Composite polymer electrolytes(CPEs)offer a promising solution for all-solid-state lithium-metal batteries(ASSLMBs).However,conventional nanofillers with Lewis-acid-base surfaces make limited contribution to improving...Composite polymer electrolytes(CPEs)offer a promising solution for all-solid-state lithium-metal batteries(ASSLMBs).However,conventional nanofillers with Lewis-acid-base surfaces make limited contribution to improving the overall performance of CPEs due to their difficulty in achieving robust electrochemical and mechanical interfaces simultaneously.Here,by regulating the surface charge characteristics of halloysite nanotube(HNT),we propose a concept of lithium-ion dynamic interface(Li^(+)-DI)engineering in nano-charged CPE(NCCPE).Results show that the surface charge characteristics of HNTs fundamentally change the Li^(+)-DI,and thereof the mechanical and ion-conduction behaviors of the NCCPEs.Particularly,the HNTs with positively charged surface(HNTs+)lead to a higher Li^(+)transference number(0.86)than that of HNTs-(0.73),but a lower toughness(102.13 MJ m^(-3)for HNTs+and 159.69 MJ m^(-3)for HNTs-).Meanwhile,a strong interface compatibilization effect by Li^(+)is observed for especially the HNTs+-involved Li^(+)-DI,which improves the toughness by 2000%compared with the control.Moreover,HNTs+are more effective to weaken the Li^(+)-solvation strength and facilitate the formation of Li F-rich solid-electrolyte interphase of Li metal compared to HNTs-.The resultant Li|NCCPE|LiFePO4cell delivers a capacity of 144.9 m Ah g^(-1)after 400 cycles at 0.5 C and a capacity retention of 78.6%.This study provides deep insights into understanding the roles of surface charges of nanofillers in regulating the mechanical and electrochemical interfaces in ASSLMBs.展开更多
Brain-computer interfaces(BCIs)represent an emerging technology that facilitates direct communication between the brain and external devices.In recent years,numerous review articles have explored various aspects of BC...Brain-computer interfaces(BCIs)represent an emerging technology that facilitates direct communication between the brain and external devices.In recent years,numerous review articles have explored various aspects of BCIs,including their fundamental principles,technical advancements,and applications in specific domains.However,these reviews often focus on signal processing,hardware development,or limited applications such as motor rehabilitation or communication.This paper aims to offer a comprehensive review of recent electroencephalogram(EEG)-based BCI applications in the medical field across 8 critical areas,encompassing rehabilitation,daily communication,epilepsy,cerebral resuscitation,sleep,neurodegenerative diseases,anesthesiology,and emotion recognition.Moreover,the current challenges and future trends of BCIs were also discussed,including personal privacy and ethical concerns,network security vulnerabilities,safety issues,and biocompatibility.展开更多
Osteoporosis represents a prevalent and debilitating comorbidity in patients diagnosed with type 2 diabetes mellitus(T2DM),which is characterized by suppressed osteoblast function and disrupted bone microarchitecture....Osteoporosis represents a prevalent and debilitating comorbidity in patients diagnosed with type 2 diabetes mellitus(T2DM),which is characterized by suppressed osteoblast function and disrupted bone microarchitecture.In this study,we utilized male C57BL/6 J mice to investigate the role of SIRT3 in T2DM.Decreased SIRT3 expression and impaired mitochondrial quality control mechanism are observed in both in vitro and in vivo models of T2DM.Mechanistically,SIRT3 suppression results in hyperacetylation of FOXO3,hindering the activation of the PINK1/PRKN mediated mitophagy pathway and resulting in accumulation of dysfunctional mitochondria.Genetical overexpression or pharmacological activation of SIRT3 restores deacetylation status of FOXO3,thus facilitating mitophagy and ameliorating osteogenic impairment in T2DM.Collectively,our findings highlight the fundamental regulatory function of SIRT3 in mitochondrial quality control,crucial for maintaining bone homeostasis in T2DM.These insights not only enhance our understanding of the molecular mechanisms underlying diabetic osteoporosis but also identify SIRT3 as a promising therapeutic target for diabetic osteoporosis.展开更多
