bluuebunny/crossref_metadata_2025_split huggingface dataset:
Determinants of Incident Hyperglycemia 6 Years After Delivery in Young Rural Indian Mothers
Authors: Kulkarni Smita R. , Fall Caroline H.D. , Joshi Niranjan V. , Lubree Himangi G. , Deshpande Vaishali U. , Pasarkar Rashmi V. , Bhat Dattatray S. , Naik Sadanand S. , Yajnik Chittaranjan S. 
Published: September 2007

OBJECTIVE—To study determinants of incident hyperglycemia in rural Indian mothers 6 years after delivery.
RESEARCH DESIGN AND METHODS—The Pune Maternal Nutrition Study collected information in six villages near Pune on prepregnant characteristics and nutrition, physical activity, and glucose tolerance during pregnancy. An oral glucose tolerance test (OGTT) was repeated 6 years after delivery.
RESULTS—A total of 597 mothers had an OGTT at 28 weeks’ gestation; 3 had gestational diabetes (by World Health Organization 1999 criteria). Six years later, 42 of 509 originally normal glucose-tolerant mothers were hyperglycemic (8 diabetic, 20 with impaired glucose tolerance, and 14 with impaired fasting glucose). The hyperglycemic women had shorter legs and thicker skinfolds before pregnancy (P &lt; 0.01, both), were less active and more hyperglycemic (2-h plasma glucose 4.8 vs. 4.4 mmol/l, P &lt; 0.001) during pregnancy, and gained more weight during follow-up (6.0 vs. 2.7 kg, P &lt; 0.001). Multivariate analysis revealed that total leukocyte count and blood pressure during pregnancy were additional independent predictors of 2-h glucose concentration at follow-up.
CONCLUSIONS—Our results suggest that compromised linear growth, adiposity, inflammation, and less physical activity predispose to hyperglycemia in young rural Indian women. International cut points of diabetes risk factors are largely irrelevant in these women.
Effect of the composition ratio of pimelic acid/calcium stearate bicomponent nucleator and crystallization temperature on the production of β crystal form in isotactic polypropylene
Authors: Dou Qiang 
Published: September 2007

AbstractThe influence of the composition ratio of pimelic acid/calcium stearate bicomponent nucleator on the β crystal form content of isotactic polypropylene (iPP) had been studied at the crystallization temperature of 120°C and duration of 30 min. It was found that the β crystal form content increased continuously with increasing amount of calcium stearate at the constant amount of 0.15% pimelic acid. High β crystal form content polypropylene could be produced when the amount of calcium stearate was greater than 0.30% (the mass composition ratio of pimelic acid/calcium stearate was less than 1/2, the mole ratio was less than 1.89/1). It was shown that pimelic acid and calcium stearate could react to produce a high effective β nucleator (calcium pimelate) “in situ” during the melt‐mixing of iPP and the bicomponent nucleator. The influence of crystallization temperatures (100–140°C) on the β crystal form content of iPP had also been studied at the constant composition ratio of 0.15% pimelic acid/0.5% calcium stearate (the calcium pimelate produced in situ was 0.16%, which was calculated from stoichiometry). It was found that the β crystal form content increased continuously with increasing crystallization temperature and it maximized at 130°C. β Crystal form content decreased sharply at the crystallization temperature of 140°C. It was shown that β → α modification transformed between 130 and 140°C. © 2007 Wiley Periodicals, Inc. J Appl Polym Sci, 2008
Wnt signaling antagonists are potential prognostic biomarkers for the progression of radiographic hip osteoarthritis in elderly Caucasian women
Authors: Lane Nancy E. , Nevitt Michael C. , Lui Li‐Yung , de Leon Patricia , Corr Maripat 
Published: September 2007

