Search

[Display omitted] • Spices and phenols reduced the heterocyclic aromatic amines (HAAs) in roasted beef. • The HOMO/LUMO and ESP were analyzed by density functional theory (DFT). • Intermediates of HAAs exhibited intermolecular interactions with phenols. • The imino and hydroxyl group of capsaicin captured HAAs-related free radicals. • This study provided a reference for the development of DFT in the control of HAAs. The ability of spices (bay leaf, star anise, and red pepper) and their characteristic phenolic compounds (quercetin, kaempferol, and capsaicin) to inhibit Heterocyclic aromatic amines (HAAs) in roasted beef patties were compared. Density functional theory (DFT) was used to reveal phenolic compounds interacting with HAAs-related intermediates and free radicals to explore possible inhibitory mechanisms for HAAs. 3 % red chili and 0.03 % capsaicin reduced the total HAAs content by 57.09 % and 68.79 %, respectively. DFT demonstrated that this was due to the stronger interaction between capsaicin and the β-carboline HAAs intermediate (E bind = –32.95 kcal/mol). The interaction between quercetin and phenylacetaldehyde was found to be the strongest (E bind = −17.47 kcal/mol). Additionally, DFT indicated that capsaicin reduced the carbonyl content by transferring hydrogen atoms (HAT) to eliminate HO·, HOO·, and carbon-centered alkyl radicals. This study provided a reference for the development of DFT in the control of HAAs. [ABSTRACT FROM AUTHOR]

[Display omitted] • Ultrasound and carrageenan jointly improves the myofibrillar protein gel properties. • Ultrasound combined with carrageenan leads to heated rearrangement aggregation. • Carrageenan acts on protein by crosslinking and insertion. • Carrageenan competes with proteins for binding to water molecules in heating. To improve the limitation of transglutaminase on the quality of myofibrillar protein (MP) gel, this study investigated the synergistic effect of ultrasonic pretreatment in combination with carrageenan on the gel properties of transglutaminase-mediated MP gels. The synergistic effect generated gel with lower surface hydrophobicity and fluorescence intensity. Combined with the secondary structure results, it can be hypothesized that the synergistic effect caused the rearrangement of the proteins and the formation of aggregates wrapping hydrophobic groups, which changed the structure and phase behavior of the proteins. The synergistic effect also improved the formation of dense and interpenetrating gel networks, which reduced cooking loss and produced composite MP gels with optimal gel strength. Moreover, FTIR spectroscopy revealed the presence of electrostatic interactions in the hybrid gel system. This study provides a theoretical basis and experimental foundation for the effective use of high-tech composite functional components to improve the quality of gel products. [ABSTRACT FROM AUTHOR]

A series of bismuth modified bismuth iodide flower-like microspheres with rich oxygen vacancies were prepared by solvothermal method. Herein, a mixed solution of propylene glycol and ethylene glycol was used as the solvent. By adjusting the ratio of these two solutions in the solvent, it is not only possible to prepare Bi 4 O 5 I 2 microspheres containing different concentrations of oxygen vacancies, but also to control the content of Bi. The Bi/ Bi 4 O 5 I 2 photocatalyst prepared when the ratio of propylene glycol to ethylene glycol was 5:1 in solvent showed excellent optical properties, and more than 99% of E. coli could be inactivated within 30 min under visible light irradiation. The antibacterial mechanism experiment showed that reactive oxygen species were the main substances affecting the antibacterial effect of Bi/ Bi 4 O 5 I 2 , and the scavenging experiment of reactive oxygen showed that •O 2 - was the key active substance in the antibacterial process. Finally, it was verified that reactive oxygen species can act on the interior and exterior of bacteria, indicating a more effective antibacterial pathway. [Display omitted] [ABSTRACT FROM AUTHOR]

Abstract A simple and direct low-temperature hydrothermal synthesis approach (100 °C) has been developed to encapsulate Pd nanoparticles (ca. 2.3 nm) within nano-sized mesoporous TS-1 zeolite by utilizing dichloro(ethylenediamine)palladium (DEAP) and cetyltrimethylammonium bromide (CTAB) as palladium source and mesoporogen, respectively. It's demonstrated that the aging process of the mother liquid and low-temperature hydrothermal treatment can effectively inhibit the premature precipitation of metal precursor and thus the successful encapsulation of Pd nanoparticles into mesoporous TS-1 nanocrystals, so that the frequently occurring of Pd nanoparticle aggregation at high temperature was expectedly avoided. Consequently, the as-synthesized catalysts with highly thermal stability and mesoporous channels exhibit excellent catalytic activity and recyclability in the oxidation of CO with relatively low Pd content (0.53 wt% Pd) and catalytic wet air oxidation of phenol (66.2% of phenol conversion, 100 °C). Graphical abstract Image 1 Highlights • We report a direct synthesis of Pd encapsulated mesoporous TS-1 zeolite via low-temperature hydrothermal treatment. • The optimized synthesis condition (mesoporogen amount, temperature and time of hydrothermal treatment) are studied. • The small-sized Pd nanoparticles (2.3 nm) in mesoporous TS-1 show high stability at 600 °C under air/N 2 /H 2 atomsphere. • The hierarchical micro/mesoporous stucture endow the nano-sized TS-1 zeolite high mass transportation efficiency. • Excellent catalytic activities and recyclabilities of catalyst in the CO oxidation and wet air oxidation of phenol. [ABSTRACT FROM AUTHOR]

Abstract Herein, we report a one-step hydrothermal approach to synthesize hierarchical manganese-containing TS-1 zeolite (HMTS) with mesopores of 2–4 nm in diameter and uniform crystal size of 150–200 nm by employing manganese (III)-acetylacetonate and tetrabutyl titanate as manganese and titanium sources, respectively. It is demonstrated that Mn and Ti species in designed ratios have been successfully incorporated into the framework of HMTS zeolites during the hydrothermal treating processes. Moreover, the physicochemical and textural properties of HMTS can be easily tailored by simply altering the amounts of the template agents. The as-synthesized HMTS catalyst exhibits superior catalytic activity, excellent structural stability and recyclability on the selective oxidation of cyclohexanone to adipic acid under mild solvent-free conditions via a non-nitric acid route, which avoids the high energy consumption and emission of greenhouse gas (N 2 O). This work demonstrates a facile route to the direct synthesis of Mn-containing, hierarchical meso/microporous TS-1 with economized energy and time, presenting potential prospects in the field of aerobic oxidations of bulky organic compounds. Graphical abstract Image 1 Highlights • One-step synthesis of Mn-containing hierarchical TS-1 (HMTS) zeolite with uniform crystal size of 150-200 nm. • Effective incorporation of titanium and manganese species into the framework of zeolite. • The HMTS possesses high BET surface and adjustable hierarchically meso- and microporous structures. • The HMTS exhibits superior catalytic capacity and recyclability in the oxidation of cyclohexanone to adipic acid. [ABSTRACT FROM AUTHOR]

• Roasted chicken contained IQ, MeIQ, MeIQx, 4,8-DiMeIQx, PhIP, harman, and noharman. • Transportation of precursors may contribute greatly to the high HAA contents in skin. • PCA shows HAAs change significantly with the increase of temperature and time. • A HAA prediction model was built using backpropagation-artificial neural network. • This study facilitates the development of intelligent real-time HAA detection. The effects of chicken roasting temperature and time on the production of heterocyclic aromatic amines (HAAs) were investigated and an HAA prediction model based on heating conditions was established. Generally, the HAA content was significantly affected by the heating conditions in the roast chicken. Transportation of precursors from meat to skin, exposure of skin to high temperatures, and fat oxidation in the skin may result in higher HAAs than meat. Principal component analysis (PCA) showed that the effect of relatively high temperatures and long roasting times on HAAs was stronger than that of lower temperatures and shorter roasting times. In the prediction of HAA production, all regression correlation coefficient (R) values were close to one. The errors of 15 samples of experimental and predictive data were close to zero. Based on the results, backpropagation-artificial neural network (BP-ANN) has a high potential for predicting the production of HAAs under heating conditions. [ABSTRACT FROM AUTHOR]

