The rapid proliferation of Internet of Things(IoT)-enabled smart home systems necessitates next-generation indoor optical sensors with ultralow power consumption,ambient-light adaptability,and system-level integrabili...The rapid proliferation of Internet of Things(IoT)-enabled smart home systems necessitates next-generation indoor optical sensors with ultralow power consumption,ambient-light adaptability,and system-level integrability.Addressing this technological imperative,this study proposed a self-powered broadband photodetector(PD) through vertical integration of a hydrothermally synthesized Sb_(2)S_(3)single crystal with a commercial Si substrate.The Sb_(2)S_(3)/Si heterojunction PD showcases a maximum responsivity of 172 mA/W,a detectivity of 10^(10) Jones,and sub-millisecond response dynamics(172/160 μs rising/falling) upon 720 nm illumination at 0 V bias,outperforming other Sb_(2)S_(3)competitors.Such exceptional zero-bias operation enables direct compatibility with energy-autonomous IoT nodes.Particularly,the device's spectral alignment with indoor lighting harmonics and long-term drift-free operation establishes its viability for intelligent lighting control,occupancy detection,and low power consumption in residential IoT ecosystems.The synthesis innovation of Sb_(2)S_(3)monocrystalline structures provides a scalable pathway toward batteryless smart sensors for sustainable home automation.展开更多
The innate immune responses,including inflammasome activation,are paramount for host defense against pathogen infection.In contrast to canonical and noncanonical inflammasome activation,in this study,heat-killed gram-...The innate immune responses,including inflammasome activation,are paramount for host defense against pathogen infection.In contrast to canonical and noncanonical inflammasome activation,in this study,heat-killed gram-negative bacteria(HK bacteria)were identified as single-step stimulators of the NLRP3 inflammasome in human monocytes,and they caused a moderate amount of IL-1βto be released from cells.Time course experiments showed that this alternative inflammasome response was finished within a few hours.Further analysis showed that the intrinsically limited NLRP3 inflammasome activation response was due to the negative regulation of caspase-8 by the short isoform of cFLIP(cFLIPs),which was activated by NF-κB.In contrast,overexpressed cFLIPS,but not overexpressed cFLIPL,inhibited the activation of caspase-8 and the release of IL-1βin response to HK bacteria infection in human monocytes.Furthermore,we demonstrated that TAK1 activity mediated the expression of cFLIPs and was upstream and essential for the caspase-8 cleavage induced by HK bacteria in human monocytes.The functional specificity of cFLIPs and TAK1 revealed unique responses of human monocytes to a noninvasive pathogen,providing novel insights into an alternative regulatory pathway of NLRP3 inflammasome activation.展开更多
Leishmania parasites mainly infect macrophages and may cause severe immunopathologies in their host,which are called leishman-iases.In the current work,we infected human and mouse macrophages in vitro with Leishmania ...Leishmania parasites mainly infect macrophages and may cause severe immunopathologies in their host,which are called leishman-iases.In the current work,we infected human and mouse macrophages in vitro with Leishmania major,an etiological agent of cu-taneous leishmaniasis,and found that inhibition or deletion of the transforming growth factorβ–activated kinase 1(TAK1)gene re-sulted in increased parasite loads.In vivo,following a challenge with L.major,mice with a macrophage-specific deletion of TAK1 showed increased clinical signs and higher parasite loads compared with wild-type controls.TAK1 deficiency in mouse macro-phages led to biased Th2 cell responses during the acute stage of infection,characterized by a decrease in interferon-γexpression,and increased expression of IL-4,IL-5 and IL-10.Finally,we found that,in the late stage of L.major infection,excessive Th2-related cytokines led to high arginase 1 expression in mouse tissues and a significant reduction of NO production both locally and system-ically,resulting in compromised control of Leishmania.These findings suggest that TAK1 plays a vital role in host resistance to Leish-mania infection.展开更多
基金supported by the Shanghai Pujiang Programme (No.23PJD112)the National Natural Science Foundation of China (No.12374257)the Fundamental Research Funds for the Central Universities (No.NS2024062)。
文摘The rapid proliferation of Internet of Things(IoT)-enabled smart home systems necessitates next-generation indoor optical sensors with ultralow power consumption,ambient-light adaptability,and system-level integrability.Addressing this technological imperative,this study proposed a self-powered broadband photodetector(PD) through vertical integration of a hydrothermally synthesized Sb_(2)S_(3)single crystal with a commercial Si substrate.The Sb_(2)S_(3)/Si heterojunction PD showcases a maximum responsivity of 172 mA/W,a detectivity of 10^(10) Jones,and sub-millisecond response dynamics(172/160 μs rising/falling) upon 720 nm illumination at 0 V bias,outperforming other Sb_(2)S_(3)competitors.Such exceptional zero-bias operation enables direct compatibility with energy-autonomous IoT nodes.Particularly,the device's spectral alignment with indoor lighting harmonics and long-term drift-free operation establishes its viability for intelligent lighting control,occupancy detection,and low power consumption in residential IoT ecosystems.The synthesis innovation of Sb_(2)S_(3)monocrystalline structures provides a scalable pathway toward batteryless smart sensors for sustainable home automation.
