bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nucleosome‐specific antibody from an autoimmune mrl/mp‐lpr/lpr mouse
Authors: Losman Julie A. , Fasy Thomas M. , Novick Kristine E. , Massa Margherita , Monestier Marc 
Published: February 2007

AbstractObjective. To characterize the binding properties and variable‐region sequences of LG4‐1, a monoclonal antibody from an autoimmune MRL/Mp‐lpr/lpr mouse that reacts specifically with nucleosome core particles and represents a new antinuclear antibody specificity.Methods. The reactivity of the antibody against various nuclear substrates was determined using an enzymatic immunoassay, and the variable‐region genes were sequenced from messenger RNA, using the dideoxy chain termination method.Results. LG4‐1 was found to react with nucleosome core particles but not with individual histones and DNA, or with various histone–histone and histone–DNA complexes. It was demonstrated that this antibody is encoded by a combination of variable‐region genes and gene segments that have undergone few somatic mutations.Conclusion. The nucleosome core particle expresses a unique conformational autoepitope(s) resulting from the ordered association of histones and DNA.
Labial salivary gland biopsy is a reliable test for the diagnosis of primary and secondary amyloidosis. a prospective clinical and immunohistologic study in 59 patients
Authors: Hachulla Eric , Janin Anne , Flipo René Marc , Saïle Rachid , Facon Thierry , Bataille Dominique , Vanhille Philippe , Hatron Pierre‐Yves , Devulder Bernard , Duquesnoy Bernard 
Published: February 2007

AbstractObjective. Reports of the detection of amyloidosis by labial salivary gland (LSG) biopsy have been mostly anecdotal. The aim of this study was to assess the value of this method in the diagnosis of amyloidosis.Methods. LSG biopsy tissues were studied with a combination method using Congo red stain and immunohistologic characterization using an antibody directed against the serum amyloid P (SAP) component. Electron microscopy was performed in all cases. In a prospective study, we evaluated 30 patients with biopsy‐proven AA or AL amyloidosis. We compared these patients with a control group of 29 age‐matched patients without clinical or biologic evidence of amyloid disease (14 had rheumatoid arthritis and 15 had plasma cell dyscrasia).Results. In 26 of the 30 patients with known systemic amyloidosis, amyloid deposits were identified on LSG biopsy (sensitivity of 86%). In 1 of the remaining patients, amyloid deposits were identified on LSG biopsy and systemic amyloidosis was confirmed by abdominal fat biopsy and 123I‐labeled SAP scintigraphy.Conclusion. This study emphasizes the high sensitivity of LSG biopsy in the diagnosis of amyloidosis, even in the absence of oral symptoms.
Spontaneous production of epstein‐barr virus by b lymphoblastoid cell lines obtained from patients with sjögren's syndrome. possible involvement of a novel strain of epstein‐barr virus in disease pathogenesis
Authors: Tateishi Mutsuto , Saito Ichiro , Yamamoto Kohtaro , Miyasaka Nobuyuki 
Published: February 2007

AbstractObjective. To investigate the involvement of Epstein‐Barr virus (EBV) in the pathogenesis of Sjögren's syndrome (SS) and to examine whether the spontaneous production of EBV is unique to SS B cell lines.Methods. B cell lines were established from peripheral blood mononuclear cells (PBMC) of patients with systemic lupus erythematosus, rheumatoid arthritis, and SS. The cord blood immortalization assay, flow cytometric analysis, and polymerase chain reaction (PCR) were used to detect EBV production by B cell lines.Results. SS B cell lines produced EBV at a higher frequency, and in significantly larger amounts, than did other B cell lines. However, no correlation with the amount of EBV DNA in the genome of B cell lines was found. PCR analysis revealed that EBV with a B95‐8–like U2 region was dominant in SS B cell lines.Conclusion. Spontaneous, massive production of EBV by B cell lines is unique to SS, and may contribute to the polyclonal B cell activation seen in this disease.
Comparative studies of the major histocompatibility complex in french canadian and non–french canadian caucasians with systemic lupus erythematosus
Authors: Goldstein Rose , Sengar Dharmendra P. S. 
Published: February 2007

