Fabrication of Electrode Material for Textile-Based Triboelectric Nanogenerators: Research of the Relationship between Output Performance and Dielectric Material Strain.

In this work, a textile-based triboelectric nanogenerator (TENG) device was developed through electroless plating technology to prepare electrode material. Hydrophilic groups on the fiber surface are able to absorb Ag+, which could play a role in the center of a catalyst to reduce Cu2+ to fabricate Cu-coated cotton toward the fabrication of TENG electrode material. The TENG device established admirable performance and good stabilization, and a maximum voltage at 9.6 V was detected when the stress and strain on the polydimethylsiloxane layer are 82.6 kPa and 5.8%, respectively. In addition, the relationships among device properties and strain/thickness of dielectric materials have been explored in depth as well. The output voltage of the device increases gradually with the enhancement of dielectric strain and stress. As expected, the TENG as-fabricated device was installed to various physical behaviors to illustrate the harvesting of power of knee-jerk movements.

Design and Analysis of a Textured Cu-Encapsulated Ni Tube for Low-Reflection Electromagnetic Interference Shielding Material.

With the frequent increase and update of electromagnetic interference (EMI) shielding materials, a low-resolution material that can absorb most electromagnetic waves, thereby effectively reducing the secondary pollution, is urgently needed. However, the excellent performance, flexibility, and low cost of these methods are usually incompatible with current reports. To address the above dilemma, we reported a facile solution for fabricating a low-reflection and high-performance EMI shielding composite by means of electroless nickel plating (EP-Ni), electroless copper plating (EP-Cu), annealing, and coating with a polydimethylsiloxane (PDMS) polymer with the structure of a Ni@Cu tube encapsulated with PDMS. The results indicate that the active groups on vegetable wool can act as active sites for the absorption of the Pd catalyst, thereby catalyzing the reduction of Ni2+, Cu2+, and the subsequent deposition on the plant fiber surface. Notably, the Ni@Cu-encapsulated plant fibers decreased during annealing at 100 °C. According to the segregated network and synergistic effect of the porous structure, the as-fabricated EMI shielding material demonstrated high absorption and low reflection, in which the power coefficient of the T value was approximately 0.0001, the R value was about 0.1764 (a decrease of 27.5% compared that of EP-Ni cotton), and the A value was approximately 0.8235.

Mechanism Insights in Anticorrosion Performance of Waterborne Epoxy Coatings Reinforced by PEI-Functionalized Boron Nitride Nanosheets.

Functionalized hexagonal boron nitride nanosheets (BNNSs) have arisen as compelling anticorrosive additives, yet the precise mechanism of their corrosion resistance enhancement in coatings remains unclear. Here, polyethylenimine functionalized BNNSs (PEI-BNNSs) with approximately 6-11 layers were prepared through a "one-step" method. Then, the PEI-BNNSs/Waterborne epoxy (WEP) composite coatings were incorporated via the waterborne latex blending method for the anticorrosion of the Q235 substrate. The impedance modulus (|Z|f = 0.01 Hz) of 0.5 wt % PEI-BNNSs/WEP composite coating soaked in 3.5 wt % NaCl solution for 35 days increased by 4 orders of magnitude compared to pure WEP coating, exhibiting exceptional long-term resistance against corrosion. The positron annihilation lifetime spectroscopy and corrosion product analysis demonstrated that the reinforced anticorrosion capabilities are not solely ascribed to the "tortuous path effect" arising from BNNSs impermeability. These mechanisms also encompass the reduction in free volume fraction and radius of the free volume cavities within the composite coating brought about by the PEI molecules. Additionally, the increase in coating adhesion, promoted by PEI, plays an important role in augmenting the barrier properties against corrosive agents. This study provided a full comprehension of the role played by functionalized BNNSs in fortifying the anticorrosion attributes of WEP coatings.

Activation of Notch1-GATA3 pathway in asthma bronchial epithelial cells induced by acute PM2.5 exposure and the potential protective role of microRNA-139-5p.

