Lucasdemant8196

riparia had the greatest phenotypic plasticity. North American species exhibited significant differences in tooth areablade area. Intermediate developmental stages were most likely to exhibit phenotypic plasticity, and only V. amurensis exhibited phenotypic plasticity in later developmental stages. CONCLUSIONS Leaves have variable phenotypic plasticity along the vine. Environmental signal was strongest in intermediate developmental stages. This is significant for leaf physiognomic-paleoclimate proxies because these leaves are likely the most common in leaf litter and reflect leaves primarily included in paleoclimate reconstructions. Early season and early developmental stages have the potential to be confounding factors but are unlikely to exert significant influence because of differential preservation potential. © 2020 The Authors. American Journal of Botany published by Wiley Periodicals LLC on behalf of Botanical Society of America.We examined the relative contribution of genetic, shared environmental and non-shared environmental factors to the covariance between parental sensitivity and limit-setting observed twice in a longitudinal study using a child-based twin design. Parental sensitivity and parental limit-setting were observed in 236 parents with each of their same-sex toddler twin children (Mage  = 3.8 years; 58% monozygotic). Bivariate behavioral genetic models indicated substantial effects of similar shared environmental factors on parental sensitivity and limit-setting and on the overlap within sensitivity and limit-setting across 1 year. Moderate child-driven genetic effects were found for parental limit-setting in year 1 and across 1 year. Genetic child factors contributing to explaining the variance in limit-setting over time were the same, whereas shared environmental factors showed some overlap. © 2020 The Authors. WP1066 in vivo Child Development published by Wiley Periodicals LLC on behalf of Society for Research in Child Development.Early onset pancreatic cancer (EOPC) is a rare disease with a very high mortality rate. Almost nothing is known on the genetic susceptibility of EOPC, therefore we performed a genome-wide association study (GWAS) to identify novel genetic variants specific for patients diagnosed with pancreatic ductal adenocarcinoma (PDAC) at younger ages. In the first phase, conducted on 821 cases with age of onset ≤60 years, of whom 198 with age of onset ≤50, and 3227 controls from PanScan I-II, we observed four SNPs (rs7155613, rs2328991, rs4891017 and rs12610094) showing an association with EOPC risk (P  less then  1x10-4 ). We replicated these SNPs in the PANcreatic Disease ReseArch (PANDoRA) consortium and used additional in silico data from PanScan III and PanC4. Among these four variants rs2328991 was significant in an independent set of 855 cases with age of onset ≤60 years, of whom 265 with age of onset≤50, and 4142 controls from the PANDoRA consortium while in the in silico data we observed no statistically significant association. However, the resulting meta-analysis supported the association (P = 1.15x10-4 ). In conclusion we propose a novel variant rs2328991 to be involved in EOPC risk. Even though it was not possible to find a mechanistic link between the variant and the function, the association is supported by a solid statistical significance obtained in the largest study on EOPC genetics present so far in the literature. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.BACKGROUND Critically ill newborn infants undergo a variety of painful procedures or experience a variety of painful conditions during their early life in the neonatal unit. In the critically ill paediatric and neonatal population, clonidine is prescribed as an adjunct to opioids or benzodiazepines aiming to reduce the doses of these drugs that are required for analgesia or sedation, or to facilitate weaning from mechanical ventilation. It has been shown that clonidine premedication might have a positive effect on postoperative pain in children. OBJECTIVES To assess the benefit and harms of clonidine for the prevention or treatment of procedural pain; postoperative pain; or pain associated with clinical conditions in non-ventilated neonates. SEARCH METHODS We used the standard search strategy of Cochrane Neonatal to search the CENTRAL, MEDLINE via PubMed, Embase, and CINAHL to December 2018. We also searched clinical trials databases, conference proceedings, and the reference lists of retrieved articles for r procedure; for postoperative pain and for pain associated with clinical conditions, the mean values of each analgesia scale assessed at 30 minutes, three hours, and 12 hours after the administration of the intervention. We planned to use the GRADE approach to assess the quality of evidence. MAIN RESULTS Our search strategy yielded 3383 references. Two review authors independently assessed all references for inclusion. We did not find any completed studies for inclusion. We excluded three trials where clonidine was administered for spinal anaesthesia. AUTHORS' CONCLUSIONS We did not find any studies that met our inclusion criteria and hence there is no evidence to recommend or refute the use of clonidine for the prevention or treatment of procedural or postoperative pain, or pain associated with clinical conditions in neonates. Copyright © 2020 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd.SAMHD1 is an enzyme with phosphohydrolase activity. Mutations in SAMHD1 have been linked to the development of Aicardi-Goutières Syndrome in humans. This enzyme also has the capacity to restrict HIV virus replication in macrophages. Here we report that Samhd1 is highly expressed in murine macrophages and is regulated by pro-inflammatory (IFN-γ and LPS) but not by anti-inflammatory (IL-4 or IL-10) activators. The induction of Samhd1 follows the pattern of an intermediate gene that requires protein synthesis. In transient transfection experiments using the Samhd1 promoter, we found that a fragment of 27 bps of this gene, falling between -937 and -910 bps relative to the transcription start site, is required for IFN-γ-dependent activation. Using EMSAs, we determined that IFN-γ treatment led to the elimination of a protein complex. Chromatin immunoprecipitation assays and siRNA experiments revealed that IRF1 is required for IFN-γ- or LPS-induced Samhd1 expression. Therefore, our results indicate that Samhd1 is stimulated by pro-inflammatory agents IFN-γ and LPS.