bluuebunny/crossref_metadata_2025_split huggingface dataset:
Summary of potable well monitoring conducted for aldicarb and its metabolites in the United States in 2005
Authors: Jones Russell L. , Allen Richard 
Published: June 2007

Abstract
United States potable well monitoring in the Pacific Northwest, California, Texas, Mississippi delta, and the Southeast was conducted in 2005 to provide estimates of dietary exposure to aldicarb carbamate residues (aldicarb and its two carbamate metabolites) in potentially vulnerable potable wells. Samples were analyzed from 1,673 drinking water wells in nine major use areas that were within 300 m of fields treated at least once with aldicarb between 2002 and 2005. Analyses were performed with a high-performance liquid chromatography/tandem mass spectrometry analytical method with limits of quantitation of 0.021 μg/L for aldicarb and aldicarb sulfone and 0.027 μg/L for aldicarb sulfoxide. The method detection limits were 0.0070 μg/L for aldicarb and aldicarb sulfone and 0.0090 μg/L for aldicarb sulfoxide. Samples from 1,513 of the 1,673 wells contained no aldicarb carbamate residues. Only 10 wells had total aldicarb carbamate residues above 1 μg/L, the maximum being 2.9 μg/L. All residues were below the U.S. Environmental Protection Agency Health Advisory Limit (HAL) of 10 μg/L. Given the number of samples collected in this study, there is a 95% confidence level that the maximum concentration in this study exceeds the 99.8th percentile of concentrations of all potable wells located within 300 m of fields recently treated with aldicarb. Therefore, the data from this study show that the restrictions and management practices on the current product label continue to be effective in preventing residues in excess of the 10 μg/L HAL in potable wells in these use areas.
Feeding inhibition in the soil collembolanFolsomia candidaas an endpoint for the estimation of organic waste ecotoxicity
Authors: Domene Xavier , Natal-da-Luz Tiago , Alcañiz Josep M. , Andrés Pilar , Sousa José Paulo 
Published: June 2007

AbstractDespite the increasing quantities of organic wastes that are being reused in soils, there are few studies that focus on the selection of bioassays for the ecotoxicological risk assessment of organic wastes to soils. In the present study, differences in feeding inhibition in the soil collembolan Folsomia candida were evaluated as an ecotoxicological endpoint for the assessment of risk to soils amended with polluted organic wastes. Seven organic wastes (dewatered sewage sludges, thermally dried sewage sludges, composted sewage sludges, and a thermally dried pig slurry) were tested. These wastes had different origins, treatments, and pollutant burdens, and were selected as a representative sample of the wide variety of wastes currently generated. A clear dose response was observed for this parameter, with an increase in percentage of individual feeding inhibition with increased doses of organic wastes. More significantly, feeding inhibition correlated highly with mortality and reproduction inhibition in the different wastes. Composted sludges displayed the lowest toxicity, followed by thermally dried sludge and dewatered sludge. Thermally dried pig slurry showed the highest toxicity for feeding, with lower median effective concentration (EC50) values than the lowest dose tested. Among waste physicochemical parameters and pollutants, low organic matter stability appeared to be the main predictor of potential adverse effects on soil fauna, because it correlated significantly with feeding inhibition and mortality. Furthermore, feeding inhibition tests were run over a short exposure time (less than 7 d), which, together with the results obtained, makes this bioassay a good screening tool for organic waste toxicity.
Pathways to Smoking Cessation Among African American and Puerto Rican Young Adults
Authors: Marcus Stephen E. , Pahl Kerstin , Ning Yuming , Brook Judith S. 
Published: June 2007

Objectives. We examined the pathways to smoking cessation between late adolescence and young adulthood. Methods. We obtained data from a sample of urban African American and Puerto Rican young adults (N=242), mean age 19 years, who reported tobacco use and determined cessation rates between late adolescence and young adulthood. We used structural equation modeling to examine the pathways of positive family relations, family smoking, maladaptive personality attributes, and substance use to smoking cessation. Results. A mediational pathway linked the absence of positive family relations with maladaptive personality attributes, both of which were related to substance use and ultimately smoking cessation. Substance use mediated the path between family smoking and smoking cessation. Conclusions. The results suggest that a positive relationship with one’s parents, less smoking in the family, conventional personality attributes, and little or no other substance use facilitate smoking cessation among young adults.
The Influence of Subjective Social Status on Vulnerability to Postpartum Smoking Among Young Pregnant Women
Authors: Reitzel Lorraine R. , Vidrine Jennifer I. , Li Yisheng , Mullen Patricia D. , Velasquez Mary M. , Cinciripini Paul M. , Cofta-Woerpel Ludmila , Greisinger Anthony , Wetter David W. 
Published: June 2007