• FSDAF can better predict biomass changes. • Mapping the spatiotemporal distribution of grassland biomass(30 m, 8 days). • Biomass is closely related to altitude and water supply in the Xilin River Basin. • Biomass responds more to temperature changes than precipitation. Accurate estimation of aboveground biomass of grasslands is key to sustainable grassland utilization. However, most satellites cannot provide high temporal and spatial resolution data. Patterns of grassland dynamics associated with variability in climate conditions across spatiotemporal scales are yet to be adequately quantified. A spatiotemporal fusion model offers the opportunity to combine the resolution advantages of different remote sensing data to achieve a high frequency and high precision monitoring of vegetation. We test a flexible spatiotemporal data fusion (FSDAF) methodology to generate synthetic normalized difference vegetation index (NDVI) data from Moderate-Resolution Imaging Spectroradiometer (MODIS) and Landsat data sets. The methodology is tested for the semi-arid grassland of the Xilin River Basin, China. Based on NDVI data fusion and field measured aboveground biomass an aboveground biomass estimation model is established for the watershed. Exploring the temporal and spatial changes of biomass and its relationship with environmental factors. The results show that: (1) The FSDAF model performs well (R2 = 0.75) and has clear textural features. (2) The established Support Vector Machine Aboveground Biomass model not only ensured the accuracy of estimation (R2 = 0.78, RMSE = 15.43 g/m2), but also generated spatiotemporal maps of biomass with higher spatial (30 m) and temporal resolution (8 days). (3) The grassland aboveground biomass in this area decreases from southeast to northwest, and the grassland biomass reaches its peak at the end of July. The average biomass of different grasslands decreases in the order of meadow grassland > typical grassland > desert grassland. (4) Aboveground biomass increased linearly with increasing water content, organic carbon and total nitrogen, and was most sensitive to soil water content. During the early growing and rapid growing period, aboveground biomass is mainly affected by both air temperature and precipitation, while the effects of temperature and human activities gradually dominate in the middle and late growing periods. This study helps to improve the spatial and temporal resolution of dynamic monitoring of grassland biomass, and provides a scientific basis for grassland protection and management in arid and semi-arid regions. [ABSTRACT FROM AUTHOR]

• The effects of different curing methods on black pork were comparatively studied. • Ultrasonic-assisted curing effectively improved the tenderness and taste of black pork. • Ultrasonic-assisted curing was beneficial to increase the degree of protein denaturation. • Ultrasonic-assisted curing could significantly destroy the structure of muscle fiber. This study aimed to investigate the effects of standing curing (SC), tumbling curing (TC), vacuum tumbling curing (VTC) and ultrasonic-assisted curing (UAC) on the edible quality of black pork and property of myofibrillar proteins (MPs) extracted from black pork. The results showed that all curing methods could improve the marinating absorptivity and the gel water retention of black pork, the solubility and surface hydrophobicity of myofibrillar proteins, and reduce the cooking loss and shear force of black pork, the hydrogen bond content of myofibrillar proteins and the gel whiteness compared with the control group (SC). The result of sodium dodecyl sulfate–polyacrylamide gel electrophoresis (SDS-PAGE) showed that the concentration of protein bands by VTC treatment was decreased obviously. In addition, the result of the scanning electron microscope (SEM) presented that tumbling and ultrasound treatment would destroy the structure of muscle fibers and make them loose and disordered. [ABSTRACT FROM AUTHOR]

Described herein is a facile one-pot strategy to synthesize N-doped graphitic carbon-incorporated g-C 3 N 4 by adding slight amount of citric acid into urea as the precursor during thermal polymerization. The obtained materials retained the original framework of g-C 3 N 4 and show remarkably enhanced visible light harvesting and promoted photo-excited charge carrier separation and transfer. The high-resolution N 1s spectrum of XPS showed a graphitic N peak, which could be attributed to N-doped graphitic carbon. In addition to the common-recognized light harvesting enhancement and charge carrier recombination inhibition, the incorporation of N-doped graphitic carbon into the planar framework of g-C 3 N 4 is suggested to result in extended and delocalized π-conjugated system of this copolymer, thus greatly elevating the photocatalytic performance for H 2 evolution by water splitting under visible light. The H 2 evolution rate on N-doped graphitic carbon-incorporated g-C 3 N 4 reached 64 μmol h −1 , which is almost 4.3 times the rate on pure g-C 3 N 4 . This approach may provide a promising route for rational design of high performance, cost-effective and metal-free photocatalysts. [ABSTRACT FROM AUTHOR]

A series of experiments were performed to investigate the relationship between syngas composition (H 2 /CO/CO 2 /N 2 /O 2 ) and NO formation. Laser-saturated fluorescence measurements of NO in a premixed syngas flat flame from a heat flux burner were recorded for various fuel compositions, dilution ratios and equivalence ratios. Quantitative measurements were compared with the predictions from CHEMKIN software using four different chemical mechanisms, i.e., GRI mech 3.0, Chemical Reaction Engineering and Chemical Kinetics 1407, GDF-Kin 3.0, and the Mendiara and Glarborg mechanism; each mechanism included reaction subsets for NO x formation. These models were validated against a CH 4 flame; the GDF-Kin 3.0 mechanism produced the best agreement with measurements. NO measurements for CO/H 2 syngas fuel with 50% CO 2 dilution at various equivalence ratios found the maximum NO production near stoichiometry. The majority of NO produced for these conditions is predicted to come from the combination of the NNH and N 2 O pathways. Investigation of NO production during combustion of different CO/H 2 ratio syngas diluted with 60% N 2 showed that increasing the H 2 fraction decreased the total NO concentration. However, normalizing the NO production rate by the fuel mass consumption rate showed H 2 produces more NO per gram of fuel consumed. Predictions of temperature and NO rate of production along the flame axis showed that the syngas with high H 2 content had a flame front closer to the burner exit and NO production rate greater than the high CO case. Dilution of CO/H 2 syngas fuel with N 2 and CO 2 showed that CO 2 has a stronger reduction in NO emission than N 2 . GDF-Kin 3.0 predicted that dilution with CO 2 caused a greater reduction in flame temperature than the same volume of N 2 . Predicted NO rate of production and reaction sensitivity analysis predicted that the Zel’dovich pathway was dominant for undiluted syngas. However, as the flame temperature reduced, the Zel’dovich pathway was inhibited to a greater extent than the N 2 O and NNH pathways so that, at high dilution, NO production was driven by the N 2 O and NNH pathways. [ABSTRACT FROM AUTHOR]

Impaired glucose uptake is involved in Alzheimer’s disease (AD) and glucose transporter 3 (Glut3) is the major neuronal glucose transporter. Estrogens contribute its theorized protective role against AD. The present studies aimed to examine the effect of 17β-estradiol (E2, the natural estrogen) on Glut3 expression and the underlying mechanisms by using human SH-SY5Y cell line. The results demonstrated that E2 increased Glut3 expression. E2 could stimulate the activation of Akt signaling pathway and the subsequent phosphorylation of cAMP response element binding protein (CREB). Akt/CREB pathway mediated E2-induced increase in Glut3 expression. These results suggested the mechanisms underlying E2-induced increase in Glut3 expression in human SH-SY5Y cell line and might provide the new data for elucidating the neuroprotective role of E2 against AD. [ABSTRACT FROM AUTHOR]

