bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lupus and pregnancy studies
Authors: Urowitz Murray B. , Gladman Dafna D. , Farewell Vern T. , Stewart Jacqueline , Mcdonald Joanne 
Published: February 2007

AbstractObjective. To examine factors prior to pregnancy in patients with systemic lupus erythematosus (SLE) that are prognostic for the occurrence of active disease during and shortly after pregnancy.Methods. Case–control study of pregnant SLE patients and nonpregnant SLE controls, using logistic regression analyses to assess the role of prepregnancy disease activity as a prognostic factor for flare during pregnancy or the postpartum followup period.Results. Lupus flares occurred frequently and in similar percentages of pregnant SLE patients and control SLE patients. Active lupus at study entry, both in control and in pregnant patients, was not predictive of flare. Inactive lupus at onset was not protective against flare in controls but was protective in pregnant lupus patients.Conclusion. Inactive disease at the onset of pregnancy in SLE provides optimum protection against the occurrence of flare during pregnancy.
Predictors of psychosocial adjustment in systemic sclerosis
Authors: Moser Debra K. , Clements Philip J. , Brecht Mary‐Lynn , Weiner Steven R. 
Published: February 2007

AbstractObjective.To determine predictors of psychosocial adjustment in patients with systemic sclerosis (SSc).Methods.We surveyed 94 patients with SSc. Age, sex, education level, marital status, work status, income, support group attendance, length of time since diagnosis, functional status, social support, illness‐related uncertainty, and hardiness were examined as potential predictors of psychosocial adjustment. The reliability and validity of the instruments used to measure these variables have been established.Results.Only education level, functional ability, illness‐related uncertainty, hardiness, and social support were predictive of psychosocial adjustment. Education level and functional ability explained 14% of the variance in psychosocial adjustment, while illness‐related uncertainty, hardiness, and social support increased the explained variance to 38%.Conclusion.Although patients with relatively poorer psychosocial adjustment to illness have lower formal education levels and more functional disability, the majority of the explained variance in psychosocial adjustment is ascribable to illness‐related uncertainty, low level of hardiness, and less satisfaction with social support.
Autoantigenic epitopes on dna topoisomerase i
Authors: Kuwana Masataka , Kaburaki Junichi , Mimori Tsuneyo , Tojo Takeshi , Homma Mitsuo 
Published: February 2007

AbstractObjective. To elucidate the clinical and immunogenetic associations with reactivity to autoantigenic epitopes on DNA topoisomerase I (topo I) recognized by sera from patients with systemic sclerosis (SSc).Methods. Autoantigenic epitopes on topo I were identified by screening an epitope library constructed from topo I complementary DNA restriction fragments using autoimmune anti–topo I–positive sera as a probe. Epitope reactivities of sera from 43 anti–topo I–positive SSc patients were surveyed by immunoblotting, and associations with clinical symptoms and HLA–DR types were examined.Results. Four different epitope regions were identified on the topo I molecule. Immunoreactivity to the region encompassing amino acid residues 658–700, termed ER4, was found to be associated with diffuse cutaneous SSc, progressive pulmonary interstitial fibrosis, and poor prognosis for 15‐year survival. SSc patients with ER4 reactivity frequently displayed the DR2/DRw52 phenotype.Conclusion. Molecular analysis of precise antigenic epitopes on topo I is helpful in classifying clinical subsets of SSc.
Modulation of human t cell responses by nitric oxide and its derivative, s‐nitrosoglutathione
Authors: Merryman Parvin F. , Clancy Robert M. , He Xiao Yuen , Abramson Steven B. 
Published: February 2007

