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Pancreatic ductal adenocarcinoma has a high rate of neural invasion (80 to 100%) and can be associated with moderate to severe pain in pancreatic cancer. Treatment of pain with celiac plexus blockage (CPB) combined with the three-step ladder utilization of pharmaceutical analgesics following WHO guidelines is used, but the evidence in randomized controlled trials is inconsistent. This meta-analysis identified and compared seven randomized control trials of pain relief from pancreatic cancer, by treatment with medical management alone to celiac plexus blockade with medical management. While no evidence of potential publication bias was detected, group size and statistical power may account for some of the inconsistent conclusions. The combined CPB groups had a significantly lower pain score at 4 weeks, but significance was not maintained at 8 weeks. The combined CPB groups required significantly less drug use compared to the combined control groups treated with pharmaceutical analgesics.

Double B-box 1a (DBB1a) belongs to the zinc-finger family proteins in Arabidopsis thaliana. Transcriptional analysis uncovered that the DBB1a gene expression was blue light-dependently regulated, and the transcript level of DBB1a in cry1cry2 was decreased but not in phyAphyB compared to wild type under blue light conditions. Transgenic plants containing pDBB1a:GUS (β-glucuronidase) displayed GUS activity in the vascular system of leaves and petioles. Green fluorescent protein (GFP)-fused DDB1a (DBB1a-GFP) protein was found in the nucleus in transient transformation assays with onion epidermal cells as well as in stable transgenic Arabidopsis plants. To investigate the function of DBB1a, we generated DBB1a over-expressing and under-expressing transgenic Arabidopsis plants. Analysis of hypocotyl growth of these lines indicated that DBB1a promoted hypocotyl elongation under blue light condition. The phenotype of transgenic plants with DBB1a over-expression could be impaired by a gibberellin (GA)-biosynthesis inhibitor. Moreover, the expression analysis of GA metabolic and catabolic genes in DBB1a transgenic lines indicated that the DBB1a suppressed GA2-oxidase1 (GA2ox1) and GA2-oxidase8 (GA2ox8) expression, but induced GA3β-hydroxygenase1 (GA3ox1) and GA20-oxidase1 (GA20ox1) expression under blue light. Taken together, we concluded that DBB1a promotes hypocotyl elongation under blue light condition through an increase in bioactive GA levels in Arabidopsis.

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/npsi/ctrl?lang=en http://nparc.cisti-icist.nrc-cnrc.gc.ca/npsi/ctrl?lang=fr Access and use of this website and the material on it are subject to the Terms and Conditions set forth at http://nparc.cisti-icist.nrc-cnrc.gc.ca/npsi/jsp/nparc_cp.jsp?lang=en NRC Publications Archive Archives des publications du CNRCThis publication could be one of several versions: author's original, accepted manuscript or the publisher's version. / La version de cette publication peut être l'une des suivantes : la version prépublication de l'auteur, la version acceptée du manuscrit ou la version de l'éditeur. For the publisher's version, please access the DOI link below./ Pour consulter la version de l'éditeur, utilisez le lien DOI ci-dessous.http://dx.doi.org/10.1016/S0017-9310(00)00227-1International Journal of Heat and Mass Transfer, 44, 9, pp. 1803-1815, 2001 AbstractA numerical model has been developed to simulate volatile organic compound (VOC) emissions from "wet" coating materials. The model considers the VOC mass transfer process in the air and material-air interface, and diffusion in the material film and also in the substrate. Our numerical simulations confirmed that the emissions from "wet" materials applied to an absorptive substrate are dominated by evaporation at the beginning followed by internal diffusion, which had been hypothesized based on previous experimental data. The numerical model has been validated based on the data from small-scale environmental chamber tests.

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SummaryEfficient trafficking of the cystic fibrosis transmembrane conductance regulator (CFTR) to and from the cell surface is essential for maintaining channel density at the plasma membrane (PM) and ensuring proper physiological activity. The most common mutation, F508del, exhibits reduced surface expression and impaired function despite treatment with currently available pharmacological small molecules, called correctors. To gain more detailed insight into whether CFTR enters compartments that allow corrector stabilization in the cell periphery, we investigated the peripheral trafficking itineraries and kinetics of wild type (WT) and F508del in living cells using high-speed fluorescence microscopy together with fluorogen activating protein detection. We directly visualized internalization and accumulation of CFTR WT from the PM to a perinuclear compartment that colocalized with the endosomal recycling compartment (ERC) markers Rab11 and EHD1, reaching steady-state distribution by 25 minutes. Stimulation by protein kinase A (PKA) depleted this intracellular pool and redistributed CFTR channels to the cell surface, elicited by reduced endocytosis and active translocation to the PM. Corrector or temperature rescue of F508del also resulted in targeting to the ERC and exhibited subsequent PKA-stimulated trafficking to the PM. Corrector treatment (24 hours) led to persistent residence of F508del in the ERC, while thermally destabilized F508del was targeted to lysosomal compartments by 3 hours. Acute addition of individual correctors, C4 or C18, acted on peripheral trafficking steps to partially block lysosomal targeting of thermally destabilized F508del. Taken together, corrector treatment redirects F508del trafficking from a degradative pathway to a regulated recycling route, and proteins that mediate this process become potential targets for improving the efficacy of current and future correctors.