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Peat can be used as a soil amendment to ameliorate saline soils. This study explored the effects of different peat application methods on soil infiltration, phreatic evaporation, and salt accumulation in a coastal saline soil. One-dimensional vertical infiltration and phreatic evaporation experiments were carried out for 3 and 21 days, respectively. Columns were prepared using a moderately saline silty loam soil without peat amendment (control), soil mixed with peat (MP), soil containing a buried peat layer (BP), and soil containing a buried soil–peat mixture (BSP). Compared with the control, the infiltration rate was significantly reduced by 68.3% under the BP treatment. At the end of the infiltration stage, the 0–20 cm soil water content was increased by 11.9% and 10.3% under the BP and BSP treatments, respectively; however, no significant increase occurred under the MP treatment (2.9%) compared with that of the control. After evaporation, significant reductions (44–45%) were observed in the cumulative evaporation amount under the BP treatment compared with that of the control. The 0–20 cm soil water content and electrical conductivity of the BP treatment were also reduced by 47.7% and 84.2%, respectively. There were no significant differences in the soil water and salt distributions of 0–20 cm depth under the BSP and MP treatments compared with that of the control. These findings indicate that burying a peat layer in the saline soil is an effective method to reduce infiltration in the upper soil layers and simultaneously inhibit phreatic evaporation, thereby controlling salt movement in the deeper soil layers.

Lithium titanium oxide (Li2TiO3) tritium breeder ceramic plates with nano- and coarse-grain size were fabricated. The preparation methods contained CTAB-modifying precursor, combining dry-pressing with isostatically cold-pressing, and calcinating at optimized sintering temperature in turn. Then their properties were characterized after radiation by 280 keV helium (He+) ion. Extensive characterization analyses were performed to reveal the changes in nano-grained and coarse-grained Li2TiO3 after radiation. They contained glancing angle X-ray diffraction (GIXRD), atomic force microscopy (AFM), electron spin resonance (ESR), and scanning electron microscopy (SEM). The results showed as follows, GIXRD peak position of the nano-grained Li2TiO3 was more stable than the coarse-grained Li2TiO3 after radiation. Nano-grained Li2TiO3 was less rough and swollen than the coarse-grained one after radiation. Nano-grained Li2TiO3 had more excellent structural stability and less defect concentration of Eʹ-center after radiation. As a result, nano-grained Li2TiO3 might have much better radiation tolerance than the coarse-grained one by comparing characterization results.

Carbon monoxide releasing molecule-3 (CORM-3) has been shown to protect inflammatory diseases via the upregulation of heme oxygenases-1 (HO-1). However, in rat brain astrocytes (RBA-1), the mechanisms underlying CORM-3-induced HO-1 remain poorly defined. This study used western blot, real-time PCR, and promoter activity assays to determine the levels of HO-1 expression and 2 ′ ,7 ′ -dichlorodihydrofluorescein diacetate (H2DCFDA) and dihydroethidium (DHE) to measure reactive oxygen species (ROS). We found that CORM-3-induced HO-1 expression was mediated through ROS generation by Nox or mitochondria. The signaling components were differentiated by pharmacological inhibitors and small interfering RNA (siRNA). Subcellular fractions, immunofluorescent staining, and chromatin immunoprecipitation assay were used to evaluate the nuclear translocation and promoter binding activity of Nrf2 induced by CORM-3. The roles of mTOR and FoxO1 in CORM-3-stimulated responses are still unknown in RBA-1 cells. Our results demonstrated that transfection with siRNAs or pretreatment with pharmacological inhibitors attenuated the levels of HO-1 and phosphorylation of signaling components including Akt, mTOR, FoxO1, and Nrf2 stimulated by CORM-3. Moreover, pretreatment with N-acetyl-L-cysteine, diphenyleneiodonium chloride, apocynin, or rotenone blocked nuclear translocation and promoter binding activity of Nrf2 induced by CORM-3. The present study concluded that in RBA-1 cells, CORM-3-induced HO-1 expression is, at least partially, mediated through Nox and mitochondria/ROS-dependent PI3K/Akt/mTOR cascade to activate FoxO1 or ROS leading to activation of Nrf2 activity.

Several pro-inflammatory factors and proteins have been characterized that are involved in the pathogenesis of inflammatory diseases, including acute respiratory distress syndrome, chronic obstructive pulmonary disease, and asthma, induced by oxidative stress, cytokines, bacterial toxins, and viruses. Reactive oxygen species (ROS) act as secondary messengers and are products of normal cellular metabolism. Under physiological conditions, ROS protect cells against oxidative stress through the maintenance of cellular redox homeostasis, which is important for proliferation, viability, cell activation, and organ function. However, overproduction of ROS is most frequently due to excessive stimulation of either the mitochondrial electron transport chain and xanthine oxidase or reduced nicotinamide adenine dinucleotide phosphate (NADPH) by pro-inflammatory cytokines, such as interleukin-1β and tumor necrosis factor α. NADPH oxidase activation and ROS overproduction could further induce numerous inflammatory target proteins that are potentially mediated via Nox/ROS-related transcription factors triggered by various intracellular signaling pathways. Thus, oxidative stress is considered important in pulmonary inflammatory processes. Previous studies have demonstrated that redox signals can induce pulmonary inflammatory diseases. Thus, therapeutic strategies directly targeting oxidative stress may be effective for pulmonary inflammatory diseases. Therefore, drugs with anti-inflammatory and anti-oxidative properties may be beneficial to these diseases. Recent studies have suggested that traditional Chinese medicines, statins, and peroxisome proliferation-activated receptor agonists could modulate inflammation-related signaling processes and may be beneficial for pulmonary inflammatory diseases. In particular, several herbal medicines have attracted attention for the management of pulmonary inflammatory diseases. Therefore, we reviewed the pharmacological effects of these drugs to dissect how they induce host defense mechanisms against oxidative injury to combat pulmonary inflammation. Moreover, the cytotoxicity of oxidative stress and apoptotic cell death can be protected via the induction of HO-1 by these drugs. The main objective of this review is to focus on Chinese herbs and old drugs to develop anti-inflammatory drugs able to induce HO-1 expression for the management of pulmonary inflammatory diseases.

