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Objective The upregulation of long noncoding RNA intersectin 1-2 (lnc ITSN1-2) is associated with poor prognosis in acute ischemic stroke (AIS) patients, but the role and mechanism of lnc ITSN1-2 in AIS are rarely reported, which, thus, are highlighted in this study. Methods AIS cell model was constructed by oxygen glucose deprivation and reoxygenation (OGD/R). The quantitative real-time PCR was used to detect the expression of lnc ITSN1-2 in HT22 cells. The effects of lnc ITSN1-2 overexpression or knockdown on viability, LDH release, apoptosis, inflammatory and apoptotic factor expressions in OGD/R-induced HT22 cells were measured by cell counting kit-8 assay, LDH release kit, flow cytometry, ELISA and western blot, respectively. Starbase was used to screen the target genes of lnc ITSN1-2. The targeting relationship between lnc ITSN1-2 and miR-195-5p was predicted by starbase and verified by dual-luciferase report assay. The above assays were conducted again to study the function of miR-195-5p. Lastly, the levels of activated mitogen-activated protein kinases (MAPK) pathway-related proteins were determined by western blot. Results OGD/R treatment reduced the HT22 cell viability and enhanced LDH release rate and lnc ITSN1-2 expression. Lnc ITSN1-2 overexpression promoted the cell injury, apoptosis and inflammation in OGD/R-induced HT22 cells, while lnc ITSN1-2 knockdown generated the opposite effect and deactivated the MAPK pathways. However, the effect of lnc ITSN1-2 knockdown in OGD/R-induced HT22 cells was reversed by miR-195-5p inhibitor. Conclusion Lnc ITSN1-2 knockdown suppressed the inflammation and apoptosis in OGD/R-induced HT22 cells by regulating the miR-195-5p-mediated MAPK pathways.

Multitudinous people suffer from lactose intolerance which is bound up with lactose malabsorption. Enzymatic hydrolysis is the most common approach for the preparation of lactose-free products. The recycling of hydrolytic enzymes is an effective way to produce low-cost lactose-free products. Herein, a facile strategy for the preparation of the novel Fe3O4 magnetic nanoparticles-β-galactosidase-CaHPO4 hybrid nanocomplexes (β-gal MNCs) was established. β-gal MNCs were composed of amino-modified Fe3O4 magnetic nanoparticles, β-galactosidase and crystalline calcium hydrogen phosphates. Meanwhile, under the external magnetic field, the magnetic β-gal MNCs can be easily and rapidly separated from the reaction medium. In addition, the β-galactosidase maintained most of its initial activity after immobilization into the β-gal MNCs. In a continuous hydrolysis reaction, β-gal MNCs exhibited excellent reusability and good stability. Therefore, β-gal MNCs hold promising prospects in the fast and low-cost preparation of lactose-free milk.

To explore whether acupuncture can improve sleep disturbance, cognitive impairment and emotional disorders caused by sleep deprivation, and its association with the attenuation of oxidative stress injury in prefrontal cortex. Fifty-two male Sprague-Dawley rats were randomly divided into a control group (n=10), a model group (n=14), a manual acupuncture (MA) group (n=14), and a sham-MA group (n=14). All the groups were established as sleep deprivation models via the modified multiple platform method, except for the control group. Rats in both the MA group and the sham-MA group received corresponding intervention, respectively. After modeling and intervention, the four groups received three behavioral tests, namely sleep monitoring, by comprehensive lab animal monitoring system (CLAMS), Morris water maze (MWM) test and open-field test (OFT), followed by oxygen free radical level test and Western blot (WB) detection for the expression levels of Bax and Bcl-2. The MA group derived more sleep time within 24 h than either the model group or the sham-MA group (both P 0.05), and the escape latency was significantly shorter in these three groups than that in the model group (all P

In this study, CuO, ZnO, and (1 − x)ZnO − xCuO (CZO) powders were synthesized through the aqueous solution method. Sintering (separate) and direct synthesis were conducted at 500°C and 700°C, respectively, to produce CuO, ZnO, and CZO powders in different proportions. Various proportions of (1 − x)ZnO−xCuO (x = 0.33, 0.5, 0.67) powders were analyzed and compared under various temperature and process conditions. The morphology, phase structure, and photoelectromagnetic properties of CZO were analyzed to determine the influence of ZnO, CuO, and their mutual doping on the photoelectromagnetic properties. The results revealed that direct synthesis was the most effective process and that CZO powder exhibited the best electromagnetic properties when the Cu doping ratio was high—when Cu:Zn was close to 1:1. When Cu was doped excessively (x = 0.67), it resulted in the formation of the cuprous oxide phase, which is detrimental to the electrical and magnetic properties of CZO powder.

Objective: To investigate the protective effects and mechanisms of sesamin (SES) on dextran sulfate sodium (DSS)-induced experimental colitis in mice. Methods: SES (50, 100, and 200 mg kg−1) were orally administered to C57BL/6 male mice after DSS instillation. The anti-inflammatory effect of SES on colonic damage was assessed by clinical, macroscopic, microscopic, and inflammatory signaling pathways. Results and conclusions: It could be found that bodyweight and colon length of mice treated with DSS was significantly decreased while that were increased by SES treatment. SES treatment reduced the DAI values and improved the histopathology of the colon in the DSS-treated mice. SES also reduced TNF-α, IL-1β and IL-6 production caused by DSS. We also measured the expression of the phosphorylation of p65, IκB, p38, ERK and JNK protein and found that SES can alleviate colon damage via the NF-κB and MAPK signaling pathways. The findings of this study suggested that SES had anti-inflammatory effects on intestinal inflammation and can be used as a new therapeutic candidate for inflammatory bowel disease.

The sirtuins family is well known by its unique nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase function. The most-investigated member of the family, Sirtuin 1 (SIRT1), accounts for deacetylating a broad range of transcription factors and coregulators, such as p53, the Forkhead box O (FOXO), and so on. It serves as a pivotal regulator in various intracellular biological processes, including energy metabolism, DNA damage response, genome stability maintenance and tumorigenesis. Although the most attention has been focused on its intracellular functions, the regulatory effect on extracellular microenvironment remodeling of SIRT1 has been recognized by researchers recently. SIRT1 can regulate cell secretion process and participate in glucose metabolism, neuroendocrine function, inflammation and tumorigenesis. Here, we review the advances in the understanding of SIRT1 on remodeling the extracellular microenvironment, which may provide new ideas for pathogenesis investigation and guidance for clinical treatment.

