ADE-FDTD scattered-field formulation for dispersive materials

pre-printThis letter presents a scattered-field formulation for modeling dispersive media using the finite-difference time-domain (FDTD) method. Specifically, the auxiliary differential equation method is applied to Drude and Lorentz media for a scattered field FDTD model. The present technique can also be applied in a straightforward manner to Debye media. Excellent agreement is achieved between the FDTD-calculated and exact theoretical results for the reflection coefficient in half-space problems

VEGF polymorphisms in early cervical cancer susceptibility, angiogenesis, and survival

Objective. Vascular endothelial growth factor (VEGF) plays an important role in cervical carcinogenesis. We hypothesized that VEGF genetic polymorphisms may affect cancer susceptibility, angiogenesis, and survival in patients with early cervical cancer. Methods. Among 215 healthy subjects and 199 early cervical cancer patients who were treated with surgical resection, we specifically investigated four genetic polymorphisms within the VEGF gene (-2578C>A, -460 T>C, +405G>C, and +936C>T). VEGF and CD31 microvessel density (MVD) were measured using tissue microarrays constructed from 117 patients who had available tissue. Results. Risk of cervical cancer was decreased in subjects with the VEGF -2578A/A genotype (adjusted OR = 0.39, 95% CI 0.16-0.96). Angiogenesis measured by CD31 MVD was significantly decreased in patients with the VEGF +405C/C genotype and VEGF -2578C - -460T - + 405C haplotype (recessive model; adjusted OR=0.32, 95% CI 0.11-0.99, equally). Moreover, VEGF +405C/C and VEGF -2578C - 460 T - +405C haplotype were significantly related to shorter disease-free survival (adjusted HR = 3.18, 95% CI 1.13-8.94, equally) and overall survival (adjusted HR=8.86, 95% CI 1.40-56.08, equally) by multiple Cox regression analysis. Conclusion. Polymorphisms of VEGF genes may affect cancer susceptibility and survival of early cervical cancer by modulating tumor angiogenesis. Prospective study among homogeneously treated patients is warranted. (C) 2010 Elsevier Inc. All rights reserved.Randall LM, 2009, GYNECOL ONCOL, V112, P583, DOI 10.1016/j.ygyno.2008.11.013Kim YT, 2009, J GYNECOL ONCOL, V20, P1, DOI 10.3802/jgo.2009.20.1.1Schneider BP, 2008, BREAST CANCER RES TR, V111, P157, DOI 10.1007/s10549-007-9755-9Hofmann G, 2008, J CANCER RES CLIN, V134, P591, DOI 10.1007/s00432-007-0322-xHeist RS, 2008, J CLIN ONCOL, V26, P856, DOI 10.1200/JCO.2007.13.5947Kim JG, 2008, CLIN CANCER RES, V14, P62, DOI 10.1158/1078-0432.CCR-07-1537NASR HB, 2008, CLIN CHIM ACTA, V395, P124, DOI 10.1016/j.cca.2008.05.022Chen W, 2007, VIROLOGY, V367, P168, DOI 10.1016/j.virol.2007.05.030Kim JG, 2007, ANN ONCOL, V18, P1030, DOI 10.1093/annonc/mdm085Hefler LA, 2007, CLIN CANCER RES, V13, P898, DOI 10.1158/1078-0432.CCR-06-1008Tzanakis N, 2006, J SURG ONCOL, V94, P624, DOI 10.1002/jso.20619Anderson JE, 2006, DRUG RESIST UPDATE, V9, P198, DOI 10.1016/j.drup.2006.08.001Lu H, 2005, CANCER RES, V65, P5015Parkin DM, 2005, CA-CANCER J CLIN, V55, P74Hicklin DJ, 2005, J CLIN ONCOL, V23, P1011, DOI 10.1200/JCO.2005.06.081Koukourakis MI, 2004, LUNG CANCER-J IASLC, V46, P293, DOI 10.1016/j.lungcan.2004.04.037Toussaint-Smith E, 2004, ONCOGENE, V23, P2988, DOI 10.1038/sj.onc.1207442Stevens A, 2003, CANCER RES, V63, P812Lee IJ, 2002, INT J RADIAT ONCOL, V54, P768Bosch FX, 2002, J CLIN PATHOL, V55, P244Renner W, 2000, J VASC RES, V37, P443Carmeliet P, 2000, NATURE, V407, P249Watson CJ, 2000, CYTOKINE, V12, P1232Fujiwaki R, 2000, ANTICANCER RES, V20, P1317Kodama J, 1999, EUR J CANCER, V35, P485Hanahan D, 1996, CELL, V86, P353GUIDI AJ, 1995, J NATL CANCER I, V87, P1237