AbstractObjectiveTo determine whether serum levels of 2 Wnt signaling antagonists, Frizzled‐related protein (FRP) and Dkk‐1, are associated with the development and progression of radiographic hip osteoarthritis (RHOA).MethodsPelvic radiographs were obtained a mean of 8.3 years apart in 5,928 Caucasian women ≥65 years of age who were enrolled in the Study of Osteoporotic Fractures. Random sampling of this cohort was performed, with ∼180 subjects per group assigned to 2 nested case–control studies on RHOA incidence and progression. Baseline serum levels of FRP and Dkk‐1 were measured by capture enzyme‐linked immunosorbent assay. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated using logistic regression analyses with adjustment for potential covariates.ResultsThere were no differences in serum levels of FRP and Dkk‐1 between case subjects with incidence or progression of RHOA and their respective control subjects. There was a trend for higher baseline serum levels of FRP to be associated with a reduced risk of incident RHOA (age‐adjusted OR 0.59 [95% CI 0.32–1.09], P = 0.09 for women in the highest quartile versus women in the lowest quartile). There was no association of serum levels of FRP with progression of RHOA. Serum levels of Dkk‐1 did not correlate with incident RHOA. However, higher serum levels of Dkk‐1 were associated with diminished risk of RHOA progression (age‐adjusted OR 0.43 [95% CI 0.23–0.79], P = 0.007 for women in the highest quartile compared with women in the lowest quartile).ConclusionElevated circulating levels of Dkk‐1 appeared to be associated with reduced progression of RHOA in elderly women, whereas the highest quartile of serum FRP levels tended to be associated with a modest reduction in risk of incident RHOA.
Central role of the MEK/ERK MAP kinase pathway in a mouse model of rheumatoid arthritis: Potential proinflammatory mechanisms
Authors: Thiel Melissa J. , Schaefer Caralee J. , Lesch Mark E. , Mobley James L. , Dudley David T. , Tecle Haile , Barrett Stephen D. , Schrier Denis J. , Flory Craig M. 
Published: September 2007

AbstractObjectiveTo evaluate the role of the MEK/ERK MAP kinase pathway in murine collagen‐induced arthritis (CIA) using the selective MEK inhibitor PD184352. We examined the effects of the inhibitor in cytokine‐stimulated synovial fibroblasts and in cytokine‐induced arthritis in rabbits to investigate its antiinflammatory mechanisms.MethodsMurine CIA was used to assess the effects of the selective MEK inhibitor on paw edema, clinical scores, weight loss, histopathologic features, and joint levels of p‐ERK. Western blotting and immunohistochemistry techniques were used to assess p‐ERK in human and rabbit synovial fibroblasts and synovial tissue from rheumatoid arthritis (RA) patients. Interleukin‐1α (IL‐1α)–stimulated stromelysin production in rabbit synovial fibroblasts was assessed by enzyme‐linked immunosorbent assay. A rabbit IL‐1α–induced arthritis model was used to assess the effects of the inhibitor on IL‐1α–induced MEK activity, stromelysin production, and cartilage degradation.ResultsIn the CIA model, PD184352 inhibited paw edema and clinical arthritis scores in a dose‐dependent manner. Disease‐induced weight loss and histopathologic changes were also significantly improved by treatment. Inhibition of disease‐induced p‐ERK levels in the joints was seen with the inhibitor. Levels of p‐ERK in the synovium were higher in RA patients than in normal individuals. PD184352 reduced IL‐1α–induced p‐ERK levels in human RA synovial fibroblasts. The production of p‐ERK and stromelysin was also inhibited in IL‐1α–stimulated rabbit synovial fibroblasts. We observed IL‐1α–induced p‐ERK in the synovial lining, subsynovial vasculature, and articular chondrocytes. IL‐1α–induced stromelysin production and proteoglycan loss from the articular cartilage were reduced by PD184352.ConclusionThese data demonstrate the inhibition of murine CIA by PD184352, support the hypothesis that antiinflammatory activity contributes to the mechanism of action of the inhibitor, and suggest that a selective inhibitor may effectively treat RA and other inflammatory disorders.
The chemical biomarkers C2C, Coll2‐1, and Coll2‐1NO2 provide complementary information on type II collagen catabolism in healthy and osteoarthritic mice
Authors: Ameye L. G. , Deberg M. , Oliveira M. , Labasse A. , Aeschlimann J. M. , Henrotin Y. 
Published: September 2007