AbstractObjective. To examine the effects of nitric oxide (NO) and its more stable derivative, S‐nitrosoglutathione (SNO‐GSH), on the response of activated T lymphocytes.Methods. The effects of NO and SNO‐GSH on DNA synthesis, interleukin‐2 (IL‐2) production, IL‐2 receptor expression, and cGMP accumulation were determined in phytohemagglutinin–activated peripheral blood mononuclear cells (PBMC) and spleen T cells.Results. Nitric oxide (half‐life [T1/2] < 15 seconds) did not inhibit T cell proliferation. However, the derivative SNO‐GSH (25 μM) (T1/2 >2 hours) inhibited DNA synthesis by a mean ± SD of 65 ± 19.6% (P < 0.001) in PBMC and 75 ± 15% (P < 0.001) in spleen cells. Macrophage depletion of PBMC did not abrogate the inhibition. SNO‐GSH had no effect on IL‐2 production or IL‐2 receptor expression. NO (25 μM) increased the cGMP content of PBMC (0.65 ± 0.15 pmoles/106 cells; P < 0.04), as did SNO‐GSH (25 μM) in both PBMC (3.8 ± 1; P < 0.001) and spleen T cells (5.2 ± 1.2; P < 0.001). Methylene blue and hemoglobin, which are NO inhibitors, inhibited SNO‐GSH–induced cGMP accumulation (P < 0.001).Conclusion. SNO‐GSH inhibits T cell DNA synthesis independently of IL‐2 production and in association with cGMP accumulation via a NO‐dependent mechanism. We suggest that NO and its S‐nitrosothiol derivatives may act as endogenous inhibitors of T cell–mediated inflammation.
Detection of human t lymphotropic virus type i tax gene in salivary gland epithelium from two patients with sjögren's syndrome
Authors: Mariette Xavier , Agbalika Felix , Daniel Marie‐ThéRèSe , Bisson Michel , Lagrange Philippe , Brouet Jean‐Claude , Morinet Frédéric 
Published: February 2007

AbstractObjective. To investigate whether human T lymphotropic virus type I (HTLV‐I) could be involved in the pathogenesis of Sjögren's syndrome (SS).Methods. Labial salivary gland (LSG) biopsy specimens from 9 patients with SS (4 with primary SS and 5 with SS secondary to rheumatoid arthritis) and 9 controls were studied for the presence of the tax gene of HTLV‐I using in situ hybridization, and for the presence of tax, gag, pol, and env genes of HTLV‐I using the polymerase chain reaction (PCR). Testing for antibodies to HTLV‐I and examination of lymphocytes on blood smears were performed to determine whether systemic viral infection was present.Results. Using in situ hybridization and PCR, we detected the tax gene, but not the gag, pol, or env genes, of HTLV‐I in LSG sections from 2 of 9 patients with SS and from none of the control subjects. Tax DNA was present mostly in nuclei of epithelial cells, but also in some lymphoid cells. Serum of the 2 affected patients did not contain antibodies to HTLV‐I. In 1 patient, examination of blood smears revealed rare convoluted lymphocytes, sometimes with the appearance of “flower cells,” as observed in the blood of HTLV‐I–infected patients.Conclusion. None of the known endogenous retroviral sequences is homologous to the tax gene. Thus, we suggest that HTLV‐I (or another related retrovirus) can infect salivary epithelium. Transactivation properties of the tax protein could be implicated in the pathogenesis of SS. Alternatively, viral infection could cause de novo expression of HLA–DR antigens and favor the presentation of antigens by epithelial cells, leading, in some genetically predetermined subjects, to lymphoid infiltration of the gland.
A longitudinal study of subchondral plate and trabecular bone in cruciate‐deficient dogs with osteoarthritis followed up for 54 months
Authors: Dedrick D. K. , Goldstein S. A. , Brandt K. D. , O'Connor B. L. , Goulet R. W. , Albrecht M. 
Published: February 2007

AbstractObjective. To evaluate the sequence of changes in articular cartilage, trabecular bone, and subchondral plate in dogs with osteoarthritis (OA), 3 months, 18 months, and 54 months after anterior cruciate ligament transection (ACLT).Methods. Specimens of the medial tibial plateau were analyzed with microscopic computed tomography (micro‐CT) at a resolution of 60 μm, and biochemical and morphologic changes in the femoral articular cartilage were assessed.Results. At 3 months and 18 months after ACLT, the articular cartilage in the unstable knee showed histologic changes typical of early OA and increased water content and uronic acid concentration; by 54 months, full‐thickness ulceration had developed. Micro‐CT analysis showed a loss of trabecular bone in the unstable knee, compared with the contralateral knee, at all time points. At both 18 and 54 months, the differences in trabecular thickness and surface‐to‐volume ratio were greater than at 3 months. Although the mean subchondral plate thickness, especially in the medial aspect of the medial tibial plateau, was greater in the OA knee than in the contralateral knee 18 months and 54 months after ACLT, these differences were not statistically significant; however, the difference was significantly greater at 54 months than at 3 months.Conclusion. Thickening of the subchondral bone is not required for the development of cartilage changes of OA in this model. The bony changes that develop after ACLT, however, could result in abnormal transmission of stress to the overlying cartilage and thereby contribute to the progression of cartilage degeneration.
Calcific tendinitis in the proximal thigh
Authors: Hodge Jacqueline C. , Schneider Robert , Freiberger Robert H. , Magid Steven K. 
Published: February 2007

