Cellular Mechanism Underlying the Facilitation of Contractile Response Induced by Tumor Necrosis Factor-α in Mouse Tracheal Smooth Muscle.

The proinflammatory cytokine tumor necrosis factor-α (TNF-α) augments intracellular Ca2+ signaling and contractile responses of airway smooth muscles, leading to airway hyperresponsiveness. However, the underlying mechanism has not been fully elucidated. This study aimed to investigate the cellular mechanism of the potentiated contraction of mouse tracheal smooth muscle induced by TNF-α. The results showed that TNF-α triggered facilitation of mouse tracheal smooth muscle contraction in an epithelium-independent manner. The TNF-α-induced hypercontractility could be suppressed by the protein kinase C inhibitor GF109203X, the tyrosine kinase inhibitor genistein, the Src inhibitor PP2, or the L-type voltage-dependent Ca2+ channel blocker nifedipine. Following TNF-α incubation, the α1C L-type Ca2+ channel (CaV1.2) was up-regulated in cultured primary mouse tracheal smooth muscle cells. Pronounced phosphotyrosine levels were observed in mouse tracheas. In conclusion, this study shows that TNF-α enhanced airway smooth muscle contraction via protein kinase C-Src-CaV1.2 pathways, which provides novel insights into the pathologic role of proinflammatory cytokines in mediating airway hyperresponsiveness.

Direct modulation bandwidth enhancement of uncooled DFB laser operating over a wide temperature range based on groove-in-trench waveguide structure.

Uncooled direct modulation DFB laser offers high speed transmission rate over a wide temperature range with high reliability and low cost, making it a cost-effective light source choice for 5G fronthaul and data center applications. However, a significant 3dB bandwidth decrease can be observed in high temperature for conventional DFB lasers. We present an uncooled DFB laser operating up to 85°C with extended direct modulation bandwidth and high reliability based on a novel groove-in-trench ridge waveguide structure, where two narrow grooves penetrating the active layer are etched symmetrically in the two conventional trenches by deep wet etching, respectively. By optimizing the distance between the groove and the mesa stripe, we obtain a 3dB bandwidth of 15.3 GHz at 85°C, which is a 3.7 GHz improvement compared with the conventional ridge waveguide DFB laser. Transmissions of 25 Gb/s NRZ signal at 25°C and 85°C with clear eye openings have been demonstrated. It also achieves 25 Gb/s transmission over 10 km optical fiber with a low power penalty of 0.5 dB for a bit error rate of 10-12 at 85°C. In addition, the result of 2000-hour aging test shows that the proposed groove-in-trench structure DFB lasers have the same excellent reliability as the conventional ones.

Experiment demonstration of high speed 1.3 µm grating assisted surface-emitting DFB lasers.

Surface emitting lasers are attractive light sources for silicon integrated photonic circuits. High speed direct operation is of great importance for these lasers in high capacity and low cost on-chip communication system. Here, we demonstrate a 1.3 µm surface emitting ridge-waveguide distributed feedback (DFB) laser with second order grating and λ/4 phase shift grating, which can achieve a 24 Gb/s operation over a wide temperature. The fabricated lasers can achieve low threshold current as 6.8 mA, and 12.5 mA at 20, and 70°C, respectively. Stable single mode operation has been observed with high side mode suppression ratio (SMSR) > 40 dB at all temperatures (20-70 °C). Meanwhile, the surface emitting optical power can reach 1.7 mW at high temperature as 70 °C. 3 dB bandwidth of small signal response is 21 GHz and 12 GHz at 20 °C and 70 °C respectively. The far-field divergence angle of surface emitting beam is 13.4°×20.2° of 10 µm length second order grating coupler. The proposed laser may have great advantages of single mode, high speed modulation and good temperature tolerance. In addition, compared with conventional DFB lasers, the surface emitting DFB laser has no additional manufacturing process, which is simple to fabricate and easy to integrate with silicon platform.

ß2-Adrenoceptor Activation Stimulates IL-6 Production via PKA, ERK1/2, Src, and Beta-Arrestin2 Signaling Pathways in Human Bronchial Epithelia.