OBJECTIVE: PM2.5 is closed linked to asthma exacerbation. The Notch1 pathway acts as an important pathway, ultimately inducing T-helper cells that express GATA3 and its corresponding Th2 cytokines. The regulatory effects of miR-139-5p on the Notch1 pathway have been indicated in cancer. However, studies on miR-139-5p have not applied asthma-related models. The role of miR-139-5p and its regulatory effects on the Notch1-GATA3 pathway in asthma exacerbation induced by acute PM2.5 exposure has not been elucidated. We hypothesize that acute PM2.5 exposure induces asthma exacerbation by regulating the expression of miR-139-5p and activating the Notch1-GATA3 pathway. METHODS: We first employed Diseased Human Bronchial Epithelial Cells-Asthma cells to establish an in vitro model of acute exposure to PM2.5, and explored the relationship between the different concentrations and durations of acute PM2.5 exposure and the activation of Notch1-GATA3 pathway. We investigated the protein and mRNA expression changes of Notch1, upstream Jagged1, downstream GATA3, as well as the regulatory effect of miR-139-5p involved in it. RESULTS: The miR-139-5p expression increased within 24 h of PM2.5 exposure. However, if PM2.5 exposure was sustained, miR-139-5p expression turned to decrease, accompanied by upregulations of the mRNA and protein expression of Notch1-GATA3 pathway. Overexpression of miR-139-5p blocked Notch1-GATA3 pathway activation induced by acute PM2.5 exposure. CONCLUSION: Acute PM2.5 exposure can activate Notch1-GATA3 pathway in asthma bronchial epithelial cells model, which might be involved in PM2.5-induced asthma exacerbation. miR-139-5p has a potential protective role of inhibiting PM2.5-induced asthma airway inflammation by targeting Notch1.

Genetic bases of language control in bilinguals: Evidence from an EEG study.

Previous studies have debated whether the ability for bilinguals to mentally control their languages is a consequence of their experiences switching between languages or whether it is a specific, yet highly-adaptive, cognitive ability. The current study investigates how variations in the language-related gene FOXP2 and executive function-related genes COMT, BDNF, and Kibra/WWC1 affect bilingual language control during two phases of speech production, namely the language schema phase (i.e., the selection of one language or another) and lexical response phase (i.e., utterance of the target). Chinese-English bilinguals (N = 119) participated in a picture-naming task involving cued language switches. Statistical analyses showed that both genes significantly influenced language control on neural coding and behavioral performance. Specifically, FOXP2 rs1456031 showed a wide-ranging effect on language control, including RTs, F(2, 113) = 4.00, FDR p = .036, and neural coding across three-time phases (N2a: F(2, 113) = 4.96, FDR p = .014; N2b: F(2, 113) = 4.30, FDR p = .028, LPC: F(2, 113) = 2.82, FDR p = .060), while the COMT rs4818 (ts >2.69, FDR ps < .05), BDNF rs6265 (Fs >5.31, FDR ps < .05), and Kibra/WWC1 rs17070145 (ts > -3.29, FDR ps < .05) polymorphisms influenced two-time phases (N2a and N2b). Time-resolved correlation analyses revealed that the relationship between neural coding and cognitive performance is modulated by genetic variations in all four genes. In all, these findings suggest that bilingual language control is shaped by an individual's experience switching between languages and their inherent genome.

Fabrication of Textured Ni-Coated Carbon Tubes for a Flexible Strain Sensor: Effect of the Device Elastic Modulus on Sensor Performance.