LiV_(2)O_(4)is a spinel-structured compound that stands out as the first known 3d-electron system exhibiting typical heavy fermion behavior.A central question is how such strong mass renormalization emerges in the abs...LiV_(2)O_(4)is a spinel-structured compound that stands out as the first known 3d-electron system exhibiting typical heavy fermion behavior.A central question is how such strong mass renormalization emerges in the absence of f-electrons.In this work,we investigate the three-dimensional electronic structure of LiV_(2)O_(4)thin films using angle-resolved photoemission spectroscopy.We identify that an electron-like flat band is derived from a_(1g)orbitals,along with a highly dispersive e′_(g)band strongly coupled with phonons.The overall agreement with dynamical mean-field theory calculations highlights the essential role of inter-orbital Hund’s coupling in reducing the a_(1g)bandwidth to 25 meV,approaching a Mott state.Notably,we find that heavy-fermion behavior arises from additional renormalization at the a_(1g)band near the Fermi level,likely driven by many-body interactions at energy scales down to a few meV and potentially linked to geometric frustration inherent to the spinel lattice.These results provide crucial insights into the origin of the heavy fermion behavior in 3d-electron systems.展开更多
Polycystic ovary syndrome(PCOS)is a heterogeneous disorder with evidence of polygenetic components,and obesity may be a risk factor for hyperandrogen ism.Previous studies have shown that LHCGR is en riched in the ovar...Polycystic ovary syndrome(PCOS)is a heterogeneous disorder with evidence of polygenetic components,and obesity may be a risk factor for hyperandrogen ism.Previous studies have shown that LHCGR is en riched in the ovary and LHCGR deficiency causes infertility without typical PCOS phenotypes.ALMS1 is implicated in obesity and hyperandrogenism,the common phenotypes among PCOS patients.Through whole-exome sequencing of 22 PCOS families and targeted candidate gene sequencing of additional 65 sporadic PCOS patients,we identified potential causative mutations in LHCGR and ALMS1 in a sibling-pair PCOS family and three sporadic PCOS patients.The expression of LHCGRL638 P in granulosa-like tumor cell line(KGN)cells promoted cyclic adenosine monophosphate production and granulosa cell proliferation,indicating that LHCGRL638 P is an activating mutation.Lhcgr~(L642 P/L642 P)mice showed an irregular estrous cycle,reduced follicles with dynamic folliculogenesis,and increased testosterone(T),estradiol(E2),and dehydroepiandrosterone.Lhcgr~(+/L642 P)AIms1~(+/PB)mice displayed increased T and E2 but decreased late secondary and preovulatory follicles.We showed that activating mutation of LHCGR likely plays important roles in the pathophysiology of PCOS involving abnormal reproductive physiology,whereas ALMS1 deficiency may promote anovulatory infertility via elevated androgens,suggesting that the disturbed LHCGR and ALMS1 cooperatively induce PCOS phenotypes,characterized as anovulation and hyperandrogenemia frequently observed in PCOS patients with obesity.展开更多