AbstractObjective. To investigate and compare the predisposing role of major histocompatibility complex (MHC) genes in systemic lupus erythematosus (SLE) in French Canadian and non–French Canadian (mainly Anglo‐Saxon descent) Caucasian subjects.Methods. HLA–A, B, C (serology), DR, and DQ (restriction fragment length polymorphism [RFLP] typing) were determined. RFLP defining a large C4A,21‐OHA deletion (Taq I C4) and an Nco I tumor necrosis factor α (TNFα) RFLP were analyzed in 91 Caucasian Canadians and 91 ethnically matched control subjects.Results. In the total SLE and non–French Canadian SLE populations, HLA–B8, DR3(DR17), Dw24, DQ2, and the C4A gene deletion were associated with SLE. These HLA specificities and the C4A gene deletion were not significantly increased in French Canadian SLE patients compared with ethnically matched controls. When present in French Canadians, the C4A gene deletion was less closely associated with HLA–DR3(DR17), Dw24, DQ2 than in other Caucasians. HLA–DQ6 was associated with SLE in French Canadians. No association of the 2‐allele Nco I TNFα RFLP with SLE was found in this population, in either ethnic group.Conclusion. These results support the importance of ethnic background in the study of MHC genes and SLE. The extended HLA–B8,DR3,C4A null haplo‐type is found mainly in SLE patients of Anglo‐Saxon descent, while the DQ6 specificity is associated with SLE in French Canadians. This relatively genetically homogeneous Caucasian population offers the opportunity to study non–HLA–B8,DR3–linked MHC influence in SLE.
Synergistic effect of interleukin‐1β and tumor necrosis factor α on interleukin‐8 gene expression in synovial fibroblasts. evidence that interleukin‐8 is the major neutrophil‐activating chemokine released in response to monokine activation
Authors: Rathanaswami Palaniswami , Hachicha Mohamed , Wong Wai Lee , Schall Thomas J. , Mccoll Shaun R. 
Published: February 2007

AbstractObjective. To investigate both the involvement of chemokines in general and the relative importance of specific chemokines in rheumatoid arthritis (RA), we characterized the effect of the monokines tumor necrosis factor α (TNFα) and interleukin‐1β (IL‐1β) on the synthesis of neutrophil‐activating factors by synovial fibroblasts isolated from the joints of patients with RA.Methods. Neutrophil‐stimulating activity was assessed by determining intracellular calcium mobilization. IL‐8 synthesis and secretion was assessed by specific enzyme‐linked immunosorbent assay, and IL‐8 messenger RNA (mRNA) levels were determined by Northern blot.Results. Treatment of synovial fibroblasts with IL‐1β and TNFα resulted in the production of an activity which induced intracellular calcium mobilization in peripheral blood neutrophils. The 2 monokines combined had a synergistic effect on the release of the neutrophil‐stimulating activity. The effect of the 2 monokines required gene transcription and translation, and closely mimicked the pattern of IL‐8 secretion induced in these cells by the monokines. We confirmed that the majority of the neutrophil‐stimulating activity was IL‐8 by 3 different approaches: cross‐desensitization experiments with IL‐8, melanoma growth‐stimulatory activity, and neutrophil‐activating peptide 2, stimulation of calcium mobilization in cells transfected with the IL‐8 receptor complementary DNA, and inhibition of the activity following pretreatment of the supernatants with an anti‐IL‐8 antibody. TNFα and IL‐1β induced a time‐ and dose‐dependent release of immunoreactive IL‐8. A synergistic effect of TNFα and IL‐1β was also observed for both IL‐8 production and accumulation of IL‐8 mRNA.Conclusion. These results indicate that the monokines TNFα and IL‐1β synergistically activate IL‐8 expression and protein secretion by synovial fibroblasts, and that under these conditions, IL‐8 appears to be the major neutrophil‐activating factor released.
In vitro release of prostaglandins and leukotrienes from synovial tissue, cartilage, and bone in degenerative joint diseases
Authors: Wittenberg Ralf H. , Willburger Roland E. , Kleemeyer Karin S. , Peskar Bernhard A. 
Published: February 2007

AbstractObjective. To determine the major source of eicosanoid release in arthritic joint tissues and to examine the modulation of this release by indomethacin and diclofenac.Methods. Release of prostaglandin E2 (PGE2), 6‐keto‐PGF1α, leukotriene B4 (LTB4), and LTC4 was measured in supernatants of synovial tissue, cartilage, and bone incubates from patients with osteoarthritis, active rheumatoid arthritis (RA), inactive RA, and pseudogout. Radioimmunoassay (RIA) was used to determine the levels of the eicosanoids.Results. Addition of the divalent cation ionophore A23187 resulted in significant release of all eicosanoids measured from synovial tissue, but not from cartilage, cortical bone, or cancellous bone. PG release was significantly inhibited by the addition of indomethacin or diclofenac at either 10–5 moles/liter or 10–7 moles/liter. The amount of LTC4 released from cartilage and bone was only slightly above the detection limit of the RIA, whereas large amounts were released from synovial tissue. Neither indomethacin nor diclofenac had an effect on LTC4 release. LTC4 release from synovial tissue of patients with inactive RA was significantly decreased in comparison with the levels from synovial tissue of patients with the other joint diseases. There was no significant difference in PG release among patients in the various disease groups.Conclusion. Synovial tissue appears to be the major source of eicosanoids in synovial fluid. Indomethacin and diclofenac inhibit the release of PG, but not LT, from various joint tissues.
The course of skin involvement in systemic sclerosis over three years in a trial of chlorambucil versus placebo
Authors: Clements Philip , Lachenbruch Peter , Furst Daniel , Paulus Harold 
Published: February 2007

