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This article examines US airline mergers between 1993 and 2018 and studies their impact on the labor market. Our difference‐in‐differences estimates indicate a significant reduction in the merging airlines' long‐term wage and fringe benefits following the mergers. The effect is particularly salient among large‐scale mergers involving major airlines and low cost carriers. The results also suggest a negative short‐term employment impact of mergers that varies by occupation types. Our findings are consistent with the impact of merger‐induced monopsony power discussed in recent literature and offer important policy implications regarding how to account for employer monopsony power during mergers and acquisitions.

When the president of the United States tweets, do investors respond? We analyze the impact of tweets from President Donald J. Trump's official Twitter accounts from November 9, 2016 to December 31, 2017 that include names of publicly traded companies. We find that these tweets move company stock prices and increase trading volume, volatility, and institutional investor attention, with a stronger impact before the presidential inauguration. There is some evidence that the initial impact of the presidential tweets on stock prices is reversed in the next few trading days.

Using micro‐level thermostat data from 27,000 U.S. households, we analyze how home heating/cooling decisions respond to weather. Responses are greater for extreme heat than for extreme cold and persist for at least 30 days after exposure, due in part to transaction costs but also to changes in intrinsic preferences. Failure to understand habit can lead us to overestimate the impact of short‐term policy nudges but underestimate the long‐run impact of small changes. Higher frequency estimates of how behavior responds to weather improve our understanding of climate adaptation as climate change affects not only mean temperatures but also variances. (JEL C55, D03, Q4)

© 2018 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. Neovascularization, increased basal membrane thickness and increased airway smooth muscle (ASM) bulk are hallmarks of airway remodelling in asthma. In this study, we examined connective tissue growth factor (CTGF) dysregulation in human lung tissue and animal models of allergic airway disease. Immunohistochemistry revealed that ASM cells from patients with severe asthma (A) exhibited high expression of CTGF, compared to mild and non-asthmatic (NA) tissues. This finding was replicated in a sheep model of allergic airways disease. In vitro, transforming growth factor (TGF)-β increased CTGF expression both in NA- and A-ASM cells but the expression was higher in A-ASM at both the mRNA and protein level as assessed by PCR and Western blot. Transfection of CTGF promoter-luciferase reporter constructs into NA- and A-ASM cells indicated that no region of the CTGF promoter (−1500 to +200 bp) displayed enhanced activity in the presence of TGF-β. However, in silico analysis of the CTGF promoter suggested that distant transcription factor binding sites may influence CTGF promoter activation by TGF-β in ASM cells. The discord between promoter activity and mRNA expression was also explained, in part, by differential post-transcriptional regulation in A-ASM cells due to enhanced mRNA stability for CTGF. In patients, higher CTGF gene expression in bronchial biopsies was correlated with increased basement membrane thickness indicating that the enhanced CTGF expression in A-ASM may contribute to airway remodelling in asthma.

Nature builds biological materials from limited ingredients, however, with unparalleled mechanical performances compared to artificial materials, by harnessing inherent structures across multi-length-scales. In contrast, synthetic material design overwhelmingly focuses on developing new compounds, and fails to reproduce the mechanical properties of natural counterparts, such as fatigue resistance. Here, a simple yet general strategy to engineer conventional hydrogels with a more than 100-fold increase in fatigue thresholds is reported. This strategy is proven to be universally applicable to various species of hydrogel materials, including polysaccharides (i.e., alginate, cellulose), proteins (i.e., gelatin), synthetic polymers (i.e., poly(vinyl alcohol)s), as well as corresponding polymer composites. These fatigue-resistant hydrogels exhibit a record-high fatigue threshold over most synthetic soft materials, making them low-cost, high-performance, and durable alternatives to soft materials used in those circumstances including robotics, artificial muscles, etc.

4D printing is an emerging fabrication technology that enables 3D printed structures to change configuration over "time" in response to an environmental stimulus. Compared with other soft active materials used for 4D printing, shape-memory polymers (SMPs) have higher stiffness, and are compatible with various 3D printing technologies. Among them, ultraviolet (UV)-curable SMPs are compatible with Digital Light Processing (DLP)-based 3D printing to fabricate SMP-based structures with complex geometry and high-resolution. However, UV-curable SMPs have limitations in terms of mechanical performance, which significantly constrains their application ranges. Here, a mechanically robust and UV-curable SMP system is reported, which is highly deformable, fatigue resistant, and compatible with DLP-based 3D printing, to fabricate high-resolution (up to 2 µm), highly complex 3D structures that exhibit large shape change (up to 1240%) upon heating. More importantly, the developed SMP system exhibits excellent fatigue resistance and can be repeatedly loaded more than 10 000 times. The development of the mechanically robust and UV-curable SMPs significantly improves the mechanical performance of the SMP-based 4D printing structures, which allows them to be applied to engineering applications such as aerospace, smart furniture, and soft robots.