The exploration of flexible resistive sensors with excellent performance remains a challenge. In this paper, a nickel-coated carbon tube with a textured structure was prepared as a conductive sensitive material and inserted into the poly(dimethylsiloxane) (PDMS) polymer; interestingly, the sensor performance was controlled by the elastic modulus of the matrix resin. The results show that Pd2+ may be adsorbed by the active groups on the surface of a plant fiber as a catalytic center for the reduction of Ni2+. After 300 °C annealing, the inner plant fiber would be carbonized and attached to the outside of the nickel tube; to be precise, the textured Ni-encapsulated C tube was fabricated successfully. It is worth noting that the C tube serves as a layer of support for the external Ni coating, providing sufficient mechanical strength. In addition, resistance sensors with different properties were prepared by controlling the elasticity modulus of the PDMS polymer by introducing different contents of curing agents. The limit uniaxial tensile strain was enhanced from 42 to 49% and sensitivity reduced from 0.2 to 2.0% with the elasticity modulus of the matrix resin increasing from 0.32 to 2.2 MPa. As expected, the sensor is obviously appropriate for the detection of elbow joints, human speaking, and human joints with the reduction of the elasticity modulus of the matrix resin. To be precise, the optimal elastic modulus of the sensor matrix resin would facilitate the improvement of its sensitivity to monitor different human behaviors.

Fabrication of Ni-Encapsulated Carbon Tube/Poly(dimethylsiloxane) Composite Materials for Lightweight and Flexible Electromagnetic Interference Shielding Material.

The exploration of flexible and lightweight electromagnetic interference (EMI) shielding materials with excellent shielding effectiveness, as a means to effectively alleviate electromagnetic pollution, is still a tremendous challenge. This paper proposes a conducting material named the textured Ni-encapsulated carbon tube, which can be applied in EMI shielding material by being inserted in the center of a poly(dimethysiloxane) (PDMS) polymer. We demonstrated that Pd2+ could be absorbed by the active groups on the plant fiber surface to catalyze the reduction of Ni2+ as a catalytic center by means of a textured Ni-encapsulated plant fiber. Owing to the outstanding heat-conducting capability of the Ni coating, the inner plant fiber was carbonized and attached to the Ni-tube inside the surface during annealing. To be precise, the textured Ni-encapsulated C tube was fabricated successfully after annealing at 300 °C. On further increasing the annealing temperature, the C tube disappeared gradually with the Ni coating being oxidized to NiO. Of note, the C tube acted as a support layer for the external Ni coating, providing sufficient mechanical strength. When combined with the coating PDMS layer, a flexible and lightweight EMI shielding material is fabricated successfully. It displays an outstanding EMI shielding effectiveness of 31.34 dB and a higher specific shielding efficiency of 27.5 dB·cm3/g, especially showing excellent mechanical property and flexibility with only 2 mm thickness. This study provides a new method to fabricate outstanding EMI shielding materials.

The N6-methyladenosine demethylase FTO is required for odontoblast differentiation in vitro and dentine formation in mice by promoting RUNX2 exon 5 inclusion through RBM4.

