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Nonalcoholic fatty liver disease (NAFLD) is characterized by excessive lipid accumulation in hepatocytes. CD38 was initially identified as a lymphocyte surface antigen and then has been found to exist in a variety of cell types. Our previous studies showed that CD38-/- mice were resistant to high-fat diet (HFD)-induced obesity. However, the role and mechanism of CD38 in HFD-induced NAFLD is still unclear. Here, we reported that CD38-/- mice significantly alleviated HFD-induced hepatic steatosis. HFD or oleic acid (OA) remarkably increased the mRNA and protein expressions of CD38 in mouse hepatic tissues and primary hepatocytes or hepatic cell lines in vitro and in vivo, suggesting that CD38 might play a role in HFD-induced hepatic steatosis. We observed that CD38 deficiency markedly decreased HFD- or OA-induced the lipid accumulation and oxidative stress in CD38-/- livers or primary hepatocytes, respectively. In contrast, overexpression of CD38 in Hep1-6 cells aggravated OA-induced lipid accumulation and oxidative stress. Furthermore, CD38 deficiency markedly inhibited HFD- or OA-induced the expressions of NOX4, and increased the expression of PPARα, CPT1, ACOX1 and SOD2 in liver tissue and hepatocytes from CD38-/- mice, indicating that CD38 deficiency-mediated the enhancement of fatty acid oxidation and the inhibition of oxidative stress contributed to protecting NAFLD. More importantly, Ex527 (Sirt1 inhibitor) and 3-TYP (Sirt3 inhibitor) significantly enhanced OA-induced lipid accumulation and oxidative stress in CD38-/- primary hepatocytes, suggesting that the anti-lipid accumulation of CD38 deficiency might be dependent on NAD/Sirtuins-mediated enhancement of FAA β-oxidation and suppression of oxidative stress in hepatocytes. In conclusion, we demonstrated that CD38 deficiency protected mice from HFD-induced NAFLD by reducing lipid accumulation and suppressing oxidative stress via activating NAD/Sirtuins signaling pathways.

We compared the methods of electrocardiogram (ECG) and X-ray localization of the peripherally inserted central catheter (PICC) tip position, in order to find a more convenient, practical, and safe method.To investigate the value of applying electrocardiographic localization of the PICC tip position in critically ill patients with advanced cancer in Hebei Province, China.Enrolled 137 advanced cancers requiring PICC placement. The position of the catheter tip was localized with the bedside electrocardiogram in real time. Then, the localization was performed using a chest X-ray (the gold standard). The accuracy of electrocardiographic location was checked.Specific P waves were observed in 130 patients. No change in the P waves was observed for the remaining seven patients. The age of the latter group of patients was more advanced (87.29 [5.15] years), a significant difference to that of the 130 patients with specific P waves (71.58 [14.84] years) (t = -6.704, p .001). Specific P waves not only involve ascendance in P waves but also ascendance in QRS waves.The use of an ECG to localize the PICC tip in critically ill patients with advanced cancer may replace the unnecessary use of chest X-rays. Specific P waves not only involve an increase in P waves but also an increase in QRS waves. If there is no change in the P wave, a chest X-ray film must be obtained. In elderly patients, because there is a possibility of catheter tip malposition, a comprehensive evaluation should be performed before surgery.

Endothelial activation plays an essential role in the pathogenesis of sepsis-induced acute lung injury, however, the detailed regulatory mechanisms remain largely unknown. Here, we reported that TRIM47, an E3 ubiquitin ligase of the tripartite motif-containing protein family, was highly expressed in vascular endothelial cells. TRIM47-deficient mice were effectively resistant to lipopolysaccharide (LPS)-induced acute lung injury and death by attenuating pulmonary inflammation. TRIM47 was upregulated during TNFα-induced endothelial activation in vitro. Knockdown of TRIM47 in endothelial cells inhibited the transcription of multiple pro-inflammatory cytokines, reduced monocyte adhesion and the expression of adhesion molecules, and suppressed the secretion of IL-1β and IL-6 in endothelial cells. By contrast, overexpression of TRIM47 promoted inflammatory response and monocyte adhesion upon TNFα stimulation. In addition, TRIM47 was able to activate the NF-κB and MAPK signaling pathways during endothelial activation. Furthermore, our experiments revealed that TRIM47 resulted in endothelial activation by promoting the K63-linked ubiquitination of TRAF2, a key component of the TNFα signaling pathway. Taken together, our studies demonstrated that TRIM47 as a novel activator of endothelial cells, promoted LPS-induced pulmonary inflammation and acute lung injury through potentiating the K63-linked ubiquitination of TRAF2, which in turn activates NF-κB and MAPK signaling pathways to trigger an inflammatory response in endothelial cells.

