐I retroviral coinfection.
Elevated levels of the soluble form of bone marrow stromal cell antigen 1 in the sera of patients with severe rheumatoid arthritis
Authors: Lee Byung Ok , Ishihara Katsuhiko , Denno Kakuro , Kobune Yoshiko , Itoh Motoyuki , Muraoka Osamu , Kaisho Tsuneyasu , Sasaki Takeshi , Ochi Takahiro , Hirano Toshio 
Published: February 2007

AbstractObjective. Bone marrow stromal cell antigen 1 (BST‐1) is a novel glycosyl phosphatidylinositol–anchored ectoenzyme, which is overexpressed on bone marrow stromal and synovial cell lines derived from patients with rheumatoid arthritis (RA). To investigate the pathophysiologic roles of BST‐1 in RA, we established an enzyme‐linked immunosorbent assay (ELISA) system to detect the soluble form of BST‐1 (sBST‐1) and examined levels of sBST‐1 in the sera of RA patients.Methods. Concentrations of sBST‐1 in sera from healthy donors and from patients with RA, osteoarthritis, Sjögren's syndrome, and systemic lupus erythematosus were measured with the ELISA.Results. In 7% of the RA patient samples (10 of 143), concentrations of serum sBST‐1 were higher (∼30–50‐fold) than in non‐RA samples. Serum sBST‐1 concentrations showed no correlation with age, C‐reactive protein level, or rheumatoid factor level. All RA patients with high concentrations of serum sBST‐1 had severe disease with involvement of several large joints.Conclusion. We believe the measurement of serum sBST‐1 may have prognostic value, but further analysis is necessary to clarify the clinical significance of elevated sBST‐1 in RA.
Accelerated generation of CD14+ monocyte‐lineage cells from the bone marrow of rheumatoid arthritis patients
Authors: Hirohata Shunsei , Yanagida Tamiko , Itoh Kenji , Nakamura Hiroshi , Yoshino Shin'Ichi , Tomita Tetsuya , Ochi Takahiro 
Published: February 2007

AbstractObjective. To examine the capacity of bone marrow progenitor cells to generate CD14+ cells, in order to assess the role of bone marrow in the pathogenesis of rheumatoid arthritis (RA).Methods. CD14‐ cells purified from bone marrow specimens of 11 patients with active RA and 8 control patients (osteoarthritis or trauma) were cultured in the presence or absence of granulocyte–macrophage colony‐stimulating factor (GM‐CSF; 100 pg/ml). After incubation for various lengths of time, the cells were analyzed by flow cytometry for expression of CD14 and HLA‐DR.Results. The spontaneous generation of CD14+ cells from bone marrow CD14‐ progenitor cells was accelerated in RA patients compared with control patients. Moreover, the expression of HLA–DR on the bone marrow–derived CD14+ cells was also accelerated in RA patients compared with controls. GM‐CSF significantly enhanced the generation of CD14+ cells, as well as the expression of HLA–DR, on CD14+ cells of control patients, but not those of RA patients. GM‐CSF levels in the culture supernatants of bone marrow CD14‐ cells were not significantly different between RA patients and control patients (undetectable in most cases).Conclusion. These observations strongly support the hypothesis that the accelerated generation of CD14+ cells from bone marrow progenitor cells and the accelerated maturation of such CD14+ cells into HLA–DR+ cells play an important role in the pathogenesis of RA. Moreover, the data suggest a functional alteration of RA bone marrow CD14‐ cells in their responsiveness to GM‐CSF.
Outcome in patients with early rheumatoid arthritis treated according to the “sawtooth” strategy
Authors: Möttönen Timo , Paimela Leena , Ahonen Jari , Helve Tapani , Hannon Pekka , Leirisalo‐Repo Marjatta 
Published: February 2007