基金supported by grants from the Natural Science Foundation of China(81830049,92269202),National Key R&D Program(2022YFC2304700,2022YFC2303200,2018YFA0507300)Strategic Priority Research Program(XDB29030303)and International Partnership Program(153831KYSB20190008)of the Chinese Academy of Sciences,Shanghai Municipal Science and Technology Major Project(2019SHZDZX02)and Research Leader Program(20XD1403900),as well as the Innovation Capacity Building Project of Jiangsu Province(BM2020019).
文摘The innate immune responses,including inflammasome activation,are paramount for host defense against pathogen infection.In contrast to canonical and noncanonical inflammasome activation,in this study,heat-killed gram-negative bacteria(HK bacteria)were identified as single-step stimulators of the NLRP3 inflammasome in human monocytes,and they caused a moderate amount of IL-1βto be released from cells.Time course experiments showed that this alternative inflammasome response was finished within a few hours.Further analysis showed that the intrinsically limited NLRP3 inflammasome activation response was due to the negative regulation of caspase-8 by the short isoform of cFLIP(cFLIPs),which was activated by NF-κB.In contrast,overexpressed cFLIPS,but not overexpressed cFLIPL,inhibited the activation of caspase-8 and the release of IL-1βin response to HK bacteria infection in human monocytes.Furthermore,we demonstrated that TAK1 activity mediated the expression of cFLIPs and was upstream and essential for the caspase-8 cleavage induced by HK bacteria in human monocytes.The functional specificity of cFLIPs and TAK1 revealed unique responses of human monocytes to a noninvasive pathogen,providing novel insights into an alternative regulatory pathway of NLRP3 inflammasome activation.
基金supported by grants from the Institute Pasteur International Direction,International Partnership Program(153831KYSB20190008)the Strategic Priority Research Program of the Chinese Academy of Sciences(XDB29030303)+4 种基金the National Key Basic Research Program(2018YFA0507300,2022YFC2304700,2022YFC2303200)the National Natural Science Foundation of China(81830049,92269202)the Shanghai Municipal Science and Technology Major Project(#2019SHZDZX02)the Research Leader Program(#20XD1403900)the Innovation Capacity Building Project of Jiangsu province(BM2020019)。
文摘Leishmania parasites mainly infect macrophages and may cause severe immunopathologies in their host,which are called leishman-iases.In the current work,we infected human and mouse macrophages in vitro with Leishmania major,an etiological agent of cu-taneous leishmaniasis,and found that inhibition or deletion of the transforming growth factorβ–activated kinase 1(TAK1)gene re-sulted in increased parasite loads.In vivo,following a challenge with L.major,mice with a macrophage-specific deletion of TAK1 showed increased clinical signs and higher parasite loads compared with wild-type controls.TAK1 deficiency in mouse macro-phages led to biased Th2 cell responses during the acute stage of infection,characterized by a decrease in interferon-γexpression,and increased expression of IL-4,IL-5 and IL-10.Finally,we found that,in the late stage of L.major infection,excessive Th2-related cytokines led to high arginase 1 expression in mouse tissues and a significant reduction of NO production both locally and system-ically,resulting in compromised control of Leishmania.These findings suggest that TAK1 plays a vital role in host resistance to Leish-mania infection.