Endothelial activation plays an essential role in the pathology of sepsis-induced acute lung injury, but the detailed regulatory mechanisms remain largely unknown. Here, we demonstrated that TRIM47, an ubiquitin E3 ligase of tripartite protein family, is highly expressed in vascular endothelial cells and is up-regulated during TNFα-induced endothelial activation. Knockdown of TRIM47 in endothelial cells prevents the transcription of multiple pro-inflammatory cytokines, reduces monocyte adhesion and the expression of adhesion molecules, and inhibits the secretion of IL-1β and IL-6 into the supernatant. By contrast, overexpression of TRIM47 promotes inflammatory response and monocyte adhesion upon TNFα stimulation. TRIM47 modulates the activation of NF-κB and MAPK signaling pathways during endothelial activation. Further experiment confirmed that TRIM47 interacts with TRAF2 and mediates K63-linked ubiquitination. In addition, TRIM47-deficient mice are more resistant to lipopolysaccharide-induced acute lung injury and death, due to attenuated pulmonary inflammation. Taken together, our studies suggest that TRIM47 promotes pulmonary inflammation and injury at least partly through potentiating the K63-linked ubiquitination of TRAF2, which in turn activates NF-κB and MAPK signaling pathways to trigger inflammatory response in endothelial cells.

Nonalcoholic fatty liver disease (NAFLD) is characterized by excessive lipid accumulation in hepatocytes. CD38 was initially identified as a lymphocyte surface antigen and then has been found to exist in a variety of cell types. Our previous studies showed that CD38-/- mice were resistant to high-fat diet (HFD)-induced obesity. However, the role and mechanism of CD38 in HFD-induced NAFLD is still unclear. Here, we reported that CD38-/- mice significantly alleviated HFD-induced hepatic steatosis. HFD or oleic acid (OA) remarkably increased the mRNA and protein expressions of CD38 in mouse hepatic tissues and primary hepatocytes or hepatic cell lines in vitro and in vivo, suggesting that CD38 might play a role in HFD-induced hepatic steatosis. We observed that CD38 deficiency markedly decreased HFD- or OA-induced the lipid accumulation and oxidative stress in CD38-/- livers or primary hepatocytes, respectively. In contrast, overexpression of CD38 in Hep1-6 cells aggravated OA-induced lipid accumulation and oxidative stress. Furthermore, CD38 deficiency markedly inhibited HFD- or OA-induced the expressions of NOX4, and increased the expression of PPARα, CPT1, ACOX1 and SOD2 in liver tissue and hepatocytes from CD38-/- mice, indicating that CD38 deficiency-mediated the enhancement of fatty acid oxidation and the inhibition of oxidative stress contributed to protecting NAFLD. More importantly, Ex527 (Sirt1 inhibitor) and 3-TYP (Sirt3 inhibitor) significantly enhanced OA-induced lipid accumulation and oxidative stress in CD38-/- primary hepatocytes, suggesting that the anti-lipid accumulation of CD38 deficiency might be dependent on NAD/Sirtuins-mediated enhancement of FAA β-oxidation and suppression of oxidative stress in hepatocytes. In conclusion, we demonstrated that CD38 deficiency protected mice from HFD-induced NAFLD by reducing lipid accumulation and suppressing oxidative stress via activating NAD/Sirtuins signaling pathways.

Background Obesity is a metabolic disorder syndrome characterized by excessive fat accumulation that is related to many diseases. Human amniotic mesenchymal stem cells (hAMSCs) have a great potential for cell-based therapy due to their characteristics such as pluripotency, low immunogenicity, no tumorigenicity, potent paracrine effects, and no ethical concern. Recently, we observed that both hAMSCs and their conditioned medium (hAMSCs-CM) efficiently repaired skin injury, inhibited hepatocellular carcinoma, and alleviated high-fat diet (HFD)-induced diabetes. However, the effects and the underlying mechanisms of hAMSCs-CM on high-fat diet (HFD)-induced obesity were not explored. Methods The characteristics of hAMSCs were confirmed by flow cytometry, RT-PCR, and immunofluorescence. Obese mice were induced by administrating HFD for 15 weeks and simultaneously, the mice were intraperitoneally injected with hAMSCs-CM weekly to evaluate the effects of hAMSCs-CM on HFD-induced obesity. GTT and ITT assays were used to assess the effects of hAMSCs-CM on HFD-induced glucose tolerance and insulin resistance. The lipid accumulation and adipocytes hypertrophy in mouse adipose tissues were determined by histological staining, in which the alterations of blood lipid, liver, and kidney function were also examined. The role of hAMSCs-CM in energy homeostasis was monitored by examining the oxygen consumption (VO2), carbon dioxide production (VCO2), and food and water intake in mice. Furthermore, the expressions of the genes related to glucose metabolism, fatty acid β oxidation, thermogenesis, adipogenesis, and inflammation were determined by western blot analysis, RT-PCR, and immunofluorescence staining. The roles of hAMSCs-CM in adipogenesis and M1/M2 macrophage polarization were investigated with 3T3-L1 preadipocytes or RAW264.7 cells in vitro. Results hAMSCs-CM significantly restrained HFD-induced obesity in mice by inhibiting adipogenesis and lipogenesis, promoting energy expenditure, and reducing inflammation. The underlying mechanisms of the anti-obesity of hAMSCs-CM might be involved in inhibiting PPARγ and C/EBPα-mediated lipid synthesis and adipogenesis, promoting GLUT4-mediated glucose metabolism, elevating UCP1/PPARα/PGC1α-regulated energy expenditure, and enhancing STAT3-ARG1-mediated M2-type macrophage polarization. Conclusion Our studies demonstrated that hAMSCs significantly alleviated HFD-induced obesity through their paracrine effects. Obviously, our results open up an attractive therapeutic modality for the prevention and treatment of obesity and other metabolic disorders clinically. Graphic Abstract The cytokines, exosomes, or micro-vesicles secreted from hAMSCs significantly inhibited HFD-induced obesity in mice by inhibiting lipid production and adipogenesis, promoting energy consumption, and reducing inflammation.