AIM: To investigate whether the regulation of aquaporin 3 (AQP3) and AQP9 induced by Auphen and dibutyryl cAMP (dbcAMP) inhibits hepatic tumorigenesis.METHODS: Expression of AQP3 and AQP9 was detected by Western blot,...AIM: To investigate whether the regulation of aquaporin 3 (AQP3) and AQP9 induced by Auphen and dibutyryl cAMP (dbcAMP) inhibits hepatic tumorigenesis.METHODS: Expression of AQP3 and AQP9 was detected by Western blot, immunohistochemistry (IHC), and RT-PCR in HCC samples and paired non-cancerous liver tissue samples from 30 hepatocellular carcinoma (HCC) patients. A xenograft tumor model was used in vivo. Nine nude mice were divided into control, Auphen-treated, and dbcAMP-treated groups (n = 3 for each group). AQP3 and AQP9 protein expression after induction of xenograft tumors was detected by IHC and mRNA by RT-PCR analysis. The terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay and histological evaluation were used to detect apoptosis of tumor cells, and the concentration of serum α-fetoprotein (AFP) was measured using RT-PCR and an ELISA kit.RESULTS: The volumes and weights of tumors decreased significantly in the Auphen- and dbcAMP-treated mice compared with the control mice (P < 0.01). The levels of AQP3 were significantly lower in the Auphen treatment group, and levels of AQP9 were significantly higher in thedbcAMP treatment mice than in the control mice (P < 0.01). The reduction of AQP3 by Auphen and increase of AQP9 by dbcAMP in nude mice suppressed tumor growth of HCC, which resulted in reduced AFP levels in serum and tissues, and apoptosis of tumor cells in the Auphen- and dbcAMP-treated mice, when compared with control mice (P < 0.01). Compared with para-carcinoma tissues, AQP3 expression increased in tumor tissues whereas the expression of AQP9 decreased. By correlating clinicopathological and expression levels, we demonstrated that the expression of AQP3 and AQP9 was correlated with clinical progression of HCC and disease outcomes.CONCLUSION: AQP3 increases in HCC while AQP9 decreases. Regulation of AQP3 and AQP9 expression by Auphen and dbcAMP inhibits the development and growth of HCC.展开更多
基金the financial support from the National Natural Science Foundation of China(52203123 and 52473248)State Key Laboratory of Polymer Materials Engineering(sklpme2024-2-04)+1 种基金the Fundamental Research Funds for the Central Universitiessponsored by the Double First-Class Construction Funds of Sichuan University。
文摘Composite polymer electrolytes(CPEs)offer a promising solution for all-solid-state lithium-metal batteries(ASSLMBs).However,conventional nanofillers with Lewis-acid-base surfaces make limited contribution to improving the overall performance of CPEs due to their difficulty in achieving robust electrochemical and mechanical interfaces simultaneously.Here,by regulating the surface charge characteristics of halloysite nanotube(HNT),we propose a concept of lithium-ion dynamic interface(Li^(+)-DI)engineering in nano-charged CPE(NCCPE).Results show that the surface charge characteristics of HNTs fundamentally change the Li^(+)-DI,and thereof the mechanical and ion-conduction behaviors of the NCCPEs.Particularly,the HNTs with positively charged surface(HNTs+)lead to a higher Li^(+)transference number(0.86)than that of HNTs-(0.73),but a lower toughness(102.13 MJ m^(-3)for HNTs+and 159.69 MJ m^(-3)for HNTs-).Meanwhile,a strong interface compatibilization effect by Li^(+)is observed for especially the HNTs+-involved Li^(+)-DI,which improves the toughness by 2000%compared with the control.Moreover,HNTs+are more effective to weaken the Li^(+)-solvation strength and facilitate the formation of Li F-rich solid-electrolyte interphase of Li metal compared to HNTs-.The resultant Li|NCCPE|LiFePO4cell delivers a capacity of 144.9 m Ah g^(-1)after 400 cycles at 0.5 C and a capacity retention of 78.6%.This study provides deep insights into understanding the roles of surface charges of nanofillers in regulating the mechanical and electrochemical interfaces in ASSLMBs.
基金supported by the National Key R&D Program of China(2021YFF1200602)the National Science Fund for Excellent Overseas Scholars(0401260011)+3 种基金the National Defense Science and Technology Innovation Fund of Chinese Academy of Sciences(c02022088)the Tianjin Science and Technology Program(20JCZDJC00810)the National Natural Science Foundation of China(82202798)the Shanghai Sailing Program(22YF1404200).
