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| 1 | Polymer solar cells with an inverted device configuration using polyhedral oligomeric silsesquioxane-[60]fullerene dyad as a novel electron acceptor显示文摘A polyhedral oligomeric silsesquioxane-[60]fullerene (POSS-C60) dyad was designed and used as a novel electron acceptor for bulk heterojunction (BHJ) polymer solar cells (PSCs) with an inverted device configuration. The studies of time-resolved photoinduced absorption of the pristine thin film of poly[(4,4'-bis(2-ethylhexyl)dithieno[3,2-b:2',3'-d]silole)-2,6-diyl-alt-(4,7-bis (2-thienyl)-2,1,3-benzothiadiazole)-5,5'-diyl] (SiPCPDTBT) and the composite thin film of SiPCPDTBT:POSS-C60 indicated efficient electron transfer from SiPCPDTBT to POSS-C60 with inhibited back-transfer. BHJ PSCs made by SiPCPDTBT mixed with POSS-C60 yielded the power conversion efficiencies (PCEs) of 1.50%. Under the same operational conditions, PCEs observed from BHJ PSCs made by SiPCPDTBT mixed with [6,6]-phenyl-C61-butyric acid methyl ester were 0.92%. These results demonstrated that POSS-C60 is a potentially good electron acceptor for inverted BHJ PSCs. | ZHANG Wen-Bin TU YingFeng SUN Hao-Jan YUE Kan GONG Xiong CHENG Stephen Z. D. | 2012 | Science China Chemistry2012，55，5： | 3 |
| 2 | Controlling Morphology of Active Layer by Tuning Coplanarity of the Centrality in Acceptor-Donor-Acceptor Small Molecules for Photovoltaic Application显示文摘一系列 acceptor-donor-acceptor 选择小分子被综合包含 phenothiazine, 2,7-carbazole 和 thieno 的捐赠电子的中央大楼一半[3,4-b ] thiophene 和双方上的 tetrazine 的接受电子的一半。中央块的各种各样的符合构造,与在 phenothiazine 的一份订单的共面 < 2,7-carbazole < thieno [3,4-b ] thiophene,在光、电气化学的性质和小分子的 crystallinity 上有明显的影响。另外,混合在小分子之间拍摄,从制服变化并且(6,6 )-phenyl-C61-butyric 酸甲基酉旨提供了 signi ? cantly 各种各样的形态学出现到贯穿的网络。作为结果,光电的设备基于三个小分子提供了的体积异质接面改变了性能,并且最高共面的分子基于展出的设备最好的光电的表演。 | Pan Zhang Chao Li Yue Zhao Yaowen Li Yingfeng Tu | 2013 | Chinese Journal of Chemistry2013，31，11： | 2 |
| 3 | No Evidence for the Compensation Hypothesis in the Swelled Vent Frog(Feirana quadranus)显示文摘The compensation hypothesis predicts that if the left testis is defective e.g.due to developmental stress,the increased right testis serves a compensatory role,and thereby displaying testes asymmetry which can be a reliable indicator of male body condition.Here,to test the prediction of the compensation hypothesis,we analyzed difference in size between left testis and right testis and the relationship between testes asymmetry and male body condition in the swelled vent frog(Feirana quadranus).We found that the left testis was larger than right testis,displaying a significant directional asymmetry in testes size.Although testes mass was correlated with body condition,testes asymmetry was not correlated with body condition,which cannot provide evidence that the right testis had a compensatory function.Our findings suggest no evidence for the compensation hypothesis in this species due to lacking the compensatory function in right testis. | Yingfeng YUE Long JIN Chunlan MAI Xiaofu HUANG Wenbo LIAO | 2020 | Asian Herpetological Research2020，11，3： | 0 |
| 4 | RIPK3 promotes hantaviral replication by restricting JAK-STAT signaling without triggering necroptosis显示文摘Hantaan virus(HTNV)is a rodent-borne virus that causes hemorrhagic fever with renal syndrome(HFRS),resulting in a high mortality rate of 15%.Interferons(IFNs)play a critical role in the anti-hantaviral immune response,and IFN pretreatment efficiently restricts HTNV infection by triggering the expression of a series of IFNstimulated genes(ISGs)through the Janus kinase-signal transducer and activator of transcription 1(JAK-STAT)pathway.However,the tremendous amount of IFNs produced during late infection could not restrain HTNV replication,and the mechanism remains unclear.Here,we demonstrated that receptor-interacting protein kinase 3(RIPK3),a crucial molecule that mediates necroptosis,was activated by HTNV and contributed to hantavirus evasion of IFN responses by inhibiting STAT1 phosphorylation.RNA-seq analysis revealed the upregulation of multiple cell death-related genes after HTNV infection,with RIPK3 identified as a key modulator of viral replication.RIPK3 ablation significantly enhanced ISGs expression and restrained HTNV replication,without affecting the expression of pattern recognition receptors(PRRs)or the production of type I IFNs.Conversely,exogenously expressed RIPK3 compromised the host's antiviral response and facilitated HTNV replication.RIPK3^(-/-)mice also maintained a robust ability to clear HTNV with enhanced innate immune responses.Mechanistically,we found that RIPK3 could bind STAT1 and inhibit STAT1 phosphorylation dependent on the protein kinase domain(PKD)of RIPK3 but not its kinase activity.Overall,these observations demonstrated a noncanonical function of RIPK3 during viral infection and have elucidated a novel host innate immunity evasion strategy utilized by HTNV. | Yue Si Haijun Zhang Ziqing Zhou Xudong Zhu Yongheng Yang He Liu Liang Zhang Linfeng Cheng Kerong Wang Wei Ye Xin Lv Xijing Zhang Wugang Hou Gang Zhao Yingfeng Lei Fanglin Zhang Hongwei Ma | 2023 | Virologica Sinica2023，38，5： | 0 |
| 5 | STING strengthens host anti-hantaviral immunity through an interferon-independent pathway显示文摘Hantaan virus(HTNV),the prototype virus of hantavirus,could escape innate immunity by restraining type I interferon(IFN)responses.It is largely unknown whether there existed other efficient anti-hantaviral tactics in host cells.Here,we demonstrate that the stimulator of interferon genes(STING)strengthens the host IFNindependent anti-hantaviral immunity.HTNV infection activates RIG-I through IRE1-XBP 1-mediated ER stress,which further facilitates the subcellular translocation and activation of STING.During this process,STING triggers cellular autophagy by interacting with Rab7A,thus restricting viral replication.To note,the anti-hantaviral effects of STING are independent of canonical IFN signaling.Additionally,neither application of the pharmacological antagonist nor the agonist targeting STING could improve the outcomes of nude mice post HTNV challenge in vivo.However,the administration of plasmids exogenously expressing the mutant C-terminal tail(ΔCTT)STING,which would not trigger the type I IFN responses,protected the nude mice from lethal HTNV infection.In summary,our research revealed a novel antiviral pathway through the RIG-I-STING-autophagy pathway,which offered novel therapeutic strategies against hantavirus infection. | Kerong Wang Jian Zhang Yongheng Yang Yue Si Ziqing Zhou Xudong Zhu Sushan Wu He Liu Hui Zhang Liang Zhang Linfeng Cheng Wei Ye Xin Lv Yingfeng Lei Xijing Zhang Shilin Cheng Lixin Shen Fanglin Zhang Hongwei Ma | 2023 | Virologica Sinica2023，38，4： | 0 |
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