AIM: Fat mass and obesity-associated (FTO) protein, the first discovered N6-methyladenine (m6A) demethylase, played positive roles in bone formation. In this study, the aim was to investigate the function and potential mechanism of Fto in dentine formation. METHODOLOGY: In vivo model, postnatal 12-day (PN12), 4-week-old (4 wk), 6-week-old (6 wk) healthy male C57BL/6J were randomly divided into Fto knockout (Fto-/- ) mice and wild-type (WT) littermates according to their genotypes, with 3-5 mice in each group. The mandibles of Fto-/- mice and WT control littermates were isolated for analysis by micro-computed tomography (micro-CT), 3-dimensional reconstruction and Haematoxylin-eosin (HE) staining. In vitro, mouse dental papilla cells (mDPCs) and human dental stem pulp cells (hDPSCs) were cultured with odontogenetic medium to evaluate differentiation capacity; expression levels of odontoblastic related genes were evaluated using quantitative real-time polymerase chain reaction (qRT-PCR). The inclusion levels of Runt-related transcription factor 2 (RUNX2) exon 5 in mDPCs and hDPSCs were detected by semiquantitative real-time polymerase chain reaction (RT-PCR). The RNA binding motif protein 4 (RBM4) m6A site was verified through m6A methylated RNA immunoprecipitation (MeRIP) and the stability of RBM4 mRNA influenced by FTO knockdown was measured by mRNA stability assay. Differences with p values < .05 were regarded as statistically significant. RESULTS: We discovered that Fto-/- mice showed significant dentine formation defects characterized by widened pulp cavity, enlarged pulp-tooth volume ratio, thinned dentine and pre-dentine layer of root (p < .05). Fto-/- mDPCs and FTO-silencing hDPSCs not only exhibited insufficient mineralization ability and decreased expression levels of odontoblastic mineralization related genes (p < .05), but showed significantly reduced Runx2 exon 5 inclusion level (p < .05). FTO knockdown increased the m6A level of RBM4 and destabilized the mRNA of RBM4, thus contributing to the reduced RBM4 expression level. Moreover, Rbm4 overexpression in Fto-/- mDPCs can partly restore Runx2 exon 5 inclusion level and the differentiation ability disrupted by Fto knockout. CONCLUSION: Thus, within the limitations of this study, the data suggest that FTO promotes odontoblastic differentiation during dentine formation by stabilizing RBM4 mRNA to promote RUNX2 exon 5 inclusion.

Coptisine attenuates sepsis lung injury by suppressing LPS-induced lung epithelial cell inflammation and apoptosis.

OBJECTIVE: This study aimed to investigate the functioning and mechanism of coptisine in acute lung injury (ALI). METHODS: Murine Lung Epithelial 12 (MLE-12) cells were stimulated with lipopolysaccharide (LPS) to construct an in vitro pulmonary injury model to study the functioning of coptisine in sepsis-induced ALI. The viability of MLE-12 cells was assessed by the cell counting kit-8 assay. The cytokine release of tumor necrosis factor-α (TNF-α), interleukin 6 (IL-6), and IL-1ß was measured by enzyme-linked-immunosorbent serologic assay. The relative expression levels of TNF-α, IL-6, and IL-1ß mRNA were examined by reverse transcription-quantitative polymerase chain reaction. The cell apoptosis of MLE-12 cells was determined by Annexin V/propidium iodide staining and analyzed by flow cytometry. The expressions of apoptosis-related proteins Bax and cleaved Caspase-3 were observed by Western blot analysis. The activation of nuclear factor kappa B (NF-κB) signaling pathway was discovered by the determination of phospho-p65, p65, phospho-nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha (IκBα), and IκBα through Western blot analysis. RESULTS: Coptisine treatment could significantly restore decrease in MLE-12 cell viability caused by LPS stimulation. The release of TNF-α, IL-6, and IL-1ß was significantly inhibited by coptisine treatment. Coptisine treatment inhibited MLE-12 cell apoptosis induced by LPS, and also inhibited the expression levels of Bax and cleaved Caspase-3. Coptisine treatment along with LPS stimulation, significantly reduced the protein level of phospho-IκBα, increased the level of IκBα, and reduced phospho-p65-p65 ratio. CONCLUSION: These results indicated that coptisine attenuated sepsis lung injury by suppressing lung epithelial cell inflammation and apoptosis through NF-κB pathway. Therefore, coptisine may have potential to treat sepsis-induced ALI.

Fine particulate pollution driven by nitrate in the moisture urban atmospheric environment in the Pearl River Delta region of south China.