AbstractCalcific tendinitis of the proximal thigh is a benign entity that may cause significant pain. It must be distinguished from chronic or malignant disorders, such as arthritis, infection, and soft tissue/cortical neoplasms. Although it may be self‐limited, some patients will benefit from medical intervention. In such cases, we recommend computed tomography–guided percutaneous steroid injection. Herein we describe the clinical and radiographic features of calcific tendinitis of the proximal thigh in 5 patients.
“Chronic lyme disease” as the incorrect diagnosis in patients with fibromyalgia
Authors: Hsu Vivien M. , Patella Sondra J. , Sigal Leonard H. 
Published: February 2007

AbstractObjective. To evaluate a large number of patients referred with persistent symptoms thought to represent chronic Lyme disease.Methods. We retrospectively reviewed the charts of nearly 800 patients referred with persisting nonspecific musculoskeletal and/or neurologic symptoms thought to represent chronic Lyme disease.Results. Seventy‐seven patients were found to have fibromyalgia, not ongoing Lyme disease, as the explanation of their chronic symptoms. Many had received multiple courses of antibiotic therapy for symptoms of fibromyalgia mistakenly attributed to chronic Lyme disease. No patient reported permanent and/or total resolution of fibromyalgia symptoms following antibiotic therapy. Appropriate therapy for fibromyalgia in those who remained compliant, however, was often effective in improving some if not all of the chronic symptoms.Conclusion. Fibromyalgia is a treatable and potentially curable disorder, and should be considered in the evaluation of patients with “refractory Lyme disease.”
Sulfasalazine in early rheumatoid arthritis. A 48‐week double‐blind, prospective, placebo‐controlled study
Authors: Hannonen Pekka , Möttönen Timo , Hakola Mikko , Oka Martti 
Published: February 2007

AbstractObjective.To investigate the efficacy and tolerability of sulfasalazine (SSZ) in the treatment of early rheumatoid arthritis (RA).Methods.Eighty patients (symptomatic disease < 12 months) were randomly assigned to treatment with SSZ or placebo for 48 weeks. Clinical, laboratory, and scintigraphic data were used to determine the effects of treatment.Results.SSZ was superior to placebo in reducing the laboratory features of inflammation, the clinical parameters of disease activity, as well as the scintigraphic activity in the joints. Furthermore, fewer erosive changes developed in the joints of patients receiving active treatment, but the difference between treatment groups did not reach statistical significance.Conclusion.SSZ is effective in the treatment of RA, and its onset of action is rapid. The results support the view that SSZ retards the development of joint erosions. However, like other conventional disease‐modifying antirheumatic drugs, its remission‐inducing ability is insufficient.
The effect of rheumatoid arthritis and steroid therapy on bone density in postmenopausal women
Authors: Hall Gerard M. , Spector Tim D. , Jane Griffin A. , S. M. Jawad Ali , Hall Margaret L. , Doyle David V. 
Published: February 2007

AbstractObjective. To assess bone mineral density (BMD) in postmenopausal women with rheumatoid arthritis (RA) and the relative effects of disease activity, disability, and past and current use of corticosteroids.Methods. One hundred ninety‐five postmenopausal patients with RA were compared with 597 postmenopausal control subjects. Bone density was measured at the lumbar spine and the proximal femur using dual x‐ray absorptiometry. Patients were divided into 3 groups according to corticosteroid use, i.e., never users (61%), current users (21%), and ex‐users (18%).Results. Compared with controls, the never users had no difference in BMD at the lumbar spine, but a 6.9% reduction at the femur (95% confidence interval [95% CI] 3.4–10.3%). In current users (mean daily prednisolone dosage 6.9 mg), BMD was reduced by 6.5% at the spine (95% CI 0–13.0%) and by 7.4% at the hip (95% CI 1.2–13.6%) compared with never users, after adjustment for age, weight, duration of menopause, and functional disability. Mean BMD was similar in the ex‐user and never user groups. Results were confirmed in 54 patients who had whole‐body BMD measurements. There were inverse correlations between BMD and Health Assessment Questionnaire scores (femoral BMD r = –0.23, P < 0.01; whole‐body BMD r = –0.40, P < 0.01) and between BMD and cumulative steroid dose (femoral BMD r = –0.32, P < 0.01; whole‐body BMD r = –0.72, P < 0.01).Conclusion. Osteoporosis in postmenopausal women with RA is more evident at the hip than the spine, and the most important determinants of bone loss are disability and cumulative corticosteroid dose. Low‐dose steroids cannot be used with complacency, but recovery after discontinuation of use may be possible.
Up‐regulation by tumor necrosis factor α of intercellular adhesion molecule 1 expression and function in synovial fibroblasts and its inhibition by glucocorticoids
Authors: Bsc Philippe Tessier, , Audette Marie , Bsc Paola Cattaruzzi, , Mccoll Shaun R. 
Published: February 2007

