The effects of Zn content on the microstxucture and the mechanical and corrosion properties of as-cast low-alloyed Mg-xZn~.2Ca alloys (x = 0.6wt%, 2.0wt%, 2.5wt%, hereafter denoted as 0.6Zn, 2.0Zn, and 2.5Zn alloys, ...The effects of Zn content on the microstxucture and the mechanical and corrosion properties of as-cast low-alloyed Mg-xZn~.2Ca alloys (x = 0.6wt%, 2.0wt%, 2.5wt%, hereafter denoted as 0.6Zn, 2.0Zn, and 2.5Zn alloys, respectively) axe investigated. The results show that the Zn content not only influences grain refinement but also induces different phase precipitation behaviors. The as-cast microstxucture of the 0.6Zn alloy is composed of ct-Mg, Mg2Ca, and Ca2Mg6Zn3 phases, whereas 2.0Zn and 2.5Zn alloys only contain ct-Mg and Ca2Mg6Zn3 phases, as revealed by X-ray diffraction (XRD) and txonsmission electron microscopy (TEM) analyses. Moreover, with in- creasing Zn content, both the ultimate tensile strength (UTS) and the elongation to fracture first increase and then decrease. Among the three investigated alloys, the largest UTS (178 MPa) and the highest elongation to fracture (6.5%) are obtained for the 2.0Zn alloy. In addition, the corrosion rate increases with increasing Zn content. This paper provides on updated investigation of the alloy composi- tion-microstxucture-property relationships of different Zn-containing Mg-Zn-Ca alloys.展开更多
The effect of fly ash on controlling alkail-silica rection (ASR) in simudated alkali solution was studied. The expausion of mortar bars and the content of Ca( OH)2 in cement paste cured at 80 °G for 91 d were...The effect of fly ash on controlling alkail-silica rection (ASR) in simudated alkali solution was studied. The expausion of mortar bars and the content of Ca( OH)2 in cement paste cured at 80 °G for 91 d were measured. Traasmission electron microscopy (TEM) and high-resolution transmission electron microscot9 (HRTEM) were employed to study the microstructure of C-S-H. TEM/ energy dispersive spectroscopy (EDS) leas then used to determine the composition of C-S-H. The pore structure of the paste was analyzed by mercury intntsion porosimetry (MIP). The results show that the contents of fly ash of 30% and 45% can well inhibit ASR. And the content of Ca(OH) 2 decreases with the increase of fly ash. That fly ash reacted with Ca(OH)2 to produce C-S-H with a low Ca/Si molar ratio could bind more Na^+ and K^+ ious, and produce a reduction in the amount of soluble alkali available for ASR. At the same time, the C- S- H produced by pozzolanic reaction converted large pores to snudler ones ( gel pores smaller than 10 nm ) to deusify the pore structure. Perhaps that could inhibit alkali trausport to aggregate for ASR.展开更多
Glutathione(GSH) is a tripeptide that constitutes one of the main intracellular reducing compounds. The normal content of GSH in the intestine is essential to optimize the intestinal Ca2+ absorption. The use of GSH de...Glutathione(GSH) is a tripeptide that constitutes one of the main intracellular reducing compounds. The normal content of GSH in the intestine is essential to optimize the intestinal Ca2+ absorption. The use of GSH depleting drugs such as DL-buthionine-S,R-sulfoximine, menadione or vitamin K3, sodium deoxycholate or diets enriched in fructose, which induce several features of the metabolic syndrome, produce inhibition of the intestinal Ca2+ absorption. The GSH depleting drugs switch the redox state towards an oxidant condition provoking oxidative/nitrosative stress and inflammation, which lead to apoptosis and/or autophagy of the enterocytes. Either the transcellular Ca2+ transport or the paracellular Ca2+ route are altered by GSH depleting drugs. The gene and/or protein expression of transporters involved in the transcellular Ca2+ pathway are decreased. The flavonoids quercetin and naringin highly abrogate the inhibition of intestinal Ca2+ absorption, not only by restoration of the GSH levels in the intestine but also by their anti-apoptotic properties. Ursodeoxycholic acid, melatonin and glutamine also block the inhibition of Ca2+ transport caused by GSH depleting drugs. The use of any of these antioxidants to ameliorate the intestinal Ca2+ absorption under oxidant conditions associated with different pathologies in humans requires more investigation with regards to the safety, pharmacokinetics and pharmacodynamics of them.展开更多
