ALBERT

Description: Many remarkable properties of graphene are derived from its large energy window for Dirac-like electronic states and have been explored for applications in electronics and photonics. In addition, strong electron-phonon interaction in graphene has led to efficient photo-thermo energy conversions, which has been harnessed for energy applications. By combining the wavelength independent absorption property and the efficient photo-thermo energy conversion, here we report a new type of applications in sound wave generation underlined by a photo-thermo-acoustic energy conversion mechanism. Most significantly, by utilizing ultrafast optical pulses, we demonstrate the ability to control the phase of sound waves generated by the photo-thermal-acoustic process. Our finding paves the way for new types of applications for graphene, such as remote non-contact speakers, optical-switching acoustic devices, etc. Scientific Reports 5 doi: 10.1038/srep10582

Description: SBF-1 exerts strong anticervical cancer effect through inducing endoplasmic reticulum stress-associated cell death via targeting sarco/endoplasmic reticulum Ca2+-ATPase 2 Cell Death and Disease 5, e1581 (December 2014). doi:10.1038/cddis.2014.538 Authors: W Li, Z Ouyang, Q Zhang, L Wang, Y Shen, X Wu, Y Gu, Y Shu, B Yu, X Wu, Y Sun & Q Xu

Description: Journal of the American Chemical Society DOI: 10.1021/ja3048128

Description: The tripartite motif (TRIM)-containing proteins are a family of proteins that have been known to be involved in divergent biological processes, including important roles in immune responses through regulating various signaling pathways. In this study, we identified a member of the TRIM family, TRIM8, as a positive regulator of tumor necrosis factor-α (TNFα) and interleukin-1β (IL-1β)–triggered NF-κB activation. Overexpression of TRIM8 activated NF-κB and potentiated TNFα- and IL-1β–induced activation of NF-κB, whereas knockdown of TRIM8 had opposite effects. Coimmunoprecipitations indicated that TRIM8 interacted with TGFβ activated kinase 1 (TAK1), a serine/threonine kinase essential for TNFα- and IL-β–induced NF-κB activation. Furthermore, we found that TRIM8 mediated K63-linked polyubiquitination of TAK1 triggered by TNFα and IL-1β. Our findings demonstrate that TRIM8 serves as a critical regulator of TNFα- and IL-1β–induced NF-κB activation by mediating K63-linked polyubiquitination of TAK1.

Description: Intracellular accumulation of the abnormally modified tau is hallmark pathology of Alzheimer’s disease (AD), but the mechanism leading to tau aggregation is not fully characterized. Here, we studied the effects of tau SUMOylation on its phosphorylation, ubiquitination, and degradation. We show that tau SUMOylation induces tau hyperphosphorylation at multiple AD-associated...

Description: An avian-origin human-infecting influenza (H7N9) virus was recently identified in China. We have evaluated the viral hemagglutinin (HA) receptor-binding properties of two human H7N9 isolates, A/Shanghai/1/2013 (SH-H7N9) (containing the avian-signature residue Gln(226)) and A/Anhui/1/2013 (AH-H7N9) (containing the mammalian-signature residue Leu(226)). We found that SH-H7N9 HA preferentially binds the avian receptor analog, whereas AH-H7N9 HA binds both avian and human receptor analogs. Furthermore, an AH-H7N9 mutant HA (Leu(226) --〉 Gln) was found to exhibit dual receptor-binding property, indicating that other amino acid substitutions contribute to the receptor-binding switch. The structures of SH-H7N9 HA, AH-H7N9 HA, and its mutant in complex with either avian or human receptor analogs show how AH-H7N9 can bind human receptors while still retaining the avian receptor-binding property.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shi, Yi -- Zhang, Wei -- Wang, Fei -- Qi, Jianxun -- Wu, Ying -- Song, Hao -- Gao, Feng -- Bi, Yuhai -- Zhang, Yanfang -- Fan, Zheng -- Qin, Chengfeng -- Sun, Honglei -- Liu, Jinhua -- Haywood, Joel -- Liu, Wenjun -- Gong, Weimin -- Wang, Dayan -- Shu, Yuelong -- Wang, Yu -- Yan, Jinghua -- Gao, George F -- New York, N.Y. -- Science. 2013 Oct 11;342(6155):243-7. doi: 10.1126/science.1242917. Epub 2013 Sep 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Research Network of Immunity and Health, Beijing Institutes of Life Science, Chinese Academy of Sciences, Beijing, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24009358" target="_blank"〉PubMed〈/a〉