Objectives. Associations between subjective social status, a subjective measure of socioeconomic status, and predictors of risk for postpartum smoking were examined among 123 pregnant women (aged 18–24 years) who stopped smoking because of pregnancy. The goal was to identify how subjective social status might influence the risk for postpartum smoking and to elucidate targets for intervention.Methods. We used multiple regression equations to examine the predictive relations between subjective social status and tobacco dependence, self-rated likelihood of postpartum smoking, confidence, temptations, positive and negative affect, depression, stress, and social support. Adjusted analyses were also conducted with control for race/ethnicity, education, income, and whether participant had a partner or not (partner status).Results. In unadjusted and adjusted analyses, subjective social status predicted tobacco dependence, likelihood of postpartum smoking, confidence, temptations, positive affect, negative affect, and social support. Adjusted analyses predicting depression and stress approached significance.Conclusions. Among young pregnant women who quit smoking because of pregnancy, low subjective social status was associated with a constellation of characteristics indicative of increased vulnerability to postpartum smoking. Subjective social status provided unique information on risk for postpartum smoking over and above the effects of race/ethnicity, objective socioeconomic status, and partner status.
Prospective Predictors of Long-Term Abstinence Versus Relapse Among Smokers Who Quit as Young Adults
Authors: Macy Jonathan T. , Seo Dong-Chul , Chassin Laurie , Presson Clark C. , Sherman Steven J. 
Published: June 2007

Objectives. We sought to identify prospective predictors of long-term abstinence versus relapse among individuals who quit smoking as young adults. Methods. Participants from an ongoing longitudinal study of smoking who had quit for at least 1 year between the ages of 18 and 24 years (n=327) were divided into those who later reported not smoking for more than 5 years (long-term abstinence) or reported current smoking, defined as smoking at least monthly (relapse). Logistic regression was used to examine odds ratios (ORs) of prospective predictors of long-term abstinence versus relapse. Results. Overall, 67% of participants maintained long-term abstinence and 33% relapsed. The strongest predictor of avoiding relapse was marrying a nonsmoker (adjusted OR [AOR]=0.07; 95% confidence interval [CI]=0.03, 0.21). Other predictors included making 1 lifetime quit attempt (AOR=0.13; 95% CI=0.04, 0.44), having as a young adult only 1 parent who smoked (AOR=0.23; 95% CI=0.06, 0.93), and working in a completely smoke-free building (AOR=0.13; 95% CI=0.03, 0.58). Conclusions. The factors related to smoking in the social environment played the largest role in predicting long-term abstinence versus relapse.
Effects of anti–glutamic acid decarboxylase antibodies associated with neurological diseases
Authors: Manto Mario‐Ubaldo , Laute Marie‐Aline , Aguera Michèle , Rogemond Véronique , Pandolfo Massimo , Honnorat Jérome 
Published: June 2007

AbstractObjectiveGlutamic acid decarboxylase (GAD) catalyzes the conversion of glutamic acid into GABA. GAD autoantibodies (GAD‐Ab) have been described in diabetes mellitus and in diseases involving the central nervous system such as stiff‐person syndrome and cerebellar ataxia. However, the pathogenic role of GAD‐Ab in neurological diseases remains a matter of debate.MethodsUsing neurophysiological and neurochemical methods, we analyzed the effects of intracerebellar and paraspinal administration of GAD‐Ab in rats.ResultsIntracerebellar administration of IgG from patients with GAD‐Ab and neurological involvement (IgG‐GAD) blocked the potentiation of the corticomotor response normally associated with trains of repetitive peripheral nerve stimulation. When injected in the lumbar paraspinal region, IgG‐GAD induced continuous motor activity with repetitive discharges, abnormal exteroceptive reflexes, and increased excitability of anterior horn neurons, as assessed by F/M ratios. Furthermore, IgG‐GAD significantly reduced the N‐methyl‐D‐aspartate–mediated production of nitric oxide in cerebellar nuclei and impaired the synaptic regulation of glutamate after N‐methyl‐D‐aspartate administration. These effects were not observed after administration of IgG from the following groups: (1) patients with GAD‐Ab, diabetes mellitus, and without neurological complications; and (2) control patients.InterpretationThese results indicate that stiff‐person syndrome and cerebellar ataxia are the direct consequence of antibody‐mediated neuronal dysfunction. Ann Neurol 2007;61:544–551
Endogenous HLA–DR–restricted presentation of the cartilage antigens human cartilage gp‐39 and melanoma inhibitory activity in the inflamed rheumatoid joint
Authors: van Lierop M. J. C. , den Hoed L. , Houbiers J. , Vencovsky J. , Ruzickova S. , Krystufkova O. , van Schaardenburg M. , van den Hoogen F. , Vandooren B. , Baeten D. , de Keyser F. , Sønderstrup G. , Bos E. , Boots A. M. 
Published: June 2007