AbstractObjective. To describe the course of cutaneous involvement in systemic sclerosis (SSc; scleroderma) over 3 years, in the context of a placebo‐controlled drug trial.Methods. The course of skin tethering (assessed by a semiquantitative skin scoring technique) was documented annually for 3 years in 64 SSc patients with early (< 3 years duration at entry), intermediate (3–8 years duration), or late (>8 years duration) diffuse or limited SSc.Results. Mean ± SD entry skin scores were significantly greater in the 33 diffuse SSc patients (13.1 ± 5.0) than in the 31 limited SSc patients (4.3 ± 2.1) (P < 0.001). In patients with diffuse SSc, the skin score remained stable for the first 12 months, but had decreased significantly by 24 months (P < 0.022) and 36 months (P < 0.004). In those with limited SSc, the skin score did not change significantly over 3 years.Conclusion. Trials of treatments designed to affect skin thickening/tethering should be conducted in patients who have diffuse SSc (of short, intermediate, or long duration) at entry. The best time to study therapies designed to affect skin thickening may be in the first year after entry.
Immunohistochemical analysis of 3‐b‐3(–) and 7‐d‐4 epitope expression in canine osteoarthritis
Authors: Visco Denise M. , Johnstone Brian , Hill Michael A. , Jolly Grant A. , Caterson Bruce 
Published: February 2007

AbstractObjective. To examine the distribution of the 3‐B‐3(–) and 7‐D‐4 epitopes in proteoglycans from morphologically normal and osteoarthritic (OA) canine articular cartilage.Methods. Cartilage samples from the femurs of stable and destabilized stifle joints of 9 dogs that had undergone transection of the cranial cruciate ligament were examined by immunohistochemistry.Results. The 3‐B‐3(–) and 7‐D‐4 epitopes were expressed in the superficial zone of cartilage from the destabilized femorotibial joints in the early stages of developing OA. The staining patterns with these two antibodies differed, with 3‐B‐3(–) reactivity confined to the superficial and upper middle zones of the articular cartilage, and 7‐D‐4 reactivity more prominent in the matrix, extending into the deeper zones and increasing with progression of the lesion. Both epitopes were also expressed in the superficial and upper middle zones of areas peripheral to the lesions and were detectable before the loss of matrix and proteoglycans could be identified by histochemical staining with toluidine blue.Conclusion. In this study, the expression of atypical chondroitin sulfate proteoglycans was demonstrated in osteoarthritic canine cartilage, and the pattern of expression changed as the lesions progressed. The occurrence of 3‐B‐3(–) and 7‐D‐4 epitopes appears to be associated with changes in chondrocyte metabolism in the early stages of cartilage degeneration in experimental osteoarthritis.
High Frequency of Silent Inflammatory Bowel Disease in Spondylarthropathy
Authors: Leirisalo‐Repo Marjatta , Turunen Ulla , Stenman Svante , Helenius Petri , Seppälä Kari 
Published: February 2007

AbstractObjective. To search for an association between gut infection, gut inflammation, and spondylarthropathies.Methods. Ileocolonoscopy was performed in 118 patients with various inflammatory and noninflammatory joint diseases and in 24 patients with uncomplicated acute bacterial gastroenteritis.Results. Endoscopic lesions were more frequent in patients with spondylarthropathy (44%) compared with those with other inflammatory arthritides (6%; P = 0.001). Ileal changes were observed only in patients with spondylarthropathy (20% versus 0%; P = 0.01). Inflammatory bowel disease was the endoscopic diagnosis in 19% of the arthritis patients. Possible or definite Crohn's disease was diagnosed in 26% of patients with chronic spondylarthropathy, and ulcerative colitis in 1 patient with rheumatoid arthritis and in 1 with chronic uroarthritis. Histologic evidence of inflammation differed less distinctly than endoscopy findings between patient groups. There was no association of gut lesions with the use of nonsteroidal antiinflammatory drugs or with the presence of HLA‐B27.Conclusion. Gut inflammation is frequent in patients with spondylarthropathy, and one‐fourth of the patients who have chronic disease have early features of Crohn's disease.
HIP Osteonecrosis Secondary to the Administration of Corticosteroids for Feigned Bronchial Asthma
Authors: Alarcön Graciela S. , Mikhail Isis , Jaffe Kenneth A. , Bradley Laurence A. , Bailey William C. 
Published: February 2007

