Sivertsenjordan3093

Pollination is the transfer of pollen grains from the stamens to the stigma, an essential requirement of sexual reproduction in flowering plants. Cross-pollination increases genetic diversity and is favored by selection in the majority of situations. Flowering plants have evolved a wide variety of traits that influence pollination success, including those involved in optimization of self-pollination, attraction of animal pollinators, and the effective use of wind pollination. In this review we discuss our current understanding of the molecular basis of the development and production of these various traits. We conclude that recent integration of molecular developmental studies with population genetic approaches is improving our understanding of how selection acts on key floral traits in taxonomically diverse species, and that further work in nonmodel systems promises to provide exciting insights in the years to come. Expected final online publication date for the Annual Review of Plant Biology, Volume 71 is April 29, 2020. Please see http//www.annualreviews.org/page/journal/pubdates for revised estimates.OBJECTIVE Our study was conducted with an attempt to investigate the diagnostic analysis of abnormal increase of fetal pulmonary artery systolic pressure (PASP) in middle and late pregnancy by color Doppler echocardiography. METHODS From August 2017 to January 2019, 52 fetuses with moderate or greater tricuspid high-speed regurgitation were retrospectively analyzed and selected as Group A. Seliciclib nmr 88 fetuses with full-color blood flow of the two ventricles and symmetrical sizes of the cardiac cavities on both sides harboring tricuspid valve and mild regurgitation or a small amount of regurgitation were selected as Group B. The pulmonary artery blood flow acceleration time (AT) and right ventricular ejection time (ET) was measured, and the PASP was calculated. RESULTS The tricuspid regurgitation velocity, tricuspid regurgitation pressure difference and PASP in Group A were higher than those in Group B (p 20 mmHg regurgitation pressure difference should be followed up in clinic. If PASP was ≥70 mmHg with symptoms of right heart failure, fetuses should be closely observed until 35-36 weeks old to ensure fetal safety and early delivery would be recommended.The incidence of asthma has increased from 5.5% to near 8% of the population, which is a major health concern. The hallmarks of asthma include eosinophilic airway inflammation that is associated with chronic airway remodeling. link2 Allergic airway inflammation is characterized by a complex interplay of resident and inflammatory cells. MicroRNAs (miRNAs) are small noncoding RNAs that function as post-transcriptional modulators of gene expression. However, the role of miRNAs, specifically miR-451, in the regulation of allergic airway inflammation is unexplored. Our previous findings showed that oxidant stress regulates miR-451 gene expression in macrophages during an inflammatory process. In this paper, we examined the role of miR-451 in regulating macrophage phenotype using an experimental poly-allergenic murine model of allergic airway inflammation. We found that miR-451 contributes to the allergic induction of CCL17 in the lung, and plays a key role in pro-asthmatic macrophage activation. Remarkably, administration of a Sirt2 inhibitor diminished alternate macrophage activation and markedly abrogated DRA-induced lung inflammation. These data demonstrate a role for miR-451 in modulating allergic inflammation by influencing allergen-mediated macrophages phenotype.The lungs, the immune and nervous systems functionally interact to respond to respiratory environmental exposures and infections. The lungs are innervated by vagal sensory neurons of the jugular and nodose ganglia, fused together in smaller mammals as the jugular-nodose complex (JNC). While the JNC shares properties with the other sensory ganglia, the trigeminal (TG) and dorsal root ganglia (DRG), these sensory structures express differential sets of genes that reflect their unique functionalities. Here, we used RNAseq in mice to identify the differential transcriptomes of the three sensory ganglia types. Using a fluorescent retrograde tracer and fluorescence-activated cell sorting we isolated a defined population of airway-innervating JNC neurons and determined their differential transcriptional map after pulmonary exposure to lipopolysaccharide (LPS), a major mediator of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) after infection with Gram-negative bacteria or inhalation of organic dust. JNC neurons activated an injury response program leading to increased expression of gene products such as the G-protein coupled receptors, Cckbr, inducing functional changes in neuronal sensitivity to peptides, and Gpr151, also rapidly induced upon neuropathic nerve injury in pain models. Unique JNC-specific transcripts, present at only minimal levels in TG, DRG and other organs, were identified. These included TMC3, encoding for a putative mechanosensor, and Urotensin 2B, a hypertensive peptide. These findings highlight the unique properties of the JNC and reveal that ALI/ARDS rapidly induce a nerve-injury related state changing vagal excitability.Idiopathic pulmonary fibrosis (IPF) results in scarring of the lungs by excessive extracellular matrix (ECM) production. Resident fibroblasts are the major cell type involved in ECM deposition. link3 The biochemical pathways that facilitate pathological fibroblast activation leading to aberrant ECM deposition are not fully understood. Tank Binding Protein Kinase-1 (TBK1), is a kinase that regulates multiple signaling pathways, and was recently identified as a candidate regulator of fibroblast activation in a large-scale siRNA screen. In order to