From plasmon-enhanced molecular spectroscopy to plasmon-mediated chemical reaction

该论文在田中群教授指导下完成，第一作者为iChEM中心2013级博士生战超。 表面等离激元效应可以在时间和空间上实现光子、电子和热能的重新分配。表面等离激元增强分子光谱由于其具有超高的灵敏度在过去四十年里引起了人们的广泛关注并得到快速发展。近年，表面等离激元效应介导的化学反应得到广泛的关注。该综述系统介绍了表面等离激元效应、表面等离激元增强分子光谱和表面等离激元介导化学反应的背景和基础理论，并与传统热化学、光化学和光催化进行对比。通过将表面等离激元介导化学反应与表面等离激元增强分子光谱以及其它反应类型进行比较，归纳出表面等离激元介导化学反应的独特科学内涵，展示了较完整的表面等离激元介导化学反应的物理化学图像。系统深入地分析了表面等离激元介导化学反应的特色和优势、影响因素及其之间的关联性，进而讨论高效利用表面等离激元来介导化学反应的策略，并对该领域做了展望。【Abstract】The excitation of surface plasmons (SPs), collective oscillation of conduction electrons in nanostructures, can redistribute photon, electron and heat energy in time and space. Making use of this ability, plasmon-enhanced molecular spectroscopies (PEMS) with ultra-high sensitivity and surface selectivity have attracted much attention and developed significantly in the past four decades. Recently, SPs have impacted the discipline of chemistry, through plasmon-mediated chemical reactions (PMCR). PMCR exhibit some obvious differences from, and potential advantages over traditional thermal-chemistry, photo-chemistry and photo-catalysis. Our physicochemical understanding of PMCR is still far from complete. In this review, we analyze the common ground and distinctive features of PEMS and PMCR; comparing as well, PMCR and traditional photo-chemical and thermal-chemical reactions. We then discuss how to advance PMCR by rationally designing and fabricating plasmonic nanostructures, selecting suitable surface/interface mediators and teaming them synergistically.We are deeply grateful to M. Moskovits for his very helpful suggestions and careful academic and English editing throughout the manuscript. This work is financially supported by the National Natural Science Foundation of China (21533006, 21621091, 91427304 and 21403180) and the Ministry of Science and Technology of China (2015CB932300). 研究工作得到国家自然科学基金委(21533006、21621091、91427304）和科技部重大科学研究计划（2015CB932300）的支持

Plasmon-Mediated Chemical Reactions on Nanostructures Unveiled by Surface-Enhanced Raman Spectroscopy.

Surface plasmons (SPs) originating from the collective oscillation of conduction electrons in nanostructured metals (Au, Ag, Cu, etc.) can redistribute not only the electromagnetic fields but also the excited carriers (electrons and holes) and heat energy in time and space. Therefore, SPs can engage in a variety of processes, such as molecular spectroscopy and chemical reaction. Recently, plenty of demonstrations have made plasmon-mediated chemical reactions (PMCRs) a very active research field and make it as a promising approach to facilitate light-driven chemical reactions under mild conditions. Concurrently, making use of the same SPs, surface-enhanced Raman spectroscopy (SERS) with a high surface sensitivity and energy resolution becomes a powerful and commonly used technique for the in situ study of PMCRs. Typically, various effects induced by SPs, including the enhanced electromagnetic field, local heating, excited electrons, and excited holes, can mediate chemical reactions. Herein, we use the para-aminothiophenol (PATP) transformation as an example to elaborate how SERS can be used to study the mechanism of PMCR system combined with theoretical calculations. First, we distinguish the chemical transformation of PATP to 4,4’-dimercaptoazobenzene (DMAB) from the chemical enhancement mechanism of SERS through a series of theoretical and in situ SERS studies. Then, we focus on disentangling the photothermal, hot electrons, and "hot holes" effects in the SPs-induced PATP-to-DMAB conversion. Through varying the key reaction parameters, such as the wavelength and intensity of the incident light, using various core-shell plasmonic nanostructures with different charge transfer properties, we extract the key factors that influence the efficiency and mechanism of this reaction. We confidently prove that the transformation of PATP can occur on account of the oxygen activation induced by the hot electrons or because of the action of hot holes in the absence of oxygen and confirm the critical effect of the interface between the plasmonic nanostructure and reactants. The products of these two process are different. Furthermore, we compare the correlation between PMCRs and SERS, discuss different scenario of PMCRs in situ studied by SERS, and provide some suggestions for the SERS investigation on the PMCRs. Finally, we comment on the mechanism studies on how to distinguish the multieffects of SPs and their influence on the PMCRs, as well as on how to power the chemical reaction and regulate the product selectivity in higher efficiencies

