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991.
A selective and sensitive fluorescent sensor for cysteine detection based on bi‐8‐carboxamidoquinoline derivative and Cu2+ complex
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Guoping Chai Qingwen Liu Qiang Fei Jinling Zhang Xiaoxiao Sun Hongyan Shan Guodong Feng Yanfu Huan 《Luminescence》2018,33(1):153-160
In this paper, a novel fluorescent sensor 1 for selective and sensitive detection of cysteine was developed based on a complex between bi‐8‐carboxamidoquinoline derivative ligand ( L ) and Cu2+. The interaction of Cu2+ with the ligand causes a dramatic fluorescence quenching most likely due to its high affinity towards Cu2+ and a ligand–metal charge transfer (LMCT) process. The in situ generated L–Cu 2 complex was utilized as a chemosensing ensemble for cysteine. In the presence of cysteine, the fluorophore, L , was released from L–Cu 2 complex because of the strong affinity of cysteine to Cu2+ via the Cu–S bond, leading to the fluorescence recovery of the ligand. The proposed displacement mechanism was confirmed by the results of mass spectrometry (MS) study. Under optimized conditions, the recovered fluorescence intensity is linear with cysteine concentrations in the range 1 × 10?6 mol/l to 8 × 10?6 mol/l. The detection limit for cysteine is 1.92 × 10?7 mol/l. Furthermore, the established method showed a highly sensitive and selective response to cysteine among the 20 fundamental α‐amino acids used as the building blocks of proteins, after Ni2+ was used as a masking agent to eliminate the interference of His. The proposed sensor is applicable in monitoring cysteine in practical samples with good recovery rate. 相似文献
992.
Zhixiong Zhou Lin Chen Chuanju Dong Wenzhu Peng Shengnan Kong Jinsheng Sun Fei Pu Baohua Chen Jianxin Feng Peng Xu 《Marine biotechnology (New York, N.Y.)》2018,20(5):573-583
Common carp (Cyprinus carpio) is one of the most widely studied fish species due to its great economic value and strong environmental adaptability. Scattered scale, a typical phenotype of the mirror carp that is derived from Europe, has never been observed in the Yellow River carp previously. We recently identified approximately one fourth of the F1 progenies displaying scattered scale in a full-sib Yellow River carp family in our breeding program, despite both parents that showed wild type with normal scale patterns. This family provides us unique materials to investigate the genetic basis underlying the abnormal scale mutant in Yellow River carp population. Genome-wide association study (GWAS) and association mapping were performed based on genome-wide single nucleotide polymorphisms (SNP) genotyped with common carp 250 K SNP genotyping array in 82 samples of the Yellow River carp family. We identified a 1.4 Mb genome region that was significantly associated with abnormal scattered scale patterns. We further identified a deletion mutation in fibroblast growth factor receptor 1 a1 (fgfr1a1) gene within this genome region. Amplification and sequencing analysis of this gene revealed a 311-bp deletion in intron 10 and exon 11, which proved that fgfr1a1 could be the causal gene responsible for abnormal scattered scale in the Yellow River carp family. Since similar fragment mutation with 306-bp and 310-bp deletions had been previously reported as causal mutation of scattered scale patterns in the mirror carp, we speculate that either the deletion mutation was introduced from Europe-derived mirror carp or the deletion independently occurred in the mutation hotspot in fgfr1a1 gene. The results provided insights into the genetic basis of scale pattern mutant in Yellow River carp population, which would help us to eliminate the recessive allele of the abnormal scale patterns in Yellow River carp population by molecular marker-assisted breeding. 相似文献
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996.
Exploring Inorganic Binary Alkaline Halide to Passivate Defects in Low‐Temperature‐Processed Planar‐Structure Hybrid Perovskite Solar Cells
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Xu Liu Yuanfang Zhang Lei Shi Ziheng Liu Jialiang Huang Jae Sung Yun Yiyu Zeng Aobo Pu Kaiwen Sun Ziv Hameiri John A. Stride Jan Seidel Martin A. Green Xiaojing Hao 《Liver Transplantation》2018,8(20)
Planar perovskite solar cells obtained by low‐temperature solution processing are of great promise, given a high compatibility with flexible substrates and perovskite‐based tandem devices, whilst benefitting from relatively simple manufacturing methods. However, ionic defects at surfaces usually cause detrimental carrier recombination, which links to one of dominant losses in device performance, slow transient responses, and notorious hysteresis. Here, it is shown that several different types of ionic defects can be simultaneously passivated by simple inorganic binary alkaline halide salts with their cations and anions. Compared to previous literature reports, this work demonstrates a promising passivation technology for perovskite solar cells. The efficient defect passivation significantly suppresses the recombination at the SnO2/perovskite interface, contributing to an increase in the open‐circuit voltage, the fast response of steady‐state efficiency, and the elimination of hysteresis. By this strong leveraging of multiple‐element passivation, low‐temperature‐processed, planar‐structured perovskite solar cells of 20.5% efficiencies, having negligible hysteresis, are obtained. Moreover, this defect‐passivation enhances the stability of solar cells with efficiency beyond 20%, retaining 90% of their initial performance after 30 d. This approach aims at developing the concept of defect engineering, which can be expanded to multiple‐element passivation from monoelement counterparts using simple and low‐cost inorganic materials. 相似文献
997.