Exaggerated cytokine secretion drives pathogenesis of a number of chronic inflammatory diseases, including asthma. Anti-inflammatory pharmacotherapies, including corticosteroids, are front-line therapies and although they have proven clinical utility, the molecular mechanisms responsible for their actions are not fully understood. The corticosteroid-inducible gene, mitogen-activated protein kinase (MAPK) phosphatase 1 (MKP-1, DUSP1) has emerged as a key molecule responsible for the repressive effects of steroids. MKP-1 is known to deactivate p38 MAPK phosphorylation and can control the expression and activity of the mRNA destabilizing protein-tristetraprolin (TTP). But whether corticosteroid-induced MKP-1 acts via p38 MAPK-mediated modulation of TTP function in a pivotal airway cell type, airway smooth muscle (ASM), was unknown. While pretreatment of ASM cells with the corticosteroid dexamethasone (preventative protocol) is known to reduce ASM synthetic function in vitro, the impact of adding dexamethasone after stimulation (therapeutic protocol) had not been explored. Whether dexamethasone modulates TTP in a p38 MAPK-dependent manner in this cell type was also unknown. We address this herein and utilize an in vitro model of asthmatic inflammation where ASM cells were stimulated with the pro-asthmatic cytokine tumor necrosis factor (TNF) and the impact of adding dexamethasone 1 h after stimulation assessed. IL-6 mRNA expression and protein secretion was significantly repressed by dexamethasone acting in a temporally distinct manner to increase MKP-1, deactivate p38 MAPK, and modulate TTP phosphorylation status. In this way, dexamethasone-induced MKP-1 acts via p38 MAPK to switch on the mRNA destabilizing function of TTP to repress pro-inflammatory cytokine secretion from ASM cells. J. Cell. Physiol. 231: 2153-2158, 2016. © 2016 Wiley Periodicals, Inc.

BACKGROUND AND PURPOSE Airway remodelling is a consequence of long-term inflammation and MAPKs are key signalling molecules that drive pro-inflammatory pathways. The endogenous MAPK deactivator – MAPK phosphatase 1 (MKP-1) – is a critical negative regulator of the myriad pro-inflammatory pathways activated by MAPKs in the airway. EXPERIMENTAL APPROACH Herein we investigated the molecular mechanisms responsible for the upregulation of MKP-1 in airway smooth muscle (ASM) by the corticosteroid dexamethasone and the β2-agonist formoterol, added alone and in combination. KEY RESULTS MKP-1 is a corticosteroid-inducible gene whose expression is enhanced by long-acting β2-agonists in an additive manner. Formoterol induced MKP-1 expression via the β2-adrenoceptor and we provide the first direct evidence (utilizing overexpression of PKIα, a highly selective PKA inhibitor) to show that PKA mediates β2-agonist-induced MKP-1 upregulation. Dexamethasone activated MKP-1 transcription in ASM cells via a cis-acting corticosteroid-responsive region located between −1380 and −1266 bp of the MKP-1 promoter. While the 3′-untranslated region of MKP-1 contains adenylate + uridylate elements responsible for regulation at the post-transcriptional level, actinomycin D chase experiments revealed that there was no increase in MKP-1 mRNA stability in the presence of dexamethasone, formoterol, alone or in combination. Rather, there was an additive effect of the asthma therapeutics on MKP-1 transcription. CONCLUSIONS AND IMPLICATIONS Taken together, these studies allow us a greater understanding of the molecular basis of MKP-1 regulation by corticosteroids and β2-agonists and this new knowledge may lead to elucidation of optimized corticosteroid-sparing therapies in the future.

Transforming growth factor (TGF) beta 1 increases pro-inflammatory cytokines and contractile protein expression by human airway smooth muscle (ASM) cells, which could augment airway inflammation and hyperresponsiveness. Phosphoinositide 3' kinase (PI3K) is one of the signaling pathways implicated in TGF beta 1 stimulation, and may be altered in asthmatic airways. This study compared the expression of PI3K isoforms by ASM cells from donors with asthma (A), chronic obstructive pulmonary disease (COPD), or neither disease (NA), and investigated the role of PI3K isoforms in the production of TGF beta 1 induced pro-inflammatory cytokine and contractile proteins in ASM cells. A cells expressed higher basal levels of p110d mRNA compared to NA and COPD cells; however COPD cells produced more p110d protein. TGF beta 1 increased 110d mRNA expression to the same extent in the three groups. Neither the p110d inhibitor IC87114 (1, 10, 30?mu M), the p110 beta inhibitor TGX221 (0.1, 1, 10?mu M) nor the PI3K pan inhibitor LY294002 (3, 10?mu M) had any effect on basal IL-6, calponin or smooth muscle a-actin (a-SMA) expression. However, TGF beta 1 increased calponin and a-SMA expression was inhibited by IC87114 and LY294002 in all three groups. IC87114, TGX221, and LY294002 reduced TGF beta 1 induced IL-6 release in a dose related manner in all groups of ASM cells. PI3K p110d is important for TGF beta 1 induced production of the contractile proteins calponin and a-SMA and the proinflammatory cytokine IL-6 in ASM cells, and may therefore be relevant as a potential therapeutic target to treat both inflammation and airway remodeling. J. Cell. Physiol. 227: 30443052, 2012. (c) 2011 Wiley Periodicals, Inc.

A hybrid nanoarchitecture aerogel composed of WS2 nanosheets and carbon nanotube-reduced graphene oxide (CNT-rGO) with ordered microchannel three-dimensional (3D) scaffold structure was synthesized by a simple solvothermal method followed by freeze-drying and post annealing process. The 3D ordered microchannel structures not only provide good electronic transportation routes, but also provide excellent ionic conductive channels, leading to an enhanced electrochemical performance as anode materials both for lithium-ion batteries (LIBs) and sodium-ion batteries (SIBs). Significantly, WS2/CNT-rGO aerogel nanostructure can deliver a specific capacity of 749 mA h g−1 at 100 mA g−1 and a high first-cycle coulombic efficiency of 53.4% as the anode material of LIBs. In addition, it also can deliver a capacity of 311.4 mA h g−1 at 100 mA g−1, and retain a capacity of 252.9 mA h g−1 at 200 mA g−1 after 100 cycles as the anode electrode of SIBs. The excellent electrochemical performance is attributed to the synergistic effect between the WS2 nanosheets and CNT-rGO scaffold network and rational design of 3D ordered structure. These results demonstrate the potential applications of ordered CNT-rGO aerogel platform to support transition-metal-dichalcogenides (i.e., WS2) for energy storage devices and open up a route for material design for future generation energy storage devices.