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In this Letter, the CH3NH3PbBr3 nanocrystals (NCs) are embedded into the interstices of the fluorine (polyvinyl fluoride/polyvinylidene fluoride, PVF/PVDF) matrix on polyethylene terephthalate (PET) substrate to introduce new advantages, such as being flexible and waterproof, while maintaining the high optical performance of perovskites. The sample's photoluminescence (PL) spectra under 325â nm laser is a green emission peaked at 537â nm with full width at half maximum (FWHM) of about 21.2â nm and a fast PL decay time. As a color converter, it shows high optical absorption and can transform light from solar-blind ultraviolet to a blue region into a green region in air, water, and bending conditions. While excited by a 270â nm ultraviolet light-emitting diode (LED), the system's observed -3â dB bandwidth with the color converter is near 4.4â MHz in air and water conditions with well-eye diagrams at a data rate of 30â Mbps. Finally, we demonstrate an audio transmission application with an ultraviolet light source, a color conversion layer, and a low-cost silicon-based photodetector.
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In this work, we design, fabricate, and characterize a different-mode (waveguide-connected) power splitter ((W)PS) by what we believe to be a novel multi-dimension direct-binary-search algorithm that can significantly balance the device performance, time cost, and fabrication robustness by searching the state-dimension, rotation-dimension, shape-dimension, and size-dimension parameters. The (W)PS can simultaneously generate the fundamental transverse electric (TE0) and TE1 mode with the 1:1 output balance. Compared with the PS, the WPS can greatly shorten the adiabatic taper length between the single-mode waveguide and the grating coupler. The measured results of the different-mode (W)PS indicate that the insertion loss and crosstalk are less than 0.9 (1.3) dB and lower than -17.8 (-14.9) dB from 1540â nm to 1560â nm. In addition, based on the tunable tap couplers, the different-mode (W)PS can be extended to multiple output ports with different modes and different transmittances.
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Integrated Sensing and Communication (ISAC) involves incorporating wireless sensing capabilities into communication systems. The integration of ISAC affords improvements in the performance of the communication system, as well as the ability to perform high-precision motion detection, positioning, imaging, and other related functions. Therefore, it is highly valuable to develop an ISAC terminal device that has a high degree of integration and energy efficiency. Here, we propose an ISAC chip that utilizes the coexistence of luminescence and detection properties of III-nitride multiple quantum wells for motion detection and visible light communication. The ISAC chip includes both a transmitter and a receiver of visible light and is fabricated on a sapphire wafer with InGaN/GaN multiple quantum wells. A rotating mirror is used as the object for motion detection and modulates the light signal emitted by the transmitter in a reflected light path. The variation period of the photocurrent curve generated by the modulated light signal is consistent with the rotation period of the mirror. We also investigate the performance of this chip as a transmitter and transceiver terminal of visible light communication systems. The results of the study provide a promising approach for the integration of motion sensing and visible light communication.
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Silicon-based gallium nitride lasers are considered potential laser sources for on-chip integration. However, the capability of on-demand lasing output with its reversible and wavelength tunability remains important. Herein, a Benz-shaped GaN cavity is designed and fabricated on a Si substrate and coupled to a Ni metal wire. Under optical pumping, excitation position-related lasing and exciton combination properties of pure GaN cavity are studied systematically. Under electrically driven, joule thermal of Ni metal wire makes it easy to change the temperature of the cavity. And then, we demonstrate a joule heat-induced contactless lasing mode manipulation in the coupled GaN cavity. The driven current, coupling distance, and excitation position influence the wavelength tunable effect. Compared with other positions, the outer ring position has the highest lasing properties and lasing mode tuning abilities. The optimized structures demonstrate clear wavelength tuning and an even mode switch. The thermal reduction of the band gap is identified to account for the modification of the lasing profile, but the thermo-optic effect is non-negligible under a high-driven current.