文摘Brain-computer interfaces(BCIs)represent an emerging technology that facilitates direct communication between the brain and external devices.In recent years,numerous review articles have explored various aspects of BCIs,including their fundamental principles,technical advancements,and applications in specific domains.However,these reviews often focus on signal processing,hardware development,or limited applications such as motor rehabilitation or communication.This paper aims to offer a comprehensive review of recent electroencephalogram(EEG)-based BCI applications in the medical field across 8 critical areas,encompassing rehabilitation,daily communication,epilepsy,cerebral resuscitation,sleep,neurodegenerative diseases,anesthesiology,and emotion recognition.Moreover,the current challenges and future trends of BCIs were also discussed,including personal privacy and ethical concerns,network security vulnerabilities,safety issues,and biocompatibility.
基金supported by the National Key Research and Development Project (2021YFA1201404)National Natural Science Foundation of China Major Project (81991514)+6 种基金General Project (82272530, 82372459)Jiangsu Province Medical Innovation Center of Orthopedic Surgery (CXZX202214)Jiangsu Provincial Key Medical Center FoundationJiangsu Provincial Medical Outstanding Talent FoundationJiangsu Provincial Medical Youth Talent FoundationJiangsu Provincial Key Medical Talent Foundationthe Fundamental Research Funds for the Central Universities (14380493, 14380494)
文摘Osteoporosis represents a prevalent and debilitating comorbidity in patients diagnosed with type 2 diabetes mellitus(T2DM),which is characterized by suppressed osteoblast function and disrupted bone microarchitecture.In this study,we utilized male C57BL/6 J mice to investigate the role of SIRT3 in T2DM.Decreased SIRT3 expression and impaired mitochondrial quality control mechanism are observed in both in vitro and in vivo models of T2DM.Mechanistically,SIRT3 suppression results in hyperacetylation of FOXO3,hindering the activation of the PINK1/PRKN mediated mitophagy pathway and resulting in accumulation of dysfunctional mitochondria.Genetical overexpression or pharmacological activation of SIRT3 restores deacetylation status of FOXO3,thus facilitating mitophagy and ameliorating osteogenic impairment in T2DM.Collectively,our findings highlight the fundamental regulatory function of SIRT3 in mitochondrial quality control,crucial for maintaining bone homeostasis in T2DM.These insights not only enhance our understanding of the molecular mechanisms underlying diabetic osteoporosis but also identify SIRT3 as a promising therapeutic target for diabetic osteoporosis.
基金support of Dr.Z.T.Liu,Dr.Z.C.Jiang,Dr.Marta Zonno,and Dr.Sergey Gorovikovsupported in part by the National Key R&D Program of the MOST of China(Grant No.2023YFA1406300)+4 种基金the National Natural Science Foundation of China(Grant Nos.12274085,12422404,and 92477206)the New Cornerstone Science Foundation,the Innovation Program for Quantum Science and Technology(Grant No.2021ZD0302803)Shanghai Municipal Science and Technology Major Project(Grant No.2019SHZDZX01)The ARPES measurements used Beamlines 09U and 03U of the SSRF and Beamline QMSC of Canadian Light sourcesupported by the ME2 project from the National Natural Science Foundation of China(Contract No.11227902).
文摘LiV_(2)O_(4)is a spinel-structured compound that stands out as the first known 3d-electron system exhibiting typical heavy fermion behavior.A central question is how such strong mass renormalization emerges in the absence of f-electrons.In this work,we investigate the three-dimensional electronic structure of LiV_(2)O_(4)thin films using angle-resolved photoemission spectroscopy.We identify that an electron-like flat band is derived from a_(1g)orbitals,along with a highly dispersive e′_(g)band strongly coupled with phonons.The overall agreement with dynamical mean-field theory calculations highlights the essential role of inter-orbital Hund’s coupling in reducing the a_(1g)bandwidth to 25 meV,approaching a Mott state.Notably,we find that heavy-fermion behavior arises from additional renormalization at the a_(1g)band near the Fermi level,likely driven by many-body interactions at energy scales down to a few meV and potentially linked to geometric frustration inherent to the spinel lattice.These results provide crucial insights into the origin of the heavy fermion behavior in 3d-electron systems.