Inflammation-induced activation and dysfunction of endothelial cells play an important role in the pathology of multiple vascular diseases. Nicaraven, a potent hydroxyl radical scavenger, has recently been found to have anti-inflammatory roles; however, the mechanism of its action is not fully understood. Here we investigated the effects of Nicaraven on tumor necrosis factor α (TNFα) – induced inflammatory response in human umbilical vein endothelial cells and we explore the underlying mechanisms related to the nuclear factor-κB (NF-κB) signaling pathway. Our results showed that Nicaraven significantly reduced the reactive oxygen species production after TNFα stimulation. Nicaraven suppressed TNFα-induced mRNA expression of multiple adhesion molecules and pro-inflammatory cytokines, including vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), E-selectin, MCP-1, TNFα, interleukin-1β (IL-1β), IL-6, and IL-8. In addition, Nicaraven inhibited monocyte adhesion and reduced the protein levels of VCAM-1 and ICAM-1. Mechanistically, Nicaraven prevented TNFα-induced activation of NF-κB signaling pathway by suppressing the phosphorylation of NF-κB p65, IκBα, and IκB kinase (IKK)α/β, stabilizing IκBα, and inhibiting the translocation of p65 from cytosol to nucleus. Finally, we showed that Nicaraven improved the functions of endothelial cells, seen as the upregulation of endothelial nitric oxide synthase and increased nitric oxide levels. Our findings indicated that Nicaraven effectively inhibits TNFα-induced endothelial activation and inflammatory response at least partly through inhibiting NF-κB signaling pathway.

New carbon-loaded nickel chalcogenide electrode materials (NiS

CD38 is the main enzyme for nicotinamide adenine dinucleotide (NAD) degradation in mammalian cells. Decreased NAD levels are closely related to metabolic syndromes and aging-related diseases. Our study showed that CD38 deficiency significantly alleviated angiotensin II (Ang II)-induced vascular remodeling in mice, as shown by decreased blood pressures; reduced vascular media thickness, media-to-lumen ratio, and collagen deposition; and restored elastin expression. However, our bone marrow transplantation assay showed that CD38 deficiency in lymphocytes led to lack of protection against Ang II-induced vascular remodeling, suggesting that the effects of CD38 on Ang II-induced vascular remodeling might rely primarily on vascular smooth muscle cells (VSMCs), not lymphocytes. In addition, we observed that CD38 deficiency or NAD supplementation remarkably mitigated Ang II-induced vascular senescence by suppressing the biogenesis, secretion, and internalization of senescence-associated small extracellular vesicles (SA-sEVs), which facilitated the senescence of neighboring non-damaged VSMCs. Furthermore, we found that the protective effects of CD38 deficiency on VSMC senescence were related to restoration of lysosome dysfunction, particularly with respect to the maintenance of sirtuin-mediated mitochondrial homeostasis and activation of the mitochondria–lysosomal axis in VSMCs. In conclusion, our findings demonstrated that CD38 and its associated intracellular NAD decline are critical for Ang II-induced VSMC senescence and vascular remodeling.

Background/Aims: Previous studies showed that CD38 deficiency protected heart from ischemia/reperfusion injury and high fat diet (HFD)-induced obesity in mice. However, the role of CD38 in HFD-induced heart injury remains unclear. In the present study, we have investigated the effects and mechanisms of CD38 deficiency on HFD-induced heart injury. Methods: The metabolites in heart from wild type (WT) and CD38 knockout (CD38-/-) mice were examined using metabolomics analysis. Cell viability, lactate hydrogenase (LDH) release, super oxide dismutase (SOD) activity, reactive oxygen species (ROS) production, triglyceride concentration and gene expression were examined by biochemical analysis and QPCR. Results: Our results revealed that CD38 deficiency significantly elevated the intracellular glutathione (GSH) concentration and GSH/GSSG ratio, decreased the contents of free fatty acids and increased intracellular NAD+ level in heart from CD38-/- mice fed with HFD. In addition, in vitro knockdown of CD38 significantly attenuated OA-induced cellular injury, ROS production and lipid synthesis. Furthermore, the expression of mitochondrial deacetylase Sirt3 as well as its target genes FOXO3 and SOD2 were markedly upregulated in the H9C2 cell lines after OA stimulation. In contrast, the expressions of NOX2 and NOX4 were significantly decreased in the cells after OA stimulation. Conclusion: Our results demonstrated that CD38 deficiency protected heart from HFD-induced oxidative stress via activating Sirt3/FOXO3-mediated anti-oxidative stress pathway.