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The kidney regulates blood pressure through salt/water reabsorption affected by tubular sodium transporters. Expanding our prior research on placental cluster of differentiation 81 (CD81), this study explores the interaction of renal CD81 with sodium transporters in preeclampsia (PE). Effects of renal CD81 with sodium transporters were determined in lipopolysaccharide (LPS)-induced PE rats and immortalized mouse renal distal convoluted tubule cells. Urinary exosomal CD81, sodium potassium 2 chloride cotransporter (NKCC2), and sodium chloride cotransporter (NCC) were measured in PE patients. LPS-PE rats had hypertension from gestational days (GD) 6 to 18 and proteinuria from GD9 to GD18. Urinary CD81 in both groups tented to rise during pregnancy. Renal CD81, not sodium transporters, was higher in LPS-PE than controls on GD14. On GD18, LPS-PE rats exhibited higher CD81 in kidneys and urine exosomes, higher renal total and phosphorylated renal NKCC2 and NCC with elevated mRNAs, and lower ubiquitinated NCC than controls. CD81 was co-immunoprecipitated with NKCC2 or NCC in kidney homogenates and co-immunostained with NKCC2 or NCC in apical membranes of renal tubules. In plasma membrane fractions, LPS-PE rats had greater amounts of CD81, NKCC2, and NCC than controls with enhanced co-immunoprecipitations of CD81 with NKCC2 or NCC. In renal distal convoluted tubule cells, silencing CD81 with siRNA inhibited NCC and prevented LPS-induced NCC elevation. Further, PE patients had higher CD81 in original urines, urine exosomes and higher NKCC2 and NCC in urine exosomes than controls. Thus, the upregulation of renal CD81 on NKCC2 and NCC may contribute to the sustained hypertension observed in LPS-PE model. Urine CD81 with NKCC2 and NCC may be used as biomarkers for PE.
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Hipertensão , Pré-Eclâmpsia , Gravidez , Camundongos , Humanos , Ratos , Feminino , Animais , Simportadores de Cloreto de Sódio-Potássio/metabolismo , Simportadores de Cloreto de Sódio/genética , Simportadores de Cloreto de Sódio/metabolismo , Lipopolissacarídeos/toxicidade , Lipopolissacarídeos/metabolismo , Cloretos/metabolismo , Pré-Eclâmpsia/induzido quimicamente , Pré-Eclâmpsia/metabolismo , Membro 1 da Família 12 de Carreador de Soluto/metabolismo , Placenta/metabolismo , Túbulos Renais Distais/metabolismo , Hipertensão/metabolismo , Sódio/metabolismo , Potássio/metabolismo , Tetraspanina 28/metabolismoRESUMO
Exogenous hydrogen sulfide (H2 S) protects kidneys from diabetic injuries in animal models. In order to explore the role of endogenous H2 S in diabetic nephropathy, we determined the renal H2S producing enzymes in vivo and in vitro. In diabetic mice, H2 S levels in blood and kidney were decreased while cystathionine ß-synthase (CBS), mainly located in mouse renal proximal convoluted tubules (PCT), was reduced selectively. In cultured mouse PCT cells treated with high glucose, CBS protein and activity was reduced while ubiquitinated CBS was increased, which was abolished by a proteasome inhibitor MG132 at 1 hour; high glucose drove CBS colocalized with proteasome 26S subunit ATPase6, indicating an involvement of ubiquitination proteasome degradation. At 48 hours, high glucose also selectively decreased CBS protein, concentration-dependently, but increased the ubiquitination of CBS; silence of CBS by siRNA increased nitrotyrosine, a marker for protein oxidative injury. Nitrotyrosine was also increased by high glucose treatments. The increases of nitrotyrosine either by cbs-siRNA or by glucose were restored by GYY4137, indicating that the H2 S donor may protect kidney from oxidative injury induced by CBS deficiency. In diabetic kidneys, ubiquitinated CBS and nitrotyrosine were increased but restored by GYY4137. The treatment also ameliorated albuminuria and renal morphologic changes in diabetic mice. Our findings suggest that high glucose induces reduction of renal CBS protein and activity in vivo and in vitro that is critical to the pathogenesis of diabetic kidney disease.
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Cistationina beta-Sintase/deficiência , Diabetes Mellitus Experimental/complicações , Nefropatias Diabéticas/patologia , Glucose/farmacologia , Sulfeto de Hidrogênio/metabolismo , Animais , Nefropatias Diabéticas/etiologia , Nefropatias Diabéticas/metabolismo , Camundongos , Camundongos Endogâmicos C57BLRESUMO
Female ovaries degenerate about 20 years earlier than testes leading to reduced primordial follicle reserve and a reduction in oocyte quality. Here we found that bridge integrator 2 (BIN2) is enriched in mouse ovaries and oocytes and that global knockout of this protein improves both female fertility and oocyte quality. Quantitative ovarian proteomics and phosphoproteomics showed that Bin2 knockout led to a decrease in phosphorylated ribosomal protein S6 (p-RPS6), a component of the mammalian target of rapamycin pathway and greatly increased nicotinamide nucleotide transhydrogenase (NNT), the free-radical detoxifier. Mechanistically, we find that phosphorylation of BIN2 at Thr423 and Ser424 leads to its translocation from the membrane to the cytoplasm, subsequent phosphorylation of RPS6 and inhibition of Nnt translation. We synthesized a BIN2-penetrating peptide (BPP) designed to inhibit BIN2 phosphorylation and found that a 3-week BPP treatment improved primordial follicle reserve and oocyte quality in aging and after chemotherapy-induced premature ovarian failure without discernible side effects.