Propofol Inhibits Proliferation, Migration, Invasion and Promotes Apoptosis Through Down-Regulating miR-374a in Hepatocarcinoma Cell Lines

Background: Propofol is a commonly used anaesthetic with controversial effects on cancer cells. We aimed to explore the functional roles of propofol in hepatocellular carcinoma (HCC) cells as well as the underlying mechanisms. Methods: HepG2 and SMMC-7721 cells were used in this study. Firstly, the effects of propofol on cell viability, migration, invasion, apoptosis, and involved proteins were assessed by Cell Counting Kit-8 assay, Transwell assay, flow cytometry assay and Western blot analysis, respectively. Subsequently, alteration of miR-374a after stimulation of propofol was analyzed by qRT-PCR. miR-374a was overexpressed and the alteration of proteins in the Wnt/β-catenin and PI3K/AKT pathways was detected by Western blot analysis. The downstream factor of miR-374a was finally studied. Results: Propofol inhibited cell viability, migration and invasion but promoted apoptosis of HepG2 and SMMC-7721 cells. Meanwhile, cyclinD1, matrix metalloproteinase (MMP)-2 and MMP-9 were down-regulated while Bax/Bcl-2, cleaved caspase-3 and cleaved caspase-9 were up-regulated by propofol. Then, miR-374a level was reduced by propofol. Expression of Wnt3a, β-catenin, p-PI3K and p-AKT was decreased by propofol, whereas these decreases were reversed by miR-374a overexpression. Finally, TP53 was proven to be target of miR-374a in HepG2 cells. Conclusion: Propofol inhibited cell proliferation, migration and invasion while promoted cell apoptosis of HepG2 and SMMC-7721 cells through inhibiting the Wnt/β-catenin and PI3K/ AKT pathways via down-regulation of miR-374a. Besides, miR-374a affected propofol-treated HepG2 cells by targeting TP53

Burden of Pneumonia and Meningitis Caused by Streptococcus pneumoniae in China among Children under 5 Years of Age: A Systematic Literature Review

BACKGROUND AND METHODS: To understand the burden and epidemiology of Streptococcus pneumoniae disease among children between 1 and 59 months of age in China, we conducted a review of literature published between 1980 and 2008 applying standardized algorithms. Because of the absence of population-based surveillance for pneumococcal disease (PD), we identified all-cause pneumonia, bacteremia and meningitis burden, syndromes most commonly associated with S. pneumoniae, and applied the proportion of disease attributable to S. pneumoniae from studies that determined the etiology of these three syndromes to calculate PD burden. Because of the microbiologic difficulties in identifying S. pneumoniae-attributable pneumonia which likely underestimates the pneumonia burden, we also used the proportion obtained from vaccine efficacy trials. RESULTS: Between 1980 and 2008, there were 12,815 cases/100,000/year of all-cause pneumonia among children between 1 month and 59 months, with 526 deaths/100,000 annually. There were 14 meningitis cases/100,000/year. We estimate that as of 2000, there were 260,768 (113,000 to 582,382) and 902 (114-4,463) cases of pneumococcal pneumonia and meningitis, respectively with 10,703 (4,638-23,904) and 75 (9-370) pneumococcal pneumonia and meningitis deaths, respectively. Pneumococcal pneumonia cases and deaths were more than two-fold higher, 695,382 (173,845-1,216,918) and 28,542 (7,136-49,949), respectively, when parameters from efficacy trials were used. Serotypes 19F, 19A and 14 were the most common serotypes obtained from pneumonia/meningitis patients. Currently available vaccines are expected to cover 79.5% to 88.4% of the prevalent serotypes. With high antibiotic resistance, introducing pneumococcal vaccines to the routine immunization program should be considered in China. Population-based studies are warranted

PCBP-1 regulates alternative splicing of the CD44 gene and inhibits invasion in human hepatoma cell line HepG2 cells