基金jointly supported by the National Key Research and Development Program of China(2018YFC1002104 to L.W.,2018YFC1004904 to B.-L.W.and J.F.,2016YFC1000500 to H.Y.W.and W.F.T.)the National Natural Science Foundation of China([81930036,31521003,31771669]to H.Y.W.)+1 种基金the Commission for Science and Technology of Shanghai Municipality(17JC1400902to H.Y.W.)the MDA-CHB Research Grant to B.-L.W。
文摘Polycystic ovary syndrome(PCOS)is a heterogeneous disorder with evidence of polygenetic components,and obesity may be a risk factor for hyperandrogen ism.Previous studies have shown that LHCGR is en riched in the ovary and LHCGR deficiency causes infertility without typical PCOS phenotypes.ALMS1 is implicated in obesity and hyperandrogenism,the common phenotypes among PCOS patients.Through whole-exome sequencing of 22 PCOS families and targeted candidate gene sequencing of additional 65 sporadic PCOS patients,we identified potential causative mutations in LHCGR and ALMS1 in a sibling-pair PCOS family and three sporadic PCOS patients.The expression of LHCGRL638 P in granulosa-like tumor cell line(KGN)cells promoted cyclic adenosine monophosphate production and granulosa cell proliferation,indicating that LHCGRL638 P is an activating mutation.Lhcgr~(L642 P/L642 P)mice showed an irregular estrous cycle,reduced follicles with dynamic folliculogenesis,and increased testosterone(T),estradiol(E2),and dehydroepiandrosterone.Lhcgr~(+/L642 P)AIms1~(+/PB)mice displayed increased T and E2 but decreased late secondary and preovulatory follicles.We showed that activating mutation of LHCGR likely plays important roles in the pathophysiology of PCOS involving abnormal reproductive physiology,whereas ALMS1 deficiency may promote anovulatory infertility via elevated androgens,suggesting that the disturbed LHCGR and ALMS1 cooperatively induce PCOS phenotypes,characterized as anovulation and hyperandrogenemia frequently observed in PCOS patients with obesity.
基金Supported by Science and Technology Commission of Shanghai,No.13ZR1406700 and No.13DZ1930908
文摘AIM: To investigate whether the regulation of aquaporin 3 (AQP3) and AQP9 induced by Auphen and dibutyryl cAMP (dbcAMP) inhibits hepatic tumorigenesis.METHODS: Expression of AQP3 and AQP9 was detected by Western blot, immunohistochemistry (IHC), and RT-PCR in HCC samples and paired non-cancerous liver tissue samples from 30 hepatocellular carcinoma (HCC) patients. A xenograft tumor model was used in vivo. Nine nude mice were divided into control, Auphen-treated, and dbcAMP-treated groups (n = 3 for each group). AQP3 and AQP9 protein expression after induction of xenograft tumors was detected by IHC and mRNA by RT-PCR analysis. The terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay and histological evaluation were used to detect apoptosis of tumor cells, and the concentration of serum α-fetoprotein (AFP) was measured using RT-PCR and an ELISA kit.RESULTS: The volumes and weights of tumors decreased significantly in the Auphen- and dbcAMP-treated mice compared with the control mice (P < 0.01). The levels of AQP3 were significantly lower in the Auphen treatment group, and levels of AQP9 were significantly higher in thedbcAMP treatment mice than in the control mice (P < 0.01). The reduction of AQP3 by Auphen and increase of AQP9 by dbcAMP in nude mice suppressed tumor growth of HCC, which resulted in reduced AFP levels in serum and tissues, and apoptosis of tumor cells in the Auphen- and dbcAMP-treated mice, when compared with control mice (P < 0.01). Compared with para-carcinoma tissues, AQP3 expression increased in tumor tissues whereas the expression of AQP9 decreased. By correlating clinicopathological and expression levels, we demonstrated that the expression of AQP3 and AQP9 was correlated with clinical progression of HCC and disease outcomes.CONCLUSION: AQP3 increases in HCC while AQP9 decreases. Regulation of AQP3 and AQP9 expression by Auphen and dbcAMP inhibits the development and growth of HCC.