To identify potential sources of fine particles (PM2.5, with aerodynamic diameter (Da) ≤ 2.5 µm) in urban Dongguan of south China, a comprehensive campaign was carried out in the whole 2019. Hourly PM2.5 and its dominant chemical components including organic carbon (OC), elemental carbon (EC), water-soluble inorganic ions (WSIIs) and thirteen elements were measured using online instruments. Gaseous pollutants including NH3, HNO3, NO2, NO and O3 and meteorological parameters were also synchronously measured. PM2.5 was dominated by carbonaceous aerosols in summer and by WSIIs in the other seasons. PM2.5 and its dominant chemical components mostly peaked around noon (10:00-14:00 LST). Furthermore, high PM2.5 levels during the daytime were closely related with the increased NO3- levels. The high mass concentrations of NO3- in urban Dongguan during the daytime were likely related with regional transport of NO3- from suburban Dongguan, which was originated from the reaction between NO2 and O3 under the moisture condition during the nighttime. Seven major source factors for PM2.5 including secondary sulfate, ship emission, traffic emission, secondary nitrate, industrial processes, soil dust and coal combustion were identified by positive matrix factorization (PMF) analysis, which contributed 26 ± 14%, 16 ± 16%, 16 ± 10%, 14 ± 11%, 12 ± 11%, 8 ± 6% and 8 ± 6%, respectively, to annual PM2.5 mass concentration. Although secondary sulfate contributed much more than secondary nitrate to PM2.5 on annual basis, the latter exceeded the former source factor when daily PM2.5 mass concentration was higher than 60 µg m-3, indicating the critical role nitrate played in PM2.5 episode events.

High serum uric acid may associate with the increased risk of colorectal cancer in females: A prospective cohort study.

Elevated serum uric acid (SUA) levels have been previously reported to play a role in multiple types of cancers. However, epidemiological studies evaluating SUA levels and colorectal cancer risk remain sparse. This cohort study included 444 462 participants between the ages of 40 and 69 years from the UK Biobank, followed up from 2006 to 2010. Multivariable adjusted Cox regression models were used to estimate hazard ratios (HRs). During a mean follow-up of 6.6 years, 2033 and 855 cases of colon and rectal cancers, respectively, were diagnosed. The multivariable-adjusted HRs for risks of colon cancer in the lowest uric acid categories (≤3.5 mg/dL) compared with the reference groups were 1.31 (95% confidence interval [CI] = 0.75-2.29) in males and 1.26 (95% CI = 1.03-1.55) in females. The HRs in the highest uric acid groups (>8.4 mg/dL) were 1.16 (95% CI = 0.83-1.63) in males and 2.00 (95% CI = 1.02-3.92) in females. The corresponding HRs of rectal cancer in the lowest uric acid groups compared with the reference group were 2.21 (95% CI = 1.15-4.23) in males and 0.98 (95% CI = 0.66-1.45) in females. The HRs in the highest uric acid groups were 1.35 (95% CI = 0.82-2.23) in males and 3.81 (95% CI = 1.38-10.56) in females. In conclusion, SUA showed a U-shaped association with colon cancer risk in both male and female populations. The same pattern was observed in male patients with rectal cancer. However, SUA levels were positively associated with occurrence of rectal cancer in female subjects.

Outdoor air pollution and the risk of asthma exacerbations in single lag0 and lag1 exposure patterns: a systematic review and meta-analysis.