Description: The emergence of the H7N9 influenza virus in humans in Eastern China has raised concerns that a new influenza pandemic could occur. Here, we used a ferret model to evaluate the infectivity and transmissibility of A/Shanghai/2/2013 (SH2), a human H7N9 virus isolate. This virus replicated in the upper and lower respiratory tracts of the ferrets and was shed at high titers for 6 to 7 days, with ferrets showing relatively mild clinical signs. SH2 was efficiently transmitted between ferrets via direct contact, but less efficiently by airborne exposure. Pigs were productively infected by SH2 and shed virus for 6 days but were unable to transmit the virus to naive pigs or ferrets. Under appropriate conditions, human-to-human transmission of the H7N9 virus may be possible.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhu, H -- Wang, D -- Kelvin, D J -- Li, L -- Zheng, Z -- Yoon, S-W -- Wong, S-S -- Farooqui, A -- Wang, J -- Banner, D -- Chen, R -- Zheng, R -- Zhou, J -- Zhang, Y -- Hong, W -- Dong, W -- Cai, Q -- Roehrl, M H A -- Huang, S S H -- Kelvin, A A -- Yao, T -- Zhou, B -- Chen, X -- Leung, G M -- Poon, L L M -- Webster, R G -- Webby, R J -- Peiris, J S M -- Guan, Y -- Shu, Y -- HSN266200700005C/PHS HHS/ -- New York, N.Y. -- Science. 2013 Jul 12;341(6142):183-6. doi: 10.1126/science.1239844. Epub 2013 May 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Joint Influenza Research Centre [Shantou University Medical College/University of Hong Kong], Shantou University, Shantou, PR China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23704376" target="_blank"〉PubMed〈/a〉

Description: Upregulated long non-coding RNA AGAP2-AS1 represses LATS2 and KLF2 expression through interacting with EZH2 and LSD1 in non-small-cell lung cancer cells Cell Death and Disease 7, e2225 (May 2016). doi:10.1038/cddis.2016.126 Authors: W Li, M Sun, C Zang, P Ma, J He, M Zhang, Z Huang, Y Ding & Y Shu

Description: A novel H7N9 influenza A virus first detected in March 2013 has since caused more than 130 human infections in China, resulting in 40 deaths. Preliminary analyses suggest that the virus is a reassortant of H7, N9 and H9N2 avian influenza viruses, and carries some amino acids associated with mammalian receptor binding, raising concerns of a new pandemic. However, neither the source populations of the H7N9 outbreak lineage nor the conditions for its genesis are fully known. Using a combination of active surveillance, screening of virus archives, and evolutionary analyses, here we show that H7 viruses probably transferred from domestic duck to chicken populations in China on at least two independent occasions. We show that the H7 viruses subsequently reassorted with enzootic H9N2 viruses to generate the H7N9 outbreak lineage, and a related previously unrecognized H7N7 lineage. The H7N9 outbreak lineage has spread over a large geographic region and is prevalent in chickens at live poultry markets, which are thought to be the immediate source of human infections. Whether the H7N9 outbreak lineage has, or will, become enzootic in China and neighbouring regions requires further investigation. The discovery here of a related H7N7 influenza virus in chickens that has the ability to infect mammals experimentally, suggests that H7 viruses may pose threats beyond the current outbreak. The continuing prevalence of H7 viruses in poultry could lead to the generation of highly pathogenic variants and further sporadic human infections, with a continued risk of the virus acquiring human-to-human transmissibility.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3801098/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3801098/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lam, Tommy Tsan-Yuk -- Wang, Jia -- Shen, Yongyi -- Zhou, Boping -- Duan, Lian -- Cheung, Chung-Lam -- Ma, Chi -- Lycett, Samantha J -- Leung, Connie Yin-Hung -- Chen, Xinchun -- Li, Lifeng -- Hong, Wenshan -- Chai, Yujuan -- Zhou, Linlin -- Liang, Huyi -- Ou, Zhihua -- Liu, Yongmei -- Farooqui, Amber -- Kelvin, David J -- Poon, Leo L M -- Smith, David K -- Pybus, Oliver G -- Leung, Gabriel M -- Shu, Yuelong -- Webster, Robert G -- Webby, Richard J -- Peiris, Joseph S M -- Rambaut, Andrew -- Zhu, Huachen -- Guan, Yi -- 092807/Wellcome Trust/United Kingdom -- 095831/Wellcome Trust/United Kingdom -- 260864/European Research Council/International -- BB/E009670/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- HHSN266200700005C/AI/NIAID NIH HHS/ -- HSN266200700005C/PHS HHS/ -- England -- Nature. 2013 Oct 10;502(7470):241-4. doi: 10.1038/nature12515. Epub 2013 Aug 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Joint Influenza Research Centre (SUMC/HKU), Shantou University Medical College, Shantou 515041, China.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23965623" target="_blank"〉PubMed〈/a〉