Emerging evidence has suggested the functions of exosomes in allergic diseases including asthma. By using a mouse model with asthma induced by ovalbumin (OVA), we explored the roles of M2 macrophage-derived exosomes (M2Φ-Exos) in asthma progression. M2Φ-Exos significantly alleviated OVA-induced fibrosis and inflammatory responses in mouse lung tissues, as well as inhibited abnormal proliferation, invasion, and fibrosis-related protein production in platelet derived growth factor (PDGF-BB) treated primary mouse airway smooth muscle cells (ASMCs). The OVA administration in mice or the PDGF-BB treatment in ASMCs reduced the expression of miR-370, which was detected in M2Φ-Exos by miRNA sequencing. However, treating the mice or ASMCs with M2Φ-Exos reversed the inhibitory effect of OVA or PDGF-BB on miR-370 expression. We identified that the target of miR-370 was fibroblast growth factor 1 (FGF1). Downregulation of miR-370 by Lv-miR-370 inhibitor or overexpression of FGF1 by Lv-FGF1 blocked the protective roles of M2Φ-Exos in asthma-like mouse and cell models. M2Φ-Exos were found to inactivate the MAPK signaling pathway, which was recovered by miR-370 inhibition or FGF1 overexpression. Collectively, we conclude that M2Φ-Exos carry miR-370 to alleviate asthma progression through downregulating FGF1 expression and the MAPK/STAT1 signaling pathway. Our study may offer a novel insight into asthma treatment.

Endoplasmic reticulum (ER) type I signal peptidases (ER SPases I) are vital proteases that cleave signal peptides from secreted proteins. However, the specific function of ER SPase I in plants has not been genetically characterized, and the substrate is largely unknown. Here, we report the identification of a maize (Zea mays) miniature seed6 (mn6) mutant. The loss-of-function mn6 mutant exhibited severely reduced endosperm size. Map-based cloning and molecular characterization indicated that Mn6 is an S26-family ER SPase I, with Gly102 (box E) in Mn6 critical for protein function during processing. Mass spectrometric and immunoprecipitation analyses revealed that Mn6 is predominantly involved in processing carbohydrate synthesis-related proteins, including the cell wall invertase miniature seed1 (Mn1), which is specifically expressed in the basal endosperm transfer layer. RNA and protein expression levels of Mn1 were both significantly downregulated in the mn6 mutant. Due to the significant reduction in cell wall invertase activity in the transfer cell layer, mutation of Mn6 caused dramatic defects in endosperm development. These results suggest that proper maturation of Mn1 by Mn6 may be a crucial step for proper seed filling and maize development.

DNA damage signals transducer RING finger protein 8 (RNF8) is involved in maintaining genomic stability by facilitating the repair of DNA double-strand breaks (DSB) via ubiquitin signaling. By analyzing the TCGA database and colon cancer tissue microarrays, we found that the expression level of RNF8 was positively correlated with that of c-Myc in colon cancer, which were closely associated with poor survival of colon cancer patients. Furthermore, overexpressing and knocking down RNF8 increased and decreased the expression of c-Myc in colon cancer cells, respectively. In addition, RNF8 interacted with β-catenin and facilitated its nuclear translocation by conjugating K63 polyubiquitination on it. These observations suggested a de novo role of RNF8 in promoting the progression of colon cancer by inducing β-catenin-mediated c-Myc expression.

Baicalin is a plant-derived flavonoid from Scutellaria baicalensis Georgi with multiple bioactivities and has a protective effect against avian pathogenic Escherichia coli (APEC) infection. However, the underlying mechanism of baicalin against APEC infection is still unknown. Therefore, we aimed to explore whether the protective effects and mechanisms of baicalin on APEC-induced lung inflammation were related to the regulation of gut microbiota. The results showed that baicalin significantly reduced APEC colonization and pro-inflammatory cytokines production, and additionally recovered air-blood barrier integrity in the lungs after APEC challenge. However, depletion of gut microbiota significantly weakened the protective effects of baicalin against APEC infection as mentioned above. Furthermore, baicalin markedly restored the dysbiosis of gut microbiota induced by APEC as well as increased the abundance of short chain fatty acid (SCFA)-producing bacteria and the production of SCFAs including acetic acid, propionic acid and butyric acid, especially acetic acid. In addition, the concentrations of acetic acid and its receptor free fatty acid receptor 2 (FFAR2) were significantly upregulated in the lung tissues after baicalin treatment. In conclusion, gut microbiota played a key role in the pharmacological action of baicalin against APEC-induced lung inflammation. Baicalin remodeled the dysbiosis of gut microbiota caused by APEC and increased the production of SCFAs, especially acetic acid in the gut, and then the increased acetate may circulate to the lungs to activate FFAR2 to defend APEC infection. Together, our study suggested that baicalin inhibited APEC infection through remodeling the gut microbiota dysbiosis and increasing the SCFA production. Furthermore, baicalin may serve as an alternative antibiotic and a novel therapeutic drug to prevent or treat APEC infection.

Lignin is a complex polymer in plant cell walls whose proportion is second only to that of cellulose and plays an important role in the mechanical properties of wood and stress resistance of plants. Here, we induced tension wood (TW) formation in Catalpa bungei by artificial bending and analyzed the lignin metabolism of the TW. LC-MS analysis showed that a significantly higher content of coniferyl aldehyde was observed in the TW cell wall than in the opposite wood (OW) and normal wood (NW) cell walls. TW had significantly lower contents of coniferyl alcohol than OW and NW. Raman spectroscopy results indicated that TW had lower total lignin than OW and NW. The transcription and translation levels of most of the differentially expressed genes (DEGs) involved in lignin monomer biosynthesis indicated upregulation in TW/OW and TW/NW. We found no significant difference in the transcription levels of three collision gases (CADs) between TW and OW or between NW, but their translation levels were significantly downregulated in TW, suggesting post-transcriptional control for CAD. We predicted and analyzed transcription factors that could target DEGs involved in lignin monomer biosynthesis in TW. Based on the analysis of the relationships of targeting and coexpression, we found that NAC (evm.model.group1.695) could potentially target 4CLs and CCoAOMT, that HD-Zip (evm.model.group7.1157) had potential targeting relationships with CCoAOMT, F5H, and CCR, and that their expression levels were significantly positive. It is speculated that the upregulation of NAC and HD-ZIP transcription factors activates the expression of downstream target genes, which leads to a significant increase in coniferyl aldehyde in TW. However, the decrease in total lignin in TW may be caused by the significant downregulation of CAD translation and the significant decrease in precursors (coniferyl alcohol). Whether the expression of CAD genes is regulated by post-transcriptional control and affects TW lignin metabolism needs further study.

