| 7 | 基于超强拉曼增强金纳米粒子修饰的过渡金属双硫属化合物纳米片的分子检测(英文)显示文摘本文报道用不同尺寸的金纳米粒子(AuNPs)来修饰单层WS2和MoS2纳米片,通过表面增强拉曼散射(SERS)技术检测微量的罗丹明6G染料,并对比了它们在不同波长的激光激发下的等离子体特性。AuNPs在WS2和MoS2纳米片上的均匀沉积是通过种子介导的生长方法还原HAuCl4来实现的。我们进一步使用扫描电子显微镜和拉曼光谱对所制备的异质结构进行了表征。几种优化结构的拉曼增强因子接近108,几乎达到检测单分子需要的灵敏度。我们的研究结果表明,通过贵金属纳米粒子对超薄过渡金属双硫属元素化合物进行可控修饰是完全可行的。这个策略也适合于制备高效且灵活的基底,用在新一代基于表面增强拉曼散射的化学传感器和生物传感器上。Jason D Orlando 1,Ethan Kahn 2,Cindy Y Wong 3,Yin-ting Yeh 4,5,Tej B Limbu 1,Basant Chitara 1,Ana L Elias 4,5,Mauricio Terrones 4,5,YAN Fei(1.Department of Chemistry and Biochemistry,North Carolina Central University,Durham,NC.27707,USA;2.Department of Materials Science and Engineering,The Pennsylvania State University,University Park,PA.16802,USA;3.School for Engineering of Matter,Transport and Energy,Arizona State University,Tempe,AZ.85287,USA;4.Department of Physics,The Pennsylvania State University,University Park,PA.16802,USA;5.Center for Nanoscale Science,The Pennsylvania State University,University Park,PA.16802,USA) | Jason D Orlando Ethan Kahn Cindy Y Wong Yin-ting Yeh Tej B Limbu Basant Chitara Ana L Elias Mauricio Terrones 鄢非 | 2019 | 分析科学学报2019，35，6： | 0 |
| 8 | Human IgG1 antibodies suppress angiogenesis in a target-independent manner显示文摘Aberrant angiogenesis is implicated in diseases affecting nearly 10%of the world’s population.The most widely used antiangiogenic drug is bevacizumab,a humanized IgG1 monoclonal antibody that targets human VEGFA.Although bevacizumab does not recognize mouse Vegfa,it inhibits angiogenesis in mice.Here we show bevacizumab suppressed angiogenesis in three mouse models not via Vegfa blockade but rather Fc-mediated signaling through FcγRI(CD64)and c-Cbl,impairing macrophage migration.Other approved humanized or human IgG1 antibodies without mouse targets(adalimumab,alemtuzumab,ofatumumab,omalizumab,palivizumab and tocilizumab),mouse IgG2a,and overexpression of human IgG1-Fc or mouse IgG2a-Fc,also inhibited angiogenesis in wild-type and FcγR humanized mice.This anti-angiogenic effect was abolished by Fcgr1 ablation or knockdown,Fc cleavage,IgG-Fc inhibition,disruption of Fc-FcγR interaction,or elimination of FcRγ-initated signaling.Furthermore,bevacizumab’s Fc region potentiated its anti-angiogenic activity in humanized VEGFA mice.Finally,mice deficient in FcγRI exhibited increased developmental and pathological angiogenesis.These findings reveal an unexpected anti-angiogenic function for FcγRI and a potentially concerning off-target effect of hIgG1 therapies. | Sasha Bogdanovich Younghee Kim Takeshi Mizutani Reo Yasuma Laura Tudisco Valeria Cicatiello Ana Bastos-Carvalho Nagaraj Kerur Yoshio Hirano Judit Z Baffi Valeria Tarallo Shengjian Li Tetsuhiro Yasuma Parthasarathy Arpitha Benjamin J Fowler Charles B Wright Ivana Apicella Adelaide Greco Arturo Brunetti Menotti Ruvo Annamaria Sandomenico Miho Nozaki Ryo Ijima Hiroki Kaneko Yuichiro Ogura Hiroko Terasaki Balamurali K Ambati Jeanette HW Leusen Wallace Y Langdon Michael R Clark Kathryn L Armour Pierre Bruhns J Sjef Verbeek Bradley D Gelfand Sandro De Falco Jayakrishna Ambati | 2016 | Signal Transduction and Targeted Therapy2016，1，1： | 0 |
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