Heme oxygenase-1 (HO-1) has been shown to exert as an antioxidant and anti-inflammatory enzyme in cardiovascular inflammatory diseases. Flavonoids have been demonstrated to display anti-inflammatory and antioxidant effects through the induction of HO-1. 5,8-Dihydroxy-4 ′ ,7-dimethoxyflavone (DDF), one of the flavonoid compounds, is isolated from Reevesia formosana. Whether DDF induced HO-1 expression on human cardiac fibroblasts (HCFs) remained unknown. Here, we found that DDF time- and concentration-dependently induced HO-1 protein and mRNA expression, which was attenuated by pretreatment with reactive oxygen species (ROS) scavenger N-acetyl cysteine (NAC) in HCFs. DDF-enhanced ROS generation was attenuated by NAC, but not by either diphenyleneiodonium chloride (DPI, Nox inhibitor) or MitoTempol (mitochondrial ROS scavenger). Interestingly, pretreatment with glutathione (GSH) inhibited DDF-induced HO-1 expression. The ratio of GSH/GSSG was time-dependently decreased in DDF-treated HCFs. DDF-induced HO-1 expression was attenuated by an inhibitor of p38 MAPK (p38i VIII) or siRNA, but not by MEK1/2 (PD98059) or JNK1/2 (SP600125). DDF-stimulated p38 MAPK phosphorylation was inhibited by GSH or p38i VIII. Moreover, DDF-induced HO-1 expression was mediated through Nrf2 phosphorylation and translocation into the nucleus which was attenuated by NAC or p38 siRNA. DDF also stimulated antioxidant response element (ARE) promoter activity which was inhibited by NAC, GSH, or p38i VIII. Interaction between Nrf2 and the ARE-binding sites on the HO-1 promoter was revealed by chromatin immunoprecipitation assay, which was attenuated by NAC, GSH, or p38i VIII. We further evaluated the functional effect of HO-1 expression on the thrombin-induced fibrotic responses. Our result indicated that the induction of HO-1 by DDF can attenuate the thrombin-induced connective tissue growth factor expression. These results suggested that DDF-induced HO-1 expression is, at least, mediated through the activation of the ROS-dependent p38 MAPK/Nrf2 signaling pathway in HCFs. Thus, the upregulation of HO-1 by DDF could be a candidate for the treatment of heart fibrosis.

Purpose Neuroinflammation, characterized by the increased expression of inflammatory proteins such as matrix metalloproteinases (MMPs), plays a critical role in neurodegenerative disorders. Lipopolysaccharide (LPS) has been shown to upregulate MMP-9 expression through the activation of various transcription factors, including activator protein 1 (AP-1) and forkhead box protein O1 (FoxO1). The flavonoid 3,5,7-trihydroxy-2-phenyl-4H-1-benzopyran-4-one (galangin) has been demonstrated to possess antioxidant and anti-inflammatory properties in various types of cells. Here, we investigated the mechanisms underlying the inhibitory effect of galangin on LPS-induced MMP-9 expression in rat brain astrocytes (RBA-1 cells). Methods Pharmacological inhibitors and siRNAs were employed to explore the effects of galangin on LPS-challenged RBA-1 cells. Gelatin zymography, Western blotting, real-time PCR, and a luciferase reporter assay were used to detect MMP-9 activity, protein expression, mRNA levels, and promoter activity, respectively. The protein kinases involved in the LPS-induced MMP-9 expression were determined by Western blot. A chromatin immunoprecipitation (ChIP) assay was employed to evaluate the activity of c-Jun at the MMP-9 promoter. Results Galangin treatment attenuated the LPS-mediated induction of MMP-9 protein and mRNA expression, as well as the activity at the MMP-9 promoter. In addition, galangin exerted its inhibitory effects on MMP-9 expression through suppressing the LPS-stimulated activation of proline-rich tyrosine kinase (Pyk2), platelet-derived growth factor receptor beta (PDGFRβ), phosphoinositide 3-kinase (PI3K), protein kinase B (Akt), mammalian target of rapamycin (mTOR), and mitogen-activated protein kinases (MAPKs). Pretreatment with galangin attenuated the LPS-induced phosphorylation of c-Jun and FoxO1. LPS-induced cell migration was also suppressed by galangin pretreatment. Conclusion Galangin attenuates the LPS-induced inflammatory responses, including the induction of MMP-9 expression and cell migration, via inhibiting Pyk2/PDGFRβ/PI3K/Akt/mTOR/JNK1/JNK2 and p44/p42 MAPK cascade-dependent AP-1 and FoxO1 activities. These results provide new insights into the mechanisms through which galangin mitigates LPS-induced inflammatory responses, and suggest novel strategies for the management of LPS-related brain diseases.

Three different alumina/aluminum bi-layer armors having different striking faces, i.e., monolithic alumina, mosaic alumina, and mosaic alumina enhanced by aluminum honeycomb, were fabricated and tested under the impact of the flat projectile. The ballistic performance of each armor type was also investigated using three-dimensional (3D) finite element (FE) simulations. Upon validating the FE simulation results with experimental measurements, the ballistic limit velocity and failure mechanisms for each type of armor, as well as the influence of ceramic tile size, impact position, border effect, and inter tile gap width were quantified. For the enhanced mosaic armor, the metallic honeycomb lattice performed as a cellular skeleton to confine the ceramic tiles and fragments, leading to enhanced ballistic resistance. Besides, the honeycomb enhanced mosaic armor was also found to have much improved multi-hit ballistic resistance in comparison with monolithic and mosaic alumina. The honeycomb preserved the structural integrity of the mosaic armor so that a high level of residual ballistic resistance remained even after impact. With the extended reliability calculation method, single shot ballistic data were used to estimate the performance of the honeycomb enhanced mosaic armor under multiple projectile impacts.