Acute liver injury can be caused by chemicals and can lead to liver failure. We investigated the protective effect of helicid (HEL) on acute liver injury caused by CCl4 in mice. We found that ALT and AST levels as well as hepatic pathological damage in mice treated with CCl4 was increased significantly, while the effects were decreased by HEL treatment. HEL treatment increased the activity of T-SOD, GSH and CAT and reduced the level of MDA in CCl4 treated mice. HEL improved the histopathology of liver caused by CCl4. HEL also reduced TNF-α, IL-1β and IL- 6 activity caused by CCl4. We investigated the phosphorylation of p65 and IκB protein and found that HEL can alleviate liver damage via the NF-κB signaling pathway. Our findings indicate that HEL protects against acute liver injury induced by CCl4. The protective effect of HEL appears to be due to its antioxidative and anti-inflammatory properties through the NF-κB signaling pathway.

Highlights Highly sensitive and selective room-temperature NO2 gas sensors by sensitizing MoS2 nanosheets with PbS quantum dots were demonstrated. In this device architecture, the receptor and transduction function as well as the utility factor of semiconductor gas sensors could be enhanced simultaneously.The strategy of sensitizing 2D semiconductors with quantum dots as sensitive and selective receptors for gas molecules may offer a powerful new degree of freedom to the surface and interface engineering of semiconductor gas sensors. Electronic supplementary material The online version of this article (10.1007/s40820-020-0394-6) contains supplementary material, which is available to authorized users., The Internet of things for environment monitoring requires high performance with low power-consumption gas sensors which could be easily integrated into large-scale sensor network. While semiconductor gas sensors have many advantages such as excellent sensitivity and low cost, their application is limited by their high operating temperature. Two-dimensional (2D) layered materials, typically molybdenum disulfide (MoS2) nanosheets, are emerging as promising gas-sensing materials candidates owing to their abundant edge sites and high in-plane carrier mobility. This work aims to overcome the sluggish and weak response as well as incomplete recovery of MoS2 gas sensors at room temperature by sensitizing MoS2 nanosheets with PbS quantum dots (QDs). The huge amount of surface dangling bonds of QDs enables them to be ideal receptors for gas molecules. The sensitized MoS2 gas sensor exhibited fast and recoverable response when operated at room temperature, and the limit of NO2 detection was estimated to be 94 ppb. The strategy of sensitizing 2D nanosheets with sensitive QD receptors may enhance receptor and transducer functions as well as the utility factor that determine the sensor performance, offering a powerful new degree of freedom to the surface and interface engineering of semiconductor gas sensors. Electronic supplementary material The online version of this article (10.1007/s40820-020-0394-6) contains supplementary material, which is available to authorized users.

In this study, CuZnO (CZO) films were fabricated by two-stage magnetron sputtering. The film crystallization and the diffusion of the copper layer were enhanced by 1 h heat treatment (500 ℃); then the nanowire was grown from the CZO film system using an aqueous solution method. After 2 h of heat treatment (500 ℃), the film and the nanowire system were observed. The morphology and microstructure were analyzed and their optical and electromagnetic properties were analyzed. The CZO thin film is doped with copper atoms by zinc oxide so that the concentration of the carrier is increased and the ferromagnetism is enhanced and the electrical properties are improved. There are many oxygen vacancies and interstitial zinc on the nanowire, which increases the concentration of zinc oxide carriers. The carriers improve electrical and magnetic properties. After heat treatment, copper atoms were diffused into the ZnO film layer in ZnO/CuZnO system, which can greatly improve the electrical and magnetic properties of the structure.

In this study, wire is made of nanometer flash-gold (Au) film deposited onto the surface of Ag-2.5 wt% Pd-1.5 wt% Au wire (APA wire), denoted as AAPA wire. The flash-Au film increases the resistance to chlorination and sulfidation of the silver (Ag) alloy wire, which is susceptible to deterioration in a chlorine- and sulfur-rich environment. In the chlorination test, the mechanical properties of the AAPA wire were better than those of the APA wire. Chloride ions corrode the wire along grain boundaries, resulting in a change from ductile fracture to brittle fracture in the tensile test. Chloride ions preferentially corroded the aluminum (Al) pad, greatly decreasing the reliability of the ball bond. The wedge bond did not fail due to the use of Au pad. In the sulfidation test, the average diameter of the wire increased with increasing sulfidation time. After sulfidation, the electrical conductivity decreased due to the thickening of Ag2S, whose resistance is high, and a decrease in the effective channel of the electric current. In addition, the formation of Ag2S caused a consumption of Ag atoms in the Ag wire, and thus formed voids at the interface between the sulfide layer and the Ag wire. The fracture of the sulfided ball bond was located in the heat-affected zone after the tensile test. The results show that the AAPA wire has better resistance in chlorination and sulfidation environment.

In this paper, a quartz crystal microbalance (QCM)-based humidity sensor has been fabricated by colloidal tin oxide (SnO2) nanowires. The SnO2 nanowires were synthesized via a colloidal process that employing SnCl4 ethanol solutions mixed with oleic acid (OA) and oleylamine (OLA). The spin-coating method was chosen to deposit the sensitive film at room temperature without high-temperature sintering. Furthermore, the Cu(NO3)2 methanol solution was used to remove the organic long chains coated on the surface of the colloidal SnO2 nanowires and expose more adsorption sites. The characterizations of the material were studied by means of FTIR, XRD, and FE-SEM. The saturated salt solution method was used to investigate the humidity sensing performance (response, recovery, repeatability, etc.) of the QCM sensor in the range of 11%–97%. The results showed that the sample with 12 h synthesis has the best humidity response. This may be attributed to the larger specific surface area which makes the material provide more adsorption sites for water molecules, and more (110) planes formed which could absorb more water molecules proved by the Density Functional Theory (DFT) calculation.