AbstractObjectiveCompared with wild‐type (WT) mice, biglycan/fibromodulin double‐deficient mice develop severe knee osteoarthritis. We undertook this study to compare type II collagen catabolism in the 2 genotypes and to compare the usefulness of 3 biomarkers of collagen degradation (C2C [also known as Col2‐3/4Clong mono] as well as the peptide Coll2‐1 and its nitrated form, Coll2‐1NO2) for evaluating collagen catabolism in vivo.MethodsIn 15 WT mice and 15 biglycan/fibromodulin double‐deficient mice, we determined serum levels of C2C at ages 66 and 141 days, and we determined serum levels of Coll2‐1 and Coll2‐1NO2 at ages 49, 81, 95, and 141 days. Expression of the biomarkers in knee sections was examined using immunohistochemistry.ResultsThe mean concentrations of C2C and Coll2‐1 were higher in biglycan/fibromodulin double‐deficient mice at all time points. For C2C and Coll2‐1, the ratio of the serum concentration in biglycan/fibromodulin double‐deficient mice to that in WT mice (the double‐deficient:WT ratio) was constant over time and was ∼1.63 and ∼1.15, respectively. In contrast, the double‐deficient:WT ratio for Coll2‐1NO2 varied and, depending on age, was >1 or <1. No significant correlation was found between the expression of the different biomarkers, except for a weak, negative correlation between Coll2‐1NO2 and C2C. In both genotypes, antibodies to each biomarker labeled some fibroblasts in the tendons and menisci as well as chondrocytes above the tidemark in articular cartilage. Growth plates were unstained. For each biomarker, extracellular staining was limited to fibrocartilage areas in the tendons and menisci in all mice and was limited to some focal lesions of the cartilage in biglycan/fibromodulin double‐deficient mice.ConclusionThe different double‐deficient:WT ratios observed with C2C, Coll2‐1, and Coll2‐1NO2 in the absence of any correlation between the expression of the 3 biomarkers indicate that these biomarkers give complementary, rather than redundant, information about in vivo type II collagen catabolism.
Systemic autoimmune disease mortality and occupational exposures
Authors: Gold L. S. , Ward M. H. , Dosemeci M. , Roos A. J. De 
Published: September 2007

AbstractObjectiveTo generate hypotheses regarding occupational exposures that may cause systemic autoimmune diseases.MethodsBased on examination of US death certificates, we identified deaths in 26 states for which a cause was listed as rheumatoid arthritis (RA) (n = 36,178), systemic lupus erythematosus (SLE) (n = 7,241), systemic sclerosis (n = 5,642), or other systemic autoimmune disease (n = 4,270). Odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated to estimate associations between occupation and death from any systemic autoimmune disease, and from RA, SLE, and systemic sclerosis, specifically. Additionally, we estimated risks associated with occupational exposures, which were assigned using job‐exposure matrices.ResultsA broad array of occupations was associated with death from systemic autoimmune diseases, including several of a priori interest. Farming occupation was associated with death from any systemic autoimmune disease (OR 1.3 [95% CI 1.2–1.4]), and increased risk was also seen with occupational exposure to animals and pesticides. Several industrial occupations were associated with death from any systemic autoimmune disease, including mining machine operators (OR 1.3 [95% CI 1.1–1.5]), miscellaneous textile machine operators (OR 1.2 [95% CI 1.0–1.4]), and hand painting, coating, and decorating occupations (OR 1.8 [95% CI 1.0–2.9]). These occupations were also significantly associated with death from the specific autoimmune diseases examined. Certain occupations entailing exposure to the public, such as teachers, were associated with systemic autoimmune disease–related death, whereas others, such as waiters and waitresses, were not.ConclusionOur results suggest that death from systemic autoimmune diseases may be associated with occupational exposures encountered in farming and industry. The hypotheses generated in this study provide leads for future research on determinants of these diseases.
Variation in the relative copy number of the TLR7 gene in patients with systemic lupus erythematosus and healthy control subjects
Authors: Kelley James , Johnson Martin R. , Alarcón Graciela S. , Kimberly Robert P. , Edberg Jeffrey C. 
Published: September 2007

AbstractObjectiveTo determine whether there is an increase in the number of TLR7 gene copies in patients diagnosed as having systemic lupus erythematosus (SLE) and whether gene amplification influences the autoantibody profiles in SLE patients, as has recently been reported in the BXSB/Yaa mouse model of lupus.MethodsWe used a modified real‐time quantitative polymerase chain reaction protocol to calculate the relative TLR7 gene copy number according to the comparative 2 method in 99 SLE patients and 91 healthy controls matched for sex and ethnicity. Autoantibody profiles were determined by standard methods.ResultsThe relative number of TLR7 gene copies in SLE patients and healthy controls varied; however, no significant concordance between the number of relative gene copies and the SLE phenotype was found. There was also no difference in variation by ethnic group. Comparison of the relative gene copy numbers according to the presence or absence of antinuclear antibodies (ANAs), the ANA staining patterns, and the presence or absence of anti‐RNA–associated antigen antibody showed no statistically significant difference in the SLE patients.ConclusionWe determined that although the relative gene copy number of TLR7 varied in both SLE patients and healthy controls, it was not significantly increased among our SLE patients as compared with our controls. We found no detectable trend for an association between the relative gene copy number and the autoantibody profile in SLE patients.
Role of subchondral bone in osteoarthritis development: A comparative study of two strains of guinea pigs with and without spontaneously occurring osteoarthritis
Authors: Muraoka Tomoya , Hagino Hiroshi , Okano Toru , Enokida Makoto , Teshima Ryota 
Published: September 2007

