| 2 | Polyoxometalate derived p-n heterojunction for optimized reaction interface and improved HER显示文摘MoS_(2) is a typical electrocatalyst for hydrogen evolution reaction(HER),but the HER activity is spoilt by intensive adsorption towards H^(*),which requires further improvement.For n-type MoS_(2),the construction of p-n heterojunction with p-type MoO_(3) can reverse this situation,because inner electronic field in p-n heterojunction can facilitate H^(*) desorption.Based on this hypothesis,p-n heterojunction is built between MoS_(2) and MoO_(3) with polyoxometalate compound as precursor.The obtained MoO_(3)/MoS_(2) exhibits excellent HER activity,which only requires 68 mV to obtain 10 mA/cm^(2).With MoO_(3)/MoS_(2) as cathode material and Zn slice as anode,Zn-H^(+)battery is assembled.Its open circuit voltage achieves 1.11 V with short circuit current 151.4 mA/cm^(2).The peak power density of this Zn-H^(+) battery reaches 47.6 mW/cm^(2).When discharge at 10 mA/cm^(2),the specific capacity and energy density reach 728 mAh/g and 759 Wh/kg.In this process,H_(2) production rate of Zn-H^(+) battery achieves 364μmol/h with Faradic efficiency 97.8%.It realizes H_(2) production and electricity generation simultaneously. | Xiaoli Cui Yunmeng Sun Xinxin Xu | 2023 | Chinese Chemical Letters2023，34，3： | 0 |
| 3 | Growth differentiation factor 11 promotes macrophage polarization towards M2 to attenuate myocardial infarction via inhibiting Notch1 signaling pathway显示文摘Background:Myocardial infarctions(MI)is a major threat to human health especially in people exposed to cold environment.The polarization of macrophages towards different functional phenotypes(M1 macrophages and M2 macrophages)is closely related to MI repairment.The growth differentiation factor 11(GDF11)has been reported to play a momentous role in inflammatory associated diseases.In this study,we examined the regulatory role of GDF11 in macrophage polarization and elucidated the underlying mechanisms in MI.Methods:In vivo,the mice model of MI was induced by permanent ligation of the left anterior descending coronary artery(LAD),and mice were randomly divided into the sham group,MI group,and MI+GDF11 group.The protective effect of GDF11 on myocardial infarction and its effect on macrophage polarization were verified by echocardiography,triphenyl tetrazolium chloride staining and immunofluorescence staining of heart tissue.In vitro,based on the RAW264.7 cell line,the effect of GDF11 in promoting macrophage polarization toward the M2 type by inhibiting the Notch1 Signaling pathway was validated by qRT-PCR,Western blot,and flow cytometry.Results:We found that GDF11 was significantly downregulated in the cardiac tissue of MI mice.And GDF11 supplementation can improve the cardiac function.Moreover,GDF11 could reduce the proportion of M1 macrophages and increase the accumulation of M2 macrophages in the heart tissue of MI mice.Furthermore,the cardioprotective effect of GDF11 on MI mice was weakened after macrophage clearance.At the cellular level,application of GDF11 could inhibit the expression of M1 macrophage(classically activated macrophage)markers iNOS,interleukin(IL)-1β,and IL-6 in a dose-dependent manner.In contrast,GDF11 significantly increased the level of M2 macrophage markers including IL-10,CD206,arginase 1(Arg1),and vascular endothelial growth factor(VEGF).Interestingly,GDF11 could promote M1 macrophages polarizing to M2 macrophages.At the molecular level,GDF11 significantly down-regulated the Notch1 signaling pathway,the activation of which has been demonstrated to promote M1 polarization in macrophages.Conclusions:GDF11 promoted macrophage polarization towards M2 to attenuate myocardial infarction via inhibiting Notch1 signaling pathway. | Manyu Gong Xuewen Yang Yaqi Wang Yanying Wang Dongping Liu Haodong Li Yunmeng Qu Xiyang Zhang Yanwei Zhang Han Sun Lei Jiao Ying Zhang | 2023 | Frigid Zone Medicine2023，3，1： | 0 |
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