AbstractObjective. To examine the regulation of the intercellular adhesion molecule 1 (ICAM‐1) gene in cultured human synovial fibroblasts in response to tumor necrosis factor α (TNFα), and investigate its modulation by the synthetic glucocorticoid, dexamethasone.Methods. Cell surface expression of ICAM‐1 was determined by flow cytometry, enzyme immunoassay, and immunoprecipitation. ICAM‐1 messenger RNA (mRNA) levels were monitored by Northern blot. ICAM‐1 function was determined by measuring the adhesion of monocytes to synovial fibroblasts.Results. ICAM‐1 expression on unstimulated cells was weak but was rapidly enhanced in both a time‐ and dose‐dependent manner following exposure to TNFα. Treatment of the cells with TNFα also resulted in both a time‐ and dose‐dependent increase in steady‐state ICAM‐1 mRNA levels, as determined by Northern blot. The increased expression of ICAM‐1 was inhibited by cycloheximide and actinomycin D. Cultured synovial fibroblasts from patients with rheumatoid and nonrheumatoid arthropathies responded similarly to TNFα. Adhesion studies demonstrated that ICAM‐1 is involved in the adherence of peripheral blood monocytes to TNFα‐activated synovial fibroblasts. In addition, dexamethasone inhibited TNFα‐induced surface expression of ICAM‐1, accumulation of ICAM‐1 mRNA, and adhesion of monocytes to TNFα‐activated synovial fibroblasts.Conclusion. These combined results provide further evidence of an important role of ICAM‐1 in inflammatory synovitis, as well as a potentially novel site of antiinflammatory action of glucocorticoids.
Differential in vivo expression of collagenase messenger RNA in synovium and cartilage. Quantitative comparison with stromelysin messenger rna levels in human rheumatoid arthritis and osteoarthritis patients and in two animal models of acute inflammatory arthritis
Authors: Wolfe Ms Gloria C. , , Macnaul Bs Karen L. , , Buechel Frederick F. , Mcdonnell Joseph , Hoerrner Bs Lori A. , , Lark Michael W. , Moore Vernon L. , Hutchinson Nancy I. 
Published: February 2007

AbstractObjective. To compare quantitatively the in vivo expression of collagenase messenger RNA (mRNA) and stromelysin mRNA in the joint tissues of human osteoarthritis (OA) and rheumatoid arthritis (RA) patients and in two animal models of acute inflammatory arthritis.Methods. In vivo levels of metalloproteinase mRNA and protein were determined by quantitative Northern hybridization and by enzyme‐linked immunosorbent assay, respectively.Results. In synovium, mean levels of collagenase mRNA were similar to those of stromelysin mRNA; however, in cartilage, mean levels of collagenase mRNA were significantly lower. The ratios of collagenase mRNA to stromelysin mRNA levels in RA and OA cartilage reflected similar ratios of collagenase protein to stromelysin protein levels in synovial fluid.Conclusion. The regulation of collagenase mRNA expression in cartilage is distinct from that of stromelysin, suggesting distinct roles for these two metalloproteinases in normal and abnormal physiologic functioning of cartilage.
A distinctive autoantibody profile in black female patients with lupus nephritis
Authors: Mccarty G. A. , Harley J. B. , Reichlin M. 
Published: February 2007

AbstractObjective. Lupus nephritis has often been associated with anti‐DNA, but, based on the findings in eluate studies, it appears that other antigen–antibody reactions, such as those involving anti–Ro/SS‐A, antinuclear RNP (anti‐nRNP), and/or anti‐Sm, may also contribute to the pathogenesis of nephritis. In the present investigation, we identified and further studied a distinctive precipitin profile present in black women with nephritis.Methods. Longitudinal clinical and serologic studies of a cohort of university‐based systemic lupus erythematosus (SLE) patients (n = 120) were carried out over an 8‐year period.Results. A subset of 20 black female patients was identified, of whom 8 had lupus nephritis (group I) and 12 did not (group II). Group I was characterized by a distinct precipitin profile consisting of anti–Ro/SS‐A, anti‐Sm, and anti‐nRNP, but no anti–La/SS‐B. SLE disease duration at presentation was significantly shorter in group I than in group II (mean 1.94 years versus 5.21 years; P = 0.02). The distinctive precipitin profile of anti–Ro/SS‐A, anti‐Sm, and anti‐nRNP occurred exclusively in group I patients (6 of 8, versus 0 of 12 in group II; P < 0.001). In white lupus nephritis patients, this precipitin profile was not seen.Conclusion. While the mechanism responsible for the relationship of this distinctive serologic profile to the development of nephritis in black female lupus patients remains to be determined, its presence may be used as a marker for severe and progressive renal disease.
Low levels of total cholesterol, high‐density lipoprotein, and apolipoprotein a1 in association with anticardiolipin antibodies in patients with systemic lupus erythematosus
Authors: Lahita R. G. , Rivkin E. , Cavanagh Ms I. , , Romano P. 
Published: February 2007