OBJECTIVE To determine the functional role of hydrogen sulfide(H_2S) in protecting against mitochondrial dysfunction in heart failure through the inhibition of Ca^(2+)/calmodulin-dependent protein kinaseⅡ(Ca MKⅡ) us...OBJECTIVE To determine the functional role of hydrogen sulfide(H_2S) in protecting against mitochondrial dysfunction in heart failure through the inhibition of Ca^(2+)/calmodulin-dependent protein kinaseⅡ(Ca MKⅡ) using wild type and CSE knockout mouse models.METHODS Continuous subcutaneous injection isoprenaline(7.5 mg·kg^(-1) per day),once a day for 4 weeks to induce heart failure in male C57BL/6(6-8 weeks old) mice and CSE-/-mice.150 μmol·L^(-1) H_2O_2 was used to induce oxidative stress in H9c2 cells.Echocardiograph was used to detect cardiac parameters.H&E stain and Masson stain was to observation histopathological changes.Western blot was used to detect protein expression and activity.The si RNA was used to silence protein expression.HPLC was used to detect H_2S level.Biotin assay was used to detect the level of S-sulfhydration protein.RESULTS Treatment with S-propyl-L-cysteine(SPRC) or sodium hydrosulfide(Na HS),modulators of blood H_2S levels,attenuated the development of heart failure in animals,reduced lipid peroxidation,and preserved mitochondrial function.The inhibition Ca MKⅡ phosphorylation by SPRC and Na HS as demonstrated using both in vivo and in vitro models corresponded with the cardioprotective effects of these compounds.Interestingly,Ca MKⅡ activity was found to be elevated in CSE-/-mice as compared to wild type animals and the phosphorylation status of Ca MK Ⅱ appeared to relate to the severity of heart failure.Importantly,in wild type mice SPRC was found to promote S-sulfhydration of Ca MKⅡ leading to reduced activity of this protein however,in CSE-/-mice S-sulfhydration was abolished following SPRC treatment.CONCLUSION A novel mechanism depicting a role of S-sulfhydration in the regulation of Ca MKⅡ is presented.SPRC mediated S-sulfhydration of Ca MKⅡ was found to inhibit Ca MKⅡ activity and to preserve cardiovascular homeostasis.展开更多
基金supported by the National Natural Science Foundation of China(No.51671017)Fundamental Research Funds for the Central Universities(No.FRF-GF-17-B3)+1 种基金Beijing Laboratory of Metallic Materials and Processing for Modern Transportation,the Opening Research Fund of State Key Laboratory for Advanced Metals and Materials(Nos.2016Z-11,2017Z-08)State's Key Project of Research and Development Plan(No.2016YFB0300801)
文摘The effects of Zn content on the microstxucture and the mechanical and corrosion properties of as-cast low-alloyed Mg-xZn~.2Ca alloys (x = 0.6wt%, 2.0wt%, 2.5wt%, hereafter denoted as 0.6Zn, 2.0Zn, and 2.5Zn alloys, respectively) axe investigated. The results show that the Zn content not only influences grain refinement but also induces different phase precipitation behaviors. The as-cast microstxucture of the 0.6Zn alloy is composed of ct-Mg, Mg2Ca, and Ca2Mg6Zn3 phases, whereas 2.0Zn and 2.5Zn alloys only contain ct-Mg and Ca2Mg6Zn3 phases, as revealed by X-ray diffraction (XRD) and txonsmission electron microscopy (TEM) analyses. Moreover, with in- creasing Zn content, both the ultimate tensile strength (UTS) and the elongation to fracture first increase and then decrease. Among the three investigated alloys, the largest UTS (178 MPa) and the highest elongation to fracture (6.5%) are obtained for the 2.0Zn alloy. In addition, the corrosion rate increases with increasing Zn content. This paper provides on updated investigation of the alloy composi- tion-microstxucture-property relationships of different Zn-containing Mg-Zn-Ca alloys.
