64 research outputs found

    The economics of hardwood management in the United States: 1950-1995, an annotated bibliography

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    This bibliography includes journal articles, published reports, conference proceedings articles, and academic theses and dissertations dated between 1950 and 1995 that concern economic aspects of managing hardwood tree species for timber production in the United States. The articles and reports were identified through keyword searches of computer databases available through the Mississippi State University computer system. Keywords used included individual species names as well as economic terms such as costs, returns, investment, and profit. The specific databases included the 1) USDA Agricultural Library - AGRICOLA CD-ROMs, 2) Colorado Alliance of Research Libraries System, 3) EBSCO Dissertation Abstracts, and 4) the Social Sciences in Forestry Bibliography maintained at the University of Minnesota Library. Additional references were acquired by examining the literature cited pages of the articles found through computer search

    Depression and anxiety symptoms at TNF inhibitor initiation are associated with impaired treatment response in axial spondyloarthritis

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    Acknowledgment We are grateful to Professor Gary Macfarlane for commenting on the manuscript. We are grateful to the staff of the BSRBR-AS register and to the recruiting staff at the clinical centres, details of which are available at: www.abdn.ac.uk/bsrbr-as. We also thank Dr Lewis Carpenter for suggesting splines for modelling time. Contribution: SSZ analysed the data and wrote the manuscript with significant input from all co- authors. GTJ is the Deputy Chief Investigator on BSRBR-AS and designed the study and oversaw its conduct. In the current project they discussed results and provided input into drafts of the manuscript. Funding: The BSRBR-AS is funded by the British Society for Rheumatology (BSR) who have received funding for this from Pfizer, AbbVie and UCB. These companies receive advance copies of manuscripts for comments. They have no input in determining the topics for analysis or work involved in undertaking it.Peer reviewedPublisher PD

    Comorbidity and response to TNF inhibitors in axial spondyloarthritis : longitudinal analysis of the BSRBR-AS

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    Acknowledgements: Funding: The BSRBR-AS is funded by the British Society for Rheumatology (BSR) who have received funding for this from Pfizer, AbbVie and UCB. These companies receive advance copies of manuscripts for comments. They have no input in determining the topics for analysis or work involved in undertaking it. Disclosures: The authors declare no conflicts of interest. Contribution: SSZ analysed the data and wrote the manuscript, with significant input from all coauthors. GJM and GTJ are Chief Investigator and Deputy Chief Investigator respectively on BSRBR-AS and designed the study and oversaw its conduct. In the current project they discussed results and provided input into drafts of the manuscript. Data availability: Data from the British Society for Rheumatology Biologics Register for Ankylosing Spondylitis are available to external investigators, on reasonable request. For information on how to access data, see: http://www.rheumatology.org.uk. We are grateful to the staff of the BSRBR-AS register and to the recruiting staff at the clinical centres, details of which are available at: www.abdn.ac.uk/bsrbr-asPeer reviewedPublisher PD

    Association between comorbidities and disease activity in axial spondyloarthritis : results from the BSRBR-AS

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    Funding: The BSRBR-AS is funded by the British Society for Rheumatology (BSR) who have received funding for this from Pfizer, AbbVie and UCB. These companies receive advance copies of manuscripts for comments. They have no input in determining the topics for analysis or work involved in undertaking it. We are grateful to the staff of the BSRBR-AS register and to the recruiting staff at the clinical centres, details of which are available at: http://www.abdn.ac.uk/bsrbr-as S.S.Z. analysed the data and wrote the manuscript, with significant input from all co-authors. G.J.M. and G.T.J. are Chief Investigator and Deputy Chief Investigator, respectively, on BSRBR-AS and designed the study and oversaw its conduct. In the current project they discussed results and provided input into drafts of the manuscript. Disclosure statement: The authors have declared no conflicts of interest.Peer reviewedPublisher PD

    Comorbidity burden in axial spondyloarthritis: a cluster analysis

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    Objectives To examine how comorbidities cluster in axial spondyloarthritis (axSpA) and whether these clusters are associated with quality of life, global health and other outcome measures. Methods We conducted a cross-sectional study of consecutive patients meeting ASAS criteria for axSpA in Liverpool, UK. Outcome measures included quality of life (EQ5D), global health and disease activity (BASDAI). We used hierarchical cluster analysis to group patients according to 38 pre-specified comorbidities. In multivariable linear models, the associations between distinct comorbidity clusters and each outcome measure were compared, using axSpA patients with no comorbidities as the reference group. Analyses were adjusted for age, gender, symptom duration, BMI, deprivation, NSAID-use and smoking. Results We studied 419 patients (69% male, mean age 46 years). 255 patients (61%) had at least one comorbidity, among whom the median number was 1 (range 1–6). Common comorbidities were hypertension (19%) and depression (16%). Of 15 clusters identified, the most prevalent clusters were hypertension-coronary heart disease and depression-anxiety. Compared with patients with no comorbidities, the fibromyalgia-irritable bowel syndrome cluster was associated with adverse patient-reported outcome measures; these patients reported 1.5-unit poorer global health (95%CI 0.01, 2.9), reduced quality of life (0.25-unit lower EQ5D; 95%CI −0.37, −0.12) and 1.8-unit higher BASDAI (95% CI 0.4, 3.3). Similar effect estimates were found for patients in the depression-anxiety cluster. Conclusion Comorbidity is common among axSpA patients. The two most common comorbidities were hypertension and depression. Patients in the depression-anxiety and fibromyalgia-IBS clusters reported poorer health and increased axSpA severity

    Biologic monotherapy in the biologic naive patient with rheumatoid arthritis (RA): results from an observational study

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    In the original article, the corresponding author's given name and middle name were interchanged

    The β-isoform of BCCIP promotes ADP release from the RAD51 presynaptic filament and enhances homologous DNA pairing

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    Homologous recombination (HR) is a template-driven repair pathway that mends DNA double-stranded breaks (DSBs), and thus helps to maintain genome stability. The RAD51 recombinase facilitates DNA joint formation during HR, but to accomplish this task, RAD51 must be loaded onto the single-stranded DNA. DSS1, a candidate gene for split hand/split foot syndrome, provides the ability to recognize RPA-coated ssDNA to the tumor suppressor BRCA2, which is complexed with RAD51. Together BRCA2-DSS1 displace RPA and load RAD51 onto the ssDNA. In addition, the BRCA2 interacting protein BCCIP normally colocalizes with chromatin bound BRCA2, and upon DSB induction, RAD51 colocalizes with BRCA2-BCCIP foci. Down-regulation of BCCIP reduces DSB repair and disrupts BRCA2 and RAD51 foci formation. While BCCIP is known to interact with BRCA2, the relationship between BCCIP and RAD51 is not known. In this study, we investigated the biochemical role of the β-isoform of BCCIP in relation to the RAD51 recombinase. We demonstrate that BCCIPβ binds DNA and physically and functionally interacts with RAD51 to stimulate its homologous DNA pairing activity. Notably, this stimulatory effect is not the result of RAD51 nucleoprotein filament stabilization; rather, we demonstrate that BCCIPβ induces a conformational change within the RAD51 filament that promotes release of ADP to help maintain an active presynaptic filament. Our findings reveal a functional role for BCCIPβ as a RAD51 accessory factor in HR
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