Both the stress-response protein, SIRT1, and the cell cycle checkpoint kinase, CHK2, play critical roles in aging and cancer via the modulation of cellular homeostasis and the maintenance of genomic integrity. However, the underlying mechanism linking the two pathways remains elusive. Here, we show that SIRT1 functions as a modifier of CHK2 in cell cycle control. Specifically, SIRT1 interacts with CHK2 and deacetylates it at lysine 520 residue, which suppresses CHK2 phosphorylation, dimerization, and thus activation. SIRT1 depletion induces CHK2 hyperactivation-mediated cell cycle arrest and subsequent cell death. In vivo, genetic deletion of Chk2 rescues the neonatal lethality of Sirt1−/− mice, consistent with the role of SIRT1 in preventing CHK2 hyperactivation. Together, these results suggest that CHK2 mediates the function of SIRT1 in cell cycle progression, and may provide new insights into modulating cellular homeostasis and maintaining genomic integrity in the prevention of aging and cancer.

Al-Si alloys exhibit promising wear resistance, thus being mainly employed to weld Al alloy parts and processed into components of equipment. During the new continuous casting direct rolling (CCDR) process, the raw material gradually cools and solidifies, simultaneously plastically deformed. Hence, the materials manufactured through the CCDR process presented an unparalleled microstructure. The experimental results indicated that the strength of the CCDR Al-Si alloy can be increased through cold rolling. A two-stage heat treatment (solid solution and aging treatment) was introduced to improve the ductility and satisfy the industrial application. Furthermore, the erosion wear characteristics and fracture mechanism of the CCDR Al-Si alloy dominated by the ductility were confirmed. Both cold rolling specimens (FR) and those with heat treatment (FRH) showed greater wear resistance than as-manufactured (F). The FR specimens exhibited greater wear resistance owing to a higher Al matrix strength at a lower impact angle, on the other hand, at a higher impact angle, the FRH specimens with a softer Al matrix presented better wear resistance due to the formation of a lip structure to reduce material removal. The TEM results confirmed that the nanoscale grains formation was induced in the erosion-affected region and affected the Si concentration. Conclusively, the heat-treated CCDR Al-Si alloy possessed excellent erosion resistance and workability, which can serve as a reference processed as wear-resistant mechanical parts.

The faithful DNA replication is a critical event for cell survival and inheritance. However, exogenous or endogenous sources of damage challenge the accurate synthesis of DNA, which causes DNA lesions. The DNA lesions are obstacles for replication fork progression. However, the prolonged replication fork stalling leads to replication fork collapse, which may cause DNA double-strand breaks (DSB). In order to maintain genomic stability, eukaryotic cells evolve translesion synthesis (TLS) and template switching (TS) to resolve the replication stalling. Proliferating cell nuclear antigen (PCNA) trimer acts as a slide clamp and encircles DNA to orchestrate DNA synthesis and DNA damage tolerance (DDT). The post-translational modifications (PTMs) of PCNA regulate these functions to ensure the appropriate initiation and termination of replication and DDT. The aberrant regulation of PCNA PTMs will result in DSB, which causes mutagenesis and poor response to chemotherapy. Here, we review the roles of the PCNA PTMs in DNA duplication and DDT. We propose that clarifying the regulation of PCNA PTMs may provide insights into understanding the development of cancers.

Background Bone morphogenetic protein 5 (BMP5) has been identified as one of the important risk factors for microtia; however, the link between them has yet to be clarified. In this study, we aimed to demonstrate the relationship of BMP5 with mitochondrial function and investigate the specific role of mitochondria in regulating microtia development. Methods BMP5 expression was measured in auricular cartilage tissues from patients with and without microtia. The effects of BMP5 knockdown on cellular function and mitochondrial function were also analyzed in vitro. Changes in genome-wide expression profiles were measured in BMP5-knockdown cells. Finally, the specific impact of BMP5 down-regulation on mitochondrial fat oxidation was analyzed in vitro. Results BMP5 expression was down-regulated in the auricular cartilage tissues of microtia patients. BMP5 down-regulation inhibited various cellular functions in vitro, including cell proliferation, mobility, and cytoactivity. The functional integrity of mitochondria was also damaged, accompanied by a decrease in mitochondrial membrane potential, reactive oxygen species (ROS) neutralization, and reduced adenosine triphosphate (ATP) production. Carnitine O-palmitoyltransferase 2 and diacylglycerol acyltransferase 2, two of the key regulators of mitochondrial lipid oxidation, were also found to be decreased by BMP5 down-regulation. Conclusions Down-regulation of BMP5 affects glycerolipid metabolism and fatty acid degradation, leading to mitochondrial dysfunction, reduced ATP production, and changes in cell function, and ultimately resulting in microtia. This research provides supporting evidence for an important role of BMP5 down-regulation in affecting mitochondrial metabolism in cells, and sheds new light on the mechanisms underlying the pathogenesis of microtia.

To properly understand cotton responses to potassium (K+) deficiency and how its shoot feedback regulates K+ uptake and root growth, we analyzed the changes in root transcriptome induced by low K+ (0.03 mM K+, lasting three days) in self-grafts of a K+ inefficient cotton variety (CCRI41/CCRI41, scion/rootstock) and its reciprocal grafts with a K+ efficient variety (SCRC22/CCRI41). Compared with CCRI41/CCRI41, the SCRC22 scion enhanced the K+ uptake and root growth of CCRI41 rootstock. A total of 1968 and 2539 differently expressed genes (DEGs) were identified in the roots of CCRI41/CCRI41 and SCRC22/CCRI41 in response to K+ deficiency, respectively. The overlapped and similarly (both up- or both down-) regulated DEGs in the two grafts were considered the basic response to K+ deficiency in cotton roots, whereas the DEGs only found in SCRC22/CCRI41 (1954) and those oppositely (one up- and the other down-) regulated in the two grafts might be the key factors involved in the feedback regulation of K+ uptake and root growth. The expression level of four putative K+ transporter genes (three GhHAK5 and one GhKUP3) increased in both grafts under low K+, which could enable plants to cope with K+ deficiency. In addition, two ethylene response factors (ERFs), GhERF15 and GhESE3, both down-regulated in the roots of CCRI41/CCRI41 and SCRC22/CCRI41, may negatively regulate K+ uptake in cotton roots due to higher net K+ uptake rate in their virus-induced gene silencing (VIGS) plants. In terms of feedback regulation of K+ uptake and root growth, several up-regulated DEGs related to Ca2+ binding and CIPK (CBL-interacting protein kinases), one up-regulated GhKUP3 and several up-regulated GhNRT2.1s probably play important roles. In conclusion, these results provide a deeper insight into the molecular mechanisms involved in basic response to low K+ stress in cotton roots and feedback regulation of K+ uptake, and present several low K+ tolerance-associated genes that need to be further identified and characterized.