We previously observed that disruption of FK506‐binding protein 12.6 (FKBP12.6) gene resulted in cardiac hypertrophy in male mice. Studies showed that overexpression of FKBP12.6 attenuated thoracic aortic constriction (TAC)‐induced cardiac hypertrophy in mice, whereas the adenovirus‐mediated overexpression of FKBP12.6 induced hypertrophy and apoptosis in cultured neonatal cardiomyocytes, indicating that the role of FKBP12.6 in cardiac hypertrophy is still controversial. In this study, we aimed to investigate the roles and mechanisms of FKBP12.6 in angiotensin II (AngII)‐induced cardiac hypertrophy using various transgenic mouse models in vivo and in vitro. FKBP12.6 knockout (FKBP12.6−/−) mice and cardiac‐specific FKBP12.6 overexpressing (FKBP12.6 TG) mice were infused with AngII (1500 ng/kg/min) for 14 days subcutaneously by implantation of an osmotic mini‐pump. The results showed that FKBP12.6 deficiency aggravated AngII‐induced cardiac hypertrophy, while cardiac‐specific overexpression of FKBP12.6 prevented hearts from the hypertrophic response to AngII stimulation in mice. Consistent with the results in vivo, overexpression of FKBP12.6 in H9c2 cells significantly repressed the AngII‐induced cardiomyocyte hypertrophy, seen as reductions in the cell sizes and the expressions of hypertrophic genes. Furthermore, we demonstrated that the protection of FKBP12.6 on AngII‐induced cardiac hypertrophy was involved in reducing the concentration of intracellular Ca2+ ([Ca2+]i), in which the protein significantly inhibited the key Ca2+/calmodulin‐dependent signalling pathways such as calcineurin/cardiac form of nuclear factor of activated T cells 4 (NFATc4), calmodulin kinaseII (CaMKII)/MEF‐2, AKT/Glycogen synthase kinase 3β (GSK3β)/NFATc4 and AKT/mTOR signalling pathways. Our study demonstrated that FKBP12.6 protects heart from AngII‐induced cardiac hypertrophy through inhibiting Ca2+/calmodulin‐mediated signalling pathways.

Transition metal materials, NiS, NiO and NiSe2, with a uniform hollow-structure were obtained based on NiS2 hollow spheres, and were successfully synthesized with an L-cysteine assisted hydrothermal method at 120 °C. The electrochemical properties of the NiS2, NiS, NiO and NiSe2 hollow sphere electrodes were investigated by cyclic voltammetry, galvanostatic charge–discharge and electrochemical impedance spectroscopy tests. Firstly, the cyclic voltammetry curves of the four materials all displayed pseudo-capacitance behaviour. Moreover, the galvanostatic charge–discharge tests showed that the specific capacitance of the NiS2, NiS, NiO and NiSe2 electrodes was 1643 F g−1, 1076 F g−1, 581 F g−1 and 341 F g−1, respectively, at a current density of 1 A g−1. After 1000 cycles, the specific capacitance of the NiS2, NiS, NiO and NiSe2 electrodes was retained at 455 F g−1, 368 F g−1, 246 F g−1 and 269 F g−1, respectively. The results implied that both the NiS2 and NiS electrodes exhibited higher specific capacitance, while the NiO and NiSe2 electrodes showed a longer cycling life. This work highlights the advantageous electrochemical performance of the different nickel compounds, and contributes to providing a good reference for the preparation of superior supercapacitor materials with high performance.

Our previous research showed that CD38 played vital roles in Ang-II induced hypertrophy and high fat diet induced heart injury. However, the role of CD38 in heart aging is still unknown. In the present study, we reported that CD38 knockdown significantly protected cardiomyocytes from D-galactose (D-gal)-induced cellular senescence. Cellular senescence was evaluated by β-galactosidase staining, the expressions of genes closely related to aging including p16 and p21, and the ROS production, MDA content and the expressions of oxidant stress related genes were examined by biochemical analysis, Western blot and QPCR. Our results showed that the expression of CD38 was increased in H9c2 cells after D-gal treatment and the expressions of NAMPT and Sirt1 were downregulated in heart tissue from old mice. CD38 knockdown significantly reduced the number of SA-β-gal-positive cells and the expressions of p16 and p21 in H9c2 cells with or without D-gal treatment. The acetylation level of total protein was decreased in CD38 knockdown group, but the expression of Sirt3 was increased in CD38 knockdown group treated with D-gal. In addition, knockdown of CD38 significantly attenuated D-gal induced ROS production, MDA content and NOX4 expression in the cells. Inhibition Sirt1 partially reversed the effects of CD38 knockdown on D-gal induced senescence and oxidative stress. Furthermore, NAD+ supplementation reduced D-gal induced cellular senescence, ROS production and MDA content. The expression of SOD2 was increased and the NOX4 expression was decreased in H9c2 cells after NAD+ supplementation. Taken together, our results demonstrated that CD38 knockdown alleviated D-gal induced cell senescence and oxidative stress via NAD+/Sirt1 signaling pathway.