Objective: To synthesize evidence regarding the relationship between outdoor air pollution and risk of asthma exacerbations in single lag0 and lag1 exposure patterns.Methods: We performed a systematic literature search using PubMed, Embase, Cochrane Library, Web of Science, ClinicalTrials, China National Knowledge Internet, Chinese BioMedical, and Wanfang databases. Articles published until August 1, 2020 and the reference lists of the relevant articles were reviewed. Two authors independently evaluated the eligible articles and performed structured extraction of the relevant information. Pooled relative risks (RRs) and 95% confidence intervals (CIs) of lag0 and lag1 exposure patterns were estimated using random-effect models.Results: Eighty-four studies met the eligibility criteria and provided sufficient information for meta-analysis. Outdoor air pollutants were associated with increased risk of asthma exacerbations in both single lag0 and lag1 exposure patterns [lag0: RR (95% CI) (pollutants), 1.057(1.011, 1.103) (air quality index, AQI), 1.007 (1.005, 1.010) (particulate matter of diameter ≤ 2.5 µm, PM2.5), 1.009 (1.005, 1.012) (particulate matter of diameter, PM10), 1.010 (1.006, 1.014) (NO2), 1.030 (1.011, 1.048) (CO), 1.005 (1.002, 1.009) (O3); lag1:1.064(1.022, 1.106) (AQI), 1.005 (1.002, 1.008) (PM2.5), 1.007 (1.004, 1.011) (PM10), 1.008 (1.004, 1.012) (NO2), 1.025 (1.007, 1.042) (CO), 1.010 (1.006, 1.013) (O3)], except SO2 [lag0: RR (95% CI), 1.004 (1.000, 1.007); lag1: RR (95% CI), 1.003 (0.999, 1.006)]. Subgroup analyses revealed stronger effects in children and asthma exacerbations associated with other events (including symptoms, lung function changes, and medication use).Conclusion: Outdoor air pollution increases the asthma exacerbation risk in single lag0 and lag1 exposure patterns.Trial registration: PROSPERO, CRD42020204097. https://www.crd.york.ac.uk/.Supplemental data for this article is available online at https://doi.org/10.1080/02770903.2021.2008429 .

The rescue intervention strategy for asthma patients under severe air pollution: a single-center prospective randomized controlled trial.

OBJECTIVE: The aim of our study is to provide a novel strategy to administer treatment at the first signs of severe air pollution and before patients experience symptoms for preventing airway damage. METHODS: This single-center, prospective, randomized and standard treatment parallel control clinical trial recruited adult asthma patients. The patients were randomized into either the rescue intervention strategy (RIS) group or control group. The rescue intervention strategy for the RIS group included budesonide/formoterol plus the original treatment until the severe pollution ended. The control group was maintained on the original treatment. The follow-up observation period was 1 year. RESULTS: Overall, 22 participants were enrolled and 20 completed the follow-up (11 in the RIS group and 9 in the control group). Two participants dropped out of the trial for personal reasons before the first follow-up. In the intention-to-treat analysis, the frequency of asthma exacerbations per year was significantly lower in the RIS group than in the control group (RIS vs. control, 0.55 vs. 2.67; risk rate [RR] [95% confidence interval {CI}], 0.21 [0.08-0.50]; p = 0.001). The mean number of unplanned outpatient visits per person per year was also lower in the RIS group than in the control group (RIS vs. control, 0.18 vs. 1.11; RR [95% CI], 0.16 [0.04-0.75]; p = 0.019). CONCLUSION: A novel strategy to administer treatment at the first signs of severe air pollution and before patients experience symptoms may decrease the risk of asthma exacerbations and negative outcomes under severe air pollution conditions. TRIAL REGISTRATION: ChiCTR, ChiCTR1900026757. http://www.chictr.org.cn.

Source apportionment of carbonaceous aerosols using hourly data and implications for reducing PM2.5 in the Pearl River Delta region of South China.

Ambient fine particulate matter (PM2.5) levels in South China have been decreasing in the past decade, but the decreasing rates differed between its major chemical components, e.g., with much small rates for carbonaceous aerosols than for secondary inorganic aerosols. To investigate the sources of carbonaceous aerosols in this region, a comprehensive campaign was carried out in urban Guangzhou in the winter of 2019-2020 using a combination of various instruments. Data generated from this campaign include hourly total carbon (TC), black carbon (BC), criteria air pollutants and meteorological parameters, 4-hourly particle-bound elements, and chemically-resolved daily PM2.5. Similar diurnal patterns were observed for TC, CO and NO2, suggesting TC was very likely related to vehicle exhaust emission. Secondary organic carbon (SOC) estimated using the Minimum R squared (MRS) method accounted for 35 ± 17% of OC, indicating strong atmospheric oxidation capacity. Four major source factors for carbonaceous aerosols were identified by positive matrix factorization (PMF) model, including coal combustion, traffic emissions, soil dust and ship emissions, which accounted for 37 ± 23%, 39 ± 23%, 14 ± 10% and 10 ± 13%, respectively, of TC mass concentration, 38 ± 24%, 38 ± 23%, 14 ± 10% and 10 ± 12%, respectively, of OC mass concentration, and 29 ± 21%, 43 ± 22%, 14 ± 11% and 14 ± 15%, respectively, of EC mass concentration. Among these sources, traffic emission was the most important one, suggesting the necessity for promoting clean energy vehicles and relieving urban traffic congestion.