<p>Abstract</p> <p>Background</p> <p>PCBP1 (or alpha CP1 or hnRNP E1), a member of the PCBP family, is widely expressed in many human tissues and involved in regulation of transcription, transportation process, and function of RNA molecules. However, the role of PCBP1 in CD44 variants splicing still remains elusive.</p> <p>Results</p> <p>We found that enforced PCBP1 expression inhibited CD44 variants expression including v3, v5, v6, v8, and v10 in HepG2 cells, and knockdown of endogenous PCBP1 induced these variants splicing. Invasion assay suggested that PCBP1 played a negative role in tumor invasion and re-expression of v6 partly reversed the inhibition effect by PCBP1. A correlation of PCBP1 down-regulation and v6 up-regulation was detected in primary HCC tissues.</p> <p>Conclusions</p> <p>We first characterized PCBP1 as a negative regulator of CD44 variants splicing in HepG2 cells, and loss of PCBP1 in human hepatic tumor contributes to the formation of a metastatic phenotype.</p

Proteomic screen defines the hepatocyte nuclear factor 1α-binding partners and identifies HMGB1 as a new cofactor of HNF1α

Hepatocyte nuclear factor (HNF)-1α is one of the liver-enriched transcription factors involved in many tissue-specific expressions of hepatic genes. The molecular mechanisms for determining HNF1α-mediated transactivation have not been explained fully. To identify unknown proteins that interact with HNF1α, we developed a co-IP-MS strategy to search HNF1α interactions, and high mobility group protein-B1 (HMGB1), a chromosomal protein, was identified as a novel HNF1α-interacting protein. In vitro glutathione S-transferase pull-down and in vivo co-immunoprecipitation studies confirmed an interaction between HMGB1 and HNF1α. The protein–protein interaction was mediated through the HMG box domains of HMGB1 and the homeodomain of HNF1α. Furthermore, electrophoretic mobility shift assay and chromatin-immunoprecipitation assay demonstrated that HMGB1 was recruited to endogenous HNF1α-responsive promoters and enhanced HNF1α binding to its cognate DNA sequences. Moreover, luciferase reporter analyses showed that HMGB1 potentiated the transcriptional activities of HNF1α in cultured cells, and downregulation of HMGB1 by RNA interference specifically affected the HNF1α-dependent gene expression in HepG2 cell. Taken together, these findings raise the intriguing possibility that HMGB1 is a new cofactor of HNF1α and participates in HNF1α-mediated transcription regulation through protein–protein interaction

3-(3-Pyridylmethylidene)-2-indolinone Reduces the Severity of Colonic Injury in a Murine Model of Experimental Colitis

Nrf2 is the key transcription factor regulating the antioxidant response which is crucial for cytoprotection against extracellular stresses. Numerous in vivo studies indicate that Nrf2 plays a protective role in anti-inflammatory response. 3-(3-Pyridylmethylidene)-2-indolinone (PMID) is a synthesized derivative of 2-indolinone compounds. Our previous study suggested that PMID induces the activation of Nrf2/ARE pathway, then protecting against oxidative stress-mediated cell death. However, little is known regarding the anti-inflammatory properties of PMID in severe inflammatory phenotypes. In the present study we determined if PMID treatment protects mice from dextran sodium sulphate- (DSS-) induced colitis. The result suggests that treatment with PMID prior to colitis induction significantly reduced body weight loss, shortened colon length, and decreased disease activity index compared to control mice. Histopathological analysis of the colon revealed attenuated inflammation in PMID pretreated animals. The levels of inflammatory markers in colon tissue and serum were reduced associated with inhibition of NF-κB activation. The expression levels of Nrf2-dependent genes such as HO-1, NQO1, and Nrf2 were increased in PMID pretreated mice. However, PMID pretreatment did not prevent DSS-induced colitis in Nrf2 knockout mice. These data indicate that PMID pretreatment in mice confers protection against DSS-induced colitis in Nrf2-dependent manner, suggesting a potential role of PMID in anti-inflammatory response