Purpose Neuroinflammation plays a crucial role in neurodegenerative diseases. Matrix metalloproteinases (MMPs) are a landmark of neuroinflammation. Lipopolysaccharide (LPS) has been demonstrated to induce MMP-9 expression. The mechanisms underlying LPS-induced MMP-9 expression have not been completely elucidated in astrocytes. Nuclear factor-kappaB (NF-κB) is well known as one of the crucial transcription factors in MMP-9 induction. Moreover, reactive oxygen species (ROS) could be an important mediator of neuroinflammation. Here, we differentiated whether ROS and NF-κB contributed to LPS-mediated MMP-9 expression in rat brain astrocytes (RBA-1). Besides, pristimerin has been revealed to possess antioxidant and anti-inflammatory effects. We also evaluated the effects of pristimerin on LPS-induced inflammatory responses. Methods RBA-1 cells were used for analyses. Pharmacological inhibitors and siRNAs were used to evaluate the signaling pathway. Western blotting and gelatin zymography were conducted to evaluate protein and MMP-9 expression, respectively. Real-time PCR was for mRNA expression. Wound healing assay was for cell migration. 2',7'-dichlorodihydrofluorescein diacetate (H2DCF-DA) and dihydroethidium (DHE) staining were for ROS generation. Immunofluorescence staining was conducted to assess NF-κB p65. Promoter-reporter gene assay and chromatin immunoprecipitation (ChIP) assay were used to detect promoter activity and the association of nuclear proteins with the promoter. Results Our results showed that the increased level of ROS generation was attenuated by edaravone (a ROS scavenger), apocynin (APO; an inhibitor of p47Phox), diphenyleneiodonium (DPI; an inhibitor of NOX), and pristimerin in RBA-1 cells exposed to LPS. Besides, pretreatment with APO, DPI, edaravone, Bay11-7082, and pristimerin also inhibited the phosphorylation, nuclear translocation, promoter binding activity of NF-κB p65 as well as upregulation of MMP-9 expression-mediated cell migration in RBA-1 cells challenged with LPS. Conclusion These results suggested that LPS enhances the upregulation of MMP-9 through nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX)/ROS-dependent NF-κB activity. These results also provide new insights into the mechanisms by which pristimerin attenuates LPS-mediated MMP-9 expression and neuroinflammatory responses.

A major cause of late-life health complications is the cardiovascular disease known as atherosclerosis. The process of atherogenesis is marked by endothelial cell dysfunction, the development of atherogenic lesions, and plaque buildup on the intima of the arterial endothelium. This process is fueled primarily by the adhesion of monocytes to endothelial cells via the actions of the cellular adhesion molecules VCAM-1 and E-selectin. When expressed at their basal levels, these molecules are vital to various cellular processes, but when in a state of overproduction, they drive the progression of atherosclerosis by recruiting monocytes to roll along and adhere to the endothelium. TNF-α is theorized to play a causal role in the development of atherosclerosis, but the exact mechanism remains poorly understood. This cytokine is known to upregulate various factors associated with inflammation and oxidative stress, both of which greatly contribute to endothelial dysfunction and atherogenesis. In the present study, we aimed to elucidate the effect of butyrate on these atherogenic processes. Previously not known to have atheroprotective effects, this natural compound shows promise as a treatment for atherosclerosis. In the present study, we found butyrate to exert various anti-inflammatory and downstream regulatory effects. Namely, butyrate ameliorated the overproduction of adhesion molecules, including VCAM-1 and E-selectin, reduced oxidative stress by reducing the levels of ROS and 4-HNE, and suppressed inflammation via inhibition of MCP-1 and IL-8. Additionally, butyrate rescued the reduced expression of the protective factor KLF2, which was mediated through the ERK5 pathway. Thus, butyrate may serve as a promising treatment against atherosclerosis.

The traditional separator plays a significant role in rechargeable lithium-ion batteries due to the customized features that allow ions to transfer freely with low energy barriers. However, in the lithium–sulfur battery, the commercial separator shows feeble ability for promoting the conversion of accumulated long-chain polysulfides to the short-chain polysulfides on the surface of the cathode. In this work, a carbon-intercalated montmorillonite is designed to release the imprisoned capacity of the sulfur cathode by activating the accumulated long-chain polysulfides on the surface of the cathode. Benefiting from the advantages of carbon-intercalated montmorillonite, the lithium–sulfur battery achieves a high discharge capacity of 818 mAh g–1 over 300 cycles at a current density of 1 mA cm–2 with a sulfur loading of 2.6 mg cm–2. The systematic analyses by cyclic voltammetry and AC impedance reveal that the regulation of redox environment on the cathode surface by reducing the accumulated long-chain polysulfides to short-chain sulfides is a scalable solution for constructing the actual lithium–sulfur batteries.

A novel mass production method of lithium titanite (Li2TiO3) tritium breeder ceramic pebbles using polyvinyl alcohol (PVA) and polyvinyl pyrrolidone (PVP) assisted granulation method (APG) was proposed. A binder solution of polyvinyl alcohol (PVA) was used to modify the Li2TiO3 precursor powder. The powders with adhesive properties were prilled to form green pebbles (GPs) by spheronization at a low rotation speed and spraying with polyvinyl pyrrolidone (PVP), in several cycles. Then, the density and the crush load of the GPs were improved by high-speed rolling. Finally, the ceramic pebbles were produced by sintering. The phase, the microstructure, and the crush load of the ceramic pebbles were characterized by X-ray diffraction (XRD), scanning electron microscopy (SEM), and with a universal tester, respectively.

A simple one-step molten salt method was used to synthesize micron-sized single primary particle LiNi0.8Co0.1Mn0.1O2 (NCM811) cathode material. XRD, SEM, cycle performance, rate capability, differential capacity curves, 0.1 C charge/discharge curves, and EIS were carried out to research the mechanism regarding the influence of Li/transition metal (Li/TM) ratio, sinter temperature, and sinter time on the morphology and electrochemical properties of micron-sized single primary particle LiNi0.8Co0.1Mn0.1O2 materials. Any one of these three factors increases exceeding certain limit and it will lead to the degradation of active structure evolution during the charge/discharge process, resulting in decreasing electrochemical performance of the cathode material. The micron-sized single primary particle NCM811 cathode material with little aggregation and primary particle size of ~ 1–2 μm was produced successfully under the condition of heating at 850 °C for 16 h with Li/TM = 1.15. This work will be helpful for the synthesis of micron-sized single primary particle NCM cathode materials for lithium-ion batteries.