OBJECTIVE: ß2-Adrenoceptor agonists are widely used to treat asthma because of their bronchial-dilation effects. We previously reported that isoprenaline, via the apical and basolateral ß2-adrenoceptor, induced Cl- secretion by activating cyclic AMP (cAMP)-dependent pathways in human bronchial epithelia. Despite these results, whether and how the ß2-adrenoceptor-mediated cAMP-dependent pathway contributes to pro-inflammatory cytokine release in human bronchial epithelia remains poorly understood. METHODS: We investigated ß2-adrenoceptor-mediated signaling pathways involved in the production of two pro-inflammatory cytokines, interleukin (IL)-6 and IL-8, in 16HBE14o- human bronchial epithelia. The effects of isoprenaline or formoterol were assessed in the presence of protein kinase A (PKA), exchange protein directly activated by cAMP (EPAC), Src, and extracellular signal-regulated protein kinase (ERK)1/2 inhibitors. The involvement of ß-arrestin2 was examined using siRNA knockdown. RESULTS: Isoprenaline and formoterol (both ß2 agonists) induced IL-6, but not IL-8, release, which could be inhibited by ICI 118,551 (ß2 antagonist). The PKA-specific inhibitor, H89, partially inhibited IL-6 release. Another intracellular cAMP receptor, EPAC, was not involved in IL-6 release. Isoprenaline-mediated IL-6 secretion was attenuated by dasatinib, a Src inhibitor, and PD98059, an ERK1/2 inhibitor. Isoprenaline treatment also led to ERK1/2 phosphorylation. In addition, knockdown of ß-arrestin2 by siRNA specifically suppressed cytokine release when a high concentration of isoprenaline (1 mM) was used. CONCLUSION: Our results suggest that activation of the ß2-adrenoceptor in 16HBE14o- cells stimulated the PKA/Src/ERK1/2 and/or ß-arrestin2 signaling pathways, leading to IL-6 release. Therefore, our data reveal that ß2-adrenoceptor signaling plays a role in the immune regulation of human airway epithelia.

ß2 adrenoceptor signaling regulates ion transport in 16HBE14o- human airway epithelial cells.

We investigated the regulation of Cl- secretion by adrenoceptors in polarized 16HBE14o- human bronchial epithelial cells. Treatment with the nonselective ß adrenoceptor agonist isoprenaline stimulated an increase in short-circuit current (ISC ), which was inhibited by the ß adrenoceptor blocker propranolol. Treatment with procaterol, an agonist specific for the ß2 adrenoceptor subtype, stimulated a similar increase in ISC , which was inhibited by the ß2 adrenoceptor antagonist ICI 118551. Inhibitors of cystic fibrosis transmembrane conductance regulator (CFTR) and calcium-activated Cl- channel (CaCC), but not K+ channel blockers, were able to inhibit the increase in ISC . "Trimultaneous" recording of ISC and intracellular cyclic adenosine monophosphate (cAMP) and Ca2+ levels in 16HBE14o- epithelia confirmed that the ISC induced by isoprenaline or procaterol involved both cAMP and Ca2+ signaling. Our results demonstrate that ß2 adrenoceptors regulate Cl- secretion in the human airway epithelium by activating apical CFTRs and CaCCs via cAMP-dependent and intracellular Ca2+ -dependent mechanisms, respectively.

Preparation of tannin-immobilized gelatin/PVA nanofiber band for extraction of uranium (VI) from simulated seawater.

A novel gelatin/PVA composite nanofiber band loaded with bayberry tannin (GPNB-BT) was prepared by electrostatic spinning and crosslinking for extraction of uranium (VI) from simulated seawater. The influential factors of tannin loaded on the nanofiber band were investigated in detail. Surface morphology and fiber diameter of GPNB-BT were studied by Scanning Electron Microscopy (SEM). Functional groups of GPNB-BT were investigated by Fourier Transform Infrared Spectrometer (FTIR). The adsorption process and mechanism of uranium on GPNB-BT was characterized by Energy Dispersive X-ray (EDX) and X-ray Photoelectron Spectroscopy (XPS). The results revealed that the BT had been stably solidified on the GPNB. Compared with other tannin-immobilized membranes, the nano-network structure of GPNB-BT with 200-400 nm diameter of fibers can promote solidification of tannins and improve adsorption capacity of GPNB-BT for uranium. The maximum adsorption capacity of the GPNB-BT for uranium is 170 mg/g at the optimal pH of 5.5 in 80 mg/L of initial uranium concentration and 1.4 µg/g even at extremely low initial concentration of 3 µg/L in the simulated seawater for 24 h. The GPNB-BT with good hydraulic properties, floatability and adsorption capacity for uranium is expected to be widely used in separation and enrichment of uranium in seawater and radioactive waste water.