Ischemia/reperfusion (I/R) injury induces irreversible oxidative stress damage to the cardiac muscle. We previously observed that CD38 deficiency remarkably protects mouse embryonic fibroblasts (MEFs) from oxidative stress-induced injury. However, whether CD38 deficiency protects from I/R injury in the heart is not explored. Here, we showed that the hearts of CD38 deficient mice or wild type mice supplied with exogenous NAD were significantly protected from ischemia/reperfusion injury, seen as reduction of the myocardial infarct sizes when the mice were subjected to 30 min ischemia followed by 24 hours of reperfusion. Consistently, the protection of CD38 deficiency on hypoxia/reoxygenation (H/R) injury was confirmed with a CD38 knockdown H9c2 stable cell line. Furthermore, we observed that knockdown of CD38 remarkably inhibited ROS generation and intracellular Ca2+overloading induced by H/R in H9c2 cells. The FOXO1 and FOXO3 expressions were significantly elevated by H/R injury in CD38 knockdown cells compared with normal H9c2 cells. The cell immunofluorescence assay showed that FOXO1 nuclear translocation was significantly increased in CD38 knockdown H9c2 cells. In addition, we demonstrated that the increase of FOXO1 nuclear translocation was associated with the increased expressions of antioxidant catalase and SOD2 and the attenuated expression of the ROS generation enzyme NOX4. In conclusion, our results provide new evidence that CD38 deficiency protects the heart from I/R injury through activating SIRT1/FOXOs-mediated antioxidative stress pathway.

One-dimensional (1D) porous NixSy nanostructures have been successfully fabricated by two-step method consisting of solvothermal and subsequent annealing process. The suitable heat treatment temperature and reaction time play crucial roles in the final structure, morphology, as well as performance. The uniform and perfect porous NixSy nanostructures obtained at 310 °C exhibit outstanding microwave absorption performances. A minimum reflection loss of −35.6 dB is achieved at 8.5 GHz, and the effective absorption bandwidth almost covers 14.5 GHz with the absorber thickness range of 2.0−5.0 mm. It can be supposed that this porous structure with rough surface which is favor for increasing the microwave multiple reflection and scattering, contributes a high-performance electromagnetic absorption.

Background/Aims: Our and other studies showed that CD38 deficiency protected heart from ischemia/reperfusion injury and high fat diet (HFD)-induced obesity in mice, respectively. However, the roles of CD38 in lipid overload-induced heart injury were not evaluated. In the present study, we investigated the preventive effects and mechanisms of CD38 deficiency on mouse heart injury induced by HFD. Methods: The discrepant metabolites in heart from wild type (WT) and CD38 knockout (CD38 -/- ) mice fed with HFD were examined using metabolomics analysis. The cell viability, the lactate hydrogenase (LDH) release, super oxide dismutase (SOD) activity, reactive oxygen species (ROS) production, triglyceride concentration and the expressions of various corresponding genes were examined for evaluating the effects of CD38 on oleic acid (OA)-induced cell injury using CD38 knockdown H9C2 stable cell line. Results: Our results revealed that CD38 deficiency significantly elevated the intracellular glutathione (GSH) concentration and GSH/GSSG ratio, decreased the contents of various free fatty acids and increased intracellular NAD + level in heart of CD38 -/- mice fed with HFD. Knockdown of CD38 significantly attenuated OA-induced cell injury, ROS production and lipid synthesis, seen as enhancing cell viability, reducing LDH release, elevating SOD activity, and decreasing triglyceride content and expressions of FASN in the CD38 knockdown H9C2 stable cell line. In addition, we also observed that the mitochondrial deacetylase Sirt3 and its target genes FOXO3 and SOD2 were upregulated in the stable cell lines after OA stimulation. Furthermore, the expressions of NOX2 and NOX4 were attenuated, accompanied by decreasing Bax expression and increasing Bcl-2 expression in the cells after OA stimulation. Conclusions: Our results demonstrated that CD38 deficiency protected heart from HFD-induced oxidative stress via activating Sirt3/FOXO3-mediated anti-oxidative stress pathway.

Here we reported a coordinating etching and precipitating method to synthesize a complex binary metal oxides hollow cubic structure. A novel NiCoO

The molecular structural information on a kerogen isolated from Huadian oil shale was obtained using solid-state 13C nuclear magnetic resonance (NMR), X-ray photoelectron spectroscopy (XPS), Fourier transform infrared (FTIR), and X-ray diffraction (XRD) techniques. Then, a series of Huadian kerogen isomers were constructed on the basis of these structural data. The possible carbon skeleton isomer and the substituted position effects of the aromatic ring, aliphatic ether bond, carboxylic acid, and carboxylic acid derivative as well as the quantity of tertiary and quaternary carbons on Huadian kerogen model stability have been systematically studied on the basis of density functional theory (DFT) calculations. For the carbon skeleton isomer, the calculated total energy decreases with the increasing number of the closed annular space (grid), which is constituted by connecting the aliphatic chain to the aromatic cluster or other aliphatic chain. DFT calculations show an about 16.8 kcal mol–1 decrease in total...