AbstractObjectiveThe cartilage proteins melanoma inhibitory activity (MIA) and human cartilage gp‐39 (HC gp‐39) are candidate autoantigens in rheumatoid arthritis (RA). The present study was undertaken to investigate the endogenous HLA–DR4–restricted presentation of these self proteins, in order to seek in vivo evidence in support of their potential immunologic role.MethodsMIA and HC gp‐39 were assessed in synovial fluid (SF) by enzyme‐linked immunosorbent assay and in synovial tissue (ST) by immunohistochemistry. Presentation by SF cells was investigated using specific, HLA–DR–restricted T cell hybridomas.ResultsMIA and HC gp‐39 were detected in RA SF and ST, as well as in specimens from patients with other forms of arthritis. When HC gp‐39–specific and MIA‐specific HLA–DR4–restricted T cell hybridomas raised in HLA–DR4–transgenic mice were incubated with RA SF cells as antigen‐presenting cells in the presence of HC gp‐39 or MIA peptides, the corresponding T cell hybridomas showed strong responses, which were blocked by anti–HLA–DR antibodies. Weaker but qualitatively similar responses were observed with exogenous protein, indicating uptake and processing of these antigens by SF cells. More importantly, without addition of peptide or protein, endogenous presentation of MIA and HC gp‐39 was detected in SF cells from 53% and 80% of HLA–DRB1*0401–positive RA patients, respectively. In addition, SF cells from 3 of 10 patients with spondylarthritis exhibited endogenous HC gp‐39 presentation.ConclusionThese data indicate that immunodominant epitopes of MIA and HC gp‐39 are actively presented in an HLA–DR–restricted manner in the inflamed RA joint. The question remains as to whether this leads to activation of autoreactive T cells, which could play a role in either the immunopathology or the immunomodulation of arthritis.
Autoimmune diseases in a Danish cohort of 4,866 carriers of constitutional structural chromosomal rearrangements
Authors: Bache Iben , Nielsen Nete M. , Rostgaard Klaus , Tommerup Niels , Frisch Morten 
Published: June 2007

AbstractObjectiveConstitutional structural chromosomal rearrangements (CSCRs) have facilitated the identification of genes associated with early‐onset monogenic disorders and, more recently, genes associated with common and late‐onset disorders. In an attempt to find genetic clues to their etiologies, we studied the risk of autoimmune diseases in a Danish cohort of CSCR carriers.MethodsWe followed up 4,866 CSCR carriers over 71,230 person‐years (1980 through 2004) for autoimmune diseases recorded in the Danish Hospital Discharge Register. Standardized incidence ratios (SIRs) and 95% confidence intervals (95% CIs) served as measures of the relative risk. To identify possible candidate loci for autoimmune diseases, the reported chromosomal breakpoints and deletions in CSCR carriers who developed autoimmune diseases were compared with previously suggested loci for these diseases.ResultsThe overall risk of any autoimmune disease among CSCR carriers was inconspicuous (SIR 1.2 [95% CI 0.95–1.5]; n = 74 cases observed versus 61.3 expected), but carriers of rearrangements involving chromosomes 2, 19, and 21 were at significantly increased risk. For the specific autoimmune diseases studied, cohort members were at significantly increased risk of Dupuytren's contracture, pernicious anemia, and juvenile rheumatoid arthritis (JRA). Sixteen carriers who developed an autoimmune disease had a chromosomal breakpoint or deletion coinciding with a previously suggested locus, including deletions 18p11, 18q22, and 22q11 associated with JRA.ConclusionCSCR carriers do not have a generalized predisposition to autoimmune diseases. However, we confirmed a number of reported susceptibility loci for JRA, and we suggest new susceptibility loci on chromosomes 5 and 11 for Dupuytren's contracture, and 19p13 as a possible shared susceptibility locus for a range of autoimmune diseases.
Aspirin for primary thrombosis prevention in the antiphospholipid syndrome: A randomized, double‐blind, placebo‐controlled trial in asymptomatic antiphospholipid antibody–positive individuals
Authors: Erkan Doruk , Harrison Melanie J. , Levy Roger , Peterson Margaret , Petri Michelle , Sammaritano Lisa , Unalp‐Arida Aynur , Vilela Veronica , Yazici Yusuf , Lockshin Michael D. 
Published: June 2007

