We extend our previous gas-kinetic theory analysis of drag force in a uniform temperature field [Li and Wang, Phys. Rev. E. 68, 061206 (2003); 68, 061207 (2003)] to particle transport in fluids with nonuniform temperature. Formulations for drag and thermophoretic forces are proposed for nanoparticle transport in low-density gases. We specifically consider the influence of nonrigid body collision due to van der Waals or other forces between the particle and gas molecules and find that these forces play a notable role for particles a few nanometers in size. It is shown that the present formulations can be easily reduced to the classical result of Waldmann [Z. Naturforsch. A 14a, 589 (1959)] by assuming rigid body collision. From the force formulations we also obtain the equation governing the thermophoretic velocity. This velocity is found to be highly sensitive to the potential energy of interactions between gas molecules and particle, and as such Waldmann's thermophoretic velocity is not expected to be accurate for nanosized particles.
// Qi Song 1, * , Yalan Liu 1, * , Dongxian Jiang 1 , Haixing Wang 1 , Jie Huang 1 , Yifan Xu 1 , Akesu Sujie 1 , Haiying Zeng 1 , Chen Xu 1 and Yingyong Hou 1, 2 1 Department of Pathology, Zhongshan Hospital, Fudan University, Shanghai 200032, P. R. China 2 Department of Pathology, School of Basic Medical Sciences & Zhongshan Hospital, Fudan University, Shanghai 200032, P. R. China * These authors have contributed equally to this work Correspondence to: Yingyong Hou, email: houyingyong@aliyun.com Chen Xu, email: xu.chen@zs-hospital.sh.cn Keywords: FGFR1 high amplification, clinical stage, disease free survival time, prognostic marker, ESCC Received: October 17, 2016 Accepted: June 29, 2017 Published: August 12, 2017 ABSTRACT Amplification of the fibroblast growth factor receptor 1 ( FGFR1 ) is believed to predict response to FGFR inhibitors. The aim of this study was to investigate the frequency and the prognostic impact of FGFR1 amplification in patients with resected esophageal squamous cell carcinoma (ESCC) by using fluorescent in situ hybridization. Microarrayed paraffin embedded blocks were constructed, and the cohort of tissues came from 506 patients with ESCC. FGFR1 high amplification ( FGFR1 high ) was defined by an FGFR1 /centromere 8 ratio of ≥ 2.0, or average number of FGFR1 signals/tumor cell nucleus ≥ 6.0, or percentage of tumor cells containing ≥ 15 FGFR1 signals, or large cluster in ≥ 10% of cancer cells. FGFR1 low amplification was defined by ≥ 5 FGFR1 signals in ≥ 50% of cancer cells. Kaplan-Meier curves with log-rank tests and Cox proportional hazards model were used to analyze patients' survival. Among 506 patients, high amplification, low amplification, and disomy were detected in 8.7%, 3.6% and 87.7%, respectively. In general, the FGFR1 high group trended towards worse disease-free survival (DFS) and overall survival (OS) compared to the FGFR1 low amplification/disomy ( FGFR1 low/disomy ) group (DFS, P =0.108; OS, P =0.112), but this trend was amplified for patients with DFS ≥ 30 months (DFS, P =0.009; OS, P =0.007). Furthermore, when patients were stratified into stage I-II and stage III-IV, the FGFR1 high group directly presented with adverse DFS and OS than the FGFR1 low/disomy group in stage I-II patients (DFS, P =0.019; OS, P =0.034), especially with DFS ≥ 30 months (DFS, P =0.002; OS, P =0.001). However, for patients in stage III-IV, FGFR1 high had no effect on prognosis regardless of DFS time. FGFR1 high occurs in a minority of ESCC, and it predicts delayed poor prognosis in stage I and II ESCC patients.
Electronic structure of four prototypical Cvetanovic diradicals, species derived by addition of O(3P) to unsaturated compounds, is investigated by high-level electronic structure calculations and kinetics modeling. The main focus of this study is on the electronic factors controlling the rate of inter-system crossing (ISC), minimal energy crossing points (MECPs) and spin-orbit couplings (SOCs). The calculations illuminate significant differences in the electronic structure of ethylene- and acetylene-derived compounds and a relatively minor effect due to methylation. The computed MECPs heights and SOCs reveal different mechanisms of ISC in ethylene- and acetylene-derived species, thus explaining variations in the observed branching ratios between singlet and triplet products and a puzzling effect of the methyl substitution. In the ethylene- and propylene-derived species, the MECP is very low and the rate is controlled by the SOC variations, whereas in the acetylene- and propyne-derived species the MECP is high and the changes in the ISC rate due to methyl substitutions are driven by the variations in MECP heights.
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