A series of graphene-based materials composed of flower-like CuS/ZnS (CZS) microspheres and reduced graphene oxide (rGO) with different weight ratios have been fabricated via a two-step approach, in which CZS was synthesized first by a hydrothermal method, and then combined with rGO via a sonochemical process to form CuS/ZnS/rGO (CZS/rGO) composites. The photocatalytic activity was studied by photodegradation of methylene blue (MB) in the presence of hydrogen peroxide (H2O2). The results showed that all the graphene-based photocatalysts exhibited enhanced catalytic activity, compared to pure CuS/ZnS (CZS) composites. When the weight ratio of graphene in the composite materials was 20 wt%, the composite presented the highest photocatalytic efficiency, which could eliminate more than 99% of MB within 20 min and the photocatalytic efficiency could be kept at about 99% of the original photocatalytic efficiency after three cycles.

Tungsten oxide (WO

Amino-bacterial cellulose (amino-BC) was prepared by chemical modification of bacterial cellulose(BC). The adsorption characteristics and mechanism of amino-BC were studied. The results show that adsorption data can be fitted well by Langmuir equation and the pseudo-second order kinetics, indicating that the adsorption of amino-BC would obey monolayer molecule adsorption and the main action was chemisorption. Meanwhile, the adsorption process was studied by the Elovich equation and the intra-particle diffusion model, indicating that the absorption characteristics of metal ions on amino-BC is controlled by both film diffusion and particle diffusion. The increase of reaction temperature will accelerate the adsorbing rate because of endothermic reaction.

A series of CuS/ZnS nanocomposites (CZS) with a novel 3D hierarchical structure were obtained by a simple hydrothermal method. The effects of Zn2+ content, surfactant, reaction temperature and time on the morphology of the samples was studied. The products were characterized in detail and their photocatalytic performance in the degradation of methylene blue (MB) and microwave absorption properties as an absorber were also investigated. The results indicate that CZS0.4 presented an outstanding photocatalytic degradation rate of more than 97% for MB in the first twenty minutes, and MB was degraded almost completely in the presence of each of the six samples alone 70 minutes after photocatalytic reaction. CZS0.3 exhibited excellent microwave absorption properties, presenting a reflection loss as much as −22.6 dB at 9.7 GHz with a thickness of 3 mm, which is much better than that of pure CuS.

Background Nonalcoholic fatty liver disease is one of the most common liver diseases in the world and is a typical hepatic manifestation of metabolic syndrome which is characterized with lipid accumulation in liver. Nicotinamide phosphoribosyltransferase (NAMPT) has been recently identified as an enzyme involved in nicotinamide adenine dinucleotide (NAD+) biosynthesis and plays an important role in cellular metabolism in variety of organs in mammals. The aim of this study was to investigate the effects of NAMPT on high fat diet-induced hepatic steatosis. Methods Hepatic steatosis model was induced by high fat diet (HFD) in C57BL/6 mice in vivo. HepG2 and Hep1-6 hepatocytes were transfected with NAMPT vector plasmid or treated with NAMPT inhibitor FK866 and then incubated with oleic acid. Lipids accumulation was examined by HE staining or oil red staining. Quantitative RT-PCR and Western blot were used to measure expressions of the genes involved in lipogenic synthesis. Results FK866 significantly promoted liver steatosis in the mice fed with HFD and hepatic lipid accumulation in vitro, accompanied by the increases of the expressions of lipogenic genes such as sterol regulatory element-binding protein 1 (SREBP1) and fatty acid synthase (FASN). Nicotinamide mononucleotide (NMN) and NAD+ significantly rescued the actions of FK866 in vitro. In contrast, overexpression of NAMPT in HepG2 and Hep1-6 hepatocytes ameliorated hepatic lipid accumulation. In addition, FK866 decreased the protein levels of Sirt1 and phospho-AMPKα in liver of the HFD fed mice. Furthermore, Resveratrol, a Sirt1 activator, significantly reduced lipogenic gene expressions, while EX-527, a Sirt1 specific inhibitor, had the opposite effects. Conclusion Our results demonstrated that inhibition of NAMPT aggravated the HFD- or oleic acid-induced hepatic steatosis through suppressing Sirt1-mediated signaling pathway. On the one hand, the inhibition of NAMPT reduced the production of NAD+ through inhibiting the NAD+ salvage pathway, resulting in the decrease of Sirt1 activity, and then attenuated the deacetylation of SREBP1 in which the inhibition of SREBP1 activity promoted the expressions of FASN and ACC. On the other hand, the reduced Sirt1 activity alleviated the activation of AMPKα to further enhance SREBP1 activities. Electronic supplementary material The online version of this article (doi:10.1186/s12944-017-0464-z) contains supplementary material, which is available to authorized users.