determine the effect of TBK1 on fibroblast activation, TBK1 was inhibited pharmacologically (MRT68601) and genetically (siRNA) in normal and IPF human lung fibroblasts. Reducing the activity or expression of TBK1 led to reduction in α-SMA stress fiber levels by 40-60% and deposition of ECM components collagen I and fibronectin by 50% in TGF-β stimulated normal and IPF fibroblasts. YAP and TAZ are homologous mechanoregulatory, profibrotic transcription co-factors known to regulate fibroblast activation. TBK1 knockdown or inhibition decreased the total and nuclear protein levels of YAP/TAZ. Additionally, low cell-cell contact and increased ECM substrate stiffness augmented the phosphorylation and activation of TBK1, consistent with cues that regulate YAP/TAZ. The action of TBK1 towards YAP/TAZ activation was independent of LATS1/2 and canonical downstream TBK1 signaling mediator IRF3, but dependent on proteasomal machinery of the cell. This study identifies TBK1 as a fibrogenic activator of human pulmonary fibroblasts, suggesting TBK1 may be a novel therapeutic target in pulmonary fibrosis.INTRODUCTION Neutrophil extracellular traps (NETs) provide host defense, but can contribute to the pathobiology of diverse human diseases. We sought to determine the extent and mechanism by which NETs contribute to human airway cell inflammation. METHODS Primary normal human bronchial epithelia (HBEs) grown at air liquid interface and wtCFBE41o- cells (expressing wtCFTR) were exposed to cell-free NETs from unrelated healthy volunteers for 18 hours in vitro. Cytokines were measured in the apical supernatant by Luminex and the effect on the HBE transcriptome was assessed by RNA seq. RESULTS NETs consistently stimulated IL-8, TNF-α and IL-1α secretion by HBEs from multiple donors, with variable effects on other cytokines (IL-6, G-CSF, GM-CSF). HBE RNAs encoding IL-1 family cytokines, particularly IL-36 subfamily members, were increased in response to NETs. NET exposure in the presence of anakinra (recombinant human IL-1RA) dampened NET-induced changes in IL-8 and TNF-α proteins as well as IL-36α RNA. RhIL-36RA limited the increase in proinflammatory cytokine RNAs in HBEs exposed to NETs. CONCLUSION NETs selectively upregulate an IL-1 family cytokine response in HBEs, which enhances IL-8 production and is limited by rhIL-1RA. Present findings describe a unique mechanism by which NETs may contribute to inflammation in human lung disease in vivo. NET-driven IL-1 signaling may represent a novel target for modulating inflammation in diseases characterized by a substantial NET burden.If a molecular dication is produced on a repulsive potential energy surface (PES), it normally dissociates. Before that, however, ultrafast nuclear dynamics can change the PES and significantly influence the fragmentation pathway. Here, we investigate the electron-impact-induced double ionization and subsequent fragmentation processes of the ethanol molecule using multiparticle coincident momentum spectroscopy and ab initio dynamical simulations. For the electronic ground state of the ethanol dication, we observe several fragmentation channels that cannot be reached by direct Coulomb explosion (CE) but require preceding isomerization. Our simulations show that ultrafast hydrogen or proton transfer (PT) can stabilize the repulsive PES of the dication before the direct CE and form intermediate H2 or H2O. These neutrals stay in the vicinity of the precursor, and roaming mechanisms lead to isomerization and finally PT resulting in emission of H3+ or H3O+. The present findings can help to understand the complex fragmentation dynamics of molecular cations.Reducing sugars may be directly converted into the corresponding para-nitrophenyl (pNP) glycosides using 2-chloro-1,3-dimethylimidazolinium chloride (DMC), para-nitrophenol, and a suitable base in aqueous solution. The reaction is stereoselective for sugars with either a hydroxyl or an acetamido group at position 2, yielding the 1,2-trans pNP glycosides. A judicious choice of base allows extension to di- and oligosaccharide substrates, including a complex N-glycan oligosaccharide isolated from natural sources, without the requirement of any protecting group manipulations.A direct coupling of arylboronic acids with allylic fluorides was carried out in water without additives using a rhodium(III) catalyst (Cp*RhCl2)2. The transformation proceeded with excellent γ-selectivity to afford major allyl-aryl coupling products (Z) γ-substituted α,β-unsaturated amides. The reactions of α-chiral allylic fluorides took place with excellent α-to-γ chirality transfer to give allylated arenes with a stereogenic center at the benzylic and allylic position.The stability and the structure of adducts formed between four substituted phosphanes (PX3, XH, F, Cl, and NMe2) and 11 different carbenes have been investigated by DFT calculations. In most cases, the structure of the adducts depends strongly on the stability of the carbene itself, exhibiting a linear correlation with the increasing dissociation energy of the adduct. Carbenes of low stability form phosphorus ylides (F), which can be described as phosphane → carbene adducts supported with some back-bonding. The most stable carbenes, which have high energy lone pair, do not form stable F-type structures but carbene → phosphane adducts (E-type structure), utilizing the low-lying lowest unoccupied molecular orbital (LUMO) of the phosphane (with electronegative substituents), benefiting also from the carbene-pnictogen interaction. Especially noteworthy is the case of PCl3, which has an extremely low energy LUMO in its T-shaped form. Although this PCl3 structure is a transition state of rather high energy, the large stabilization energy of the complex makes this carbene-phosphane adduct stable.