AbstractWe describe the case of a woman who developed hip osteonecrosis after prolonged use of corticosteroids for feigned bronchial asthma. This type of musculoskeletal manifestation of the factitious disorders has not been reported previously.
Expression of L‐Selectin, CD43, and CD44 in Synovial Fluid Neutrophils from Patients with Inflammatory Joint Diseases
Authors: Humbría Alicia , Díaz‐González Federico , Campanero Miguel R. , Arroyo Alicia G. , Laffón Armando , González‐Amaro Roberto , Sánchez‐Madrid Francisco 
Published: February 2007

AbstractObjective. To study the expression of L‐selectin, CD43, and CD44 on peripheral blood (PB) and synovial fluid (SF) neutrophils from patients with inflammatory joint diseases, and to investigate the presence of soluble L‐selectin in both SF and plasma from patients with acute and chronic arthritis.Methods. PB and SF neutrophils were isolated from 13 patients with rheumatoid arthritis (RA) and 17 patients with various inflammatory joint diseases other than RA. Expression of L‐selectin, CD43, CD44, CD11a, and CD11b was determined in both unstimulated and in vitro—activated cells by immunofluorescence flow cytometry. Soluble L‐selectin levels were estimated in SF and plasma by a semiquantitative radioimmunoassay.Results. Neutrophils from SF showed diminished expression of L‐selectin compared with PB neutrophils; CD43 expression and CD44 expression were decreased in SF neutrophils from most patients. In contrast, SF neutrophils exhibited significantly increased expression of CD11b, to an extent similar to that seen with in vitro—activated PB neutrophils. Soluble L‐selectin was detected at similar levels in SF and PB.Conclusion. The phenotypic profile of SF neutrophils (low levels of L‐selectin, CD43, and CD44, and high levels of CD11b) from most patients with RA or other inflammatory joint conditions resembles that observed in in vitro—activated neutrophils. Our results suggest that SF neutrophils are activated to a similar degree in inflammatory joint diseases with different pathogenic mechanisms.
Effects of Peripheral Cold Exposure on Microvascular Dynamics in Systemic Sclerosis
Authors: Grassi Walter , Core Paolo , Carlino Giorgio , Cervini Claudio 
Published: February 2007

AbstractObjective. To determine the influence of cold exposure on microvascular permeability in systemic sclerosis (SSc).Methods. Thirteen patients with SSc were studied by dynamic fluorescence videomicroscopy under basal conditions and after exposure to cold.Results. Exposure to cold caused a significant reduction in the interstitial concentration of sodium fluorescein (P < 0.05 to 0.001).Conclusion. Our findings show that cold exposure has a striking effect on microvascular dynamics in SSc.
Inhibition of Collagenase Activity by N‐Chlorotaurine, a Product of Activated Neutrophils
Authors: Davies Joanna M. S. , Horwitz David A. , Davies Kelvin J. A. 
Published: February 2007

AbstractObjective. To study the effects of N‐chlorotaurine on collagenase activity, as a model of the effects of neutrophil activation in inflammatory arthritis.Methods. Collagen degradation by collagenase was measured by the release of acid‐soluble counts from 3H‐collagen.Results. N‐chlorotaurine inhibited the degradation of collagen by bacterial collagenase. This result is explained by a direct inhibition/inactivation of collagenase, since N‐chlorotaurine had no effect on the proteolytic susceptibility of collagen itself. The effect appears to be specific to N‐chlorotaurine since N‐chloroalanine, N‐chloroleucine, and HOCl/OCl‐ failed to inhibit collagenase; in fact, N‐chloroalanine and N‐chloroleucine actually increased the proteolytic susceptibility of collagen.Conclusion. N‐chlorotaurine may minimize damage to cartilaginous joint structures in inflammatory arthritis by inhibiting/inactivating collagenase.
Safe and effective isokinetic knee extension training in rheumatoid arthritis
Authors: Lyngberg Kirsten K. , Ramsing Benedicte U. , Nawrocki Anette , Harreby Mette , Danneskiold‐Samsøe Bente 
Published: February 2007