The electronic structure and bonding feature of a series of mono-ruthenium-substituted Keggin-type polyoxometalates (POMs) have been investigated by using density functional theory (DFT) calculation, natural bond orbital (NBO) analysis and energy-decomposition analysis (EDA). A comparison of the electronic properties of two known dimethyl sulfoxide (DMSO)-supported mono-ruthenium-substituted Keggin-type POMs shows that both complexes have the analogous frontier-molecular orbital feature. One of them possesses a relatively small HOMO–LUMO gap because of the high HOMO energy level. This difference comes from a high composition of POM ligand with antibonding feature in HOMO. In addition, three typical Keggin-type POM complexes [{PW11O39}RuII/III(L)]n− (L = H2O, C5H5N, NH3) have also been explored according to our computational studies. The NBO analysis shows that the RuII/III–L bond comes from donor–acceptor interactions between the end ligand and the ruthenium (II/III) centre. The EDA shows that the POM com...

The electronic structure and second-order nonlinear optical (NLO) property of a series of monoruthenium-substituted Keggin-type polyoxometalates (POMs) have been studied by using density functional theory (DFT) and time-dependent (TD)DFT calculations. The DFT calculation supports that these POM complexes possess donor-π-conjugated bridge-acceptor (D-π-A) structure, which the ruthenium atom acts as the role of electron donor and the three vanadium atoms in cap region of Keggin-type POM act as the role of electron acceptor. It is well-known that D-π-A structure, as a simple molecular scheme, has been successfully used in the development of organic NLO materials. However, the totally inorganic molecule having D-π-A structure is very rare. Thereby the second-order NLO properties of these POM complexes have been analyzed in this work. According to the calculations, introduction of the electron acceptor leads to a substantial enhancement on the second-order NLO response. The calculated βHRS(−2ω; ω, ω) value of ...

Cardiac hypertrophy is an early hallmark during the clinical course of heart failure and regulated by various signalling pathways. Recently, we observed that mouse embryonic fibroblasts from CD38 knockout mice were significantly resistant to oxidative stress such as H2O2‐induced injury and hypoxia/reoxygenation‐induced injury. In addition, we also found that CD38 knockout mice protected heart from ischaemia reperfusion injury through activating SIRT1/FOXOs‐mediated antioxidative stress pathway. However, the role of CD38 in cardiac hypertrophy is not explored. Here, we investigated the roles and mechanisms of CD38 in angiotensin II (Ang‐II)‐induced cardiac hypertrophy. Following 14 days of Ang‐II infusion with osmotic mini‐pumps, a comparable hypertension was generated in both of CD38 knockout and wild‐type mice. However, the cardiac hypertrophy and fibrosis were much more severe in wild‐type mice compared with CD38 knockout mice. Consistently, RNAi‐induced knockdown of CD38 decreased the gene expressions of atrial natriuretic factor (ANF) and brain natriuretic peptide (BNP) and reactive oxygen species generation in Ang‐II‐stimulated H9c2 cells. In addition, the expression of SIRT3 was elevated in CD38 knockdown H9c2 cells, in which SIRT3 may further activate the FOXO3 antioxidant pathway. The intracellular Ca2+ release induced by Ang‐II markedly decreased in CD38 knockdown H9c2 cells, which might be associated with the decrease of nuclear translocation of NFATc4 and inhibition of ERK/AKT phosphorylation. We concluded that CD38 plays an essential role in cardiac hypertrophy probably via inhibition of SIRT3 expression and activation of Ca2+‐NFAT signalling pathway. Thus, CD38 may be a novel target for treating cardiac hypertrophy.

Transition metal phosphoraniminato derivatives of Keggin-type polyoxometalates (POMs) are important intermediates in N-transfer reactions. Density functional theory (DFT) has been employed to calculate the electronic structures, bonding features and redox properties of the iron and ruthenium phosphoraniminato derivatives of Keggin-type POMs, [PW11O39{MVNPPh3}]3− (M = Fe, Ru). Our DFT calculations show that both anions have the same qualitative M-N single bond features. However, the calculations predict that the FeN system possesses a lower energy and more accessible metal-nitrogen antibonding orbital than the RuN system. This results in a greater weakening of the Fe-N bond in the reduction process, and thus enhances its N-transfer reactivity.

In this paper, electronic structures and third-order nonlinear optical (NLO) properties of a series of Pt–Pt bond-containing metal complexes have been calculated by using the density functional theory (DFT) combining with the sum-over-states (SOS) method. In order to check the reliability of this method, the electron correlations and basis sets have been compared. Our calculated results show that introduction of electron donor, thiophene ring and lengthing of organic conjugated ligand can enhance third-order NLO responses. The electronic structure analysis shows that the [Pt–Pt(H2P(CH2)PH2)2] fragment displays strong electron-withdrawing character in these systems. Meanwhile, the third-order NLO response of Pt–Pt bond also has been estimated by using TDDFT–SOS method. An enhancement of third-order NLO response has been observed because of the introduction of the Pt–Pt bond. This is mainly due to the intense and low-lying metal-to-ligand charge transfer (MLCT) and intraligand (IL) CT transitions.