Description: Understanding the spatiotemporal patterns of emergence and circulation of new human seasonal influenza virus variants is a key scientific and public health challenge. The global circulation patterns of influenza A/H3N2 viruses are well characterized, but the patterns of A/H1N1 and B viruses have remained largely unexplored. Here we show that the global circulation patterns of A/H1N1 (up to 2009), B/Victoria, and B/Yamagata viruses differ substantially from those of A/H3N2 viruses, on the basis of analyses of 9,604 haemagglutinin sequences of human seasonal influenza viruses from 2000 to 2012. Whereas genetic variants of A/H3N2 viruses did not persist locally between epidemics and were reseeded from East and Southeast Asia, genetic variants of A/H1N1 and B viruses persisted across several seasons and exhibited complex global dynamics with East and Southeast Asia playing a limited role in disseminating new variants. The less frequent global movement of influenza A/H1N1 and B viruses coincided with slower rates of antigenic evolution, lower ages of infection, and smaller, less frequent epidemics compared to A/H3N2 viruses. Detailed epidemic models support differences in age of infection, combined with the less frequent travel of children, as probable drivers of the differences in the patterns of global circulation, suggesting a complex interaction between virus evolution, epidemiology, and human behaviour.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4499780/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4499780/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bedford, Trevor -- Riley, Steven -- Barr, Ian G -- Broor, Shobha -- Chadha, Mandeep -- Cox, Nancy J -- Daniels, Rodney S -- Gunasekaran, C Palani -- Hurt, Aeron C -- Kelso, Anne -- Klimov, Alexander -- Lewis, Nicola S -- Li, Xiyan -- McCauley, John W -- Odagiri, Takato -- Potdar, Varsha -- Rambaut, Andrew -- Shu, Yuelong -- Skepner, Eugene -- Smith, Derek J -- Suchard, Marc A -- Tashiro, Masato -- Wang, Dayan -- Xu, Xiyan -- Lemey, Philippe -- Russell, Colin A -- 093488/Wellcome Trust/United Kingdom -- 093488/Z/10/Z/Wellcome Trust/United Kingdom -- 095831/Wellcome Trust/United Kingdom -- 260864/European Research Council/International -- MR/J008761/1/Medical Research Council/United Kingdom -- R01 AI 107034/AI/NIAID NIH HHS/ -- R01 AI107034/AI/NIAID NIH HHS/ -- R01 TW008246/TW/FIC NIH HHS/ -- R01 TW008246-01/TW/FIC NIH HHS/ -- U01 GM110721/GM/NIGMS NIH HHS/ -- U01 GM110721-01/GM/NIGMS NIH HHS/ -- U117512723/Medical Research Council/United Kingdom -- U54 GM111274/GM/NIGMS NIH HHS/ -- England -- Nature. 2015 Jul 9;523(7559):217-20. doi: 10.1038/nature14460. Epub 2015 Jun 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. ; 1] MRC Centre for Outbreak Analysis and Modelling, Department of Infectious Disease Epidemiology, School of Public Health, Imperial College London, London SW7 2AZ, UK [2] Fogarty International Center, National Institutes of Health, Bethesda, Maryland 20892, USA. ; World Health Organization (WHO) Collaborating Centre for Reference and Research on Influenza, Melbourne, Victoria 3000, Australia. ; SGT Medical College, Hospital and Research Institute, Village Budhera, District Gurgaon, Haryana 122505, India. ; National Institute of Virology, Pune 411001, India. ; WHO Collaborating Center for Reference and Research on Influenza, Centers for Disease Control and Prevention, Atlanta, Georgia 30329, USA. ; WHO Collaborating Center for Reference and Research on Influenza, Medical Research Council National Institute for Medical Research (NIMR), London NW7 1AA, UK. ; King Institute of Preventive Medicine and Research, Guindy, Chennai 600032, India. ; 1] World Health Organization (WHO) Collaborating Centre for Reference and Research on Influenza, Melbourne, Victoria 3000, Australia [2] Melbourne School of Population and Global Health, University of Melbourne, Parkville, Victoria 3010, Australia. ; Department of Zoology, University of Cambridge, Cambridge CB2 3EJ, UK. ; WHO Collaborating Center for Reference and Research on Influenza, National Institute for Viral Disease Control and Prevention, China CDC, Beijing 102206, China. ; WHO Collaborating Center for Reference and Research on Influenza, National Institute of Infectious Diseases, Tokyo 208-0011, Japan. ; 1] Fogarty International Center, National Institutes of Health, Bethesda, Maryland 20892, USA [2] Institute of Evolutionary Biology, University of Edinburgh, Edinburgh EH9 3JT, UK [3] Centre for Immunology, Infection and Evolution, University of Edinburgh, Edinburgh EH9 3FL, UK. ; 1] Department of Zoology, University of Cambridge, Cambridge CB2 3EJ, UK [2] Department of Viroscience, Erasmus Medical Center, 3015 Rotterdam, The Netherlands. ; 1] Department of Biostatistics, UCLA Fielding School of Public Health, University of California, Los Angeles, California 90095, USA [2] Department of Biomathematics, David Geffen School of Medicine at UCLA, University of California, Los Angeles, California 90095, USA [3] Department of Human Genetics, David Geffen School of Medicine at UCLA, University of California, Los Angeles, California 90095, USA. ; Department of Microbiology and Immunology, Rega Institute, KU Leuven - University of Leuven, 3000 Leuven, Belgium. ; Department of Veterinary Medicine, University of Cambridge, Cambridge CB3 0ES, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26053121" target="_blank"〉PubMed〈/a〉