• Designing tumor microenvironment-responsive and sono-responsive two-dimensional heterojunction nanostructure. • Achieving chemoreactive and sonocatalytic cancer nanotherapy triggered by tumor microenvironment and ultrasound. • Superior performance of anti-tumor effect with high biosafety enabled by chemoreactive and sonocatalytic nanotherapy. Ultrasound (US)-activated sonodynamic therapy (SDT) has been extensively explored as an effective therapeutic modality for cancer treatment due to its noninvasiveness, physical targeting and deep tissue penetration. However, the inorganic semiconductor sonosensitizer-enabled SDT still suffers from the low therapeutic efficacy because of tumor hypoxia and low separation efficiency of electrons (e−) and holes (h+) from the energy-band structure of these inorganic sonosensitizers. Herein, the two-dimensional (2D) TiO 2 @MnO 2-x heterojunction nanostructure was rationally designed and engineered for simultaneously modulating the tumor hypoxic microenvironment and augmenting the therapeutic efficacy of SDT against tumor. The MnO 2-x component was heterogeneously grown onto the surface of initially synthesized 2D TiO 2 nanosheets (NSs), which not only acted as the catalysts for converting tumor-overexpressed hydrogen peroxide into oxygen and subsequently modulating the tumor hypoxia, but also catalyzed the Fenton reaction for the production of hydroxyl radicals. The heterojunction design of TiO 2 @MnO 2-x nanostructure effectively augmented the SDT efficacy of TiO 2 -based sonosensitizers under ultrasound activation by facilitating the separation of e−/h+ pairs. The simultaneously endowed tumor-hypoxia alleviation and synergistic sono/chemodynamic tumor nanotherapy achieved the high tumor cell-killing effect and tumor-suppression efficiency, as systematically demonstrated both in vitro and in vivo. This work provides a distinct paradigm of the heterojunction semiconductor nanostructure design for improving the ultrasound-based nanotherapy and achieving high tumor-treatment efficacy. [ABSTRACT FROM AUTHOR]

Abstract: Hepatic stellate cell (HSC) activation is a key cellular event in the development of liver fibrosis. Peroxisome proliferator-activated receptor-γ (PPARγ) has been shown to function as a key transcription regulator linked to suppressing HSC activation. Compelling evidence indicates that leptin plays a unique role in the development of liver fibrosis. The aim of this study is to investigate the in vivo impact of leptin on PPARγ expression in HSCs in the model of TAA-induced liver damage. The results of the present study provide the first in vivo evidence that leptin might exert an inhibitory effect on PPARγ protein expression in HSCs, which is mediated at least through leptin-induced ERK1/2 activation. Long-form leptin receptor is involved in leptin-induced ERK1/2 activation and the subsequent decline in PPARγ expression in HSCs in the model. Furthermore, the inhibitory effect of leptin on PPARγ protein expression enhances HSC activation and proliferation in this model. The in vivo findings from this report might provide additional insights into the mechanisms underlying the profibrogenic action of leptin in liver. [Copyright &y& Elsevier]

Abstract: Aims: Hepatic stellate cell (HSC) activation is a key step in the hepatic fibrogenic process. Increasing evidence demonstrates the pro-fibrogenic action of leptin in rodent liver. Peroxisome proliferator-activated receptor-γ (PPARγ) is a potential molecular target for inhibition of HSC activation. Our previous study suggested that leptin markedly down-regulated PPARγ gene expression in HSCs. The aim of this study is to explore the molecular mechanisms underlying the inhibitory effect of leptin on PPARγ expression in rat HSCs in vitro. Main methods: The effects of leptin on the expression and trans-activation activity of early growth response-1 (Egr-1) are examined by using real-time PCR, Western blotting analysis, transient transfection, and electrophoretic mobility shift assay. The role of Egr-1 in PPARγ gene expression is demonstrated by co-transfection approach, Western blotting analysis and real-time PCR. Key findings: We document that leptin increases Egr-1 expression at protein and mRNA levels, and significantly stimulates Egr-1 trans-activation activity. Moreover, leptin induces the expression and activity of Egr-1 through activation of extracellular signal-regulated kinase (ERK) or phosphatidylinositol 3-kinase/AKT signaling (PI-3K/AKT) pathway. Further investigation reveals that Egr-1 exerts a clear inhibitory effect on the promoter activity and expression of PPARγ gene and demonstrates that Egr-1 increases the expression of HSC activation markers and promotes HSC growth. Taken together, these findings suggest that Egr-1 is involved in the inhibitory effect of leptin on PPARγ expression in rat HSCs in vitro. Significance: Our results provide novel insights into the mechanisms of leptin-induced inhibition of PPARγ expression in HSCs in vitro. [Copyright &y& Elsevier]

The active polyphenol curcumin demonstrates therapeutic effects against various different diseases. Researches revealed the inhibitory roles of curcumin in hepatic stellate cell (HSC) activation and fibrogenesis. HSC activation, a key step in liver fibrogenesis, requires the remodeling of DNA methylation, which is associated with methionine adenosyltransferase II (MATII) composed of catalytic subunit MAT2A and regulatory subunit MAT2B. MATII is essential for HSC activation in vitro. The present researches aimed to investigate the effect of curcumin on MAT2B expression in HSCs in vivo and in vitro. Results demonstrated that curcumin could reduce MAT2B expression in HSCs at multiple levels. The activation of p38 MAPK pathway promoted MAT2B expression in HSCs. The effect of curcumin on MAT2B was through its interruption of p38 MAPK signaling pathway. Knockdown of MAT2B inhibited HSC activation and reduced collagen level in the model of liver fibrosis. Curcumin down-regulation of MAT2B contributed to the inhibitory role of curcumin on HSC activation and collagen expression in mouse livers. This study provided evidences for the effect of curcumin on the expression of MAT2B, an enzyme for the biosynthesis of methyl donor S-adenosylmethionine, in HSCs and demonstrated the function significance of curcumin-induced downregulation of MAT2B in curcumin inhibition of liver fibrosis. • Curcumin reduces MAT2B expression in HSCs in vivo and in vitro. • p38 MAPK pathway involves MAT2B expression. • The effect of curcumin on MAT2B is through interrupting p38 MAPK signaling. • Knockdown of MAT2B reduces HSC activation and collagen level. • Curcumin-induced downregulation of MAT2B contributes to its inhibiting liver fibrosis. [ABSTRACT FROM AUTHOR]

• Fe-leaching induces surface reconstruction of Ni-Fe alloy/NC during OER. • Fe-leaching during OER benefits the exposure of more active sites. • The high valent Ni, pyridinic N and metal-N species are the exact active centers. • The fully activated catalyst exhibits excellent OER activity. Understanding the dynamic transformation process of the oxygen evolution reaction (OER) catalysts is of importance for their rational design. Here we first report that Fe-leaching could induce the electrochemical activation of strongly coupled Ni-Fe alloy on N-doped carbon composites to boost the OER performance. It is demonstrated that the leaching of unstable FeOOH mixed layer from the surface of FeNi 3 alloy is responsible for the surface reconstruction and exposure of more active sites. Furthermore, the N-doped carbon, FeNi 3 alloy, together with the accompanying generation of Fe-doped Ni(OH) 2 , synergistically promote the OER activity after fully activation. It is also verified that the high valent Ni species, pyridinic N and the metal-N species are the exact active centers and the fully activated catalyst Fe 0.2 Ni 0.8 /NC-600-a is among the best non-noble OER catalysts to date, which exhibits superior OER performance with a low overpotential (η 20 = 290 mV) and small Tafel slope (76 mV dec−1). This study is helpful to understand the fundamentals of the Ni-Fe alloy catalysts and provides guidance to design advanced catalysts for water oxidation through in-situ electrochemical activation. [ABSTRACT FROM AUTHOR]