AbstractObjectiveTo determine the efficacy of a daily dose of 81 mg aspirin in primary thrombosis prevention in asymptomatic, persistently antiphospholipid antibody (aPL)–positive individuals (those with positive aPL but no vascular and/or pregnancy events).MethodsThe Antiphospholipid Antibody Acetylsalicylic Acid (APLASA) study was a multicenter, randomized, double‐blind, placebo‐controlled clinical trial in which asymptomatic, persistently aPL‐positive individuals were randomized to receive a daily dose of 81 mg of aspirin or placebo. In a separate observational and parallel study, asymptomatic, persistently aPL‐positive individuals who were taking aspirin or declined randomization were followed up prospectively.ResultsIn the APLASA study, 98 individuals were randomized to receive aspirin or placebo (mean ± SD followup period 2.30 ± 0.95 years), of whom 48 received aspirin and 50 received placebo. In the observational study, 74 nonrandomized individuals were followed up prospectively (mean ± SD followup period 2.46 ± 0.76 years); 61 received aspirin and 13 did not. In the APLASA study, the acute thrombosis incidence rates were 2.75 per 100 patient‐years for aspirin‐treated subjects and 0 per 100 patient‐years for the placebo‐treated subjects (hazard ratio 1.04, 95% confidence interval 0.69–1.56) (P = 0.83). Similarly, in the observational study, the acute thrombosis incidence rates were 2.70 per 100 patient‐years for aspirin‐treated subjects and 0 per 100 patient‐years for those not treated with aspirin. All but 1 patient with thrombosis in either study had concomitant thrombosis risk factors and/or systemic autoimmune disease at the time of thrombosis.ConclusionOur results suggest that asymptomatic, persistently aPL‐positive individuals do not benefit from low‐dose aspirin for primary thrombosis prophylaxis, have a low overall annual incidence rate of acute thrombosis, and develop vascular events when additional thrombosis risk factors are present.
Hsp90 mediates insulin‐like growth factor 1 and interleukin‐1β signaling in an age‐dependent manner in equine articular chondrocytes
Authors: Boehm Amber K. , Seth Mayank , Mayr Karen G. , Fortier Lisa A. 
Published: June 2007

AbstractObjectiveMany metabolic processes in chondrocytes thought to contribute to age‐related changes in the extracellular matrix are influenced by known roles of Hsp90. Age‐related decreases in the level of Hsp90 have been documented in numerous cell types and could contribute to cartilage degeneration. The aim of this study was to investigate the roles of age and Hsp90 in insulin‐like growth factor 1 (IGF‐1) and interleukin‐1β (IL‐1β) signaling in chondrocytes.MethodsLevels of Hsp90 messenger RNA (mRNA) and protein, with respect to age, were determined by quantitative real‐time polymerase chain reaction (PCR) and Western blot analysis, respectively. The Hsp90 inhibitor geldanamycin (50 nM, 100 nM, or 500 nM) was used to assess age‐related responses to Hsp90 with concurrent IGF‐1 or IL‐1β stimulation of chondrocytes. Quantitative real‐time PCR was used to measureCOL2A1and matrix metalloproteinase 13 (MMP13) gene expression; Western blot analysis was performed to determine the phosphorylation status of p42/44 and Akt/protein kinase B.ResultsThe effects of Hsp90 inhibition with geldanamycin were concentration dependent. Inhibition of Hsp90 with 100 nMor 500 nMgeldanamycin blocked IGF‐1–induced cell proliferation, Akt and p42/44 activation, andCOL2A1expression. Basal and IL‐1β–induced up‐regulation ofMMP13mRNA was blocked by all concentrations of geldanamycin tested. Gain‐of‐function assays with Hsp90 resulted in increased expression ofMMP13mRNA.ConclusionThese results suggest that Hsp90 is involved in opposing signaling pathways of cartilage homeostasis, and that catabolic responses are more sensitive to Hsp90 inhibition than are anabolic responses. Further studies are needed to determine the role of Hsp90 inhibition in osteoarthritis in order to assess its potential as a therapeutic target.
C1D is a major autoantibody target in patients with the polymyositis–scleroderma overlap syndrome
Authors: Schilders Geurt , Egberts Wilma Vree , Raijmakers Reinout , Pruijn Ger J. M. 
Published: June 2007