Stability Analysis: Rational Design of a Ag Nanoparticle/Polymer Brush for Fabricating Cu Coating on a PET Surface.

Excellent stability of a catalytic center would facilitate the prolongation of the cycle of a chemical plating bath and the reduction of environmental pollution. In this study, silane (3-aminopropyltriethoxysilane (KH550) and γ-(2,3-epoxypropoxy)propytrimethoxysilane (KH560)) was incorporated in AgNO3 solution to rationally prepare a Ag nanoparticle/polymer brush (Ag/PB) catalytic solution. The effects of the KH560 relative content on the Ag/PB structure and stability were studied. The epoxy group in the KH560 could react with an amino group in the KH550 through direct ring-opening reaction to form a secondary amino group and hydroxyl, which could coadsorb Ag nanoparticles by means of a chelating structure; hence, Ag/PB with superior Ag-adsorbed intensity was established on a polyethylene terephthalate (PET) surface. Ag particles on PB with 75% KH560 revealed the best stability of those measured, and the relative Ag surplus was 56.7% after stability testing. The generated Ag/PB that served as catalytic centers to catalyze the electroless copper plating resulted in a facile technology for preparing Cu/PET composite material. This means that the technology has potential application in a green process for preparing metal/polymer composite materials.

Genome-Wide Identification of Soybean ABC Transporters Relate to Aluminum Toxicity.

ATP-binding cassette (ABC) transporter proteins are a gene super-family in plants and play vital roles in growth, development, and response to abiotic and biotic stresses. The ABC transporters have been identified in crop plants such as rice and buckwheat, but little is known about them in soybean. Soybean is an important oil crop and is one of the five major crops in the world. In this study, 255 ABC genes that putatively encode ABC transporters were identified from soybean through bioinformatics and then categorized into eight subfamilies, including 7 ABCAs, 52 ABCBs, 48 ABCCs, 5 ABCDs, 1 ABCEs, 10 ABCFs, 111 ABCGs, and 21 ABCIs. Their phylogenetic relationships, gene structure, and gene expression profiles were characterized. Segmental duplication was the main reason for the expansion of the GmABC genes. Ka/Ks analysis suggested that intense purifying selection was accompanied by the evolution of GmABC genes. The genome-wide collinearity of soybean with other species showed that GmABCs were relatively conserved and that collinear ABCs between species may have originated from the same ancestor. Gene expression analysis of GmABCs revealed the distinct expression pattern in different tissues and diverse developmental stages. The candidate genes GmABCB23, GmABCB25, GmABCB48, GmABCB52, GmABCI1, GmABCI5, and GmABCI13 were responsive to Al toxicity. This work on the GmABC gene family provides useful information for future studies on ABC transporters in soybean and potential targets for the cultivation of new germplasm resources of aluminum-tolerant soybean.

Interactions between hydrogen sulphide and nitric oxide regulate two soybean citrate transporters during the alleviation of aluminium toxicity.