• BC/ZnO nanocomposite strengthens paper and improves aging resistance. • The nanocomposite imparts antifungal properties to paper. • The nanocomposite helps in deacidification of paper. Paper, commonly used as an information carrier, can become acidified and brittle over time. In this study, 0.3 % bacterial cellulose (BC) composite with 1.0% zinc oxide (ZnO) nanoparticles was prepared and used to coat brittle book paper for deacidification and consolidation. The BC/ZnO nanocomposite was characterized using zeta potential, micro morphology, elemental mapping, X-ray photoelectron spectra, Fourier transform infrared, and thermogravimetric analyses. The results indicated that the composite exhibited good stability. ZnO nanoparticles were bonded to the hydroxyl groups on BC, enhancing the thermal stability of BC. The composite was uniformly sprayed on the paper surface, and the mechanical properties, color difference, readability, pH, and micromorphology of the paper samples were examined before and after the treatment. The BC/ZnO nanocomposite exhibited good deacidification and consolidation effects on paper samples with low impact on the original paper appearance. Moreover, the BC/ZnO nanocomposite showed a good inhibitory effect on fungi growth on paper. [ABSTRACT FROM AUTHOR]

Epigenetic reader Bromodomain protein 4 (BrD4) functions as a global genomic regulator to direct hepatic stellate cell (HSC) activation (a key step in liver fibrogenesis) and liver fibrosis. The pivotal pro-fibrotic cytokine transforming growth factor-β1 (TGFβ1) signals through both Smad and Stat3 to elicit a wide array of biological effects. Stat3 is widely acknowledged as a regulator of gene transcription and is involved in fibrosis of multiple tissues. The present study focused on BrD4 function implication in the roles of TGFβ1-induced Stat3 signaling in HSC activation and liver fibrosis by using heterozygous TGFβ1 knockout mice and HSC culture. Results showed that Stat3 was required for TGFβ1-induced BrD4 expression in HSCs. BrD4 expression paralleled Stat3 activation in activated HSCs in human cirrhotic livers. BrD4 was involved in the roles of TGFβ1-induced Stat3 in HSC activation and liver fibrogenesis. Smad3 bound to phosphorylated-Stat3 and contributed to TGFβ1-induced Stat3 signaling. BrD4 expression induced by Stat3 signaling required the early-immediate gene Egr1. Egr1 had a positive feedback on Stat3 activation. In conclusion, a network consisting of Stat3 signaling, Smad3 signaling, Egr1, and BrD4 was involved in the effects of TGFβ1 on liver fibrosis, providing new toxicological mechanisms for TGFβ1 in liver fibrogenesis. [Display omitted] • Stat3 signaling mediates TGFβ1-induced BrD4 expression in HSCs. • Stat3 signaling required BrD4 for promoting HSC activation and liver fibrosis. • TGFβ1-stimulated Stat3 signaling promotes BrD4 expression by Egr1. • TGFβ1-induced Stat3 signaling cross-talks with Smad3 signaling in HSCs. • Egr1 had a positive feedback on Stat3 activation in HSCs. [ABSTRACT FROM AUTHOR]

A large amount of granular protrusions overlie the outer cell wall surfaces in both elongating and non-elongating stipe regions but overlie the inner cell wall surfaces only in non-elongating stipe regions. Removal of granular protrusions using alkali, amorphous materials overlying on both the inner and outer cell wall surfaces were explored in the non-elongating stipe regions. β-1,3-Glucanase treatment not only removed above those granular protrusions and underlying amorphous materials on the wall surfaces but also removed wall matrices embedding chitin microfibrils on the cell walls of most stipe regions, except for the outer cell wall surfaces of the non-elongating stipe regions where most of the wall matrices remained. The chitin microfibrils were closely and transversely arranged on both the inner and outer cell wall surfaces in the elongating apical stipe region, whereas they were loosely and transversely arranged on the inner cell wall surfaces and further became sparser and even randomly arranged on the outer cell wall surface in the non-elongating stipe regions. We propose that the surface deposition of granular protrusions and amorphous materials and the change of microfibril architecture and wall matrices may cause loss of wall plasticity and cessation of stipe elongation. [ABSTRACT FROM AUTHOR]

Abstract: Peptidoglycan recognition proteins (PGRPs) are secreted innate immunity pattern recognition molecules. In this study, a new peptidoglycan recognition protein 1 named cnPGRP1 was isolated from an antler base of sika deer Cervus nippon. The antler base antimicrobial proteins (AAP) were subjected to consecutive chromatographic methods connected to Sephadex G-25 gel filtration column (CM) anion-exchange column, and RP-HPLC. The molecular weight of cnPGRP1 was 17.2kDa under SDS-PAGE, and peptide mass fingerprint analysis by MALDI-TOF-MS as peptidoglycan recognition protein 1 matched to Dasypus novemcinctus. The matched amino acids sequences were RLYEIIQKWPHYRA. Both Gram-positive and Gram-negative bacteria can be killed by cnPGRP1 in the 50–250μg/mL range through in vitro. Furthermore, cnPGRP1 has been found to bind Gram-positive bacteria, Gram-negative bacteria, and even fungus. [Copyright &y& Elsevier]

Photothermal membrane distillation (PMD) achieves localized temperature increase by absorbing and converting light energy to drive evaporation and phase change processes. It is expected to solve the challenges of low energy conversion efficiency and fouling of traditional membrane distillation (MD). A dual-structured photothermal composite membrane was constructed by oxidatively polymerizing photothermal functional materials on an electrospinning substrate membrane. The superhydrophobic Polytetrafluoroethylene/Polyimide (PTFE/PI) substrate membranes offer a spacious pore structure and excellent mechanical properties with low mass transfer resistance and low heat loss. The presence of the densely connected region of the Polyaniline (PANI) in the photothermal layer accelerates the local photothermal conversion. The porous structure formed by interconnecting fibers loaded with PANI is conducive to the repeated refraction of light beams and thus enhances the absorption of light energy. Under 1 kW·m−2 light intensity, the permeate flux of the PTFE/PI-PI/PANI membrane is stable at 1.44 ± 0.02 L·m−2·h−1 within 480 h PMD. With the outstanding salt rejection performance of 99.99 % and high photothermal conversion efficiency of 90.3 %, the photothermal membrane can be applied in areas where fresh water and fuel resources are scarce but solar energy resources are abundant. [Display omitted] • The superhydrophobic layer prevents membrane wetting for durable PMD operation. • The hydrophilic photothermal layer mitigates the temperature polarization effect. • The dual heating mode of composite membrane boots the mass transfer driving force. • The overall porous structure expands efficient water vapor transmission channels. [ABSTRACT FROM AUTHOR]

Abstract: The second-order distorted wave Born approximation (DWBA) method is employed to investigate the triple differential cross sections (TDCS) of coplanar doubly symmetric collisions for alkali target sodium at excess energies of 6–60 eV. Comparing with the first-order DWBA calculations, the inclusion of second-order Born term in the scattering amplitude improves the degree of agreement with experiments, especially for backward scattering region of TDCS. This indicates the present second-order Born term is capable to give a reasonable correction to DWBA model in studying coplanar symmetric problems in low and intermediate energy range. [Copyright &y& Elsevier]