AbstractObjective. To investigate the outcome of early rheumatoid arthritis (RA) when treated according to the “sawtooth” strategy, and to compare the results with the findings of other studies.Methods. In this prospective study, 142 patients with early RA were treated actively with slow‐acting antirheumatic drugs (SAARDs) for an average of 6.2 years, and were closely monitored clinically. Several outcome measures were applied, and the results were compared with findings in previously described cohorts.Results. The mean cumulative number of SAARDs used during the study was 3.3. Treatment changes were made because of inefficacy more often than because of adverse events. The percentage of patients whose disease entered remission increased with time to 32% (45 of 142). Only 24% of the patients (34 of 142) had deterioration to Steinbrocker functional class III or IV. The “sawtooth” treatment strategy seemed to improve the outcome of the patients with early RA.Conclusion. In the majority of patients with early RA, “sawtooth” therapy remains beneficial for at least 6 years. However, in one‐fourth of the patients, the disease fails to respond to this drug treatment strategy.
Childhood‐onset scleroderma: Is it different from adult‐onset disease?
Authors: Vancheeswaran Rama , Black Carol M. , David Joel , Hasson Nathan , Harper John , Atherton David , Trivedi Premila , Woo Patricia 
Published: February 2007

AbstractObjective. To distinguish childhood‐onset scleroderma from adult‐onset disease.Methods. The clinical and serologic features of 58 patients with childhood‐onset scleroderma (11 patients with diffuse cutaneous systemic sclerosis [SSc], 16 with linear SSc, 14 with linear morphea, and 17 with morphea) were examined in the largest cohort of such patients studied to date. These parameters were compared with data obtained from patients with adult‐onset disease.Results. Childhood‐onset scleroderma resembled adult‐onset disease with regard to the heterogeneity of clinical expression and subsets of disease, but it also differed from adult‐onset disease in a number of clinical and laboratory parameters. The predominant childhood‐onset disease presentation was the localized form of the disease, with limited and diffuse SSc being less notable. There was a significant association of trauma with childhood‐onset scleroderma (P < 0.0001), which was not noted in adult‐onset disease. Furthermore, in contrast to adult disease, patients with childhood‐onset disease had normal levels of parameters of vascular activation (von Willebrand factor, angiotensin‐converting enzyme, E‐selectin, and endothelin‐1), T cell activation (soluble interleukin‐2 receptors), and collagen synthesis (carboxy‐terminal type I and aminoterminal type III), a notable lack of anticentromere antibodies, and abnormal coagulation indices.Conclusion. A number of features distinguish childhood‐onset scleroderma from adult‐onset disease.
Pyoderma gangrenosum in association with undifferentiated seronegative spondylarthropathy
Authors: Olivieri Ignazio , Costa Angela Maria , Cantini Fabrizio , Niccoli Laura , Marini Raffaela , Ferri Silvio 
Published: February 2007

AbstractThe cases of 2 women with pyoderma gangrenosum (PG) and undifferentiated seronegative spondylarthropathy (SpA) are described. These 2 cases, together with the recently reported case of PG and B27‐positive psoriatic spondylarthropathy, suggest that PG may also occur in association with forms of seronegative SpA that are different from primary ankylosing spondylitis (AS) and AS associated with inflammatory bowel disease.
Monoclonal cryo‐antifibrinogenemia
Authors: Euler Hans H. , Zeuner Rainald A. , Béress Rosemarie , Gutschmidt Hans J. , Christophers Enno , Schroeder Johann O. 
Published: February 2007

AbstractWe report on a 54‐year‐old female patient with arthritis and a severe cold‐induced leukocytoclastic vasculitis of the skin caused by a rare form of cryofibrinogenemia (“type II” cryofibrinogen). Affinity chromatography of cryoprecipitates from the patient's plasma revealed reversible cryoprecipitability of complexes composed of fibrinogen and a monoclonal antifibrinogen antibody (IgG3k). Conventional serum and plasma electrophoresis did not detect the paraprotein. Control of symptoms was achieved by long‐term plasmapheresis.
Inhibition of fas antigen‐mediated apoptosis of rheumatoid synovial cells in vitro by transforming growth factor β1
Authors: Kawakami Atsushi , Eguchi Katsumi , Matsuoka Naoki , Tsuboi Masahiko , Kawabe Yojiro , Aoyagi Takahiko , Nagataki Shigenobu 
Published: February 2007