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Ovário , Transdução de Sinais , Feminino , Camundongos , Animais , Ovário/metabolismo , Fosforilação , Oócitos , Fertilidade , MamíferosRESUMO
Tripartite motif-containing 22 (TRIM22) has been documented to participate in numerous cellular activities during human diseases. However, whether TRIM22 is involved in the regulation of neuronal survival during the progression of cerebral ischemia/reperfusion (I/R) injury remains unknown. In the present study, treatment of HCN-2 cells with oxygen-glucose deprivation/reoxygenation (OGD/R) markedly upregulated TRIM22 expression. A significant increase in TRIM22 expression was observed in the ischemic cortex tissues from middle cerebral artery occlusion/reperfusion mice. OGD/R inhibited the viability and induced the apoptosis of HCN-2 cells, which was accompanied by an increase in caspase-3 activity and an increase in LDH release. Furthermore, OGD/R increased the levels of tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-6, and monocyte chemoattractant protein-1 and induced NLRP3 inflammasome activation, as evidenced by increases in NACHT, LRR and PYD domains-containing protein 3, apoptosis-associated speck-like protein containing a caspase recruitment domain and cleaved caspase-1 expression and caspase-1 activity. However, these changes induced by OGD/R were blocked by silencing of TRIM22. In addition, TRIM22 regulated NF-κB activity in HCN-2 cells undergoing OGD/R stimulation. Furthermore, inhibition of NF-κB by pyrrolidine dithiocarbamate inhibited OGD/R-induced NLRP3 inflammasome activation in HCN-2 cells. Taken together, silencing of TRIM22 protects neurons against OGD/R-induced apoptosis and inflammation. The anti-inflammatory effect of TRIM22 knockdown was the consequence of inhibition of NF-κB/NLRP3 axis. TRIM22 may be a potential target for treating cerebral I/R injury.
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Apoptose , Glucose/deficiência , Inflamação/patologia , Antígenos de Histocompatibilidade Menor/metabolismo , NF-kappa B/antagonistas & inibidores , Proteína 3 que Contém Domínio de Pirina da Família NLR/antagonistas & inibidores , Oxigênio/metabolismo , Proteínas Repressoras/metabolismo , Proteínas com Motivo Tripartido/metabolismo , Animais , Linhagem Celular , Técnicas de Silenciamento de Genes , Inflamassomos/metabolismo , Masculino , Camundongos , Antígenos de Histocompatibilidade Menor/genética , NF-kappa B/metabolismo , Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo , Proteínas Repressoras/genética , Transdução de Sinais , Proteínas com Motivo Tripartido/genéticaRESUMO
BACKGROUND: Docetaxel resistance affects prognosis in advanced prostate cancer (PCa). The precise mechanisms remain unclear. Transcription factor Forkhead box M1 (FOXM1), which participates in cell proliferation and cell cycle progression, has been reported to affect the sensitivity of chemotherapy. This study explores the role of FOXM1 in PCa docetaxel resistance and its association with kinesin family member 20 A (KIF20A), which is known to promote therapeutic resistance in some cancers. METHODS: We monitored cell growth using MTT and colony formation assays, and cell apoptosis and cell cycle progression using flow cytometry. Wound-healing and transwell assays were used to detect cell invasion and migration. mRNA and protein expression were analyzed using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blotting. We monitored FOXM1 binding to the KIF20A promoter using a ChIP assay. Tumorigenicity in nude mice was used to assess in vivo tumorigenicity. RESULTS: FOXM1 knockdown induced cell apoptosis and G2/M cell cycle arrest, suppressing cell migration and invasion in docetaxel-resistant PCa cell lines (DU145-DR and VCaP-DR). Exogenous FOXM1 overexpression was found in their parental cells. Specific FOXM1 inhibitor thiostrepton significantly weakened docetaxel resistance in vitro and in vivo. We also found that FOXM1 and KIF20A exhibited consistent and highly correlated overexpression in PCa cells and tissues. FOXM1 also regulated KIF20A expression at the transcriptional level by acting directly on a Forkhead response element (FHRE) in its promoter. KIF20A overexpression could partially reverse the effect on cell proliferation, cell cycle proteins (cyclinA2, cyclinD1 and cyclinE1) and apoptosis protein (bcl-2 and PARP) of FOXM1 depletion. CONCLUSIONS: Our findings indicate that highly expressed FOXM1 may help promote docetaxel resistance by inducing KIF20A expression, providing insight into novel chemotherapeutic strategies for combatting PCa docetaxel resistance.