Carbon Monoxide Inhibits Cytokine and Chloride Secretion in Human Bronchial Epithelia.

BACKGROUND/AIMS: Carbon monoxide (CO) is an important gas produced endogenously by heme oxygenase (HO) that functions as an anti-inflammatory and in ion channel modulation, but the effects of CO on airway inflammation and ion transport remains unclear. METHODS: The effect of CO on cell damage- and nucleotide-induced pro-inflammatory cytokine release in primary human bronchial epithelia cells (HBE) and in the 16HBE14o- human bronchial epithelial cell line were investigated. The effects of CO on calcium- and cAMP-dependent chloride (Cl-) secretion were examined using a technique that allowed the simultaneous measurement and quantification of real-time changes in signalling molecules (cAMP and Ca2+) and ion transport in a polarised epithelium. RESULTS: CO suppressed the release of interleukin (IL)-6 and IL-8 and decreased the phosphorylation of ERK1/2 and NF-κB p65. Furthermore, CO inhibited UTP-induced increases in calcium and Cl- secretion, and forskolin-induced increases in cAMP and Cl- secretion. CONCLUSIONS: These findings suggest a novel anti-inflammatory role of CO in human bronchial epithelia via interactions with purinergic signalling pathways. Further, CO modulated both the Ca2+- and cAMP-dependent secretion of Cl-.

Regulation of Intracellular Calcium by Carbon Monoxide in Human Bronchial Epithelial Cells.

BACKGROUND/AIMS: Carbon monoxide (CO) is an important autocrine/paracrine messenger involved in a variety of physiological and pathological processes. This study aimed to investigate the regulatory role of CO released by CO-releasing molecule-2 (CORM-2) in a P2Y receptor-mediated calcium-signaling pathway in the human bronchial epithelial cell line, 16HBE14o-. METHODS: Intracellular calcium ([Ca2+]i) was measured by fura-2 microspectrofluorimetry. D-myo-inositol-1-phosphate (IP1) levels and cGMP-dependent protein kinase activity (PKG) were also quantified. RESULTS: The exogenous application of CORM-2 increased both intracellular Ca2+ and IP1, which are inhibited by U73122, a phospholipase C (PLC) inhibitor. In contrast, the P2Y2/P2Y4 receptor-mediated intracellular Ca2+ release and influx induced by UTP were inhibited in the presence of CORM-2. However, CORM-2 did not affect the store-operated Ca2+ entry (SOCE) induced by thapsigargin (Tg). Moreover, the inhibitory effect of CORM-2 on UTP-induced calcium increase could be attenuated by a soluble guanylyl cyclase (sGC) inhibitor, 1H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one (ODQ), or a Protein Kinase G (PKG) inhibitor, KT5823, suggesting the involvement of sGC/PKG signaling in this process. CONCLUSION: CORM-2 serves a dual role in modulating [Ca2+]i in 16HBE14o- cells. Thus, CO released by CORM-2 may act as a regulator of calcium homeostasis in human airway epithelia. These findings help further elucidate the function of CO in many physiological and pathological conditions.

Anomalously high Na+ and low Li+ mobility in intercalated Na2Ti6O13.