BACKGROUND AND PURPOSE Chicken colibacillosis, caused by avian Escherichia coli (APEC), results in huge economic losses to the poultry industry. Baicalin exerts protective effects during the development of colibacillosis. In this study, we mainly explored the mechanism of this protective effects with regard to gut microbiota. EXPERIMENTAL APPROACH The chicken colibacillosis model was established by intratracheal instillation of APEC. The gut microbiota-depleted chicken model was established with broad-spectrum antibiotics. Viscera index measurement and Haematoxylin and eosin stain were applied to assess histological changes of tissues. ELISA were used to measure the cytokines and Quantitative-PCR were used to evaluate the gene expression. The gut microbiota and its metabolite were detected by 16srDNA and ultrahigh-performance liquid chromatography (LC-MS). KEY RESULTS Depletion of gut microbiota exacerbated the tissue damage and weakened the protective effects of baicalin during APEC-induced chicken colibacillosis while pretreatment of baicalin reduced these changes and inflammatory response induced by APEC. Moreover, APEC infection led to dysbiosis of gut microbiota and its metabolites. However, the pretreatment of baicalin remodeled the gut microbiota featured with increased abundance of Intestinimonas and its associated with beneficial metabolites. CONCLUSIONS Gut microbiota played a protective role in the prevention of chicken colibacillosis and the pharmacological action of baicalin. The altered specific gut bacterial and/or metabolites may be served as indicators to predict the occurrence and prognosis of chicken colibacillosis. Our findings may provide a paradigm for the mechanistic studies of compounds and aid the exploration of the mechanisms and pathways underlying the function of herbal medicines.

Background Lodging is one of the important factors causing maize yield. Plant height is an important factor in determining plant architecture in maize (Zea mays L.), which is closely related to lodging resistance under high planting density. Coronatine (COR), which is a phytotoxin and produced by the pathogen Pseudomonas syringae, is a functional and structural analogue of jasmonic acid (JA). Results In this study, we found COR, as a new plant growth regulator, could effectively reduce plant height and ear height of both hybrids (ZD958 and XY335) and inbred (B73) maize by inhibiting internode growth during elongation, thus improve maize lodging resistance. To study gene expression changes in internode after COR treatment, we collected spatio-temporal transcriptome of inbred B73 internode under normal condition and COR treatment, including the three different regions of internode (fixed, meristem and elongation regions) at three different developmental stages. The gene expression levels of the three regions at normal condition were described and then compared with that upon COR treatment. In total, 8605 COR-responsive genes (COR-RGs) were found, consist of 802 genes specifically expressed in internode. For these COR-RGs, 614, 870, 2123 of which showed expression changes in only fixed, meristem and elongation region, respectively. Both the number and function were significantly changed for COR-RGs identified in different regions, indicating genes with different functions were regulated at the three regions. Besides, we found more than 80% genes of gibberellin and jasmonic acid were changed under COR treatment. Conclusions These data provide a gene expression profiling in different regions of internode development and molecular mechanism of COR affecting internode elongation. A putative schematic of the internode response to COR treatment is proposed which shows the basic process of COR affecting internode elongation. This research provides a useful resource for studying maize internode development and improves our understanding of the COR regulation mechanism based on plant height.

Avian pathogenic Escherichia coli (APEC), collectively known as causative agent of extraintestinal infections, is an important cause of morbidity and mortality in poultry. Currently, quorum sensing (QS), biofilm formation and virulence factors are considered as novel prospective targets for antimicrobial therapy to control APEC invasion. In addition, inflammatory responses are also served as the major pathological features of APEC invasion. This study was aimed to explore the effect of baicalin on APEC and APEC-induced inflammatory responses. After treatment with baicalin, we mainly examined the AI-2 secretion, biofilm formation, expression of virulence genes of APEC, and the levels of inflammatory cytokines, as well as the expression of NF-κB pathway. Our results showed that baicalin significantly inhibited the QS via decreasing the AI-2 secretion, biofilm formation, and the expression of virulence genes of APEC such as LsrB, LsrK, LuxS, pfs, H-NS, fimA, fimB, fyuA, csgA, csgB, and rpoS. Moreover, baicalin significantly attenuated the release of lactate dehydrogenase (LDH), and the adhesion of APEC to chicken type II pneumocytes to reduce cell damage. Furthermore, baicalin also inhibited the expression of pro-inflammatory cytokines and NF-κB activation. Thus, our data revealed that baicalin could interfere with the quorum sensing, biofilm formation and virulence genes expression to relieve the APEC pathogenicity. Additionally, baicalin decreased the inflammatory responses of chicken type II pneumocytes induced by APEC. Taken together, these data provide a novel potential pharmaco-therapeutic approach to chicken colibacillosis.

Madecassoside (MA), a crucial ingredient of Centella asiatica, has been reported to exhibit a variety of bioactivities, including antipulmonary fibrosis, and antiinflammatory effects. Here we aimed to elucidate the protective effects and underlying mechanisms of MA on LPS-induced acute lung injury (ALI). The mice were treated with MA for one week and then received intratracheal of LPS to establish the ALI model. Then we evaluated the pathological changes by haematoxylin and eosin staining and measured the levels of proinflammatory cytokines and myeloperoxidase (MPO) by ELISA, the transcriptional level of tight junction proteins by qRT-PCR, as well as the expression of Toll-like receptor4/Nuclear factor kappa-B (TLR4/NF-κB) pathway by Western blot. The results showed that MA significantly inhibited LPS-induced pathological damages, lung edema, MPO, and proinflammatory cytokines production. Furthermore, MA obviously repaired alveolar epithelium integrity showing by reduced secretion of total proteins in the BALF and enhanced mRNA expression of tight junction as Occludin and zonula occludens-1 (ZO-1) comparing to LPS. Further research showed that LPS stimulation activated the TLR4/NF-κB signaling pathway and the activation was inhibited by MA. In conclusion, these data indicated that MA had protective effects against LPS-induced ALI. The therapeutic mechanisms may be associated with reducing the alveolar epithelium permeability and inflammatory response via repressing the activation of TLR4/NF-κB pathway.