Hydrogen sulphide (H2 S) is emerging as an important signalling molecule involved in plant resistance to various stresses. However, the underlying mechanism of H2 S in aluminium (Al) resistance and the crosstalk between H2 S and nitric oxide (NO) in Al stress signalling remain elusive. Citrate secretion is a wide-spread strategy for plants against Al toxicity. Here, two citrate transporter genes, GmMATE13 and GmMATE47, were identified and characterized in soybean. Functional analysis in Xenopus oocytes and transgenic Arabidopsis showed that GmMATE13 and GmMATE47 mediated citrate exudation and enhanced Al resistance. Al treatment triggered H2 S generation and citrate exudation in soybean roots. Pretreatment with an H2 S donor significantly elevated Al-induced citrate exudation, reduced Al accumulation in root tips, and alleviated Al-induced inhibition of root elongation, whereas application of an H2 S scavenger elicited the opposite effect. Furthermore, H2 S and NO mediated Al-induced GmMATE expression and plasma membrane (PM) H+ -ATPase activity and expression. Further investigation showed that NO induced H2 S production by regulating the key enzymes involved in biosynthesis and degradation of H2 S. These findings indicate that H2 S acts downstream of NO in mediating Al-induced citrate secretion through the upregulation of PM H+ -ATPase-coupled citrate transporter cotransport systems, thereby conferring plant resistance to Al toxicity.

Baicalin inhibits pressure overload-induced cardiac fibrosis through regulating AMPK/TGF-ß/Smads signaling pathway.

AMP-activated protein kinase (AMPK) is a central regulator of multiple metabolic pathways. It has been shown that activation of AMPK could inhibit fibroblast proliferation and extracellular matrix (ECM) accumulation, thereby suppressing cardiac fibrosis. Baicalin, the major component found in skullcap, possesses multiple protective effects on the cardiovascular system. However, little is known about the effect of baicalin on cardiac fibrosis and the molecular mechanism by which baicalin exerts its anti-fibrotic effects has not been investigated. In this study, we revealed that baicalin could inhibit cell proliferation, collagen synthesis, fibronectin (FN) and Connective tissue growth factor (CTGF) protein expression in cardiac fibroblasts induced by angiotensin Ⅱ (Ang Ⅱ). It also ameliorated cardiac fibrosis in rats submitted to abdominal aortic constriction (AAC). Moreover, baicalin inhibited transforming growth factor-ß (TGF-ß)/Smads signaling pathway stimulated with Ang Ⅱ through activating AMPK. Subsequently, we also demonstrated that baicalin attenuated Ang Ⅱ-induced Smad3 nuclear translocation, and interaction with transcriptional coactivator p300, but promoted the interaction of p300 and AMPK. Taken together, these results provide the first evidence that the effect of baicalin against cardiac fibrosis may be attributed to its regulation on AMPK/TGF-ß/Smads signaling, suggesting the therapeutic potential of baicalin on the prevention of cardiac fibrosis and heart failure.

Novel naftopidil derivatives containing methyl phenylacetate and their blocking effects on α1D/1A-adrenoreceptor subtypes.

α1-Adrenoceptor (α1-AR) antagonists are considered to be the most effective monotherapy agents for lower urinary tract symptoms associated with benign prostatic hyperplasia (LUTS/BPH). In this study, we synthesized compounds 2-17, which are novel piperazine derivatives that contain methyl phenylacetate. We then evaluated the vasodilatory activities of these compounds. Among them, we found that compounds 2, 7, 12, which contain 2-OCH3, 2-CH3 or 2, 5-CH3, respectively, exhibited potent α1-blocking activity similar to protype drug naftopidil (1). The antagonistic effects of 2, 7, and 12 on the (-)-noradrenaline-induced contractile response of isolated rat prostatic vas deferens (α1A), spleen (α1B) and thoracic aorta (α1D) were further characterized to assess the sub receptor selectivity. Compared with naftopidil (1) and terazosin, compound 12 showed the most desirable α1D/1A subtype selectivity, especially improved α1A subtype selectivity, and the ratios pA2 (α1D)/pA2 (α1B) and pA2 (α1A)/pA2 (α1B) were 17.0- and 19.5-fold, respectively, indicating less cardiovascular side effects when used to treat LUTS/BPH. Finally, we investigated the chiral pharmacology of 12. We found, however, that the activity of enantiomers (R)-12 and (S)-12 are not significantly different from that of rac-12.