We report an anomalous diffusion behavior in intercalated Na2Ti6O13. Using first-principles calculations, the direct migration of inserted Na+ along the tunnel direction is predicted to have a barrier of 0.24-0.44 eV, while the migration of inserted Li+ along the tunnel direction has a barrier of 0.86-1.15 eV. Although Li+ can also diffuse along a zig-zag path in the tunnel, the barrier of 0.86-0.99 eV is still much higher than that for Na+. Our results surprisingly lead to the conclusion that the diffusion of larger Na+ is 4-8 orders of magnitude faster than Li+ in the same host lattice, and explain the experimentally observed exceptional rate capability of Na2Ti6O13 as the Na-ion battery anode. The anomalous diffusion behavior is attributed to the geometric features of Na2Ti6O13. For migration of Li+ it is necessary to weaken Li-O bonds and to overcome the repulsion between Li and host Na ions simultaneously, while for Na+ diffusion the improved Na-O bonding at the transition state partially compensates for the energy penalty from the repulsion of host Na ions.

Boron clusters as highly stable magnesium-battery electrolytes.

Boron clusters are proposed as a new concept for the design of magnesium-battery electrolytes that are magnesium-battery-compatible, highly stable, and noncorrosive. A novel carborane-based electrolyte incorporating an unprecedented magnesium-centered complex anion is reported and shown to perform well as a magnesium-battery electrolyte. This finding opens a new approach towards the design of electrolytes whose likelihood of meeting the challenging design targets for magnesium-battery electrolytes is very high.

SARS-CoV-2 spike protein receptor binding domain promotes IL-6 and IL-8 release via ATP/P2Y2 and ERK1/2 signaling pathways in human bronchial epithelia.

The spike protein of SARS-CoV-2 as well as its receptor binding domain (RBD) has been demonstrated to be capable of activating the release of pro-inflammatory mediators in endothelial cells and immune cells such as monocytes. However, the effects of spike protein or its RBD on airway epithelial cells and mechanisms underlying these effects have not been adequately characterized. Here, we show that the RBD of spike protein alone can induce bronchial epithelial inflammation in a manner of ATP/P2Y2 dependence. Incubation of human bronchial epithelia with RBD induced IL-6 and IL-8 release, which could be inhibited by antibody. The incubation of RBD also up-regulated the expression of inflammatory indicators such as ho-1 and mkp-1. Furthermore, ATP secretion was observed after RBD treatment, P2Y2 receptor knock down by siRNA significantly suppressed the IL-6 and IL-8 release evoked by RBD. Additionally, S-RBD elevated the phosphorylation level of ERK1/2, and the effect that PD98059 can inhibit the pro-inflammatory cytokine release suggested the participation of ERK1/2. These novel findings provide new evidence of SARS-CoV-2 on airway inflammation and introduce purinergic signaling as promising treatment target.

Instability of Liquid Film with Odd Viscosity over a Non-Uniformly Heated and Corrugated Substrate.

The effect of odd viscosity on the instability of liquid film along a wavy inclined bottom with linear temperature variation is investigated. By utilizing the long-wave approximation, the non-linear evolution equation of the free surface is derived. By applying the normal mode method, the linear instability of thin film flow is investigated. With the help of multi-scale analysis methods, the weakly non-linear instability of thin film flow is also investigated. The results reveal that the Marangoni effect caused by non-uniform temperature distribution promotes the instability of the liquid film, while the odd viscosity has a stabilizing effect. In addition, for a positive local inclination angle θ, an increase in bottom steepness ζ inhibits the instability of the liquid film flow. In contrast, with a negative local inclination angle θ, increased bottom steepness ζ promotes the instability of the liquid film flow. The results of the temporal linear instability analysis and the weakly non-linear instability analysis have been substantiated through numerical simulations of the non-linear evolution equations.

Pro-inflammatory action of formoterol in human bronchial epithelia.