Lingchen Gao Yichao Zhao Jie He Yang Yan Longwei Xu Nan Lin Qingqi Ji Renyang Tong Yanan Fu Yu Gao Yuanyuan Su Ancai Yuan Ben He Jun Pu 《遗传学报》2018,45(3):125-135
Sentrin-specific protease 3 (SENP3), a member of the desumoylating enzyme family, is known as a redox sensor and could regulate multiple cellular signaling pathways. However, its implication in myocardial ischemia reperfusion (MIR) injury is unclear. Here, we observed that SENP3 was expressed and upregulated in the mouse heart depending on reactive oxygen species (ROS) production in response to MIR injury. By utilizing siRNA-mediated cardiac specific gene silencing, SENP3 knockdown was demonstrated to significantly reduce MIR-induced infarct size and improve cardiac function. Mechanistic studies indicated that SENP3 silencing ameliorated myocardial apoptosis mainly via suppression of endoplasmic reticulum (ER) stress and mitochondrial-mediated apoptosis pathways. By contrast, adenovirus-mediated cardiac SENP3 overexpression significantly exaggerated MIR injury. Further molecular analysis revealed that SENP3 promoted mitochondrial translocation of dynamin-related protein 1 (Drp1) in reperfused myocardium. In addition, mitochondrial division inhibitor-1 (Mdivi-1), a pharmacological inhibitor of Drp1, significantly attenuated the exaggerated mitochondrial abnormality and cardiac injury by SENP3 overexpression after MIR injury. Taken together, we provide the first direct evidence that SENP3 upregulation pivotally contributes to MIR injury in a Drp1-dependent manner, and suggest that SENP3 suppression may hold therapeutic promise for constraining MIR injury. 相似文献
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999.
Microenvironment‐induced PIM kinases promote CXCR4‐triggered mTOR pathway required for chronic lymphocytic leukaemia cell migration
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Emilia Białopiotrowicz Patryk Górniak Monika Noyszewska‐Kania Bartosz Puła Hanna Makuch‐Łasica Grażyna Nowak Aleksandra Bluszcz Maciej Szydłowski Ewa Jabłonska Karolina Piechna Tomasz Sewastianik Anna Polak Ewa Lech‐Marańda Bożena K. Budziszewska Maja Wasylecka‐Juszczyńska Katarzyna Borg Krzysztof Warzocha Wojciech Czardybon Michał Gałęzowski Renata Windak Krzysztof Brzózka Przemysław Juszczyński 《Journal of cellular and molecular medicine》2018,22(7):3548-3559
Lymph node microenvironment provides chronic lymphocytic leukaemia (CLL) cells with signals promoting their survival and granting resistance to chemotherapeutics. CLL cells overexpress PIM kinases, which regulate apoptosis, cell cycle and migration. We demonstrate that BCR crosslinking, CD40 stimulation, and coculture with stromal cells increases PIMs expression in CLL cells, indicating microenvironment‐dependent PIMs regulation. PIM1 and PIM2 expression at diagnosis was higher in patients with advanced disease (Binet C vs. Binet A/B) and in those, who progressed after first‐line treatment. In primary CLL cells, inhibition of PIM kinases with a pan‐PIM inhibitor, SEL24‐B489, decreased PIM‐specific substrate phosphorylation and induced dose‐dependent apoptosis in leukaemic, but not in normal B cells. Cytotoxicity of SEL24‐B489 was similar in TP53‐mutant and TP53 wild‐type cells. Finally, inhibition of PIM kinases decreased CXCR4‐mediated cell chemotaxis in two related mechanisms‐by decreasing CXCR4 phosphorylation and surface expression, and by limiting CXCR4‐triggered mTOR pathway activity. Importantly, PIM and mTOR inhibitors similarly impaired migration, indicating that CXCL12‐triggered mTOR is required for CLL cell chemotaxis. Given the microenvironment‐modulated PIM expression, their pro‐survival function and a role of PIMs in CXCR4‐induced migration, inhibition of these kinases might override microenvironmental protection and be an attractive therapeutic strategy in this disease. 相似文献
1000.
本文采用辣根过氧化物酶(HRP)逆行追踪技术结合硫辛酰胺脱氨酸(NADPH-d)组织化学方法,研究正常豚鼠耳蜗核一氧化氮合酶(NOS)阳性神经元的上行投射特点。探讨耳蜗核NOS阳性神经元在听觉信号传递中的可能作用。结果表明,一侧上橄榄复合体加压注射HRP后,两侧耳蜗核均出现HRP标记细胞,同侧耳蜗核NOS-HRP双标细胞较多占82.63%,并可见HRP阳性纤维和终末包绕NOS阳性胞体,对侧耳蜗核NOS-HRP双标细胞相对较少,仅占14.87%。一侧下丘加压注入HRP后两侧耳蜗核均无HRP-NOS双标细胞。结果提示,耳蜗核NOS阳性神经元向上橄榄复合体投射,可能具有调节听觉声信号传递的作用 相似文献