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Controlling the lasing mode, emission direction, threshold, and quality factor of whispering-gallery mode lasing is important for practical applications such as optical interconnections, on-chip communications, trace detection, high-density storage, etc. In order to simultaneously control the mode and emission direction and to achieve a high-quality factor in a low-threshold whisper-gallery mode laser, such as a GaN floating microdisk, a novel fabrication design of a microdisk with a vertical slit is proposed. To demonstrate proof of concept, we experimentally measure whispering-gallery mode lasing spectra of microdisks with and without a slit. Our findings suggest that the disks can indeed operate in whispering-gallery mode, and the slit is able to change the optical path in the microcavity without breaking lasing resonance. The slit in the microdisk can also influence the lasing mode, quality factor, and directional emission. Therefore, our study provides a feasible way to control whispering-gallery mode lasing properties.
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The electrical and optical properties of micro-light emitting diodes (µ-LEDs), including current-voltage (I-V), capacitance-voltage (C-V) curves, photoluminescence (PL) as well as electroluminescence (EL) spectra have been measured and analyzed. It is found that the unit area emitting intensity of small size µ-LED is stronger that of big size µ-LED at the same conditions, due to the enhancement of both the internal quantum efficiency ηint and extraction efficiency Cex. The present method of utilizing the µ-LED for improving the unit area brightness of LEDs is applicable to high efficiency surface emitting device on GaN-on-silicon platform.
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Docetaxel-mediated chemotherapy is the first line therapy for metastatic castration-resistant prostate cancer (CRPC) patients, but its therapeutic benefit is limited by the development of resistance. Although Forkhead box protein M1 (FOXM1) has been implicated in prostate tumorigenesis and metastasis, its role in docetaxel resistance has not been studied. Here, we showed that FOXM1 expression was upregulated in the docetaxel resistant CRPC cell lines (PC3-DR and VCaP-DR) and knockdown of FOXM1 sensitized the cells to docetaxel both in vitro and in vivo. In addition, autophagy was found to be significantly enhanced in resistant cells. Moreover, FOXM1 overexpression cells showed increased autophagic flux and higher numbers of autophagosomes. Knockdown of ATG7, beclin-1 or cotreatment with chloroquine, partly restored sensitivity to docetaxel in the FOXM1-overexpressing cells. Mechanistically, FOXM1 targeted AMPK/mTOR to activate the autophagy pathway and altered docetaxel response in CRPC. These findings identify the role of FOXM1 as well as the mechanism underlying FOXM1 action in docetaxel sensitivity and may, therefore, aid in design of CRPC therapies.
