Solid-state electrolytes with high oxidation stability are crucial for achieving high power density allsolid-state lithium batteries.Halide electrolytes are promising candidates due to their outstanding compatibility ...Solid-state electrolytes with high oxidation stability are crucial for achieving high power density allsolid-state lithium batteries.Halide electrolytes are promising candidates due to their outstanding compatibility with cathode materials and high Li^(+)conductivity.However,the electrochemical stability of chloride electrolytes is still limited,leaving them unsuitable for ultrahigh voltage operation.Besides,chemical compatibility issue between sulfide and halide electrolytes affects the electrochemical performance of all-solid-state batteries.Herein,Li-ion conductor Li_(3+x)InCl_(6-x)O_(x) is designed to address these challenges.Li_(3.25)InCl_(5.75)O_(0.25)shows a Li-ion conductivity of 0.90 mS cm^(-1)at room temperature,a high onset oxidation voltage of 3.84 V,fewer by-products at ultrahigh operation voltage,and good chemical compatibility with Li_(5.5)PS_(4.5)Cl_(1.5).The Li_(3.25)InCl_(5.75)O_(0.25)@LiNi_(0.7)Co_(0.1)Mn_(0.2)O_(2)-Li_(3.25)InCl_(5.75)O_(0.25)-VGCF/Li_(3.25)InCl_(5.75)O_(0.25)/Li_(5.5)PS_(4.5)Cl_(1.5)/Li-In battery delivers good electrochemical performances at high operating voltage.This work provides a simple,economical,and effective strategy for designing high-voltage all-solid-state electrolytes.展开更多
BACKGROUND Leukemia stem cells(LSCs)are found to be one of the main factors contributing to poor therapeutic effects in acute myeloid leukemia(AML),as they are protected by the bone marrow microenvironment(BMM)against...BACKGROUND Leukemia stem cells(LSCs)are found to be one of the main factors contributing to poor therapeutic effects in acute myeloid leukemia(AML),as they are protected by the bone marrow microenvironment(BMM)against conventional therapies.Gossypol acetic acid(GAA),which is extracted from the seeds of cotton plants,exerts anti-tumor roles in several types of cancer and has been reported to induce apoptosis of LSCs by inhibiting Bcl2.AIM To investigate the exact roles of GAA in regulating LSCs under different microenvironments and the exact mechanism.METHODS In this study,LSCs were magnetically sorted from AML cell lines and the CD34+CD38-population was obtained.The expression of leucine-rich pentatricopeptide repeat-containing protein(LRPPRC)and forkhead box M1(FOXM1)was evaluated in LSCs,and the effects of GAA on malignancies and mitochondrial RESULTS LRPPRC was found to be upregulated,and GAA inhibited cell proliferation by degrading LRPPRC.GAA induced LRPPRC degradation and inhibited the activation of interleukin 6(IL-6)/janus kinase(JAK)1/signal transducer and activator of transcription(STAT)3 signaling,enhancing chemosensitivity in LSCs against conventional chemotherapies,including L-Asparaginase,Dexamethasone,and cytarabine.GAA was also found to downregulate FOXM1 indirectly by regulating LRPPRC.Furthermore,GAA induced reactive oxygen species accumulation,disturbed mitochondrial homeostasis,and caused mitochondrial dysfunction.By inhibiting IL-6/JAK1/STAT3 signaling via degrading LRPPRC,GAA resulted in the elimination of LSCs.Meanwhile,GAA induced oxidative stress and subsequent cell damage by causing mitochondrial damage.CONCLUSION Taken together,the results indicate that GAA might overcome the BMM protective effect and be considered as a novel and effective combination therapy for AML.展开更多
基金supported by the National Key Research and Development Program of China(2021YFB2500200)the National Natural Science Foundation of China(52177214,52222703)for supporting our workJiangsu Funding Program for Excellent Postdoctoral Talent for the support。
文摘Solid-state electrolytes with high oxidation stability are crucial for achieving high power density allsolid-state lithium batteries.Halide electrolytes are promising candidates due to their outstanding compatibility with cathode materials and high Li^(+)conductivity.However,the electrochemical stability of chloride electrolytes is still limited,leaving them unsuitable for ultrahigh voltage operation.Besides,chemical compatibility issue between sulfide and halide electrolytes affects the electrochemical performance of all-solid-state batteries.Herein,Li-ion conductor Li_(3+x)InCl_(6-x)O_(x) is designed to address these challenges.Li_(3.25)InCl_(5.75)O_(0.25)shows a Li-ion conductivity of 0.90 mS cm^(-1)at room temperature,a high onset oxidation voltage of 3.84 V,fewer by-products at ultrahigh operation voltage,and good chemical compatibility with Li_(5.5)PS_(4.5)Cl_(1.5).The Li_(3.25)InCl_(5.75)O_(0.25)@LiNi_(0.7)Co_(0.1)Mn_(0.2)O_(2)-Li_(3.25)InCl_(5.75)O_(0.25)-VGCF/Li_(3.25)InCl_(5.75)O_(0.25)/Li_(5.5)PS_(4.5)Cl_(1.5)/Li-In battery delivers good electrochemical performances at high operating voltage.This work provides a simple,economical,and effective strategy for designing high-voltage all-solid-state electrolytes.
文摘BACKGROUND Leukemia stem cells(LSCs)are found to be one of the main factors contributing to poor therapeutic effects in acute myeloid leukemia(AML),as they are protected by the bone marrow microenvironment(BMM)against conventional therapies.Gossypol acetic acid(GAA),which is extracted from the seeds of cotton plants,exerts anti-tumor roles in several types of cancer and has been reported to induce apoptosis of LSCs by inhibiting Bcl2.AIM To investigate the exact roles of GAA in regulating LSCs under different microenvironments and the exact mechanism.METHODS In this study,LSCs were magnetically sorted from AML cell lines and the CD34+CD38-population was obtained.The expression of leucine-rich pentatricopeptide repeat-containing protein(LRPPRC)and forkhead box M1(FOXM1)was evaluated in LSCs,and the effects of GAA on malignancies and mitochondrial RESULTS LRPPRC was found to be upregulated,and GAA inhibited cell proliferation by degrading LRPPRC.GAA induced LRPPRC degradation and inhibited the activation of interleukin 6(IL-6)/janus kinase(JAK)1/signal transducer and activator of transcription(STAT)3 signaling,enhancing chemosensitivity in LSCs against conventional chemotherapies,including L-Asparaginase,Dexamethasone,and cytarabine.GAA was also found to downregulate FOXM1 indirectly by regulating LRPPRC.Furthermore,GAA induced reactive oxygen species accumulation,disturbed mitochondrial homeostasis,and caused mitochondrial dysfunction.By inhibiting IL-6/JAK1/STAT3 signaling via degrading LRPPRC,GAA resulted in the elimination of LSCs.Meanwhile,GAA induced oxidative stress and subsequent cell damage by causing mitochondrial damage.CONCLUSION Taken together,the results indicate that GAA might overcome the BMM protective effect and be considered as a novel and effective combination therapy for AML.