基金Founded bythe National Basic Research Programof China"973"(No.2001CB610706)
文摘The effect of fly ash on controlling alkail-silica rection (ASR) in simudated alkali solution was studied. The expausion of mortar bars and the content of Ca( OH)2 in cement paste cured at 80 °G for 91 d were measured. Traasmission electron microscopy (TEM) and high-resolution transmission electron microscot9 (HRTEM) were employed to study the microstructure of C-S-H. TEM/ energy dispersive spectroscopy (EDS) leas then used to determine the composition of C-S-H. The pore structure of the paste was analyzed by mercury intntsion porosimetry (MIP). The results show that the contents of fly ash of 30% and 45% can well inhibit ASR. And the content of Ca(OH) 2 decreases with the increase of fly ash. That fly ash reacted with Ca(OH)2 to produce C-S-H with a low Ca/Si molar ratio could bind more Na^+ and K^+ ious, and produce a reduction in the amount of soluble alkali available for ASR. At the same time, the C- S- H produced by pozzolanic reaction converted large pores to snudler ones ( gel pores smaller than 10 nm ) to deusify the pore structure. Perhaps that could inhibit alkali trausport to aggregate for ASR.
文摘Glutathione(GSH) is a tripeptide that constitutes one of the main intracellular reducing compounds. The normal content of GSH in the intestine is essential to optimize the intestinal Ca2+ absorption. The use of GSH depleting drugs such as DL-buthionine-S,R-sulfoximine, menadione or vitamin K3, sodium deoxycholate or diets enriched in fructose, which induce several features of the metabolic syndrome, produce inhibition of the intestinal Ca2+ absorption. The GSH depleting drugs switch the redox state towards an oxidant condition provoking oxidative/nitrosative stress and inflammation, which lead to apoptosis and/or autophagy of the enterocytes. Either the transcellular Ca2+ transport or the paracellular Ca2+ route are altered by GSH depleting drugs. The gene and/or protein expression of transporters involved in the transcellular Ca2+ pathway are decreased. The flavonoids quercetin and naringin highly abrogate the inhibition of intestinal Ca2+ absorption, not only by restoration of the GSH levels in the intestine but also by their anti-apoptotic properties. Ursodeoxycholic acid, melatonin and glutamine also block the inhibition of Ca2+ transport caused by GSH depleting drugs. The use of any of these antioxidants to ameliorate the intestinal Ca2+ absorption under oxidant conditions associated with different pathologies in humans requires more investigation with regards to the safety, pharmacokinetics and pharmacodynamics of them.
文摘OBJECTIVE To determine the functional role of hydrogen sulfide(H_2S) in protecting against mitochondrial dysfunction in heart failure through the inhibition of Ca^(2+)/calmodulin-dependent protein kinaseⅡ(Ca MKⅡ) using wild type and CSE knockout mouse models.METHODS Continuous subcutaneous injection isoprenaline(7.5 mg·kg^(-1) per day),once a day for 4 weeks to induce heart failure in male C57BL/6(6-8 weeks old) mice and CSE-/-mice.150 μmol·L^(-1) H_2O_2 was used to induce oxidative stress in H9c2 cells.Echocardiograph was used to detect cardiac parameters.H&E stain and Masson stain was to observation histopathological changes.Western blot was used to detect protein expression and activity.The si RNA was used to silence protein expression.HPLC was used to detect H_2S level.Biotin assay was used to detect the level of S-sulfhydration protein.RESULTS Treatment with S-propyl-L-cysteine(SPRC) or sodium hydrosulfide(Na HS),modulators of blood H_2S levels,attenuated the development of heart failure in animals,reduced lipid peroxidation,and preserved mitochondrial function.The inhibition Ca MKⅡ phosphorylation by SPRC and Na HS as demonstrated using both in vivo and in vitro models corresponded with the cardioprotective effects of these compounds.Interestingly,Ca MKⅡ activity was found to be elevated in CSE-/-mice as compared to wild type animals and the phosphorylation status of Ca MK Ⅱ appeared to relate to the severity of heart failure.Importantly,in wild type mice SPRC was found to promote S-sulfhydration of Ca MKⅡ leading to reduced activity of this protein however,in CSE-/-mice S-sulfhydration was abolished following SPRC treatment.CONCLUSION A novel mechanism depicting a role of S-sulfhydration in the regulation of Ca MKⅡ is presented.SPRC mediated S-sulfhydration of Ca MKⅡ was found to inhibit Ca MKⅡ activity and to preserve cardiovascular homeostasis.