AbstractObjective. To investigate the mitogenic and anti‐apoptotic effects of transforming growth factor β1 (TGFβ) on rheumatoid synovial cells in vitro.Methods. Synovial cells were cultured with or without TGFβ1. After incubation, the proliferative response of synovial cells and the expression of Fas antigen and bcl‐2 on synovial cells were examined. Finally, Fas antigen‐mediated apoptosis of synovial cells was investigated by the addition of anti‐Fas antibody.Results. TGFβ1 enhanced the proliferation of synovial cells in a dose‐dependent manner. In addition, Fas antigen expression on synovial cells was inhibited by the addition of TGFβ1 with up‐regulation of bcl‐2 expression. The addition of anti‐Fas antibody induced synovial cell apoptosis. However, stimulation of synovial cells with TGFβ1 became markedly resistant to Fas antigen‐mediated apoptosis. The results were not affected by the addition of a neutralizing antibody to platelet‐derived growth factor type AA (PDGF‐AA), which suggests that the effect of TGFβ1 on synovial cells was promoted via PDGF‐AA‐independent mechanisms.Conclusion. Our results suggest that TGFβ1 promotes synovial cell proliferation through its mitogenic effect on synovial cells and interference with the apoptotic process mediated by the Fas antigen, resulting in the perpetuation of the synovial hyperplasia in patients with rheumatoid arthritis.
Detection of autoantibodies to nucleolar transcription factor NOR 90/hubf in sera of patients with rheumatic diseases, by recombinant autoantigen–based assays
Authors: Fujii Takao , Mimori Tsuneyo , Akizuki Masashi 
Published: February 2007

AbstractObjective. We attempted to clarify the clinical characteristics of Japanese patients with autoantibodies to nucleolar transcription factor NOR 90/hUBF (anti‐NOR 90) and to analyze the autoantigenic epitopes recognized by anti‐NOR 90.Methods. Ninety‐one patient sera containing anti‐nucleolar antibodies (ANoA) by indirect immunofluorescence were collected. Immunoblottings were performed using recombinant fusion proteins expressed from several cloned complementary DNA (cDNA) encoding the NOR 90/hUBF autoantigen.Results. Anti‐NOR 90 were detected in sera from 9 (9.9%) of 91 patients with ANoA. Seven of these patients were diagnosed as having Sjögren's syndrome, 4 had concomitant rheumatoid arthritis, I had concomitant systemic sclerosis (SSc), and 2 had SSc alone. All 9 sera were reactive with more than 2 recombinant fusion proteins from cDNA encoding separate regions on the hUBF polypeptide.Conclusion. The results suggest that while anti–NOR 90 antibodies are rare, they are associated with Sjögren's syndrome in Japanese patients, and that autoimmunity is targeted toward at least 2 separate regions (amino acids 89–310 and 310–633) of the hUBF polypeptide.
All‐trans‐retinoic acid in poems syndrome. Therapeutic effect associated with decreased circulating levels of proinflammatory cytokines
Authors: Authier François‐Jerome , Belec Laurent , Levy Yves , Lefaucheur Jean‐Pascal , Defer Gilles‐Louis , Degos Jean‐Denis , Gherardi Romain K. 
Published: February 2007