AbstractObjective. To evaluate the safety of isokinetic knee extensor strength training, and its effectiveness with regard to knee extension, in patients with rheumatoid arthritis (RA).Methods. Nine women with RA, all in functional stage II or III, underwent a low‐intensity strengthening protocol with 48 repetitions at 50% of maximal voluntary contraction, 3 times per week for 3 weeks, using an isokinetic dynamometer.Results. Five patients had knee synovitis at entry; but neither synovitis nor joint pain increased. The mean gain in strength was 21%.Conclusion. This training method was effective and safe in patients with RA.
Interleukin‐1β induces cytosolic phospholipase a2 and prostaglandin h synthase in rheumatoid synovial fibroblasts
Authors: Hulkower Keren I. , Wertheimer Stanley J. , Levin Wayne , Coffey John W. , Anderson Celia M. , Chen Ting , Dewitt David L. , Crowl Robert M. , Hope William C. , Morgan Douglas W. 
Published: February 2007

AbstractObjective. In order to investigate potential regulatory mechanisms for the increased production of prostaglandin E2 (PGE2) in interleukin‐1β (IL‐1β)–stimulated rheumatoid synovial fibroblasts (RSF), this study examined the induction of phospholipase A2 (PLA2) and prostaglandin H synthase (PGHS) enzymes and the correlation of these events with PGE2 production in IL‐1β–stimulated RSF.Methods. Protein and messenger RNA (mRNA) levels of cytosolic PLA2 (cPLA2) and PGHS‐2 enzymes in IL‐1β–stimulated RSF were measured by Western and Northern blotting, respectively, using specific antisera and complementary DNA probes. Enzymatic activity of cPLA2 was determined in cell‐free reaction mixtures utilizing mixed micelles of 14C‐phosphatidylcholine and Triton X‐100 as the substrate. PGE2 levels were quantitated using a commercial enzyme immunoassay kit.Results. Incubation of RSF with IL‐1β increased the mRNA and protein levels for the high molecular weight cPLA2 as well as for the mitogen/growth factor–responsive PGHS (PGHS‐2). The IL‐1 receptor antagonist completely abolished the induction of these two enzymes and the stimulation of PGE2 production by IL‐1β in RSF. In contrast, levels of the other known forms of these enzymes, i.e., the 14‐kd secretory group II PLA2 (sPLA2) and the constitutive form of PGHS (PGHS‐1), were unaffected by IL‐1β treatment.Conclusion. These are the first data to demonstrate the coordinate induction by IL‐1 of cPLA2 and PGHS‐2 in RSF. The time‐course for the induction of these enzymes suggests that their increase contributes to the increased production of PGE2 in IL‐1–treated RSF, and may help explain the capacity of RSF to produce large amounts of PGE2.
Modulation of helper T cell function by prostaglandins
Authors: Gold Kenneth N. , Weyand Cornelia M. , Goronzy JöRg J. 
Published: February 2007

AbstractObjective. To determine the influence of prostaglandins on the production of interleukins 2, 4, and 5 (IL‐2, IL‐4, and IL‐5), interferon‐γ (IFNγ), granulocytemacrophage colony‐stimulating factor, and transforming growth factor β1 by CD4+ T cells.
Methods. TH0, TH1, and TH2 T cell clones were stimulated in the presence and absence of the prostaglandin E1 (PGE1) analog misoprostol and PGE2. Lymphokine production was analyzed by using a semiquantitative polymerase chain reaction with lymphokine‐specific primer sets and/or by determining lymphokine activity in bioassays.
Results. PGE2 and misoprostol have distinct effects on different functional T helper cells. TH1 cells, which predominantly produce IL‐2 and IFNγ, are completely inhibited, while TH2 cells, which preferentially produce IL‐4 and IL‐5, are largely unaffected. Misoprostol and PGE2 are equivalent in their ability to modulate T cell function. In the presence of prostaglandins, THO‐like helper cells, which are characterized by the coproduction of multiple lymphokines, function as TH2 cells; however, they do not differentiate into TH2 T cells.
Conclusion. Prostaglandins that are produced in inflamed tissue can regulate the functional capabilities of infiltrating T cells. In the presence of PGE2, TH1‐like responses are suppressed and TH0‐like responses are shifted toward a TH2‐like pattern dominated by the production of IL‐4 and IL‐5. Inhibition of prostaglandin production by antiinflammatory agents might restore TH1 responses with local production of IL‐2 and IFNγ.