LIFE01200604005 Shri Somnath Ghosh - Homi Bhabha National ...

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CHAPTER 3 RESULTS Fig.3.4.5a Gene expression of NF-kB (p65) and iNOS gene in EL-4 cells which had received medium from irradiated cells. EL-4 cells cultured for 2 h in presence of different conditioned media. β-Actin gene expression in each group was used as an internal control. Ratio of intensities of NF-kB (p65) and iNOS band to that of respective β-actin band as quantified from gel pictures are shown above each gel picture. Key: Lane 1, control EL-4 cells; Lane 2, γ irradiated EL-4 cells; Lane 3, EL-4 cells receiving medium from γ irradiated EL-4 cells; Lane 4, EL-4 cells receiving medium from L-NAME treated and γ irradiated EL-4 cells; Lane 5, EL-4 cells receiving medium from cPTIO treated and γ irradiated EL-4 cells; Lane 6, EL-4 cells receiving medium from LPS-stimulated (500ng/ml), L-NAME treated and γ irradiated RAW 264.7 cells; Lane 7, EL-4 cells receiving medium from LPS-stimulated (500ng/ml), cPTIO treated and γ irradiated RAW 264.7 cells. Data represents means ± SE of three independent experiments; significantly different from unirradiated controls: *P < 0.05, **P < 0.01. 183
CHAPTER 3 RESULTS Fig.3.4.5b DNA damage in EL-4 cells cultured for 2 h in presence of different conditioned media was measured using single cell gel electrophoresis (‘comet assay’) and expressed as tail length. Key: Lane 1, control EL-4 cells; Lane 2, γ irradiated EL-4 cells; Lane 3, EL-4 cells receiving medium from γ irradiated EL-4 cells; Lane 4, EL-4 cells receiving medium from L- NAME treated and γ irradiated EL-4 cells; Lane 5, EL-4 cells receiving medium from cPTIO treated and γ irradiated EL-4 cells; Lane 6, EL-4 cells receiving medium from LPS-stimulated (500ng/ml), L-NAME treated and γ irradiated RAW 264.7 cells; Lane 7, EL-4 cells receiving medium from LPS-stimulated (500ng/ml), cPTIO treated and γ irradiated RAW 264.7 cells; Lane 8, EL-4 cells treated with L-NAME; Lane 9, EL-4 cells treated with cPTIO. Data represents means ± SE of three independent experiments; significantly different from unirradiated controls: *P < 0.05, **P < 0.01. 184
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RADIATION INDUCED SIGNALING IN MAMM
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DECLARATION I, hereby declare that
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CONTENTS Page No. SYNOPSIS………
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2.11 Measurement of NO production
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PREAMBLE SYNOPSIS Ionising radiatio
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SYNOPSIS Aims and Objectives: To St
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SYNOPSIS 2.6 Immunofluorescence sta
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SYNOPSIS ATM gene expression, which
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SYNOPSIS Percentage Survival 100 80
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SYNOPSIS Ratio of Rad52 to Actin Ra
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Relative Phosphorylation 45 40 35 3
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SYNOPSIS Fig. 3.3A Clonogenic Cell
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SYNOPSIS (A) Av No. of phospho BRCA
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SYNOPSIS Percentage Survival 120 10
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SYNOPSIS Fig.3.4B. Existance of cro
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SYNOPSIS Fig. 3.4EDNA damage in EL-
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SYNOPSIS subsequent cytotoxicity ca
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SYNOPSIS [4] Hall, E. J. Radiobiolo
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CHAPTER 1 INTRODUCTION INTRODUCTION
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CHAPTER 1 INTRODUCTION 15.8% 9.56%
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CHAPTER 1 INTRODUCTION far apart an
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CHAPTER 1 INTRODUCTION and are more
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CHAPTER 1 INTRODUCTION 1.3 DNA dama
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CHAPTER 1 INTRODUCTION associates w
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CHAPTER 1 INTRODUCTION are unable t
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CHAPTER 1 INTRODUCTION Perhaps one
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CHAPTER 1 INTRODUCTION occurs at DS
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CHAPTER 1 INTRODUCTION related prot
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CHAPTER 1 INTRODUCTION damage must
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CHAPTER 1 INTRODUCTION At the prese
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CHAPTER 1 INTRODUCTION predominant
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CHAPTER 1 INTRODUCTION provide a me
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CHAPTER 1 INTRODUCTION hypersensiti
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CHAPTER 1 INTRODUCTION cycle-specif
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CHAPTER 1 INTRODUCTION 1.4 Overview
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CHAPTER 1 INTRODUCTION 1.4.1 Radiat
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CHAPTER 1 INTRODUCTION interaction
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CHAPTER 1 INTRODUCTION p90S6 kinase
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CHAPTER 1 INTRODUCTION CD4 (formerl
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CHAPTER 1 INTRODUCTION unrepaired d
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CHAPTER 1 INTRODUCTION well to the
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CHAPTER 1 INTRODUCTION 1.6 Radiatio
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CHAPTER 1 INTRODUCTION becomes pote
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CHAPTER 2 MATERIALS AND METHODS MAT
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CHAPTER 2 MATERIALS AND METHODS 2.2
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CHAPTER 2 MATERIALS AND METHODS res
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CHAPTER 2 MATERIALS AND METHODS Arr
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CHAPTER 2 MATERIALS AND METHODS PBS
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CHAPTER 2 MATERIALS AND METHODS the
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CHAPTER 2 MATERIALS AND METHODS 2.1
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CHAPTER 3 RESULTS RESULTS 93
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CHAPTER 3 RESULTS fractionated regi
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CHAPTER 3 RESULTS On comparison of
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CHAPTER 3 RESULTS Table 3.1.2A List
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CHAPTER 3 RESULTS 80 NM_002185 IL7R
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CHAPTER 3 RESULTS SAA2 149 AU134977
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CHAPTER 3 RESULTS 221 LOC643167 RNA
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CHAPTER 3 RESULTS 299 BF244402 FBXO
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CHAPTER 3 RESULTS CDK4) 57 AU152107
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CHAPTER 3 RESULTS 134 AL045793 METT
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CHAPTER 3 RESULTS 58 AF237813 ABAT
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CHAPTER 3 RESULTS 127 AI809749 ORMD
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CHAPTER 3 RESULTS 31 BE615699 UNC84
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CHAPTER 3 RESULTS 47 AF026303 SULT1
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CHAPTER 3 RESULTS 117 BF062193 CYor
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CHAPTER 3 RESULTS 187 AL036662 ---
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CHAPTER 3 RESULTS 52 AV686514 EMP2
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CHAPTER 3 RESULTS exposed to 10 Gy
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CHAPTER 3 RESULTS Fig.3.1.4 Gene ex
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CHAPTER 3 RESULTS Fig. 3.1.6 Radiat
Page 142 and 143: CHAPTER 3 RESULTS Fig. 3.1.7 Transl
Page 144 and 145: CHAPTER 3 RESULTS 3.1.9 Stabilizati
Page 146 and 147: CHAPTER 3 RESULTS 23±1.5% (Fig. 3.