Semiconducting polymer nanoparticles (Pdots) have been demonstrated to be a promising class of probes for use in fluorometric immunochromatographic test strips (ICTS). The advantages of Pdots in ICTSs include ultrahigh brightness, minimal nonspecific adsorption, and multicolor availability, which together contribute to the high sensitivity, good specificity, and multiplexing ability. These unique properties can therefore circumvent several significant challenges of commercial ICTSs, including insufficient specificity/sensitivity and difficulty in quantitative and multiplexed detection. Here, we developed a colorimetric and fluorescent bimodal readout ICTS based on gold-Pdot nanohybrids for the determination of carcinoembryonic antigen (CEA) and cytokeratin 19 fragment (CYFRA 21-1) expressed abnormally in human blood of non-small-cell lung cancer (NSCLS). The vivid color from Au nanomaterials can be used for rapid qualitative screening (colorimetry) in 15 min, while the bright fluorescence of Pdots is ideal for the advanced quantitative measurements of CEA and CYFRA21-1 concentrations in whole blood samples. This bimodal ICTS platform possesses phenomenal detection sensitivity of 0.07 and 0.12 ng/mL for CYFRA21-1 and CEA, respectively. The accuracy and reliability of this ICTS platform were further evaluated with clinical serum samples from NSCLS patients at different stages, showing good consistency with the results from electrochemiluminescence immunoassay.

Leaf trait is an important target trait in crop breeding programs. Moderate leaf curling may be a help for improving crop yield by minimizing the shadowing by leaves. Mining locus for leaf curling trait is of significance for plant genetics and breeding researches. The present study identified a novel rapeseed accession with up-curling leaf, analyzed the up-curling leaf trait inheritance, and fine mapped the locus for up-curling leaf property (Bnuc3) in Brassica napus. Genetic analysis revealed that the up-curling leaf trait is controlled by a single dominant locus, named BnUC3. We performed an association study of BnUC3 with single nucleotide polymorphism (SNP) markers using a backcross population derived from the homozygous up-curling leaf line NJAU-M1295 and the canola variety ‘zhongshuang11’ with typical flat leaves, and mapped the BnUC3 locus in a 1.92 Mb interval of chromosome A02 of B. napus. To further map BnUC3, 232 simple sequence repeat (SSR) primers and four pairs of Insertion/Deletion (InDel) primers were developed for the mapping interval. Among them, five SSR markers and two InDel markers were polymorphic. By these markers, the mapping interval was narrowed to 92.0 kb using another F2 population. This fine mapping interval has 11 annotated genes among which BnaA02T0157000ZS were inferred to be candidate casual genes for up-curling leaf based on the cloned sequence analysis, gene functionality, and gene expression analysis. The current study laid a foundational basis for further elucidating the mechanism of BnUC3 and breeding of variety with up-curling leaf.

In this study, a case study to produce microcellular foam of a commercial thermoplastic polyurethane (TPU) through the supercritical carbon dioxide (CO2) foaming process is presented. To explore the feasibility of TPU in medical device and biomedical application, a soft TPU with Shore hardness value of 70A was selected as the model compound. The effects of saturation temperature and saturation pressure ranging from 90 to 140 °C and 90 to 110 bar on the expansion ratio, cell size and cell density of the TPU foam were compared and discussed. Regarding the expansion ratio, the effect of saturation temperature was considerable and an intermediate saturation temperature of 100 °C was favorable to produce TPU microcellular foam with a high expansion ratio. On the other hand, the mean pore size and cell density of TPU foam can be efficiently manipulated by adjusting the saturation pressure. A high saturation pressure was beneficial to obtain TPU foam with small mean pore size and high cell density. This case study shows that the expansion ratio of TPU microcellular foam could be designed as high as 4.4. The cell size and cell density could be controlled within 12–40 μm and 5.0 × 107–1.3 × 109 cells/cm3, respectively.