AbstractChronically elevated serum levels of proinflammatory cytokines is a feature of the syndrome known as POEMS (plasma cell dyscrasia with polyneuropathy, organomegaly, endocrinopathy, monoclonal [M] protein, skin changes). A patient had a POEMS syndrome with thrombocytosis and biclonal gammopathy and was treated as follows: all‐trans‐retinoic acid (tretinoin) at 90 mg/day for 50 days, no treatment for 70 days, readministration of tretinoin at 75 mg/day for 180 days. Focal bone lesion irradiation was performed from day 26 to day 50. Serum levels of interleukin‐6 (IL‐6), tumor necrosis factor a (TNFα), and IL‐1β normalized within 7 days after the first administration of tretinoin, transiently increased at the time of radiotherapy, increased again after withdrawal of the tretinoin, and decreased again after its reintroduction. The platelet count and gammopathy paralleled the changes in the cytokine levels. This study documents in vivo the ability of all‐trans‐retinoic acid to down‐regulate the release of IL‐6, IL‐1β, and TNFα, and illustrates its potential as a therapeutic agent in conditions associated with chronic overproduction of proinflammatory cytokines.
Epitope analysis of the major reactive region of the 100‐kd protein of PM‐Scl autoantigen
Authors: Ge Qun , Wu Yajuan , James Judith A. , Targoff Ira N. 
Published: February 2007

AbstractObjective. To localize the epitope(s) bound by anti–PM‐Scl antibodies in the N‐terminal half of the 100‐kd protein, the major antigen of the PM‐Scl complex.Methods. Investigations were performed by immunoblotting 20 anti–PM‐Scl positive sera against bacterially expressed, polymerase chain reaction–derived deletion mutants of the S1 fragment (amino acids 11–437), enzyme‐linked immunosorbent assay (ELISA) screening against synthesized serial octapeptides, and ELISA screening, with anti–PM‐Scl positive sera, against a synthesized 21–amino acid peptide covering the active region.Results. Anti–PM‐Scl positive sera retained full immunoblot activity with fragment 207–436 and most activity with fragment 11–241, but had markedly decreased activity against fragments 236–436 and 11–212, indicating a major epitope in the aa 207–241 region. Fusion proteins with smaller fragments localized this activity between aa 226 and aa 246. Of 42 anti–S1‐positive, anti–PM‐Scl positive sera tested by ELISA against a synthetic peptide of this region, 36 were definitely positive, 4 borderline, and 2 negative. Similar activity was seen with a peptide from which proline 228 was deleted. Three additional epitope areas were found in S1, but each reacted with only a few sera. Anti–PM‐Scl positive sera did not react with any octapeptide spanning the major epitope area (aa 207–246).Conclusion. The main immunoblot epitope of the PM‐Scl 100‐kd protein is within a central area of 21 aa (aa 226–246), but is longer than the usual linear epitope. This peptide may be useful in patient testing. Three minor epitopes in S1 may also be recognized by some sera.
Addition of corticosteroids to antibiotic treatment ameliorates the course of experimental Staphylococcus aureus arthritis
Authors: Sakiniene Egidija , Bremell Tomas , Tarkowski Andrzej 
Published: February 2007

AbstractObjective. To evaluate the combined effect of systemic corticosteroid and antibiotic therapy on the course of septic arthritis.Methods. The murine model of hematogenously acquired Staphylococcus aureus arthritis was used. Mice were treated with corticosteroids and antibiotics, and were followed up individually. Arthritis was evaluated clinically and histopathologically. Serum samples and bacterial isolates were also analyzed.Results. The prevalence of arthritis 14 days after the onset of the disease was 22% in the corticosteroid and antibiotic–treated group, as compared with 81% in the control (nontreated) group and 48% in the antibiotic‐treated group. The severity of arthritis also decreased in the corticosteroid and antibiotic‐treated group, as did the mortality rate. Immunohistochemical analysis revealed a dramatic decrease in T cells and macrophages in the synovium of mice that took the combined therapy. The mechanisms leading to this outcome include the inhibitory effect of corticosteroids on T cell and B cell proliferation and differentiation, such as suppression of interferon‐γ (IFNγ) production. Serum levels of IFNγ were decreased 4‐fold in the antibiotic‐treated group compared with the controls; a 15‐fold decrease was observed in the corticosteroid and antibiotic–treated animals. In addition, serum NO3− was significantly decreased in mice treated with antibiotics (P ≤ 0.05), as well as in mice treated with corticosteroids and antibiotics (P ≤ 0.001).Conclusion. Systemic corticosteroid administration along with antibiotic therapy had beneficial effects on the course and outcome of S aureus arthritis.