Conifers are the largest and most ubiquitous group of gymnosperms and have significant ecological significance and economic importance. However, the huge and complex genomes have hindered the sequencing and mining of conifer genomes. In this study, we identified 413 423 transposable elements (TEs) from Picea abies, Picea glauca and Pinus taeda using a combination of multiple approaches and classified them into 11 133 families. A comprehensive web-based database, ConTEdb, was constructed and served for researchers. ConTEdb enables users to browse, retrieve and download the TE sequences from the database. Several analysis tools are integrated into ConTEdb to help users mine the TE data easily and effectively. In summary, ConTEdb provides a platform to study TE biology and functional genomics in conifers.

To explore the high efficiency of the Buchwald–Hartwig amination with a wide substrate scope, easily prepared and air stable palladium precatalysts bearing rigid hindered N-heterocyclic carbenes (NHCs) were synthesized and characterized. A simple and efficient protocol for the amination of (hetero)aryl chlorides with amines is described, which revealed that sterically encumbered NHC ligands are crucial to promote the transformation. It is highlighted that the most challenging reactions could be performed between less reactive five-membered heteroaryl chlorides and heteroanilines. This methodology provides a rapid and straightforward access to a wide range of arylated amines with excellent functional group tolerance. Remarkably, the powerful synthetic utility of palladium precatalysts was further extended to the synthesis of pharmaceuticals.

In this study, a cast rod is used as the material for the forging process (without extrusion). The cast forging process is used to ameliorate the coarse grains that form in the follow-up heating process of extrusion-forged materials. Infrared (IR) heating is also used for comparison with conventional heating processes. Experimental results show that the direct forging process (without extrusion) suppress coarse grain formation and that IR heating can improve the mechanical properties of cast- and extrusion-forged materials. IR heating also enhances the tensile properties of forged materials. Keywords: Al-Mg-Si alloy, Infrared, Cast forging, Mechanical properties

Background Phytohormones are the key factors regulating vascular development in plants, and they are also involved in tension wood (TW) formation. Although the theory of hormone distribution in TW formation is widely supported, the effects of endogenous hormones on TW formation have not yet been assessed. In this study, TW formation was induced in Catalpa bungei by artificial bending. The phytohormone content of TW, opposite wood (OW) and normal wood (NW) was determined using liquid chromatography-mass spectrometry (LC-MS), and transcriptome sequencing was performed. The hormone content and related gene expression data were comprehensively analyzed. Results The results of analyses of the plant hormone contents indicated significantly higher levels of cis-zeatin (cZ), indoleacetic acid (IAA) and abscisic acid (ABA) in TW than in OW. Genes involved in the IAA and ABA synthesis pathways, such as ALDH (evm.model.group5.1511) and UGT (evm.model.scaffold36.20), were significantly upregulated in TW. and the expression levels of ARF (evm.model.group5.1332), A-ARR (evm.model.group0.1600), and TCH4 (evm.model.group2.745), which participate in IAA, cZ and Brassinolide (BR) signal transduction, were significantly increased in TW. In particular, ARF expression may be regulated by long noncoding RNAs (lncRNAs) and the HD-ZIP transcription factor ATHB-15. Conclusions We constructed a multiple hormone-mediated network of C. bungei TW formation based on hormone levels and transcriptional expression profiles were identified during TW formation.

The explosive properties of mixtures of aqueous hydrogen peroxide (H2O2) and working solution (WS), and the main components of the working solution (1, 3, 5-trimethyl benzene(TMB), trioctylphosphate (TOP)) were investigated by the drop weight test. The explosion range was interpreted by thermal calculation, and the calculated results agreed well with the experimental test. The explosion mechanism of the TMB/H2O2 mixture is the partial oxidation of TMB by H2O2, which is qualitatively obtained by analyzing the gaseous and liquid products of the TMB/ H2O2 mixture after explosion. Finally, a proposed explosion mechanism was suggested.

The microstructural characteristics, bonding force and bulk resistance of photovoltaic (PV) aluminum modules made with three hypereutectic solder alloys, namely Sn-30Zn, Sn-50Zn and Sn-70Zn, were investigated. In the dipping step, the mechanism of bonding between pure aluminum ribbons and Sn-xZn solder alloys is via the Sn-xZn solder liquid phase penetrating into aluminum grain boundaries rather than forming intermetallic compound at the interface. After reflow for connecting PV aluminum ribbon and silicon substrate with Ag paste, an AgZn3 layer, whose thickness increases with increasing reflow time, formed at the solder/Ag interface. After bias aging, the Ag paste was consumed, the thickness of AgZn3 significantly increased and the bulk resistance increased. The bulk resistance of the modules with “Ag direction” (electrons move from Al to Ag) is slightly higher than that of modules with “Al direction” (electrons move from Ag to Al) due to more formation of AgZn3, which decreases the cross-section area of electrical current and increases the path of electrical current. Sn-50Zn/Al PV modules have good stability and high conductivity, and are competitive with PV modules made with copper ribbons.

Polylactic acid (PLA), pure magnesium powder, and calcium phosphate powder were used to form a three-phase degradable biomedical composite. The effects of various powder proportions in polylactic acid–Mg–Ca3(PO4)2 composites were analyzed through mechanical and biological tests, which revealed that both the tensile and impact strength of the composite increased. Additionally, ductility presented only after a small proportion of powder was added. Hardness slightly increased because of dispersion strengthening. Furthermore, the addition of pure magnesium and calcium phosphate accelerated the degradation rate, and biocompatible salts were generated after degradation, which can improve healing and renewal in bone tissue. None of the composites exhibited cytotoxicity, meeting biological safety requirements. Overall, PLA10M10C (10 wt.% Mg, 10 wt.% Ca3(PO4)2) exhibited superior performance. Accordingly, PLA10M10C can serve as a reference for degradable biomedical material applications in orthopedic implants.