Chuen-Mao Yang,1– 3 Chien-Chung Yang,4,5 Li-Der Hsiao,1 Chia-Ying Yu,1 Hui-Ching Tseng,1 Chih-Kai Hsu,1 Jiro Hasegawa Situmorang1 1Department of Pharmacology, College of Medicine, China Medical University, Taichung, 40402, Taiwan; 2Ph.D. Program for Biotech Pharmaceutical Industry, China Medical University, Taichung, 40402, Taiwan; 3Department of Post-Baccalaureate Veterinary Medicine, College of Medical and Health Science, Asia University, Wufeng, Taichung, 41354, Taiwan; 4Department of Traditional Chinese Medicine, Chang Gung Memorial Hospital at Tao-Yuan, Kwei-San, Tao-Yuan, 33302, Taiwan; 5School of Traditional Chinese Medicine, College of Medicine, Chang Gung University, Kwei-San, Tao-Yuan, 33302, TaiwanCorrespondence: Chuen-Mao Yang No. 91, Hsueh-Shih Road, Taichung, 40402, TaiwanTel +886-4-22053366 (ext. 2229)Email chuenmao@mail.cmu.edu.twPurpose: Tumor necrosis factor-α (TNF-α) has been shown to exert as a pathogenic factor in cardiac fibrosis and heart failure which were associated with the up-regulation of cyclooxygenase (COX)-2/prostaglandin E2 (PGE2) axis. However, whether TNF-α-induced COX-2/PGE2 upregulation mediated through ROS-dependent cascade remains elusive in human cardiac fibroblasts (HCFs). This study aims to address the underlying mechanisms of TNF-α-induced COX-2/PGE2 expression.Methods: Here, we used TNF receptor neutralizing antibody (TNFR nAb), pharmacologic inhibitors, and siRNAs to dissect the involvement of signaling components examined by Western blot and ELISA in TNF-α-mediated responses in HCFs. MitoSOX Red was used to measure mitoROS generation. Isolation of subcellular fractions was performed to determine membrane translocation of PKCα. Promoter luciferase assay and chromatin immunoprecipitation (ChIP) assay were used to determine the role of transcription factor.Results: We found that TNF-α time- and concentration-dependently upregulated COX-2 protein and mRNA expression as well as PGE2 synthesis which was attenuated by TNFR1 nAb, the inhibitor of mitochondrial ROS scavenger (MitoTEMPO), protein kinase C [(PKC)α, Gö 6976], p38 MAPK [p38 inhibitor VIII, (p38i VIII)], JNK1/2 (SP600125), or forkhead box protein O1 [(FoxO1), AS1842856], and transfection with their respective siRNAs in HCFs. TNF-α-stimulated PKCα phosphorylation was inhibited by TNFR1 nAb, MitoTEMPO, or Gö 6976. TNF-α stimulated phosphorylation of p38 MAPK and JNK1/2 was attenuated by TNFR1 nAb, MitoTEMPO, Gö 6976, and their inhibitors p38i VIII and SP600125. Moreover, TNF-α-triggered FoxO1 phosphorylation was abolished by AS1842856, TNFR1 nAb, and its upstream inhibitors MitoTEMPO, Gö 6976, p38i VIII, and SP600125. Phosphorylation of FoxO1 could enhance its interaction with the COX-2 promoter element revealed by ChIP assay, which was attenuated by AS1842856.Conclusion: Our results suggested that TNF-α-induced COX-2/PGE2 upregulation is mediated through TNFR1-dependent MitoROS/PKCα/p38 MAPK and JNK1/2 cascade to activate FoxO1 binding with the COX-2 promoter in HCFs.Keywords: TNF-α, COX-2, PGE2, PKC-α, mitochondrial ROS, FoxO1

The efficacy of adiponectin (APN) in regulating bone metabolism remains controversial. This study aimed to investigate the role of APN secreted from adipose-derived stem cells on adipogenesis and osteogenesis. Human APN gene was transfected via recombinant adenovirus into adipose derived stem cells (ASCs) in vitro and were cocultured with bone marrow mesenchymal stem cells (BMSCs) in using a transwell chamber. Adipogenesis was inhibited in APN-transfected ASCs; in BMSCs, adipogenesis was inhibited, but osteogenesis was promoted in coculture with APN-transfected ASCs. Next, the same adenovirus construct was transfected into the abdominal adipose tissue of a Sprague Dawley rat in vivo, and then a tibia defect was established in the same rat. We confirmed there was higher gene and protein expression of APN in ASCs and the abdominal adipose tissue of these rat models. Development of adipocytes in abdominal adipose tissue was suppressed, and less new bone was formed in the bone defect area. In conclusion, APN secreted from ASCs could directly inhibit adipogenesis in ASCs and BMSCs and promote osteogenesis in the latter. However, APN overexpression in adipose tissue was inversely associated with bone formation in tibia defects potentially due to decreased levels of circulating bone-activating hormones.

The objective of this study was to develop the efficient methods for dialdehyde cellulose (DAC) production, in which periodate solution was used as oxidant, and an electrochemically assisted system was applied to achieve green, efficient, low-cost and sustainable oxidization of cellulose. The microcrystalline cellulose (MCC) was pre-treated by alkali or ultrasound, and then oxidized to prepare DAC in the electrolyzer with aqueous solution of sodium periodate. Finally, the DAC was obtained by centrifugation and lyophilization. The prepared DAC materials were characterized by FTIR, XRD and SEM, and analyzed via aldehyde group contents, crystallinity index, water solubility index and water retention value. The introduction of active functional groups promoted cellulose hydration and swelling. Compared to the ultrasound pretreatment, the alkaline pretreatment had a great influence on the water solubility index and water retention value of cellulose. The aldehyde group contents of DAC increased after the MCC was oxidized by sodium periodate in the electrolyzer. Electrochemically assisted oxidation significantly decreased the crystallinity of the DAC, and the surface structure was smooth and soft, which can be attributed to the electrochemically assisted reaction that could regenerate the spent periodate in anode electrolytic chamber. When DAC was prepared under optimal conditions (current density: 0.075 A/cm2, periodate concentration: 0.6 mol/L, reaction time: 30 min), the regeneration efficiency of spent periodate reached about 93.4%.

Lysophosphatidylcholine (LPC) may accumulate in the heart to cause fibrotic events, which is mediated through fibroblast activation and collagen accumulation. Here, we evaluated the mechanisms underlying LPC-mediated collagen induction via mitochondrial events in human cardiac fibroblasts (HCFs), coupling application of the pharmacologic cyclooxygenase-2 (COX-2) inhibitor, celecoxib, and genetic mutations in FOXO1 on the fibrosis pathway. In HCFs, LPC caused prostaglandin E(2) (PGE(2))/PGE(2) receptor 4 (EP(4))-dependent collagen induction via activation of transcriptional activity of forkhead box protein O1 (FoxO1) on COX-2 gene expression. These responses were mediated through LPC-induced generation of mitochondrial reactive oxygen species (mitoROS), as confirmed by ex vivo studies, which indicated that LPC increased COX-2 expression and oxidative stress. LPC-induced mitoROS mediated the activation of protein kinase C (PKC)α, which interacted with and phosphorylated dynamin-related protein 1 (Drp1) at Ser(616), thereby increasing Drp1-mediated mitochondrial fission and mitochondrial depolarization. Furthermore, inhibition of PKCα and Drp1 reduced FoxO1-mediated phosphorylation at Ser(256) and nuclear accumulation, which suppressed COX-2/PGE(2) expression and collagen production. Moreover, pretreatment with celecoxib or COX-2 siRNA suppressed WT FoxO1; mutated Ser(256)-to-Asp(256) FoxO1-enhanced collagen induction, which was reversed by addition of PGE(2). Our results demonstrate that LPC-induced generation of mitoROS regulates PKCα-mediated Drp1-dependent mitochondrial fission and COX-2 expression via a PKCα/Drp1/FoxO1 cascade, leading to PGE(2)/EP(4)-mediated collagen induction. These findings provide new insights about the role of LPC in the pathway of fibrotic injury in HCFs.

