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Antiproton identification below threshold with the AMS-02 RICH detector

Chinese Physics C 2017年第5期41卷 158-163页

作者：李紫源 Carlos Jose Delgado Mendez Francesca Giovacchini Sadakazu Haino julia hoffman School of Physics Sun Yat-Sen University Guangdong 510275 China Institute of Physics Academia Sinica Taipei 11529 China Centro de Investigaciones Energeticas Mediambientales y Tecnologicas (CIEMAT) Madrid E-28040 Spain Physics and Astronomy Department University of Hawaii Hawaii 96822 USA

The Alpha Magnetic Spectrometer（AMS-02）,which is installed on the International Space Station（ISS）,has been collecting data successfully since May *** main goals of AMS-02 are the search for cosmic anti-matter,dark matter and the precise measurement of the relative abundance of elements and isotopes in galactic cosmic *** order to identify particle properties,AMS-02 includes several specialized *** these,the AMS-02 Ring Imaging Cherenkov detector（RICH） is designed to provide a very precise measurement of the velocity and electric charge of *** describe a method to reject the dominant electron background in antiproton identification with the use of the AMS-02 RICH detector as a veto for rigidities below 3 GV.A ray tracing integration method is used to maximize the statistics of  with the lowest possible e background,providing 4 times rejection power gain for e background with respect to only 3% of  signal efficiency *** using the collected cosmic-ray data,e contamination can be well suppressed within 3% with β ≈ 1,while keeping 76% efficiency for  below the threshold.

关键词： RICH cosmic goals isotopes rejection specialized contamination maximize installed suppressed

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Fluoxetine induces cytotoxic endoplasmic reticulum stress and autophagy in triple negative breast cancer

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World Journal of Clinical Oncology 2015年第6期6卷 299-311页

作者： Michelle Bowie Patrick Pilie julia Wulfkuhle Siya Lem Abigail hoffman Shraddha Desai Emanuel Petricoin Amira Carter Adrian Ambrose Victoria Seewaldt Dihua Yu Catherine Ibarra Drendall Department of Medicine Division of Medical OncologyDuke University Medical Center Department of Internal Medicine University of Michigan Center for Applied Proteomics and Molecular Medicine George Mason University Department of Molecular and Cellular Oncology University of Texas MD Anderson Cancer Center

AIM: To investigate the mechanism of action of lipophilic antidepressant fluoxetine(FLX) in representative molecular subtypes of breast ***: The anti-proliferative effects and mechanistic action of FLX in triple-negative(SUM149PT) and luminal(T47D and Au565) cancer cells and nontransformed MCF10 A were investigated. Reverse phase protein microarray(RPPM) was performed with and without 10 μmol/L FLX for 24 and 48 h to determine which proteins are significantly changed. Viability and cell cycle analysis were also performed to determine drug effects on cell growth. Western blotting was used to confirm the change in protein expression examined by RPPM or pursue other signaling proteins. RESULTS: The FLX-induced cell growth inhibition in all cell lines was concentration- and time-dependent but less pronounced in early passage MCF10 A. In comparison to the other lines,cell growth reduction in SUM149 PT coincided with significant induction of endoplasmic reticulum(ER) stress and autophagy after 24 and 48 h of 10 μmol/L FLX,resulting in decreased translation of proteins along the receptor tyrosine kinase/Akt/mammalian target of rapamycin pathways. The increase in autophagy marker,cleaved microtubule-associated protein 1 light chain 3,in SUM149 PT after 24 h of FLX was likely due to increased metabolic demands of rapidly dividing cells and ER stress. Consequently,the unfolded protein response mediated by double-stranded RNA-dependent protein kinase-like ER kinase resulted in inhibition of protein synthesis,growth arrest at the G1 phase,autophagy,and caspase-7-mediated cell ***: Our study suggests a new role for FLX as an inducer of ER stress and autophagy,resulting in death of aggressive triple negative breast cancer SUM149 PT.

关键词： Inflammatory breast cancer Endoplasmic reticulum stress Autophagy Apoptosis Fluoxetine

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Nat Genet:科学家设计新方法找到抑制癌症发育的新基因

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现代生物医学进展 2017年第15期17卷 I0004-I0004页

作者： Jorge de la Rosa, Mathias Josef Friedrich, Yilong Li, Lena Rad, Hannes Ponstingl, Qi Liang, Sandra Bernaldo de Quirós, Imran Noorani, Emmanouil Metzakopian, Alexander Strong, Meng Amy Li, Gary J hoffman, Rocío Fuente, George S Vassiliou, Roland Rad, Allan Bradley Juan Cadiñanos Jorge de la Rosa Juan Cadiñanos Jorge de la Rosa Carlos López-Otín julia Weber Roland Rad julia Weber Roland Rad Aurora Astudillo María Teresa Fernández-García María Soledad Fernández-García Gary J hoffman Carlos López-Otín The Wellcome Trust Sanger Institute Wellcome Trust Genome Campus Hinxton UK Instituto de Medicina Oncológica y Molecular de Asturias (IMOMA) Oviedo Spain Departamento de Bioquímica y Biología Molecular Facultad de Medicina Instituto Universitario de Oncología (IUOPA) Universidad de Oviedo Oviedo Spain Department of Internal Medicine II Klinikum rechts der Isar Technische Universität München München Germany German Cancer Consortium (DKTK) German Cancer Research Center (DKFZ) Heidelberg Germany Servicio de Anatomía Patológica Hospital Universitario Central de Asturias Oviedo Spain Unidad de Histopatología Molecular Facultad de Medicina IUOPA Universidad de Oviedo Oviedo Spain School of Medicine University of Western Australia Crawley Western Australia Australia Centro de Investigación Biomédica en Red de Cáncer Spain.

英国桑格研究院的研究人员和他们的合作者们最近发现了帮助阻止前列腺癌、皮肤癌和乳腺癌发育的新基因。这些基因能够与众所周知的肿瘤抑制基因PTEN配合发挥作用，该研究还发现这些基因与人类前列腺肿瘤存在相关性。相关研究结果发表在... 详细信息

英国桑格研究院的研究人员和他们的合作者们最近发现了帮助阻止前列腺癌、皮肤癌和乳腺癌发育的新基因。这些基因能够与众所周知的肿瘤抑制基因PTEN配合发挥作用，该研究还发现这些基因与人类前列腺肿瘤存在相关性。相关研究结果发表在国际学术期刊Nature Genetics上。该研究揭示了一些参与癌症发育的新途径，这些基因有望成为治疗PTEN突变癌症的新药物靶点。这项研究开发的一些方法也可以用于发现其他协同抑制癌症生长的基因。

关键词：新基因癌症发育 Nat 科学家设计肿瘤抑制基因国际学术期刊

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