Fe3O4 nanocrystals with narrow particle size distribution (10–15 nm) were produced in high yield by using a simple solution-phase method at room temperature. In this approach, the iron oxide nanocrystals can be continually prepared through controlling the pH value of the solution. The as-synthesized Fe3O4 nanoparticles are single-crystalline and exhibit high saturation magnetization. New adsorbents of Fe3O4 nanocrystals immobilized on bacterial cellulose (FNBC) were prepared by a simple blending method in the hope of removing heavy metal ions from aqueous solutions. The FNBC showed significantly higher affinity for removing Cd2+ compared to BC. In addition, the effect of characteristic parameters such as pH value, adsorption time by simulating the adsorptive kinetics, and adsorptive isotherms were also investigated.

OBJECTIVES The purpose of this study was to compare the use of sonography and non-contrast-enhanced magnetic resonance imaging (MRI) for detection and staging of glottic carcinoma. METHODS In this study, 30 consecutive patients with glottic squamous cell carcinoma underwent high-frequency sonography and non-contrast-enhanced MRI before surgical treatment. Tumor detectability and imaging findings were evaluated independently and then compared with the surgical and postoperative pathologic findings. RESULTS Sonography showed a trend toward higher detectability than MRI in early (stage T1 and T2) glottic carcinoma (94.1% [16 of 17 patients] for sonography versus 76.5% [13 of 17 patients] for MRI; P = .335). With regard to T staging, the overall accuracy rates were 80.0% (24 of 30) for sonography and 76.7% (23 of 30) for MRI; the difference was not statistically significant (P > .99). Non-contrast-enhanced MRI was superior to sonography in showing tumor involvement in the retrolaryngeal extent of glottic carcinoma. CONCLUSIONS Sonography is suggested as a noninvasive complementary modality for detection and initial staging of glottic carcinoma.

The second-order nonlinear optical (NLO) properties of a series of expanded porphyrins, donor–acceptor-substituted hexaphyrins(1.1.1.1.1.1) and their mono- and bis-Au(III) complexes have been calculated based on density functional theory. The result shows that large-sized hexaphyrin molecules have a large static first hyperpolarizability when compared with the relatively small porphyrin molecule. However, the small porphyrin molecule is intrinsically more efficient for enhancement of the intrinsic NLO response according to intrinsic hyperpolarizability analysis. On the other hand, the switchable NLO properties of aromatic-to-antiaromatic conversion caused by two-electron oxidation/reduction processes have also been probed. The result shows that aromatic→antiaromatic reduction on the hexaphyrin core decreases the static first hyperpolarizability and the intrinsic hyperpolarizability. The value of the aromatic complex is ∼25 times larger than that of the antiaromatic complex. This indicates that the hexaphy...

The redox-switchable 2D second-order nonlinear optical (NLO) property of a series of tetrathiafulvalene (TTF) derivatives has been studied based on the density functional theory (DFT) calculations. The redox-active TTF unit has been considered as a manipulative center for switching the 2D second-order NLO properties. Our DFT calculations show that introduction of the TTF unit cannot effectively enhance the second-order NLO properties relative to the reference system 1 because the nonplane embowed arrangement of the TTF unit reduces the electron donor capacity. The electronic structure analysis shows that the TTF unit acts as the oxidized center in one- and two-electron-oxidized processes for 5. A significant transformation on the structure of the TTF unit, the TTF unit changes from the embowed structure to a planar structure, has been found in the series of oxidized processes according to DFT-optimized calculations. This leads to the low excited energy and different charge transfer features of the oxidize...

Time-dependent density functional theory (TDDFT) was employed to study second-order nonlinear optical (NLO) properties of transition metal fullerene complexes with a face to face model. The results show that the ruthenium species possesses the larger second-order NLO response than that of the iron species. Chemical modifications of the fullerene by carbon–carbon bond scission can tune charge transfer character in these complexes, and increase the static first hyperpolarizability. The electronic structure analysis and TDDFT calculations show that the open-cage complex in the ruthenium species possesses low-lying and strong charge transfer transitions, and thus give the largest second-order NLO response.

Poly(vinyl alcohol) (PVA) fibrous mats dealt with polyoxometalate containing vanadium were prepared by electrospinning method. The fibrous mats were characterized by infrared spectra, X-ray powder diffraction patterns, and scanning electron microscopy photographs. The results showed that PVA could combine with polyoxometalate by intermolecular H-bonding. The studies of the diameter distributions indicated that the average diameter of the fibrous mats was about 260–420 nm. The effects of the polyoxometalate content, electrode potential, temperature, and time on the swelling capacity of the fibrous mats in water were investigated. The existence of the polyoxometalate containing vanadium was advantaged for the crosslinking of PVA fibrous mats. The swelling degree of PVA fibrous mats containing polyoxometalate dealt with 383 K for 18 h approached zero in water. © 2007 Wiley Periodicals, Inc. J Appl Polym Sci, 2007