Chitin and chitosan are renewable biomass resources with macromolecular structures. Due to the strong intra- and inter-molecular hydrogen bonds, chitin and chitosan cannot be dissolved in water or traditional organic solvents, which tremendously limit their applications in many fields. Ionic liquid, as a novel green solvent, provides excellent solubility to chitin and chitosan. In this paper, the research progress on dissolution performance and dissolution mechanism of chitin and chitosan in ionic liquids is reviewed. Materials including fibers, films and gels created from the homogeneous solutions are summarized; meanwhile, the chemical derivatization of chitin and chitosan in ionic liquids are also discussed. Finally, the challenges and future development of ionic liquids in chitin and chitosan chemistry are proposed.

This study presents the densities and viscosities of four binary liquid mixtures containing diethyl oxalate (DEO) with the organic solvents ethanol, ethyl acetate (EA), tetrahydrofuran (THF), and t...

One potential porous scaffold material based on polyester waterborne polyurethane (PEUR) grafted with modified gelatin hydrolysate (GH) has been investigated in this research. First, the GH was modified with a silane coupling agent (KH550), and then the modified GH was mixed with pre-polymer emulsion of PEUR to obtain the PEUR grafted GH emulsion (PEUR-g-GH). The synthesized PEUR-g-GH emulsions were characterized by stability analysis and viscosity test. Moreover, the film-forming property of PEUR-g-GH has also been studied, and the PEUR-g-GH films were characterized regarding the water resistance, solvent resistance, mechanical properties, FTIR, AFM, SEM, DMA, TGA and contact angle testing. Finally, the bioactivity and biodegradation were investigated by soaking PEUR-g-GH scaffolds in simulated body fluid (SBF). The results indicated that the PEUR-g-GH emulsion has good stability, water resisting (the contact angle was over 90o), the PEUR-g-GH showed excellent film-forming, high storage modulus, good structural homogeneity and thermal stability (the temperature of maximum weight loss was over 350 °C). The freeze-dried sample showed porous structure, and the mutual crosslinking of layers can contribute to a good bearing capacity for scaffold. The SBF biodegradability revealed that the biodegradation rate and degree of films gradually increased with the content of GH increased. In addition, the cells on the material were markedly enhanced, and most of cells have proliferated and formed vesicles, which shown a good biocompatibility.

The tritium release behavior of the Li4SiO4 pebbles and Li4SiO4 + 5 mol% TiO2 pebbles with small grain sizes was investigated. The tritium release results of Li4SiO4 pebbles with different grain sizes (0.3 μm and 1.5 μm) indicated that the grain size had little effect on the tritium release regardless of the difference in gas composition of purge gas. Moreover, the tritium release of small grained pebbles was dominated by the desorption process, since the addition of H2 to purge gas substantially affected the release behavior. The modified Li4SiO4 pebbles with addition of TiO2 exhibited enhanced water formation capacity due to the increased concentration of active point as the oxygen supplier. Obvious tritiated water release peaks around 690 °C could be observed from the Li4SiO4 + 5 mol% TiO2 pebbles under 0.1%H2+He purge gas. The modified Li4SiO4 pebbles also showed improved tritium release behavior, the tritium release peaks shifted to lower temperatures compared to Li4SiO4 pebbles.

In this work, we investigate collagen protein powder (CPP) extracted from chromium leather scrap waste (CLSW). The composition and molecular weight distribution of CPP were determined by elemental analysis and sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), respectively. The microstructure and size distribution of CPP were then characterized by scanning electron microscopy (SEM) and nanometer analyzer instrument. Finally, CPP was treated with corn starch (CS), and the swelling behavior of the resulting CPP-CS blend was investigated in order to determine its range of applications. The experimental data showed that CPP contains 13 different amino-acids. CPP also displayed low mineral salt levels and a nitrogen content of 43.84%, indicating its potential use as an organic fertilizer. The molecular weight range of CPP is 6.5 to ~ 26.6 kDa. After the obtained CPP was blended with CS, the CPP-CS blend is endowed with optimal swelling properties and is able to overcome the solubility drawbacks of CPP alone. In addition, when the CPP was used as a natural fertilizer, the germination rate and height of kidney beans obviously increased.

The proliferation and adipogenesis of preadipocytes played important roles in the development of adipose tissue and contributed much to the processes of obesity. On the other hand, lipopolysaccharide (LPS), also known as endotoxin, is a key outer membrane component of gram-negative bacteria in the gut microbiota, and has a dominant role in linking inflammation to high-fat diet-induced metabolic syndrome. Studies suggested the potential roles of LPS in hepatic steatosis and in obese mice models. However, the molecular mechanisms underlying LPS-regulated obesity remained largely unknown. Here we reported that LPS stimulated expression of cyosolic phospholipase A2 (cPLA2), one of inflammation regulators of obesity, in the preadipocytes. Pretreatment the inhibitors of JAK2, STAT3, STAT5 or AMPK significantly reduced LPS-increased mRNA and protein expression of cPLA2 together with phosphorylation of JAK2, STAT3, STAT5 and AMPK, separately. Similarly, transfection of siRNA against JAK2 or AMPK abolished expression of cPLA2 and phosphorylation of JAK2 or AMPK together with downregulated expression of JAK2 and AMPK protein. LPS enhanced activation of STAT3 and STAT5 via JAK2-dependent manner in the preadipocytes. Transfection of JAK2 or AMPK siRNA further proofed the independence of JAK2 and AMPK in LPS-treated preadipocytes. In addition, LPS-increased DNA synthesis, cell numbers and cell viability of preadipocytes were attenuated by AACOCF3, AG490, BML-275, cPLA2 siRNA, JAK2 siRNA or AMPK siRNA. Attenuation JAK2/STAT or AMPK-dependent cPLA2 expression reduced LPS-mediated adipogenesis of preadipocytes. Stimulation of arachidonic acid or AMPK activator, A-769662, increased cell numbers and cell viability and promoted differentiation of preadipocytes. Collectively, these results indicated that LPS increased preadipocytes proliferation and adipogenesis via JAK/STAT and AMPK-dependent cPLA2 expression. The mechanisms of LPS-stimulated cPLA2 expression may be a link between bacteria and obesity and provides the molecular basis for preventing metabolic syndrome or hyperplasic obesity.