Single-Molecule Plasmonic Optical Trapping

人们对于在常温常压条件下尤其是溶液环境中俘获或者操控微观粒子的追求从未停止，以期不断减少可操控的微观粒子的尺寸，最终实现单分子操控的目标。化学化工学院田中群教授和洪文晶教授团队合作，利用等离激元光学纳米间隙实现单分子的直接捕获与释放。该工作由化学化工学院田中群教授、洪文晶教授以及萨本栋微米纳米科学技术研究院杨扬副教授共同指导，由化学化工学院已毕业博士生战超提出思路并设计实验、与萨本栋微米纳米研究院已毕业硕士生王干共同完成主要实验工作，已毕业博士生易骏完成理论模拟工作。魏珺颖硕士、博士生李之豪、陈招斌高工和师佳副教授参与了部分研究和课题讨论。【Abstract】The volume of the object that can be manipulated in solution is continuously decreasing toward an ultimate goal of a single molecule. However, Brownian motions suppress the molecular trapping. To date, free-molecule trapping in solution has not been accomplished. Here, we develop a strategy to directly trap, investigate, and release single molecules (∼2 nm) in solution by using an adjustable plasmonic optical nanogap, which has been further applied for selective single-molecule trapping. Comprehensive experiments and theoretical simulations demonstrated that the trapping force originated from plasmonic nanomaterials. This technique opens an avenue to manipulate single molecules and other objects in the size range of primary interest for physics, chemistry, and life and material sciences without the limitations of strong bonding group, ultra-high vacuum, and ultra-low temperature, and makes possible controllable single-molecule manipulation and investigation as well as bottom-up construction of nanodevices and molecular machines.This work is financially supported by the National Natural Science Foundation of China (21533006, 21621091, 21673195, 21973079, and 21722305), and the National Key R&D Program (2017YFA0204902, 2015CB932300). 该工作得到国家自然科学基金、国家重点研发计划课题的资助，以及固体表面物理化学国家重点实验室、能源材料化学协同创新中心的支持

Neutrino Physics with JUNO

The Jiangmen Underground Neutrino Observatory (JUNO), a 20 kton multi-purposeunderground liquid scintillator detector, was proposed with the determinationof the neutrino mass hierarchy as a primary physics goal. It is also capable ofobserving neutrinos from terrestrial and extra-terrestrial sources, includingsupernova burst neutrinos, diffuse supernova neutrino background, geoneutrinos,atmospheric neutrinos, solar neutrinos, as well as exotic searches such asnucleon decays, dark matter, sterile neutrinos, etc. We present the physicsmotivations and the anticipated performance of the JUNO detector for variousproposed measurements. By detecting reactor antineutrinos from two power plantsat 53-km distance, JUNO will determine the neutrino mass hierarchy at a 3-4sigma significance with six years of running. The measurement of antineutrinospectrum will also lead to the precise determination of three out of the sixoscillation parameters to an accuracy of better than 1\%. Neutrino burst from atypical core-collapse supernova at 10 kpc would lead to ~5000inverse-beta-decay events and ~2000 all-flavor neutrino-proton elasticscattering events in JUNO. Detection of DSNB would provide valuable informationon the cosmic star-formation rate and the average core-collapsed neutrinoenergy spectrum. Geo-neutrinos can be detected in JUNO with a rate of ~400events per year, significantly improving the statistics of existing geoneutrinosamples. The JUNO detector is sensitive to several exotic searches, e.g. protondecay via the $p\to K^++\bar\nu$ decay channel. The JUNO detector will providea unique facility to address many outstanding crucial questions in particle andastrophysics. It holds the great potential for further advancing our quest tounderstanding the fundamental properties of neutrinos, one of the buildingblocks of our Universe

Potential of Core-Collapse Supernova Neutrino Detection at JUNO

JUNO is an underground neutrino observatory under construction in Jiangmen, China. It uses 20kton liquid scintillator as target, which enables it to detect supernova burst neutrinos of a large statistics for the next galactic core-collapse supernova (CCSN) and also pre-supernova neutrinos from the nearby CCSN progenitors. All flavors of supernova burst neutrinos can be detected by JUNO via several interaction channels, including inverse beta decay, elastic scattering on electron and proton, interactions on C12 nuclei, etc. This retains the possibility for JUNO to reconstruct the energy spectra of supernova burst neutrinos of all flavors. The real time monitoring systems based on FPGA and DAQ are under development in JUNO, which allow prompt alert and trigger-less data acquisition of CCSN events. The alert performances of both monitoring systems have been thoroughly studied using simulations. Moreover, once a CCSN is tagged, the system can give fast characterizations, such as directionality and light curve