In this paper, a Schiff base (SB-1) and derivatives (SB-2 and SB-3) was synthesized and characterized by IR and 1H NMR methods, the corrosion efficiency and mechanism of carbon steel in 1: 1 hydrochloric acid was obtained by weight loss measurements, atomic absorption spectrophotometry, electrochemical measurements, atomic force microscopy studies and quantum chemical calculations. The results indicated that the inhibition efficiency was SB-3 > SB-2 > SB-1 at low concentration of inhibitors. Under high concentration, they have same efficiency. The electrochemical measurements showed that the synthesized compounds is an efficient mix-type inhibitors and its efficiency increased with the increase in inhibitor concentrations. The quantum chemical parameters were calculated using the density functional theory (DFT), and results showed that the inhibitor and the metal surface interacted with the donor-acceptor to achieve the effect of corrosion inhibition.

Two polysaccharides, GCP-I-I and GCP-II-I, were obtained from 100°C water extracts of Gentiana crassicaulis roots by DEAE anion exchange chromatography and gel filtration. The results from methanolysis, methylation, FT-IR and NMR, indicated that these two fractions are typical pectic polysaccharides, with HG and RG-I regions and AG-I/AG-II side chains, and some of the galacturonic acid units of fraction GCP-I-I were methyl esterified. Fractions GCP-I-I and GCP-II-I, both exhibited potent complement fixation, and fraction GCP-I-I was more potent than positive control BPII. The higher complement fixation activity obtained in fraction GCP-I-I may be due to the higher Mw and/or higher amount of AG-II present in fraction GCP-I-I than fraction GCP-II-I. The polysaccharides from G. crassicaulis could be used as a potential natural immunomodulator.

The major objective of the present study is to clarify the effects of rapid heat solutionizing on tensile strength of A6082 aluminum alloy. In the present investigation, grain dimensions and insoluble IMC particle were investigated both in the traditional resistance heating and in the rapidly heating specimens. Furthermore, the effect of rapid heat solutionizing on tensile strength under an identical artificial aging condition was studied pertaining to the observation on the insoluble particles present in the material due to the solidificational process and which undergone rapid heat solutionizing. The critical strain of tensile serrated flow caused by Portevin-Lechatelier (PL) effect was compared with that of the resistance heating specimens. Such rapid heating specimen is also showing larger critical onset strain in the tensile serrated flow (ɛc), suggests that the rapid heating process could offer a higher concentration on solution solutes. Hardness and tensile strength data indicated an increasing aging effect, the higher concentration of Mg and Si solid solution also lead to a shorter limiting T4/T6 process duration of A6082 aluminum alloy. A significantly shorter heat treatment time to achieve peak hardness (HRB73) without deterioration of tensile strength. The concentration of rapid heat solution was investigated using SEM and TEM, and the above results should be related to the attractive interaction between silicon and magnesium solutes since the onset strain of tensile serrated flow increases with the increasing heating rate.

The homeostatic link between oxidative stress and autophagy plays an important role in cellular responses to a wide variety of physiological and pathological conditions. However, the regulatory pathway and outcomes remain incompletely understood. Here, we show that reactive oxygen species (ROS) function as signaling molecules that regulate autophagy through ataxia‐telangiectasia mutated (ATM) and cell cycle checkpoint kinase 2 (CHK2), a DNA damage response (DDR) pathway activated during metabolic and hypoxic stress. We report that CHK2 binds to and phosphorylates Beclin 1 at Ser90/Ser93, thereby impairing Beclin 1‐Bcl‐2 autophagy‐regulatory complex formation in a ROS‐dependent fashion. We further demonstrate that CHK2‐mediated autophagy has an unexpected role in reducing ROS levels via the removal of damaged mitochondria, which is required for cell survival under stress conditions. Finally, CHK2(−/−) mice display aggravated infarct phenotypes and reduced Beclin 1 p‐Ser90/Ser93 in a cerebral stroke model, suggesting an in vivo role of CHK2‐induced autophagy in cell survival. Taken together, these results indicate that the ROS‐ATM‐CHK2‐Beclin 1‐autophagy axis serves as a physiological adaptation pathway that protects cells exposed to pathological conditions from stress‐induced tissue damage.

Catalpa bungei is an economically important tree with high-quality wood and highly valuable to the study of wood formation. In this work, the xylem microstructure of C. bungei tension wood (TW) was observed, and we performed transcriptomics, proteomics and Raman spectroscopy of TW, opposite wood (OW) and normal wood (NW). The results showed that there was no obvious gelatinous layer (G-layer) in the TW of C. bungei and that the secondary wall deposition in the TW was reduced compared with that in the OW and NW. We found that most of the differentially expressed mRNAs and proteins were involved in carbohydrate polysaccharide synthesis. Raman spectroscopy results indicated that the cellulose and pectin content and pectin methylation in the TW were lower than those in the OW and NW, and many genes and proteins involved in the metabolic pathways of cellulose and pectin, such as galacturonosyltransferase (GAUT), polygalacturonase (PG), endoglucanase (CLE) and &beta, glucosidase (BGLU) genes, were significantly upregulated in TW. In addition, we found that the MYB2 transcription factor may regulate the pectin degradation genes PG1 and PG3, and ARF, ERF, SBP and MYB1 may be the key transcription factors regulating the synthesis and decomposition of cellulose. In contrast to previous studies on TW with a G-layer, our results revealed a change in metabolism in TW without a G-layer, and we inferred that the change in the pectin type, esterification and cellulose characteristics in the TW of C. bungei may contribute to high tensile stress. These results will enrich the understanding of the mechanism of TW formation.