Despite the wide usage of ß2-adrenoceptor agonists in asthma treatment, they do have side effects such as aggravating inflammation. We previously reported that isoprenaline induced Cl- secretion and IL-6 release via cAMP-dependent pathways in human bronchial epithelia, but the mechanisms underlying the inflammation-aggravation effects of ß2-adrenoceptor agonists remain pooly understood. In this study, we investigated formoterol, a more specific ß2-adrenoceptor agonist, -mediated signaling pathways involved in the production of IL-6 and IL-8 in 16HBE14o- human bronchial epithelia. The effects of formoterol were detected in the presence of PKA, exchange protein directly activated by cAMP (EPAC), cystic fibrosis transmembrane conductance regulator (CFTR), extracellular signal-regulated protein kinase (ERK)1/2 and Src inhibitors. The involvement of ß-arrestin2 was determined using siRNA knockdown. Our results indicate that formoterol can induce IL-6 and IL-8 secretion in concentration-dependent manner. The PKA-specific inhibitor, H89, partially inhibited IL-6 release, but not IL-8. Another intracellular cAMP receptor, EPAC, was not involved in either IL-6 or IL-8 release. PD98059 and U0126, two ERK1/2 inhibitors, blocked IL-8 while attenuated IL-6 secretion induced by formoterol. Furthermore, formoterol-induced IL-6 and IL-8 release was attenuated by Src inhibitors, namely dasatinib and PP1, and CFTRinh172, a CFTR inhibitor. In addition, knockdown of ß-arrestin2 by siRNA only suppressed IL-8 release when a high concentration of formoterol (1 µM) was used. Taken together, our results suggest that formoterol stimulates IL-6 and IL-8 release which involves PKA/Src/ERK1/2 and/or ß-arrestin2 signaling pathways.

Genomic alterations associated with pseudoprogression and hyperprogressive disease during anti-PD1 treatment for advanced non-small-cell lung cancer.

Introduction: This study aimed to elucidate the relationship between dynamic genomic mutation alteration and pseudoprogression (PsPD)/hyperprogressive disease (HPD) in immunotherapy-treated advanced non-small-cell lung cancer (NSCLC), to provide clinical evidence for identifying and distinguishing between PsPD and HPD. Method: Patients with advanced NSCLC who were treated with anti-PD1 were enrolled. Whole blood was collected at baseline and post image progression. Serum was separated and sequenced using 425-panel next-generation sequencing analysis (NGS). Results: NGS revealed that not only single gene mutations were associated with PsPD/HPD before treatment, dynamic monitoring of the whole-blood genome mutation spectrum also varied greatly. Mutational burden, allele frequency%, and relative circulating tumor DNA abundance indicated that the fold change after image progression was much higher in the HPD group. Discussion: The gene mutation profiles of PsPD and HPD not only differed before treatment, but higher genome mutation spectrum post image progression indicated true disease progression in patients with HPD. This suggests that dynamic whole-genome mutation profile monitoring as NGS can distinguish PsPD from HPD more effectively than single gene detection, providing a novel method for guiding clinical immune treatment.

NONO regulates multiple cytokine production in sepsis via the ERK1/2 signaling pathway.

The massive release of pro-inflammatory cytokines is a crucial step in triggering the inflammatory cascade in sepsis. Exploring the key molecules regulating the expression and release of multiple cytokines has important value for revealing the mechanism of the cytokine storm in sepsis. This study aimed to investigate the role of multifunctional nuclear protein non-POU domain containing octamer-binding protein (NONO) in the sepsis cytokine storm and to elucidate the underlying mechanism. We found that NONO expression in tissues and cells of sepsis mice was significantly upregulated. Downregulation of NONO expression inhibited the mRNA expression of multiple cytokines, including IL-6, IL-1ß, MCP-1, MIP-1α, and MIP-1ß in inflammatory cells from mice and human leukemic monocyte-THP1 cells challenged with lipopolysaccharide (LPS), and significantly decreased the level of these cytokines and TNF-α in the supernatant of THP1 cells challenged by LPS. Nono knockout also reduced the levels of TNF-α, IL-6, MIP-1α, and MIP-1ß in serum, alleviated hepatocyte edema, and improved the survival rate of sepsis mice. Reduced NONO expression decreased the phospho-ERK1/2 level in inflammatory cells from sepsis mice or THP1 cells challenged by LPS. Phospho-ERK1/2 inhibitor decreased the mRNA expression and concentration of cytokines in the culture supernatant of LPS-induced THP1 cells, similar to the effect of NONO knockdown. After LPS challenge, the levels of phospho-ERK1/2 and NONO were increased, with obvious colocalization in the nucleus and vesicular-like organelles in macrophages. NONO knockdown decreased nuclear translocation of phospho-ERK1/2 in LPS-challenged THP1 cells. These results suggest that NONO is a potentially critical molecule involved in multiple cytokine production in sepsis. Upregulated NONO in sepsis may promote the expression and release of multiple cytokines to participate in a sepsis cytokine storm by promoting ERK1/2 phosphorylation.