Liver fibrosis is characterized by the excessive deposition of extracellular matrix in liver. Chronic liver injury induces the activation of hepatic stellate cell (HSCs), a key step in liver fibrogenesis. The activated HSC is the primary source of ECM and contributes significantly to liver fibrosis. TGFβ1 is the most potent pro-fibrotic cytokine. Bromodomain protein 4 (BrD4), an epigenetic reader of histone acetylation marks, was crucial for profibrotic gene expression in HSCs. The present study aimed to investigate the roles of BRD4 in TGFβ1-dependent HSC activation and liver fibrosis, focusing on TGFβ1-induced alterations of the levels of the fibrotic-related important proteins in HSCs by employing the heterozygous TGFβ1 knockout mice and BrD4 knockdown in vivo and in vitro. Results revealed that BrD4 protein level was significantly upregulated by TGFβ1 and BrD4 knockdown reduced TGFβ1-induced HSC activation and liver fibrosis. BrD4 was required for the influences of TGFβ1 on PDGFβ receptor and on the pathways of Smad3, Stat3, and Akt. BrD4 also mediated TGFβ1-induced increases in histone acetyltransferase p300, the pivotal pro-inflammatory NFkB p65, and tissue inhibitor of metalloproteinase 1 whereas BrD4 reduced Caspase-3 protein levels in HSCs during liver injury, independent of TGFβ1. Further experiments indicated the interaction between TGFβ1-induced BrD4 and NFkB p65 in HSCs and in liver of TAA-induced liver injury. Human cirrhotic livers were demonstrated a parallel increase in the protein levels of BrD4 and NFkB p65 in HSCs. This study revealed that BrD4 was a key molecular driver of TGFβ1-induced HSC activation and liver fibrosis. • TGFβ1 upregulates BrD4 in HSCs, contributing to TGFβ1-induced liver fibrosis. • BrD4 is involved in effects of TGFβ1 on PDGFβ receptor and the important signaling pathways associated with liver fibrosis. • BrD4 mediates TGFβ1-induced increases in p300, NFkB p65, and TIMP1 in HSCs. • BrD4 interacts with NFkB p65 in HSCs and both is parallel increased in HSCs of human cirrhotic livers. [ABSTRACT FROM AUTHOR]

• HOTAIR expression was increased in cholangiocarcinoma. • HOTAIR deletion inhibited cholangiocarcinoma progression. • HOTAIR upregulated HMGB1 expression by sponging miR-204-5p. • HOTAIR promoted cholangiocarcinoma progression via miR-204-5p/HMGB1 axis. Cholangiocarcinoma (CCA) is a malignant tumor in the world. LncRNA HOX transcript antisense intergenic RNA (HOTAIR) was identified as a crucial regulator in various cancers including CCA. This study aimed to unravel the functions of HOTAIR and its biological mechanism in CCA, hinting for the new therapeutic targets in CCA. The levels of HOTAIR, miR-204-5p and HMGB1 in CCA tissues and cell lines (HuB28 and HuCCT1) were measured by quantitative real-time polymerase chain reaction (qRT-PCR). Western blot was conducted to detect the protein levels of LC3-I, LC3-II, Beclin-1 and HMGB1. The relationships among HOTAIR, miR-204-5p and HMGB1 were examined by dual-luciferase reporter assay, RNA immunoprecipitation (RIP) assay and RNA pull down assay. Cell proliferation ability and apoptosis rate were assessed by CCK8 assay and flow cytometry, respectively. in vivo experiment was conducted to examine the bio-functions of HOTAIR in nude mice. HOTAIR and HMGB1 were over-expressed, while miR-204-5p was lowly expressed in CCA tissues and cells. The dual-luciferase reporter assay indicated that miR-204-5p was a target of HOTAIR, and HMGB1 was a target of miR-204-5p. The restoration experiments showed that HOTAIR repressed cell apoptosis, autophagy and promoted cell proliferation via miR-204-5p/HMGB1 axis. Additionally, HOTAIR silencing retarded the xenograft tumor growth by up-regulation of miR-204-5p and down-regulation of HMGB1. These data unraveled that lncRNA HOTAIR regulated HMGB1 to suppress cell apoptosis, autophagy and induce cell proliferation by sponging miR-204-5p in CCA. Thus, this new regulatory pathway may provide new therapeutic targets for CCA. [ABSTRACT FROM AUTHOR]

Obese patients usually have hyperleptinemia and are prone to develop liver fibrosis. Leptin is intimately linked to liver fibrogenesis, a multi-receptor-driven disease. Gα-Interacting Vesicle-associated protein (GIV) functions as a multimodular signal transducer and a guanine nucleotide exchange factor for Gi controling key signalings downstream of diverse receptors. This study aimed to examine the roles of GIV in leptin-caused liver fibrosis and employed the culture-activated hepatic stellate cells (HSCs) and leptin-deficient mice, respectively. Results indicated that leptin upregulated GIV expression in HSCs. GIV was involved in leptin-induced HSC activation and liver fibrosis. GIV mediated leptin regulation of TIMP1, MMP9, PDGFβ receptor and TGFβ receptor and was required for leptin stimulating the pathways of Erk1/2, Akt1, and Smad3. GIV was also a mediator for leptin-regulation of Cyclin D1 and Caspase-3 activity but GIV reduced Caspase-3 level independently of leptin in vivo. Erk1/2 signaling, Egr1 and c-Jun were associated with the effect of leptin on GIV expression in HSCs. Leptin-induced Erk1/2 signaling increased Egr1 and p-c-Jun levels and promoted their binding to GIV promoter at the sites between −190 bp and −180 bp and between −382 bp and − 376 bp, respectively. Egr1 knockdown lessened leptin-upregulation of GIV in vitro and in vivo. In human cirrhotic livers, the increase in GIV protein level parallelled with the elevated p-Erk1/2 and Egr1 levels in HSCs. In summary, the unusual signal transducer GIV was identified as an important mediator in leptin-induced liver fibrosis. GIV may have significant implications in liver fibrosis progression of obese patients with hyperleptinaemia. • GIV is involved in leptin-induced HSC activation and liver fibrosis. • Leptin requires GIV for influencing multiple molecules associated with fibrosis. • Leptin-induced Erk1/2 pathway increases Egr1 and p-c-Jun which bind GIV promoter. • Egr1 knockdown lessens leptin-upregulation of GIV in HSCs. • The levels of GIV, p-Erk1/2, and Egr1 increase parallelly in the cirrhotic liver. [ABSTRACT FROM AUTHOR]