AbstractObjective. To determine if there is an association between low levels of high‐density lipoprotein cholesterol (HDL), apolipoprotein A1 (Apo A1), total cholesterol, and anticardiolipin antibody (aCL) in patients with systemic lupus erythematosus (SLE) who are not taking corticosteroids.Methods. We studied 75 outpatients with documented SLE who were attending our hospital clinics: 57 were aCL positive and 18 were aCL negative. Both IgG and IgM aCL levels were determined by enzyme‐linked immunosorbent assay. Lipid fractions (total cholesterol, HDL, low‐density lipoprotein, very–low‐density lipoprotein, and triglycerides) were determined by standard enzymatic techniques. Apo A1 and Apo B levels were determined by nephelometry.Results. Patients with SLE who were IgG aCL + had low levels of serum cholesterol (mean ± SD 173.6 ± 34.6 mg/dl) and HDL (43.9 ± 16.3 mg/dl) compared with aCL– SLE patients, normal donors, and patients with other diseases. Apo A1 levels were also low in the aCL + group (95.5 ± 50.9 mg/dl) compared with the aCL– group (152.7 ± 32.6 mg/dl). There was no association of total cholesterol level or aCL titer with clinical activity.Conclusion. These data indicate that in SLE patients, there is an association between antibody against the phospholipid cardiolipin and low levels of cholesterol, HDL, and Apo A1.
IDENTIFICATION OF A UNIVERSAL B CELL EPITOPE ON DNA TOPOISOMERASE I, AN AUTOANTIGEN ASSOCIATED WITH SCLERODERMA
Authors: Kato Tomohiro , Yamamoto Kazuhiko , Takeuchi Hajime , Okubo Mitsuo , Hara Eiji , Nakada Susumu , Oda Kinichiro , Ito Koji , Nishioka Kusuki 
Published: February 2007

AbstractObjective. To investigate the distribution of B cell autoepitopes of human DNA topoisomerase I (topo I), an autoantigen associated with scleroderma.Methods. A complementary DNA clone, T1B, was used to produce recombinant proteins of topo I as β‐galactosidase fusion proteins. Immunoreactivity to these fusion proteins was then tested in 35 anti–topo I–positive sera from patients with scleroderma, by immunoblotting, enzyme‐linked immunosorbent assay, and double immunodiffusion.Results. One epitope was found to be universally recognized by all sera tested. Thirty‐two of the samples recognized multiple antigenic regions, but sera from the remaining 3 patients recognized only this universal epitope, and in longitudinal studies of 1 of these 3 patients, the serum recognized only this epitope for more than 2 years, even though multiple, potent, antigenic regions were found on topo I.Conclusion. Recognition of multiple epitopes in most patients suggests that the topo I molecule itself would drive the autoimmunity on topo I. However, antigen‐driven autoimmunity could not explain the production of the monoreactive anti–topo I antibody seen in the 3 patients. We thus hypothesize that there is a process whereby recognition of the universal epitope by cross‐reaction develops into antigen‐driven autoimmunity.
Phosphocitrate prevents disease progression in murine progressive ankylosis
Authors: Krug Hollis E. , Mahowald Maren L. , Halverson Paul B. , Sallis John D. , Cheung Herman S. 
Published: February 2007

AbstractObjective. Mice with progressive ankylosis, a spontaneous arthropathy, were treated with phosphocitrate (PC) in vivo to determine the effect of PC on disease progression.Methods. Two groups of mice with progressive ankylosis (matched for age, weight, and sex) were treated parenterally for 6 weeks with either PC or saline vehicle.Results. Clinically, histologically, and microradiographically, there were significant differences in disease progression and severity in the PC‐treated and the saline‐treated mice.Conclusion. PC appears to inhibit disease progression in murine progressive ankylosis.