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Proteína 7 Relacionada à Autofagia/genética , Docetaxel/farmacologia , Proteína Forkhead Box M1/genética , Neoplasias de Próstata Resistentes à Castração/tratamento farmacológico , Serina-Treonina Quinases TOR/genética , Quinases Proteína-Quinases Ativadas por AMP , Apoptose/efeitos dos fármacos , Autofagia/efeitos dos fármacos , Proteína 7 Relacionada à Autofagia/antagonistas & inibidores , Proteína Beclina-1/genética , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Cloroquina/farmacologia , Resistencia a Medicamentos Antineoplásicos/genética , Proteína Forkhead Box M1/antagonistas & inibidores , Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos , Humanos , Masculino , Neoplasias de Próstata Resistentes à Castração/genética , Neoplasias de Próstata Resistentes à Castração/patologia , Proteínas Quinases/genéticaRESUMO
ETS-domain containing protein (Elk1), which is a transcription factor, is reported to be closely related to the apoptosis of primary neurons and could be activated by hypoxia in human microvascular endothelial cells. In this study, we aimed to investigate the role of Elk1 in cortical neurons under oxygen-glucose deprivation (OGD) conditions. The OGD model of cortical neurons was established the anoxia/hypoglycemia-induced injury and the in vivo model was established by middle cerebral artery occlusion (MCAO). Elk1 mRNA and protein expression was significantly up-regulated in neurons exposed to OGD for 24â¯h, and mRNA expression was also markedly increased in cerebral cortex of rats with MCAO after 10 days. The knockdown of Elk1 in neurons without OGD obviously constrained Fra-1 and promoted Nrf2 expression. Also, Elk1 inhibition suppressed neuronal apoptosis, caspase-3 activity, LDH leakage, and MDA and SOD contents, while it increased cell viability in the neurons with OGD. The overexpression of Fra-1 showed a reverse effect on caspase-3 activity, cell viability and SOD contents in neurons under OGD conditions compared with Elk1 knockdown. Thus, Elk1 inhibition has a protective effect on neurons against OGD-induced injury.
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Glucose/farmacologia , Hipóxia/genética , Neurônios/metabolismo , Oxigênio/farmacologia , Proteínas Elk-1 do Domínio ets/genética , Animais , Apoptose/efeitos dos fármacos , Apoptose/genética , Caspase 3/genética , Caspase 3/metabolismo , Córtex Cerebral/efeitos dos fármacos , Córtex Cerebral/metabolismo , Córtex Cerebral/patologia , Transtornos Cerebrovasculares/cirurgia , Feto , Regulação da Expressão Gênica , Glucose/deficiência , Hipóxia/metabolismo , Hipóxia/patologia , Masculino , Artéria Cerebral Média/cirurgia , Fator 2 Relacionado a NF-E2/genética , Fator 2 Relacionado a NF-E2/metabolismo , Neurônios/efeitos dos fármacos , Neurônios/patologia , Cultura Primária de Células , Proteínas Proto-Oncogênicas c-fos/genética , Proteínas Proto-Oncogênicas c-fos/metabolismo , RNA Interferente Pequeno/genética , RNA Interferente Pequeno/metabolismo , Ratos , Ratos Sprague-Dawley , Transdução de Sinais , Superóxido Dismutase/genética , Superóxido Dismutase/metabolismo , Proteínas Elk-1 do Domínio ets/antagonistas & inibidores , Proteínas Elk-1 do Domínio ets/metabolismoRESUMO
Solution approaches to NiOx films for electrochromic applications are problematic due to the need of an additional high-temperature annealing treatment step in inert gas. In this study, nanostructured NiOx powder with grain size of about 10.1 nm was synthesized for fabrication of NiOx films for electrochromic application. Non-toxic dispersants of isopropanol and deionized water were used and the whole process was carried out in air. The effects of the number of spin-coating layers, annealing temperature, and the volume ratios of isopropanol to deionized water were systematically investigated. Large transmittance change of 62.3% at 550 nm, high coloration efficiency (42.8 cm²/C), rapid switching time (coloring time is 4 s, bleaching time is 3 s), and good stability were achieved in the optimized NiOx film. The optimized process only required a low processing temperature of 150 °C in air with spin-coating three times and 1:2 volume ratio of isopropanol to deionized water. Finally, good cycle durability of up to 2000 cycles without obvious degradation was demonstrated by cyclic voltammetry tests in a LiClO4/propylene carbonate electrolyte. This study provides a simple and effective approach for fabrication of NiOx films at low temperature in air, which is attractive for further commercialization of electrochromic devices.
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Placenta-specific 1 (Plac1) has been found to be essential for placentation, and abnormal Plac1 expression and distribution is highly correlated with preeclampsia and implantation failure; however, its function in mammalian oocytes has not been elucidated. Here, we report that Plac1 was more prominent in mouse oocytes and enriched at the membrane region throughout meiosis. On the one hand, Plac1 knockdown severely disrupted microvillus organization; however, on the other hand, Plac1 significantly decreased oocyte maturation and increased aneuploidy, consequently disrupting normal fertilization. On the basis of immunoprecipitate matrix-assisted laser desorption/ionization, we established a working model, then verified and suggested that, at the germinal vesicle stage, Plac1 enriches the membrane to activate furin, and active furin subsequently activates IGF-1 receptor to maintain regular microvillus organization. Upon meiosis onset, active furin/IGF-1 receptor relocates into the cytoplasm to activate (phosphorylate) Akt to promote meiosis. In summary, our finding suggests that Plac1, a protein that is crucial for placentation, is also essential for oocyte meiosis and fertilization.-Shi, L.-Y., Ma, Y., Zhu, G.-Y., Liu, J.-W., Zhou, C.-X., Chen, L.-J., Wang, Y., Li, R.-C., Yang, Z.-X., Zhang, D. Placenta-specific 1 regulates oocyte meiosis and fertilization through furin.