The thermal shrinkage of commercial polypropylene (PP) separator at high temperature seriously restricts the development of safe and stable lithium-sulfur (Li-S) batteries. To address such issue, herein, we present an interfacial engineering strategy by coating conductive polypyrrole (PPY) modified lithium-montmorillonite (PPY/Li-MMT) on the PP separator. The PPY/Li-MMT can service as an effective heat release layer to enhance the high-temperature stability of Li-S batteries. The engineered PP separator exhibits superior performance: it shows nearly no thermal shrinkage even up to 150 °C. Most importantly, the interface engineered separator has not be punctured during the hot piercing testing and the Li-S batteries deliver outstanding thermal stability even at 80 °C. In addition, the PPY/Li-MMT modified PP separator owns very high electrolyte uptake of 348.6%, large ionic conductivity of 3.63 mS cm−1 and stable performance over 600 cycles. This work provides an effective interfacial engineering strategy by coating PPY/Li-MMT interlayer to significantly improve the electrochemical performance and particularly the high-temperature stability of Li-S batteries.

Brassinosteroids (BRs) are steroid hormones that play essential roles in plant growth and development. In this study, we identified a new dwarf mutant in Brassica napus. By map-based cloning, BnaC04.BIL1 (BnaC04g41660D) gene, a BIN2-like1 (BIL1) encoding a GLYCOGEN SYNTHASE KINASE 3 (GSK3-like) protein kinase, was isolated. To date, how BIL1 involves in BR signal transduction remains uncovered. Genetic transformation experiments confirmed that the BnaC04.BIL1 is responsible for the plant dwarf phenotype in the Bndwarf2 mutants. Overexpression of BnaC04.BIL1 not only reduced plant height, but also resulted in compact plant architecture. Using CRISPR/Cas9, two sgRNAs were designed to target BnaC04.BIL1 gene. The gene editing experiments generated mutations of BnaC04.BIL1 sequence, which were stably transmitted to successive generations, and lead to restoration of plant height and plant architecture. The molecular mechanism of Bndwarf2 dwarfing was further verified by Y2H and BiFC assays. Results shown that a Thr187Ser amino acid substitution residing in the conserved region promotes the interaction between BnaC04.BIL1Mut with BnaBZR1, thus enhances the negative regulation of plant growth. The genetic and molecular evidence clarifies first the BnaC04.BIL1 can sharply change plant architecture in natural plant accessions in allotetraploid, and provides new insights into the molecular mechanisms of BR signaling.

The lithium (Li) ions uniform through the region between separator and lithium anode deliver the critical feature for the achievement of even Li deposition, which is very important for the safe operation of lithium metal batteries, especially for the Li-sulfur (Li-S) battery. The commercial separators such as polypropylene (PP) or polyethylene (PE) prepared by a wet or dry processes, however, allow the generation of plentiful porosities, resulting in the uneven Li ion stripping/platting and finally the formation of Li dendrites. Thence, we construct an atomic interlamellar ion channel by introducing the layered montmorillonite (MMT) on the surface of separator to guide the Li ion flux and achieve the stable Li deposition. The atomic interlamellar ion channel with a spacing of 1.4 nm has strong absorption capacity to the electrolyte and reserve capacity for the Li ions, thus promoting rapidly transfer of Li ions and making an even deposition of Li ions at the anode. As a result, when assembled with the proposed separator, the Coulombic efficiency (CE) of Li||Cu batteries archives 98.2 % after 200 cycles and the Li||Li symmetric batteries actualize their stable platting/stripping even after 800 h. Importantly, the proposed separator allows 140 % specific capacity increase after 190 cycles as employing the Li-S batteries.

An environmentally friendly wood adhesive developed from waterborne polyurethane (WPU) grafted gelatin (G) was investigated in this research. First, the G was extracted from chromium shavings waste, and then mixed with a prepolymer emulsion of WPU to synthesis the graft copolymer (WPUG) via a solvent-free emulsion copolymerization. The synthesized copolymer was characterized using the mechanical properties test, TGA, FT-IR, and other analysis technology. The results indicated that the WPUG had a good overall performance. Specifically, the contact angle reached 111.5°, the tensile strength reached 32.91 MPa, the temperature of the maximum weight loss was greater than 350 °C. The WPUG adhesive had excellent bonding power and mechanical properties; the dry bonding strength reached 4.21 MPa when the ratio between free amino groups of the G and isocyanate-groups of the WPU (the R value) was 1.5. This preparation of the graft copolymer not only satisfies the need of environment-friendly wood adhesives, but it also effectively improves the recyclability of chromium shavings waste.