AbstractObjectiveTo assess whether the recently discovered exosome‐associated proteins MPP6, C1D, KIAA0052/hMtr4, hSki2, and hSki8 are targeted by autoantibodies, and to determine whether these autoantibodies are accompanied by antibodies directed to the established exosome‐associated autoantigens PM–Scl‐75 and PM–Scl‐100.MethodsComplementary DNAs encoding the recently identified human exosome–associated proteins were expressed as His‐tagged fusion proteins in Escherichia coli cells. Sera obtained from patients with several different autoimmune diseases were analyzed for the presence of autoantibodies directed to these proteins, in an enzyme‐linked immunosorbent assay (ELISA). The ELISA data obtained for C1D were confirmed by Western blot analysis, using recombinant C1D.ResultsAll exosome‐associated proteins were found to be targeted by autoantibodies, although the frequency with which such antibodies occurred in patient sera was relatively low, with the exception of anti‐C1D antibodies. Autoantibodies recognizing C1D were detected in 7 of 30 patients (23%) with the polymyositis (PM)–scleroderma overlap syndrome; this frequency was similar to the frequencies for the established autoantigens PM–Scl‐75c (27%) and PM–Scl‐100 (23%). Importantly, several patients with the PM–scleroderma overlap syndrome had anti‐C1D antibodies but no anti–PM‐Scl antibodies. Anti‐C1D autoantibodies were observed in only 2 of 204 patients with other diseases, including PM, dermatomyositis, and scleroderma.ConclusionOur results demonstrate that the recently identified exosome‐associated protein C1D is a major autoantigen in patients with the PM–scleroderma overlap syndrome and suggest that the use of recombinant C1D as an autoantibody target may aid in diagnosis of the PM–scleroderma overlap syndrome.
Calcium signaling leads to mitochondrial depolarization in impact‐induced chondrocyte death in equine articular cartilage explants
Authors: Huser C. A. M. , Davies M. E. 
Published: June 2007

AbstractObjectiveChondrocyte apoptosis is an important factor in the progression of osteoarthritis. This study aimed to elucidate the mechanisms involved upstream of caspase 9 activation and, in particular, calcium signaling and mitochondrial depolarization.MethodsArticular cartilage explants obtained from healthy horses were subjected to a single impact load (500‐gm weight dropped from a height of 50 mm) and cultured in vitro for up to 48 hours. Chondrocyte death was quantified by the TUNEL method. Release of proteoglycans was determined by the dimethylmethylene blue assay. Weight change was measured, and mitochondrial depolarization was determined using JC‐1 staining. To assess the role of calcium signaling in impact‐induced chondrocyte death, explants were preincubated in culture medium containing various concentrations of calcium. Inhibitors were used to assess the role of individual signaling components in impact‐induced chondrocyte death.ResultsCalcium quenching, inhibitors of calpains, calcium/calmodulin‐regulated kinase II (CaMKII), and mitochondrial depolarization reduced impact‐induced chondrocyte death after 48 hours in culture. Transient mitochondrial depolarization was observed 3–6 hours following a single impact load. Mitochondrial depolarization was prevented by calcium quenching, inhibitors of calpain, CaMKII, permeability transition pore formation, ryanodine receptor, and the mitochondrial uniport transporter. Cathepsin B did not appear to be involved in impact‐induced chondrocyte death. The calpain inhibitor prevented proteoglycan loss, but the percentage weight gain and proteoglycan loss were unaffected by all treatments used.ConclusionFollowing a single impact load, calcium is released from the endoplasmic reticulum via the ryanodine receptor and is taken up by the mitochondria via the uniport transporter, causing mitochondrial depolarization and caspase 9 activation. In addition, calpains and CaMKII play important roles in causing mitochondrial depolarization.