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| 1 | Simulation of Typhoon-Driven Waves in the Yangtze Estuary with Multiple-Nested Wave Models显示文摘Typhoon-generated waves are simulated with two numerical wave models, the SWAN model for the coastal and Yangtze Estuary domain, nested within the WAVEWATCHIII (WW3) for the basin-scale East China Sea domain. Typhoon No. 8114 is chosen because it was very strong, and generated high waves in the Estuary. WW3 was implemented for the East China Sea coarse-resolution computational domain, to simulate the waves over a large spatial scale and provide boundary conditions for SWAN model simulations, implemented on a fine-resolution nested domain for the Yangtze Estuary area. The Takahashi wind model is applied to the simulation of the East China Sea scale (3-hourly) and Yangtze Estuary scale (1-hourly) winds. Simulations of significant wave heights in the East China Sea show that the highest waves are on the right side of the storm track, and maxima tend to occur at the eastern deep-water open boundary of the Yangtze Estuary. In the Yangtze Estuary, incoming swell is dominant over locally generated waves before the typhoon approaches the Estuary. As the typhoon approaches the Estuary, wind waves and swell coexist, and the wave direction is mainly influenced by the swell direction and the complex topography. | 徐福敏 Will Perrie 张君伦 宋志尧 Bechara Toulany | 2005 | China Ocean Engineering2005，19，4： | 11 |
| 2 | Autophagy contributes to resistance of tumor cells to ionizing radiation显示文摘 | Chaachouay H Ohneseit P Toulany M | | 0，，03： | 1 |
| 3 | Autophagy contributes to resistance of tumor cells to ionizing radiation显示文摘 | Chaachouay H Ohneseit P Toulany M | 2011 | Radiother Oncol2011，99，3： | 1 |
| 4 | Impact of onco- genie K - RAS on YB - 1 phosphorylation induced by ionizing radiation显示文摘 | Toulany M Schickfluss TA Eicheler W | 2011 | Breast Cancer Research2011，13，2： | 1 |
| 5 | Stimulated PI3K-AKT signaling mediated through hgand or radiation-induced EGFR depends indirectly, but not directly, on constitutive K-Ras activity显示文摘 | Toulany M Baumann M Rodemann HP | 2007 | Mol Cancer Res2007，5，8： | 1 |
| 6 | Blockage of epidermal growth factor receptor-phosphatidylinositol 3-kinase- AKT signaling increases radiosensitivity of K-RAS mutated human tumor cells in vitro by affecting DNA repair 显示文摘 | Toulany M Kasten-Pisula U Brammer I | 2006 | Clin Cancer Res2006，12，13： | 1 |
| 7 | PI3K-Akt signa-ling regulates basal, but MAP-kinase signaling regulates radia-tion-induced XRCC1 expression in human tumor cells in vitro显示文摘 | Toulany M Dittmann K Fehrenbacher B | 2008 | DNA Repair (Amst)2008，7，10： | 1 |
| 8 | Wind-generation waves in hurricane Juan显示文摘 | Xu F M Perrie W Toulany B | 2007 | Ocean Modeling2007，16，34： | 1 |
| 9 | ERK2--dependent reac- tivation of Akt mediates the limited response of tumor cells with constitutive K-RAS activity to PI3K inhibition 显示文摘 | Toulany M Minjgee M Saki M | 2014 | Cancer Biol Ther2014，15，3： | 1 |
| 10 | Radio-contrast media affect radiation-induced DNA damage repair in vitro and in vivo by affecting Akt signaling显示文摘 | Toulany M Kehlhach R Rodemann HP | 2010 | Radiother Oncol2010，94，1： | 1 |
| 11 | Geostrophic control on the fluctuating barotropic flow through straits显示文摘 | TOULANY GARRETT C | 1984 | Journal of Physical Oceanogra phy1984，14，： | 1 |
| 12 | Stimulated PI3K-AKT signaling mediated through ligand or radiation-in-duced EGFR depends indirectly,but not directly, on con-stitutive K-Ras activity 显示文摘 | Toulany M Baumann M Rodemann HP | 2007 | Mol Cancer Res2007，5，8： | 1 |
| 13 | Stimula- ted PI3K-AKT signaling mediated through ligand or radiation-induced EGFR depends indirectly, but not directly, on constitutive K-Ras activity显示文摘 | Toulany M Baumann M Rodemann H P | 2007 | Mol Cancer Res2007，5，8： | 1 |
| 14 | Cisplatin-mediated radiosensitization of non-small cell lung cancer cells is stimulated by ATM inhibition显示文摘 | Toulany M Mihatsch J Holler M | 2014 | Radiother Oncol2014，111，： | 1 |
| 15 | Blockage of epidermal growth factorreceptor-phosphatidylinositol 3-kinase-AKT signaling increases radiosensitivity of K-RAS mutated human tumor cells in vitro by affecting DNA repair显示文摘 | Toulany M Kasten-Pisula U Brammer I | | 0，，： | 1 |
| 16 | Radioresistance of K-ras mutated human tumor cells is mediated through EGFR-dependent acti-vation of PI3K-AKT pathway显示文摘 | Toulany M Dittmann K Kruger M | 2005 | Radiother Oncol2005，76，2： | 1 |
| 17 | Targeting of AKT1 en- hances radiation toxicity of human tumor cells by inhibiting DNA - PKcs - dependent DNA double - strand break repair显示文摘 | Toulany M Kehlbach R Florczak U | 2008 | Molec- ular cancer therapeutics2008，7，7： | 1 |
| 18 | Akt Promotes Post - Irradi- ation Survival of Human Tumor Cells through Initiation, Progres- sion, and Termination of DNA - PKcs Dependent DNA Double - Strand Break Repair 显示文摘 | Toulany M Lee KJ Fattah KR | 2012 | Molecular Cancer Researchl2012，10，7： | 1 |
| 19 | Blockage of epidermal growth factorreceptor-phosphatidylinositol 3-kinase-AKT signaling increases radiosensitivity of K-RAS mutated human tumor cells in vitro by affecting DNA repair显示文摘 | Toulany M Kasten-Pisula U Brammer I | | 0，，： | 1 |
| 20 | Blockage of epidermal growth factor receptor-phosphatidylinositol 3-kinase-AKT signaling increases radiosensitivity of K-RAS mutated human tumor cells in vitro by affecting DNA repair显示文摘 | Toulany M Kasten-Pisula U Brammer I | | 0，，13： | 1 |
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