Environmental Pollution Liability Insurance and Corporate Performance: Evidence from China in the Perspective of Green Development.

Environmental pollution is an inevitable primary responsibility in the production and management of enterprises, and it is the most severe challenge to achieving green production and sustainable development. Environmental pollution liability insurance (EPLI) can transfer corporate pollution liability to insurance companies, which affects corporate performance to a certain extent. However, the influencing factors of enterprise performance are complex, and EPLI also involves multiple subjects, so the impact of EPLI on enterprise performance is also complex. At first, this paper analyzes the possible relationship between EPLI and corporate performance based on the existing literature; subsequently, based on the list of EPLI-insured companies in 2014 and 2015 published by China's environmental protection department as a sample, this paper uses a fixed-effects model to conduct an empirical analysis, and the mediating role of corporate social responsibility (CSR) was then examined; finally, heterogeneity analysis of the initial conclusions was conducted. The following conclusions are drawn: firstly, there is a significant negative correlation between EPLI and corporate performance. Secondly, CSR played a mediating role in the effect of EPLI on corporate performance; that is, EPLI inhibited the rise of corporate performance by affecting CSR. Thirdly, the impact of EPLI on corporate performance is heterogeneous in terms of equity nature, corporate pollution level and marketization degree. The results of this paper enrich the economic impact theory of EPLI and have specific practical value for enterprise management and policymakers in the background of the green economy.

Sensitivity analysis of factors influencing pollutant removal from shallow groundwater by the PRB method based on numerical simulation.

Permeable reactive barrier (PRB) is one of the most promising in situ treatment methods for shallow groundwater pollution. However, optimal design of PRB is very difficult due to a lack of comprehensive understanding of various complex influencing factors of PRB remediation. In this study, eight of the main factors of PRB, including hydraulic gradient I, permeability coefficient KPRB of PRB material, PRB length L, PRB width W, PRB distance from pollution source Dist., the ratio of the maximum adsorption capacity to Langmuir constant of PRB material Qmax/KL, the discharge rate of pollution source DR, and recharge concentration RC were investigated, to carry out the sensitivity analysis of PRB removal efficiency. The simulation experiments for Morris analysis were designed, and pollutant removal efficiency was numerically simulated by coupling MODFLOW and MT3DMS under two scenarios of high and low permeability and dispersivity. For a typical low permeability with low dispersity medium, the sensitivity ranking of factors from high to low is DR, RC, I, W, L, Dist., Qmax/KL, and KPRB, and for a typical high permeability with a high dispersity medium, the sensitivity ranking of factors from high to low is I, W, DR, Qmax/KL, L, RC, Dist., and KPRB. When considering multiple factors in PRB design, the greater the KPRB, L, W, Qmax/KL is, the higher the removal efficiency is; the greater the RC, I is, the lower the removal efficiency is. The rest factors remain ambiguous enhancement to removal efficiency.

Conversion reaction mechanisms in lithium ion batteries: study of the binary metal fluoride electrodes.

Materials that undergo a conversion reaction with lithium (e.g., metal fluorides MF(2): M = Fe, Cu, ...) often accommodate more than one Li atom per transition-metal cation, and are promising candidates for high-capacity cathodes for lithium ion batteries. However, little is known about the mechanisms involved in the conversion process, the origins of the large polarization during electrochemical cycling, and why some materials are reversible (e.g., FeF(2)) while others are not (e.g., CuF(2)). In this study, we investigated the conversion reaction of binary metal fluorides, FeF(2) and CuF(2), using a series of local and bulk probes to better understand the mechanisms underlying their contrasting electrochemical behavior. X-ray pair-distribution-function and magnetization measurements were used to determine changes in short-range ordering, particle size and microstructure, while high-resolution transmission electron microscopy (TEM) and electron energy-loss spectroscopy (EELS) were used to measure the atomic-level structure of individual particles and map the phase distribution in the initial and fully lithiated electrodes. Both FeF(2) and CuF(2) react with lithium via a direct conversion process with no intercalation step, but there are differences in the conversion process and final phase distribution. During the reaction of Li(+) with FeF(2), small metallic iron nanoparticles (<5 nm in diameter) nucleate in close proximity to the converted LiF phase, as a result of the low diffusivity of iron. The iron nanoparticles are interconnected and form a bicontinuous network, which provides a pathway for local electron transport through the insulating LiF phase. In addition, the massive interface formed between nanoscale solid phases provides a pathway for ionic transport during the conversion process. These results offer the first experimental evidence explaining the origins of the high lithium reversibility in FeF(2). In contrast to FeF(2), no continuous Cu network was observed in the lithiated CuF(2); rather, the converted Cu segregates to large particles (5-12 nm in diameter) during the first discharge, which may be partially responsible for the lack of reversibility in the CuF(2) electrode.