Laxiflorin B is a natural ent -kaurane diterpenoid that can be isolated from the leaves of the Isodon eriocalyx var. laxiflora , a perennial shrub native to parts of China. While this compound has potent cytotoxic activity against various tumor cells, the anti-tumor targets and molecular mechanisms of Laxiflorin B are unclear. Here, we show that Laxiflorin B exhibits strong antiproliferative and proapoptotic effects on triple-negative breast cancer (TNBC) cells. At the mechanistic level, we show that β-tubulin (TUBB) is a cellular target of Laxiflorin B. By covalently binding the Cys239 and C354 residues of the TUBB colchicine-binding site, Laxiflorin B disturbs microtubule integrity and structure in vitro and in vivo. Cytotoxicity analyses also showed that the α, β-unsaturated carbonyl in the D ring of Laxiflorin B is responsible for mediating its covalent binding and anti-tumor activity. To assess the therapeutic effects of Laxiflorin B, we synthesized a Laxiflorin B-ALA pro-drug and delivered it by intraperitoneal injection (10 mg/kg) into a 4T1 orthotopic tumor mouse model. Drug treatment had anti-tumor effects without inducing notable weight loss or organ dysfunction. We conclude that Laxiflorin B is a promising colchicine binding site inhibitor that might be exploited in the context of TNBC treatment in the future. • Laxiflorin B, a natural compound from Isodon eriocalyx var. laxiflora , which can inhibit the growth of TNBC cells and promote cell apoptosis. • Laxiflorin B exerts an anti-TNBC effect by covalently targeting colchicine-sites and interfering with the microtubule dynamics of tumor cells. • Laxiflorin B, as a new tubulin inhibitor, shows remarkable effects in inhibiting tumor proliferation in the in-situ mouse model. [ABSTRACT FROM AUTHOR]

The photocatalytic activity enhancement of graphitic carbon nitride (g-C 3 N 4 ) in water splitting were commonly achieved by introducing various functional groups onto/into its planar structure. Herein, oxidized g-C 3 N 4 (CNO) was prepared via an extremely facile K 2 CO 3 activation approach. The high-resolution XPS spectra and solid-state 13 C NMR spectra confirmed the successful introduction of O-containing groups and O atoms were inherited the original molecular framework of g-C 3 N 4 , but exhibited effectively enlarged bonded with C atoms rather than N atoms in the tri-s-triazine structure of g-C 3 N 4 . CNO inherited the original molecular framework of g-C 3 N 4 , but exhibited effectively enlarged surface area and enhanced visible light absorption, and more attrractively, the band structure of g-C 3 N 4 could be well-tuned with the introduction of oxygen species. Importantly, the surface O-containing moieties could strongly interact with cocatalyst Pt and thus remarkably promote interfacial electron transfer and consequent photo-generated charge carrier separation. Consequently, the as-obtained CNO exhibited the remarkably enhanced photocatalytic performance with a H 2 evolution rate of 199.7 μmol h −1 , which is 9 times that of g-C 3 N 4 (22.2 μmol h −1 ). [ABSTRACT FROM AUTHOR]

Aims Peroxisome-proliferator activated receptor γ (PPARγ) plays a pivotal role in inhibition of hepatic stellate cell (HSC) activation, a key step for liver fibrogenesis. Adipocyte-derived hormone leptin has been shown to promote liver fibrosis in murine and human. PPARγ includes two subtypes, PPARγ1 and PPARγ2. Our previous study indicated that leptin down-regulated PPARγ1 expression in HSCs. The aim of this study was to investigate the effect of leptin on PPARγ2 expression and the underlying mechanisms in HSCs. Main methods Real-time PCR and western blot analyses were used to examine gene expression. The promoter activities were detected by luciferase assay. Key findings Leptin reduced PPARγ2 expressions at promoter level, mRNA level, and protein level in HSCs, which required β-catenin, p38 mitogen-activated protein kinase, and delta-like homolog1 (DLK1) signaling pathways. Leptin induced GATA binding protein 2 (GATA2) expression through DLK1 pathway and GATA2 reduced PPARγ2 expression. Ectopic expression of PPARγ2 reduced the protein levels of α-smooth muscle actin and α1(I)collagen in HSCs. Significance Since obese patients, often accompanied by hyperleptinemia, are more prone to liver fibrosis, the data from this study might have potential implications for clarifying the mechanisms for liver fibrogenesis in obese patients with hyperleptinemia. [ABSTRACT FROM AUTHOR]

Obese patients, often accompanied by hyperleptinemia, are more likely to develop liver fibrosis. Leptin, an adipocyte-derived hormone, augments inflammatory in liver and promotes hepatic stellate cell (HSC) activation (a key step for liver fibrogenesis) and liver fibrosis. microRNA-122 (miR-122) is the most abundant liver-specific miRNA and can attenuate liver fibrosis. This study examined the effect of leptin on miR-122 level in HSCs in vivo and in vitro . Results demonstrated that leptin reduced the levels of both miR-122 (mature miR-122) and primary miR-122 (pri-miR-122). The effects of leptin on the levels of miR-122 and pri-miR-122 were through at least hedgehog pathway. Leptin-induced decrease in sterol regulatory element-binding protein-1c (SREBP-1c) has been shown to contribute to leptin-induced HSC activation. We revealed a mutual promotional effect between SREBP-1c and miR-122. Further experiments indicated that miR-122 inhibited leptin-induced liver fibrosis in leptin-deficient mouse model. These data have potential implications for clarifying the mechanisms of hepatic fibrogenesis associated with elevated leptin level in human such as obese patients [ABSTRACT FROM AUTHOR]

Organo-lead perovskite materials as light harvesters have represented a hot field of research on high-efficiency perovskite solar cells. In such cells, the quality of organo-lead perovskite films is most critial to device performance, essentially affected by varying halide composition. Meanwhile, the understanding of formation mechanisms and basic properties of these hybrid perovskites is still ongoing. Herein, we report a one-step solution-processing strategy to investigate the role of precursor in the context of hybrid perovskites, in which the molar ratio of the methylammonium compound and lead salts is closely correlated to the characteristics of the hybrid perovskite films. We investigate the molar ratio dependence of the mixed-halides incorporation of three organolead trihalide perovskite absorbers, CH 3 NH 3 PbI 3−a Br a , CH 3 NH 3 PbI 3−a Cl a and CH 3 NH 3 PbBr 3−a Cl a , and compare them with three pure (CH 3 NH 3 PbI 3 , CH 3 NH 3 PbBr 3 , and CH 3 NH 3 PbCl 3 ) perovskites. We find the versatility of the hybrid perovskites affected by excess organic compounds. Specifically, the synergistic effect of the mixed-halides in tuning perovskite composition demonstrated that the different perovskite compositions deserved more in-depth understanding from with the varying of the crystal transformation, morphological framework, thermal decomposition and optical performance of the hybrid perovskites. Moreover, this work provides visual evidence for the design of the mixed halide perovskites based on these hybrids, which paves a way for improvements with selective properties in lead halide perovskite-based devices. [ABSTRACT FROM AUTHOR]

A novel MnO 2 /g-C 3 N 4 heterojunction composite was synthesized via a simple in-situ redox reaction between KMnO 4 and MnSO 4 ·H 2 O adsorbed on the surface of g-C 3 N 4 for the first time. MnO 2 featuring 2D δ-phase layered structure was intimately attached onto the surface of g-C 3 N 4 layers via C O bonding. Notably, the synthesized MnO 2 /g-C 3 N 4 photocatalyst showed substantially enhanced photocatalytic activity in the reduction of CO 2 than pure g-C 3 N 4 and MnO 2 . The highest CO production amount of 9.6 μmol g −1 has been obtained at an optimized loading amount of MnO 2 under 1 h irradiation of a 300 W Xe lamp. The incorporation of narrow band gap MnO 2 on the surface of g-C 3 N 4 enhanced its light harvesting ability. And the solid hetero-interface between MnO 2 and g-C 3 N 4 together with their well matched band structure was favorable for the separation of photo-induced carriers, consequently enhanced its photocatalytic activity. This novel 2D-2D MnO 2 /g-C 3 N 4 heterostructure is expected to have great potentials in CO 2 photoreduction. [ABSTRACT FROM AUTHOR]