Acute lung injury (ALI) is a common and complex inflammatory lung syndrome with higher morbidity and mortality rate. Piceatannol (PIC) has anti-inflammation and anti-oxidant properties. The study was designed to explore the effect and the action mechanisms of PIC on lipopolysaccharide (LPS)-induced ALI. Twenty-four hours after LPS challenge, mice from different treatment groups were euthanized, and the bronchoalveolar lavage fluid (BALF) and lung tissue samples were collected. Then the degree of pulmonary edema, lung pathological changes, myeloperoxidase (MPO) activity, and the production of pro-inflammatory cytokines were detected. Additionally, the messenger RNA (mRNA) expressions associated with cell adhesion molecules and tight junction were analyzed through quantitative real-time (qRT)-PCR, and the TLR4/NF-κB activation was examined by western blot. The results showed that PIC significantly inhibited LPS-induced lung edema, histopathological damage, MPO activity, cell infiltration, and pro-inflammatory cytokines production. Moreover, PIC notably suppressed mRNA expressions associated with inflammation and cell adhesion molecules. Furthermore, PIC also alleviated LPS-induced damage of air-blood barrier through reducing the levels of total proteins in BALF and recovering the expression of occludin and ZO-1 in the lung tissues. We also found that PIC remarkably restrained the LPS-induced TLR4/NF-κB pathway activation in lung tissues. In conclusion, PIC may be potential to treat LPS-induced acute lung injury (ALI) via regulating air-blood barrier and TLR4/NF-κB signaling pathway activation.

Long non-coding RNA NBR2 is a transcript of the neighbor of BRCA1 gene 2 and can regulate tumor development. However, there is little information on the role of NBR2 in the progression of thyroid cancers (TC). Here, we show that NBR2 expression is down-regulated in TC tissues and associated with histologic subtypes of TC. NBR2 expression was variably reduced in different TC cells. While NBR2 silencing significantly enhanced the malignancy of BCPAP cells by increasing cell proliferation, clonogenicity, wound healing, and invasion as well as tumor growth in vivo, and decreasing spontaneous apoptosis, NBR2 over-expression had opposite effects in BHT101 cells. Furthermore, treatment with A-769662 (a specific AMPK activator), like NBR2 over-expression, significantly attenuated the malignancy of BHT101 cells while treatment with Compound C (a specific AMPK inhibitor) significantly rescued that NBR2-reduced malignancy of BHT101 cells. In comparison with non-tumor thyroid epithelial Nthy-ori 3-1 cells, obviously increased GLUT-1 expression, but decreased AMPK and ACC phosphorylation were detected in TC cells. While NBR2 silencing further enhanced GLUT-1 expression and reduced AMPK and ACC phosphorylation as well as the EMT process in BCPAP cells. NBR2 over-expression also had opposite effects in BHT101 cells. Similar patterns of GLUT-1 expression and AMPK and ACC phosphorylation were detected in the different types of xenograft TC tumors in vivo. Therefore, such data indicated that NBR2 acted as a tumor suppressor of thyroid cancers associated with enhancing the AMPK signaling and NBR2 may be a potential biomarker and therapeutic target for thyroid cancers.

Avian pathogenic Escherichia coli (APEC) is a kind of highly pathogenic parenteral bacteria, which adheres to chicken type II pneumocytes through pili, causing inflammatory damage of chicken type II pneumocytes. Without affecting the growth of bacteria, anti-adhesion to achieve anti-inflammatory effect is considered to be a new method for the treatment of multi-drug-resistant bacterial infections. In this study, the anti-APEC activity of schizandrin was studied in vitro. By establishing the model of chicken type II pneumocytes infected with APEC-O78, the adhesion number, the expression of virulence genes, the release of lactate dehydrogenase (LDH), levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, IL-8 and activation of nuclear factor-κB (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways were detected. The results showed that schizandrin reduced the release of LDH and the adherence of APEC on chicken type II pneumocytes. Moreover, schizandrin markedly decreased the levels of IL-1β, IL-8, IL-6, and TNF-α, the mechanism responsible for these effects was attributed to the inhibitory effect of schizandrin on NF-κB and MAPK signaling activation. In conclusion, our findings revealed that schizandrin could reduce the inflammatory injury of chicken type II pneumocytes by reducing the adhesion of APEC-O78 to chicken type II pneumocytes. The results indicate that schizandrin can be a potential agent to treat inflammation caused by avian colibacillosis.

Palladium-coated copper wire with a flash-gold layer (PCA) is an oxidation-resistant fine wire that simultaneously has the properties of palladium-coated copper wire (PCC) and gold-coated copper wire. This research used an extreme sulfidation test to compare corrosion resistance between the PCC and PCA wires. In addition to closely examining the morphology of the wires, the internal matrix after the sulfidation test is also discussed. In doing so, the PCA wire was bonded onto the aluminum pads and the sulfidation test was conducted. Then, we observed its morphology and elemental distribution and found that the flash-gold layer of the PCA wire effectively enhanced resistance to sulfidation corrosion. Because the copper ball had an alloying effect on the ball bonding, it produced different shapes of sulfide after the sulfidation test. The degree of corrosion on the wedge bond was different because of the presence or absence of the coated layer. In contrast, the flash-gold layer of the PCA wire enhanced the bonding force and retained low resistance characteristics after the sulfidation test.

Recent work shows that Pockels effect and optics pump-probe measurement could be utilized as a novel method for 511 keV ionizing radiation photon detection for positron emission tomography (PET) which could potentially overcome the inherent physical limitation for coincidence time resolution of around 100 ps (Tao et al 2016 Phys. Med. Biol. 61 7600–22). In this paper, we embrace this observation and introduce a two-crossed-polarizers based setup to achieve similar detection concept, which is a simpler and more compact setup with comparable ionizing radiation detection capability as the setup used in the previously proposed work. We evaluated the performance of our experimental setup with Lithium Niobate (LiNbO(3)) and Cadmium Telluride (CdTe) detector crystals, and the desired properties of an ideal detector crystal were discussed. The modulation signal induced by 511 keV photons in both LiNbO(3) and CdTe can be detected with repeatable signal amplitude using two-crossed-polarizers based method, while CdTe could provide eight times higher detection sensitivity to 511 keV photons than LiNbO(3) under the same bias voltage, suggesting high effective Z number and high density properties of CdTe, as well as a shorter carrier lifetime and lower carrier mobility of LiNbO(3). In addition, the strength of modulation signal increased linearly with bias voltage before saturation. The modulation signal strength in LiNbO(3) continued to increase after 2000 V due to its high resistivity which could reduce the dark current in the detector, while the modulation signal of CdTe with low resistivity tended to be saturated at a bias voltage higher than 1200 V. Therefore, further increasing the bias voltage for detector crystals (especially for LiNbO(3)) may enhance the modulation strength and improve the detection sensitivity for annihilation photons.