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Fertilização/fisiologia , Furina/metabolismo , Meiose/fisiologia , Oócitos/metabolismo , Proteínas da Gravidez/metabolismo , Animais , Ativação Enzimática/fisiologia , Feminino , Furina/genética , Camundongos , Camundongos Endogâmicos ICR , Oócitos/citologia , Proteínas da Gravidez/genética , Transporte Proteico/fisiologia , Proteínas Proto-Oncogênicas c-akt/genética , Proteínas Proto-Oncogênicas c-akt/metabolismo , Receptor IGF Tipo 1/genética , Receptor IGF Tipo 1/metabolismoRESUMO
We fabricated a floating GaN microdisk supported by a silicon pillar through photolithography, dry-etching GaN, and isotropic wet-etching silicon methods. Single-mode ultraviolet whispering gallery mode (WGM) lasing was obtained from the floating GaN microdisk under optical pumping conditions at room temperature. The features of WGM lasing, i.e., the threshold, emission intensity, and lasing mode number, were characterized. A two-dimensional finite-difference time-domain simulation about the optical field contour profile also confirmed the resonance mechanism of WGM lasing. This work can help realize single-mode WGM lasing with high quality factor and low threshold.
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Transition metal dichalcogenides (TMDs) are promising candidates for flexible optoelectronic devices because of their special structures and excellent properties, but the low optical absorption of the ultrathin layers greatly limits the generation of photocarriers and restricts the performance. Here, we integrate all-inorganic perovskite CsPbBr3 nanosheets with MoS2 atomic layers and take the advantage of the large absorption coefficient and high quantum efficiency of the perovskites, to achieve excellent performance of the TMD-based photodetectors. Significantly, the interfacial charge transfer from the CsPbBr3 to the MoS2 layer has been evidenced by the observed photoluminescence quenching and shortened decay time of the hybrid MoS2/CsPbBr3. Resultantly, such a hybrid MoS2/CsPbBr3 photodetector exhibits a high photoresponsivity of 4.4 A/W, an external quantum efficiency of 302%, and a detectivity of 2.5 × 1010 Jones because of the high efficient photoexcited carrier separation at the interface of MoS2 and CsPbBr3. The photoresponsivity of this hybrid device presents an improvement of 3 orders of magnitude compared with that of a MoS2 device without CsPbBr3. The response time of the device is also shortened from 65.2 to 0.72 ms after coupling with MoS2 layers. The combination of the all-inorganic perovskite layer with high photon absorption and the carrier transport TMD layer may pave the way for novel high-performance optoelectronic devices.
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ZP3 is a principal component of the zona pellucida (ZP) of mammalian oocytes and is essential for normal fertility, and knockout of ZP3 causes complete infertility. ZP3 promotes fertilization by recognizing sperm binding and activating the acrosome reaction; however, additional cellular roles for ZP3 in mammalian oocytes have not been yet reported. In the current study, we found that ZP3 was strongly expressed in the nucleus during prophase and gradually translocated to the ZP. Knockdown of ZP3 by a specific siRNA dramatically inhibited germinal vesicle breakdown (GVBD) (marking the beginning of meiosis), significantly reducing the percentage of MII oocytes. To investigate the ZP3-mediated mechanisms governing GVBD, we identified potential ZP3-interacting proteins by immunoprecipitation and mass spectrometry. We identified Protein tyrosine phosphatase, receptor type K (Ptprk), Aryl hydrocarbon receptor-interacting protein-like 1 (Aipl1), and Diaphanous related formin 2 (Diaph2) as potential candidates, and established a working model to explain how ZP3 affects GVBD. Finally, we provided preliminary evidence that ZP3 regulates Akt phosphorylation, lamin binding to the nuclear membrane via Aipl1, and organization of the actin cytoskeleton via Diaph2. These findings contribute to our understanding of a novel role played by ZP3 in GVBD.