The economic value of haskap is low because of low utilization caused by factors such as harvesting, storage and transportation, and the sour taste. However, its value can be increased by extraction due to its large content of anthocyanins. This study helped to extract haskap by using cold plasma as pretreatment at different power (0, 100, 200, 300 W) in terms of extraction yield, monomer composition, and antioxidant capacity. It was shown that cold plasma pretreatment (CPP) degraded the cell wall components of haskap, increased its surface roughness, enhanced its hydrophilicity, improved its hydration properties, and modified its enzymatic activity. CPP significantly increased the extraction rate of anthocyanins (13.35‐20.47%), promoted the number of anthocyanin monomers, and enhanced the antioxidant activity of the extracts. These results suggest that CPP can successfully facilitate the extraction of anthocyanins and is a promising technology to add value to haskap for functional foods and nutritional products. Industrial relevance: Haskap is a good source of anthocyanins, however, conventional methods of anthocyanin extraction usually require the use of large amounts of organic solvents and are time-consuming. Cold plasma pretreatment can not only help reduce chemical pollution to the environment and improve the utilization of haskap, but also convert it into functional and nutritional food ingredients with value-added properties in a more efficient way. • A CPP method was developed for anthocyanin extraction from haskap. • The cellular structure and properties of haskap are altered by CPP. • The extraction yield of anthocyanin extracts was enhanced by CPP. • The extracts had a higher antioxidant capacity by CPP. • Extraction of anthocyanin species were promoted by CPP. [ABSTRACT FROM AUTHOR]

Leptin, an adipocyte-derived hormone, promotes liver fibrogenesis and inhibits the expression of peroxisome-proliferator activated receptor γ (PPARγ), a key transcription factor in inhibition of hepatic stellate cell (HSC) activation, in HSCs. This research aimed to further investigate the mechanisms underlying leptin regulation of PPARγ1 in HSCs in vivo and in vitro. Results demonstrated that sex-determining region Y-box 9 (Sox9) could bind to a site around − 2275 within leptin response region of PPARγ1 promoter and inhibited PPARγ1 expression. Sox9 upregulated the expressions of α1(I)collagen and alpha-smooth muscle actin in HSCs. Leptin stimulated Sox9 expression and Sox9 binding to PPARγ1 promoter. The signaling pathways of NADPH oxidase, β-catenin, and delta-like homolog1 (DLK1) mediated leptin upregulation of Sox9 expression. Moreover, there existed crosstalk between NADPH oxidase pathway and β-catenin or DLK1 signaling pathway. Human liver specimens of cirrhosis were shown to be of a large number of the positive HSCs for p47phox (playing a central role in NADPH oxidase activity), 4-hydroxynonenal (a lipid peroxidation product), Sox9, and α-smooth muscle actin whereas PPARγ-positive HSCs were rarely detected. These results might deepen understanding of the molecular mechanisms for leptin inhibition of PPARγ1 expression in HSCs and for the liver fibrosis associated with leptin. [ABSTRACT FROM AUTHOR]

Heme oxidation and loss of soluble guanylate cyclase (sGC) is thought to be an important contributor to the development of cardiovascular diseases. Nevertheless, it remains unknown why the heme loses readily in oxidized sGC. In the current study, the conformational change of sGC upon heme oxidation by ODQ was studied based on the fluorescence resonance energy transfer (FRET) between the heme and a fluorophore fluorescein arsenical helix binder (FlAsH-EDT 2 ) labeled at different domains of sGC β1. This study provides an opportunity to monitor the domain movement of sGC relative to the heme. The results indicated that heme oxidation by ODQ in truncated sCC induced the heme-associated αF helix moving away from the heme, the Per/Arnt/Sim domain (PAS) domain moving closer to the heme, but led the helical domain going further from the heme. We proposed that the synergistic effect of these conformational changes of the discrete region upon heme oxidation forces the heme pocket open, and subsequent heme loss readily. Furthermore, the kinetic studies suggested that the heme oxidation was a fast process and the conformational change was a relatively slow process. The kinetics of heme loss from oxidized sGC was monitored by a new method based on the heme group de-quenching the fluorescence of FlAsH-EDT 2 . [ABSTRACT FROM AUTHOR]

The modification of graphitic carbon nitride (g-C 3 N 4 ) for visible-light photocatalytic water splitting is a very hot topic due to the more and more serious energy and environment problems. Here we report a novel, general and cost-effective approach via Schiff base chemistry to construct aromatics-grafted g-C 3 N 4 -based copolymers. Based on this general strategy, almost all kinds of aromatics can be grafted into carbon nitride networks. As-synthesized copolymers all show remarkably enhanced and stable visible-light photocatalytic hydrogen evolution performance. In addition, the low cost and small optimized adding amounts of these co-monomers adopted here make the present strategy probably the one of most cost-effective copolymerization approach to construct g-C 3 N 4 -based copolymer photocatalysts. [ABSTRACT FROM AUTHOR]

The ozone (O 3 ) decomposition in the pre-heat zone of flames can initiate and accelerate the chain-branching reactions. In the present study, formaldehyde (CH 2 O) was investigated by both experiment and simulation methods in methane/air laminar premixed flames under atmospheric conditions. The formaldehyde concentration profiles in the flames were measured with CH 2 O-PLIF. When 4500 ppm of ozone was added, the formaldehyde concentration in Bunsen type laminar flame was enhanced by 58.5% at fuel-rich condition ( ϕ = 1.4) and 15.5% at stoichiometric condition. In the simulation work, the most recent ozone sub-mechanism was coupled with GRI-mech 3.0 kinetic mechanism. It showed that with 4500 ppm ozone addition, the formaldehyde concentration was enhanced by about 48.1% at rich condition ( ϕ = 1.4) and about 14.7% in stoichiometric mixture. The simulation suggested an early production of CH 2 O with ozone addition, especially in rich conditions. These reactions occurred at relatively low temperature, around 500 K. In order to isolate these reactions from the flame, experiments with preheated unburned mixtures were carried out. A larger amount of formaldehyde was produced in the zone far from the flame as the preheating temperature was increased. It indicated that the combustion enhancement with ozone could be caused by the additional reactions of ozone at relatively low temperature. Simulations showed that methoxy radical (CH 3 O) is the key specie for production of formaldehyde at lower temperatures. Early in the pre-heat zone of the laminar flame, formaldehyde occurs via decomposition of CH 3 O while in the pre-heated gas mixture via reaction of CH 3 O with O 2 . Furthermore, the O 3 effect on turbulent flames was investigated showing a greater enhancement in formaldehyde signal than that in the laminar cases. This difference in formaldehyde signal enhancement could be attributed to the expansion of the preheat zone, due to turbulence. [ABSTRACT FROM AUTHOR]

Curcumin exerts an inhibitory effect on hepatic stellate cell (HSC) activation, a key step for liver fibrogenesis, and on liver fibrosis by up-regulation of peroxisome proliferator-activated receptor-γ (PPARγ) expression. PPARγ plays a crucial role in suppression of HSC activation. Peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) functions as a co-activator for PPARγ. Therefore, researches on the effect of curcumin on PGC-1α might contribute to understanding of the mechanisms underlying curcumin inhibition of HSC activation and liver fibrosis through PPARγ. The present study aimed to investigate the effect of curcumin on PGC-1α expression in HSCs in vitro and examine the underlying molecular mechanisms by western blot, reat-time PCR, and transfection. Our results showed that curcumin stimulation increased PGC-1α expression and the effects of curcumin on PGC-1α expression were correlated with the activation of adenosine monophosphate-activated protein kinase (AMPK). Curcumin increased superoxide dimutase-2 (SOD2) transcription and activity by AMPK/PGC-1α axis. Moreover, PGC-1α was demonstrated to inhibit α1(I) collagen (a marker for liver fibrosis) transcription in cultured HSCs. These results demonstrated the promotion effect of curcumin on PGC-1α expression through AMPK pathway, which led to the increases in PPARγ activity and in SOD-2 transcription and activity. These data might suggest a possible new explanation for the inhibitory effect of curcumin on HSC activation and on liver fibrogenesis. [ABSTRACT FROM AUTHOR]