In the regions of tissue injuries and inflammatory diseases, sphingosine 1-phosphate (S1P), a proinflammatory mediator, is increased. S1P may induce the upregulation of cyclooxygenase-2 (COX-2)/prostaglandin E2 (PGE2) system in various types of cells to exacerbate heart inflammation. However, the detailed molecular mechanisms by which S1P induces COX-2 expression in human cardiac fibroblasts (HCFs) remain unknown. HCFs were incubated with S1P and analyzed by Western blotting, real time-Polymerase chain reaction (RT-PCR), and immunofluorescent staining. Our results indicated that S1P activated S1PR1/3-dependent transcriptional activity to induce COX-2 expression and PGE2 production. S1P recruited and activated PTX-sensitive Gi or -insensitive Gq protein-coupled S1PR and then stimulated PKCα-dependent phosphorylation of p42/p44 MAPK, p38 MAPK, and JNK1/2, leading to activating transcription factor NF-κB. Moreover, S1P-activated NF-κB was translocated into the nucleus and bound to its corresponding binding sites on COX-2 promoters determined by chromatin immunoprecipitation (ChIP) and promoter-reporter assays, thereby turning on COX-2 gene transcription associated with PGE2 production in HCFs. These results concluded that in HCFs, activation of NF-κB by PKCα-mediated MAPK cascades was essential for S1P-induced up-regulation of the COX-2/PGE2 system. Understanding the mechanisms of COX-2 expression and PGE2 production regulated by the S1P/S1PRs system on cardiac fibroblasts may provide rationally therapeutic interventions for heart injury or inflammatory diseases.

One environmental friendly wood adhesive based on waterborne polyurethane (WPU) grafted gelatin (G) was investigated in this research. The G was extracted from chromium shavings waste firstly, and then mixed with pre-polymer emulsion of WPU to synthesis the graft copolymer (WPUG) via solvent-free emulsion copolymerization. The synthesized copolymer was characterized regarding the mechanical properties test, TGA, FT-IR and other analysis technology. The results indicated that the WPUG has good stability, water resisting. The film-forming and thermal stability of G were improved after reacted with the pre-polymer of WPU, and the temperature of maximum weight loss was over 350 oC. The WPUG adhesive has excellent bonding power and mechanical properties, the dry bonding strength could reach 4.21 MPa when the R value was 1.5. The preparation of copolymer not only can perfectly satisfy the need of environment-friendly wood adhesives, but can also effectively improve the recycling use of chromium shavings waste.

Background Osteoarthritis (OA) is the most common joint disease, affecting most middle-aged and elderly people. Astilin (AST) is the main active ingredient isolated from the traditional Chinese medicine Astilbe chinensis and has anti-inflammatory and anti-arthritis effects. The purpose of this study was to investigate the effect and mechanism of AST on OA in rats mediated by papain. Methods In this study, in vivo experiments were conducted to investigate the protective effect and potential mechanism of Astilbin (AST) when it inhibited the development of osteoarthritis (OA). Results A rat model of OA is constructed. Through HE staining, it is found that AST can protect the articular surface and reduce damage. The results of immunohistochemical staining also prove that AST can inhibit the expression of prostaglandin E2 (PGE2) and has an excellent inhibitory effect on inflammatory factors. It is found that AST can significantly inhibit the protein expression of interleukin 1 beta (IL-1β), TNF-α, and NF-κB. Polymerase Chain Reaction (PCR) assay shows that the mRNA of IL-1β, TNF-α, and NF-κB is down-regulated, which also proves that the protective mechanism of AST is related to the NF-κB pathway. Conclusions In general, this study proves that AST can be a potential therapy for degenerative joint diseases, including OA.

Hetero-element doped lithium orthosilicates have been considered as advanced tritium breeders due to the superior performances. In this work, Li4Si1−xTixO4 ceramics were prepared by proprietary hydrothermal process and multistage reactive sintering. The reaction mechanism of Li4Si1−xTixO4 was put forward. XRD and SEM analyses indicate that insertion of Ti leads to lattice expansion, which promotes the grain growth and changes the fracture mode. The compressive tests show that the crush load increases almost four times by increasing x from 0 to 0.2. However, the thermal conductivity and ionic conductivity are the best when x = 0.05 and x = 0.1, respectively. Thermal cycling stability of Li4Si1−xTixO4 pebbles was further appraised through investigating the changes of microstructure and crush load. After undergoing thermal cycling, the Li4Si1−xTixO4 still show higher crush load compared with Li4SiO4, despite Ti segregation in some samples. The x = 0.05 sample exhibits excellent thermal cycling stability. In summary, proper amount of Ti doping can improve the crush load, thermal and ionic conductivity, and thermal cycling stability of Li4SiO4.

Mevastatin (MVS) has been previously shown to induce heme oxygenase (HO)-1 expression through Nox/ROS-dependent PDGFR&alpha, /PI3K/Akt/Nrf2/ARE axis in human pulmonary alveolar epithelial cells (HPAEpiCs). However, alternative signaling pathways might involve in MVS-induced HO-1 expression. We found that tumor necrosis factor &alpha, (TNF&alpha, ) induced vascular cell adhesion protein 1 (VCAM-1) expression and NF-&kappa, B p65 phosphorylation which were attenuated by pretreatment with MVS via up-regulation of HO-1, determined by Western blot and real-time qPCR. TNF&alpha, induced VCAM-1 expression was attenuated by an NF-&kappa, B inhibitor, Bay117082. The inhibitory effects of MVS were reversed by tin protoporphyrin (SnPP)IX (an inhibitor of HO-1 activity). In addition, pretreatment with the inhibitor of pan-Protein kinase C (PKC) (GF109203X), PKC&alpha, (G&ouml, 6983), Pyk2 (PF431396), p38&alpha, MAPK (SB202190), JNK1/2 (SP600125), or AP-1 (Tanshinone IIA), and transfection with their respective siRNAs abolished MVS-induced HO-1 expression in HPAEpiCs. c-Jun (one of AP-1 subunits) was activated by PKC&alpha, Pyk2, p38&alpha, MAPK, and JNK1/2, which turned on the transcription of the homx1 gene. The interaction between c-Jun and HO-1 promoter was confirmed by a chromatin immunoprecipitation (ChIP) assay, which was attenuated by these pharmacological inhibitors. These results suggested that MVS induces AP-1/HO-1 expression via PKC&alpha, /Pyk2/p38&alpha, MAPK- or JNK1/2-dependent c-Jun activation, which further binds with AP-1-binding site on HO-1 promoter and suppresses the TNF&alpha, mediated inflammatory responses in HPAEpiCs. Thus, upregulation of the AP-1/HO-1 system by MVS exerts a potentially therapeutic strategy to protect against pulmonary inflammation.