Page 148 and 149: CHAPTER 3 RESULTS whereas only the
Page 150 and 151: CHAPTER 3 RESULTS Fig.3.2.2 Gene ex
Page 152 and 153: CHAPTER 3 RESULTS Fig.3.2.4 Gene ex
Page 154 and 155: CHAPTER 3 RESULTS with equal doses
Page 156 and 157: CHAPTER 3 RESULTS Fig.3.3.1.2 Forma
Page 158 and 159: CHAPTER 3 RESULTS Fig.3.3.1.3 Phosp
Page 160 and 161: CHAPTER 3 RESULTS (7.5±0.64) (Fig.
Page 164 and 165: CHAPTER 3 RESULTS Fig.3.3.1.7b Phos
Page 166 and 167: CHAPTER 3 RESULTS 3.3.2 Oxygen beam
Page 168 and 169: CHAPTER 3 RESULTS in all the cells.
Page 170 and 171: CHAPTER 3 RESULTS 3.3.2.3 Radiation
Page 176 and 177: CHAPTER 3 RESULTS Fig.3.3.2.7 Apopt
Page 178 and 179: CHAPTER 3 RESULTS PMA stimulated U9
Page 180 and 181: CHAPTER 3 RESULTS Fig.3.4.2. Exista
Page 182 and 183: CHAPTER 3 RESULTS up-regulation of
Page 184 and 185: CHAPTER 3 RESULTS Fig.3.4.3.2 NO pr
Page 186 and 187: CHAPTER 3 RESULTS 3.4.3.4 Apoptotic
Page 188 and 189: CHAPTER 3 RESULTS 3.4.4 Bystander e
Page 190 and 191: CHAPTER 3 RESULTS Fig.3.4.4b DNA da
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Page 196 and 197: CHAPTER 4 DISCUSSION directly expos
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Page 200 and 201: CHAPTER 4 DISCUSSION A clear cause
Page 202 and 203: CHAPTER 4 DISCUSSION 4.2 Proton bea
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Page 206 and 207: CHAPTER 4 DISCUSSION Similar number
Page 208 and 209: CHAPTER 4 DISCUSSION the mechanism
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Page 214 and 215: CHAPTER 4 DISCUSSION upregulates ma
Page 216 and 217: CHAPTER 4 DISCUSSION Numerous studi
Page 218 and 219: CHAPTER 4 DISCUSSION inhibition of
Page 220 and 221: CHAPTER 4 DISCUSSION The survival o
Page 222 and 223: CHAPTER 5 REFERENCES [1] Khan, F. T
Page 224 and 225: CHAPTER 5 REFERENCES [19] Woo, R. A
Page 226 and 227: CHAPTER 5 REFERENCES [35] Nghiem, P
Page 228 and 229: CHAPTER 5 REFERENCES [52] McKay, B.
Page 230 and 231: CHAPTER 5 REFERENCES [69] Cary, R.
Page 232 and 233: CHAPTER 5 REFERENCES [84] Uziel, T.
Page 234 and 235: CHAPTER 5 REFERENCES [98] Liu, Y.;
Page 236 and 237: CHAPTER 5 REFERENCES [111] Fei, P.;
Page 238 and 239: CHAPTER 5 REFERENCES [127] Frank, K
Page 240 and 241: CHAPTER 5 REFERENCES [141] Pierce,
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CHAPTER 5 REFERENCES [156] Roots, R
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CHAPTER 5 REFERENCES [171] Xia, Z.;
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CHAPTER 5 REFERENCES (MAP) kinase c
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CHAPTER 5 REFERENCES phosphorylatio
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CHAPTER 5 REFERENCES [211] Anderson
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CHAPTER 5 REFERENCES [229] Konca, K
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CHAPTER 5 REFERENCES [245] Kastan,
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CHAPTER 5 REFERENCES [261] Miralbel
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CHAPTER 5 REFERENCES [278] Weizman,
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CHAPTER 5 REFERENCES [294] Zhou, H.
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PUBLICATIONS AND PRESENTATIONS Publ
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Mutation Research 729 (2012) 61-72
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S. Ghosh, M. Krishna / Mutation Res
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12 S. Ghosh et al. / Mutation Resea
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Cancer Invest Downloaded from infor
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1568 I. J. Radiation Oncology d Bio
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