Hepatic stellate cell (HSC) activation is a crucial step in the development of liver fibrosis. Peroxisome-proliferator activated receptor γ (PPARγ) exerts a key role in the inhibition of HSC activation. Leptin reduces PPARγ expression in HSCs and plays a unique role in promoting liver fibrosis. The present studies aimed to investigate the mechanisms underlying leptin regulation of PPARγ1 (a major subtype of PPARγ) in HSCs in vivo and in vitro. Results revealed a leptin response region in mouse PPARγ1 promoter and indicated that the region included a GATA binding protein binding site around position − 2323. GATA binding protein-2 (GATA-2) could bind to the site and inhibit PPARγ1 promoter activity in HSCs. Leptin induced GATA-2 expression in HSCs in vitro and in vivo. GATA-2 mediated leptin inhibition of PPARγ1 expression by its binding site in PPARγ1 promoter in HSCs and GATA-2 promoted HSC activation. Leptin upregulated GATA-2 expression through β-catenin and sonic hedgehog pathways in HSCs. Leptin-induced increase in GATA-2 was accompanied by the decrease in PPARγ expression in HSCs and by the increase in the activated HSC number and liver fibrosis in vivo. Our data might suggest a possible new explanation for the promotion effect of leptin on liver fibrogenesis. [ABSTRACT FROM AUTHOR]

Highlights: [•] The effect of high yield pulp (HYP) content on coated paper print quality was investigated. [•] The image quality from the two paper samples is related to the pressroom operations. [•] The coated paper containing HYP can have similar print quality. [Copyright &y& Elsevier]

Abstract: Hepatic stellate cell activation is a key cellular event in the development of liver fibrosis. Recently, Delta-like homolog 1 (DLK1) protein level has been shown to increase in HSC activation and serve as a new contributor to HSC activation and liver fibrosis. Curcumin, a natural yellow polyphenol, possesses therapeutic roles in many diseases including liver fibrosis and has long been used in traditional medicine. The present study was aimed to elucidate the effect of curcumin on DLK1 expression in HSCs in vitro and in vivo, which is still unknown. Our results demonstrated that curcumin reduced DLK1 expression in culture-activated HSCs and in rat model of liver fibrosis. The inhibitory effect of curcumin on DLK1 expression may be mediated in part by interruption of Shh signaling pathway, which contributes to the promotion effect of curcumin on the expression of PPAR-gamma, a key factor in inhibiting HSC activation. Our results in this study may reveal a new mechanisms through which curcumin exerts its inhibitory effect on HSC activation and liver fibrosis. [Copyright &y& Elsevier]

Abstract: Leptin, the adipocyte-derived hormone, plays an unique role in promoting liver fibrosis. Hepatic stellate cell (HSC) activation is the key step in liver fibrogenesis and sterol regulatory element binding protein-1c (SREBP-1c, a pivotal transcription factor for adipocyte differentiation) exerts a critical function in inhibition of HSC activation. Stat3 pathway is the main pathway induced by leptin and its role in liver fibrogenesis is controversial. Our previous results demonstrated the inhibitory effect of leptin on SREBP-1c expression in HSCs. The present study aimed to explore the role of Stat3 pathway in leptin-induced liver fibrogenesis in mouse model, focusing on examining the effect of leptin-induced Stat3 pathway on SREBP-1c expression in HSCs in vitro and in vivo. Results suggested that Stat3 pathway mediated the promotional role of leptin in liver fibrosis in mouse and was involved in leptin inhibition of SREBP-1c expression in HSCs. Leptin-induced Stat3 activation was, at least partially, ERK pathway-dependent in cultured HSCs and was correlated positively with β-catenin activity and negatively with liver X receptor α expression and activity which influenced SREBP-1c expression in HSCs. The decrease in SREBP-1c expression by leptin-induced Stat3 pathway led to the increase in the marker for HSC activation and in α1(I) collagen expression in HSCs. In summary, the effect of leptin-induced Stat3 pathway on SREBP-1c expression in HSCs might contribute to the role of leptin in liver fibrosis in mouse, thus advancing understanding of the mechanisms of liver fibrogenesis associated with leptin. [Copyright &y& Elsevier]

Soil infiltration is an inevitable process of the mutual transformation of surface water and groundwater in the ecological hydrologic cycle that helps to transport nutrients required by plants to the root system, thus promoting vegetation growth and maintaining ecological stability. It is of utmost importance to simulate the process of soil infiltration and calculate the key parameters of soil water migration accurately. Yet, a scale effect in the determination of soil infiltration can seldom be avoided. Based on the scale effect law caused by a change in the inner-ring diameter of the double-ring infiltrometer and common infiltration models, empirical models of soil infiltration scale transfer (SIST) are proposed and established to improve the simulation accuracy of the steady infiltration rate, while reducing test difficulty and consumption. The results show that the four SIST models established based on the infiltration models well simulate the infiltration process of five different sizes of double-ring infiltrometers. The simulation Adj - R 2 of the three infiltration zones in the study area was between 0.66 and 0.95, and the validation Adj - R 2 ranged from 0.72 to 0.94, indicating that the SIST models showed good applicability in the investigated semi-arid grassland. The results further showed that the double-ring infiltrometer with an inner-ring diameter larger than 90 cm and an outer ring buffer coefficient of 0.33 was not accompanied by the scale effect during measurement. Moreover, the SIST models were used to predict the steady infiltration rate in the study area, providing an accurate data basis for the establishment of regional eco-hydrological models. • SIST functions for double ring infiltration with different bi and di were proposed. • Suitable inner ring diameters can ensure the accuracy and reduce consumption. • Final infiltration rate free from infiltrometer scale effect is predicted. [ABSTRACT FROM AUTHOR]

• More NETs were found in thrombus from patients suffering from stroke associated with hyperglycemia. • Hyperglycemia primes NETosis in peri-infarction brain tissue of pMCAO mice. • Neutrophil extracellular traps exacerbate ischemic brain damage in pMCAO mice. • Inhibition of NETosis could partly eliminate the harmful effect of hyperglycemia on ischemic brain injury. Hyperglycemia is common and associated with poor outcome in acute ischemic stroke patients. Neutrophil extracellular traps (NETs) are increased either in diabetes or ischemic stroke. We aimed to determine the role of NETs in acute ischemic stroke with hyperglycemia as it has not been clarified. NETs were observed in thrombi retrieved from ischemic stroke patients undergoing endovascular treatment. Citrullinated histone H3 was much more abundant in thrombi from hyperglycemic patients than in those from normoglycemic patients. BKS-db/db and wild-type mice injected with glucose were used to establish the permanent middle cerebral artery occlusion model with hyperglycemia. NETs induced by hyperglycemia were detected in the peri-ischemic brain tissue. Inhibition of NET formation decreased the infarction volume both in db/db and wild-type mice with hyperglycemia. Neurological function deficits were alleviated by blocking NET formation. These findings suggest that NETs increased by hyperglycemia play a role in exacerbation of ischemic brain damage. [ABSTRACT FROM AUTHOR]