AbstractObjectiveTo evaluate the relationships among cartilage and subchondral bone before and after the onset of cartilage degeneration in the Hartley guinea pig model of spontaneous osteoarthritis (OA) as compared with those in Weiser‐Maple guinea pigs, which do not develop OA.MethodsMice from each strain were used at ages 2, 3, 5, and 8 months (n = 7 at each time point). The region observed was the medial tibial plateau. Cartilage degeneration was evaluated histologically. Subchondral bone structure was evaluated based on subchondral bone plate thickness and subchondral cancellous bone trabecular parameters calculated from the microfocal computed tomography 3‐dimensional reconstruction image. The bone mineral density (BMD) of the subchondral cancellous bone as well as levels of urinary N‐telopeptide of type I collagen (NTX) and serum osteocalcin (OC) were measured.ResultsIn Hartley guinea pigs, the number of chondrocytes in the surface layer started to decrease at 3 months. At 8 months, fibrillation expanded to the radial zone. In Weiser‐Maple guinea pigs, no cartilage degeneration was noted even at 8 months. Subchondral bone plate thickness was significantly lower in Hartley guinea pigs than in Weiser‐Maple guinea pigs at 2 months. The subchondral bone had a rod‐like and convex structure at 2 months in Hartley guinea pigs. BMD was significantly lower in Hartley guinea pigs than in Weiser‐Maple guinea pigs at 2 months. The serum OC level was significantly higher in Hartley guinea pigs than in Weiser‐Maple guinea pigs at 2 months and 3 months, whereas the urinary NTX level was significantly lower in Hartley guinea pigs at 3 months.ConclusionSubchondral bone is fragile, and bone formation may be promoted in subchondral bone before the onset of cartilage degeneration in Hartley guinea pigs. Subchondral bone may be involved in the development of OA.
Biomarkers predict radiographic progression in early rheumatoid arthritis and perform well compared with traditional markers
Authors: Young‐Min Steven , Cawston Tim , Marshall Nicola , Coady David , Christgau Stephan , Saxne Tore , Robins Simon , Griffiths Ian 
Published: September 2007

AbstractObjectiveTo evaluate the performance of biochemical and traditional markers in predicting radiographic progression in rheumatoid arthritis (RA).MethodsOne hundred thirty‐two patients with early RA were treated with nonbiologic therapies for 2 years and studied longitudinally. Genomic DNA was analyzed for presence of the shared epitope. Levels of matrix metalloproteinases (matrix metalloproteinase 1 [MMP‐1], MMP‐13, and MMP‐3), tissue inhibitor of metalloproteinases 1 (TIMP‐1), and cartilage oligomeric matrix protein (COMP) were assessed in serially obtained serum samples. The presence of pyridinoline (Pyr), deoxypyridinoline, glycosylated Pyr (Glc‐Gal‐Pyr), and C‐telopeptide of type II collagen (CTX‐II) was assessed in urine samples. Radiographs obtained at entry and at 2 years were evaluated using the modified Larsen score.ResultsBaseline and 2‐year radiographs were available from 118 patients. Larsen scores worsened during the 2 years in 50 patients, while 68 patients had no radiographic progression. Levels of a variety of biochemical markers, i.e., MMP‐3, CTX‐II, COMP, TIMP‐1, Pyr, and Glc‐Gal‐Pyr, correlated significantly with radiographic progression at entry and longitudinally as assessed by area under the curve (AUC). By multivariate analysis, a model including MMP‐3 and CTX‐II was identified as providing the best prediction of radiographic progression at entry (predictive accuracy by receiver operating characteristic [ROC] AUC = 0.76 [95% confidence interval 0.66–0.85]), while a combination of MMP‐3, CTX‐II, and swollen joint count formed the best longitudinal AUC model (predictive accuracy by ROC AUC = 0.81 [95% confidence interval 0.73–0.89]). Patient‐reported measures (Health Assessment Questionnaire, pain scores) were of limited use. In a subset of 50 patients who were treated with methotrexate (MTX) during the followup period, median serum MMP‐3 levels decreased after the initiation of MTX therapy (P =0.0003).ConclusionThese results indicate that biochemical markers are useful predictors of radiographic progression in RA and that serum MMP‐3 levels decrease significantly with MTX therapy. Multivariate models that include MMP‐3 and CTX‐II perform better than existing traditional markers in predicting radiographic outcome in RA.
Rate and determinants of progression of atherosclerosis in systemic lupus erythematosus
Authors: Roman Mary J. , Crow Mary K. , Lockshin Michael D. , Devereux Richard B. , Paget Stephen A. , Sammaritano Lisa , Levine Daniel M. , Davis Adrienne , Salmon Jane E. 
Published: September 2007