Regulation of smooth muscle contractility by the epithelium in rat tracheas: role of prostaglandin E2 induced by the neurotransmitter acetylcholine.

BACKGROUND: Previous studies have suggested the involvement of epithelium in modulating the contractility of neighboring smooth muscle cells. However, the mechanism underlying epithelium-derived relaxation in airways remains largely unclear. This study aimed to investigate the mechanism underlying epithelium-dependent smooth muscle relaxation mediated by neurotransmitters. METHODS: The contractile tension of Sprague-Dawley (SD) rat tracheal rings were measured using a mechanical recording system. Intracellular Ca2+ level was measured using a Ca2+ fluorescent probe Fluo-3 AM, and the fluorescence signal was recorded by a laser scanning confocal imaging system. The prostaglandin E2 (PGE2) content was measured using an enzyme-linked immunosorbent assay kit. RESULTS: We observed that the neurotransmitter acetylcholine (ACh) restrained the electric field stimulation (EFS)-induced contraction in the intact but not epithelium-denuded rat tracheal rings. After inhibiting the muscarinic ACh receptor (mAChR) or cyclooxygenase (COX), a critical enzyme in prostaglandin synthesis, the relaxant effect of ACh was attenuated. Exogenous PGE2 showed a similar inhibitory effect on the EFS-evoked contraction of tracheal rings. Moreover, ACh triggered phospholipase C (PLC)-coupled Ca2+ release from intracellular Ca2+ stores and stimulated COX-dependent PGE2 production in primary cultured rat tracheal epithelial cells. CONCLUSIONS: Collectively, this study demonstrated that ACh induced rat tracheal smooth muscle relaxation by promoting PGE2 release from tracheal epithelium, which might provide valuable insights into the cross-talk among neurons, epithelial cells and neighboring smooth muscle cells in airways.

[Potential for Phosphorus Uptake by Bed Sediments and Its Response to Carbon Additions in the Shiwuli River, Chaohu Lake Basin].

Surficial sediments were collected from five sampling sites in the mainstream of the Shiwuli River along an urban-rural gradient in the Chaohu Lake basin during July 2017 (summer) and January 2018 (winter). The total uptake (SPUlive), abiotic uptake (SPUkill), and biotic uptake (SPUbiotic) of phosphorus by sediments were measured, and uptake responses to different carbon sources (i. e., sodium acetate, glucose, and a mixture of both) were explored quantitatively through incubation experiments. The results showed that SPUlive had obviously spatiotemporal variations across the five sites, and SPUkill was higher than that of SPUbiotic. Under no carbon added, the mean values of SPUkill were 3.016 µg·(g·h)-1 and 3.368 µg·(g·h)-1, and the average values of SPUbiotic were 0.784 µg·(g·h)-1 and 0.323 µg·(g·h)-1 in summer and winter, respectively. Moreover, significant differences were found in abiotic phosphorus uptake between the two months. In the presence of carbon addition, both the value of SPUbiotic and the contribution rate of biotic phosphorus uptake showed a distinct increase. In general, the magnitude and rate of biotic uptake of phosphorus by sediments was highest when sodium acetate was added, followed by glucose, while the effect of mixed carbon was the worst. The responses of biotic phosphorus uptake to carbon addition suggested that the uptake potential of phosphorus by sediments in Shiwuli River was restricted by the carbon availability to some degree.