AbstractObjectiveTo determine the rate of atherosclerosis progression as well as the relationship of traditional risk factors, systemic lupus erythematosus (SLE)–related factors, and treatment to atherosis progression in SLE patients.MethodsOutpatients in the Hospital for Special Surgery SLE Registry underwent serial carotid ultrasound and clinical assessment in a longitudinal study.ResultsAmong 158 patients, 77 (49%) had persistent absence of atherosclerosis (carotid plaque), 36 (23%) had unchanged atherosclerosis, and 45 (28%) had progressive atherosclerosis, defined as a higher plaque score (new plaque in 25 patients and more extensive plaque in 20 patients) after a mean ± SD interval of 34 ± 9 months. Multivariate determinants of atherosclerosis progression were age at diagnosis (odds ratio [OR] 2.75, 95% confidence interval [95% CI] 1.67–4.54 per 10 years, P < 0.001), duration of SLE (OR 3.16, 95% CI 1.64–6.07 per 10 years, P < 0.001), and baseline homocysteine concentration (OR 1.24, 95% CI 1.06–1.44 per μmoles/liter, P = 0.006). SLE patients with stable plaque and progressive plaque differed only in baseline homocysteine concentration. Atherosclerosis progression was increased across tertiles of homocysteine concentration (16.2%, 36.4%, and 56.1%; P = 0.001), and homocysteine tertile was independently related to progression of atherosclerosis (OR 3.14, 95% CI 1.65–5.95 per tertile, P < 0.001). Less aggressive immunosuppressive therapy and lower average prednisone dose were associated with progression of atherosclerosis in univariate, but not multivariate, analyses. Inflammatory markers and lipids were not related to atherosclerosis progression.ConclusionAtherosclerosis develops or progresses in a substantial minority of SLE patients during short‐term followup (10% per year on average). Older age at diagnosis, longer duration of SLE, and higher homocysteine concentration are independently related to progression of atherosclerosis. These findings show that aggressive control of SLE and lowering of homocysteine concentrations are potential means to retard the development and progression of atherosclerosis in SLE.
Opsonization of late apoptotic cells by systemic lupus erythematosus autoantibodies inhibits their uptake via an Fcγ receptor–dependent mechanism
Authors: Reefman Esther , Horst Gerda , Nijk Marije T. , Limburg Pieter C. , Kallenberg Cees G. M. , Bijl Marc 
Published: September 2007

AbstractObjectiveDecreased clearance of apoptotic cells is suggested to be a major pathogenic factor in systemic lupus erythematosus (SLE). The aim of this study was to investigate whether the binding of SLE autoantibodies to apoptotic cells influences the phagocytosis of these cells by macrophages.MethodsApoptosis was induced in a human T cell line (Jurkat) and a keratinocyte cell line (HaCaT) by ultraviolet B irradiation. Binding of purified IgG from 26 SLE patients and 15 healthy controls to apoptotic cells was assessed by flow cytometry and Western blotting. Phagocytosis of IgG‐opsonized apoptotic cells by monocyte‐derived macrophages was assessed by light microscopy. Similar experiments were performed with a monoclonal antibody against SSA/Ro and IgG fractions from 5 patients with Sjögren's syndrome (SS) and 5 patients with rheumatoid arthritis (RA).ResultsIgG fractions from all 26 SLE patients bound to late apoptotic, but not early apoptotic, cells. IgG fractions isolated from SLE patients with different autoantibody profiles showed comparable levels of binding. IgG fractions from healthy controls did not bind. Opsonization of apoptotic cells with IgG fractions from SLE patients resulted in a significant inhibition of phagocytosis as compared with healthy control IgG fractions. A monoclonal antibody directed against SSA/Ro and IgG isolated from 5 antinuclear antibody (ANA)–positive patients with SS were also able to elicit these effects, whereas IgG from 5 ANA‐negative patients with RA did not. The inhibitory effect of patient IgG was abolished by blocking either the Fcγ receptors (FcγR) or the constant region of IgG, using a specific Fc‐blocking peptide.ConclusionAutoantibodies from SLE patients are able to opsonize apoptotic cells and inhibit their uptake by macrophages via an FcγR‐dependent mechanism.