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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

Pharmacological properties of N-substituted benzamides as radio- and chemosensitizers

Hua, Jianyi. January 1998 (has links)
Thesis (doctoral)--Lund University, 1998. / Added t.p. with thesis statement inserted. Includes bibliographical references.
2

Pharmacological properties of N-substituted benzamides as radio- and chemosensitizers

Hua, Jianyi. January 1998 (has links)
Thesis (doctoral)--Lund University, 1998. / Added t.p. with thesis statement inserted. Includes bibliographical references.
3

NF-кB targeting by dehydroxymethylepoxyquinomicin (DHMEQ) in nasopharyngeal carcinoma (NPC). / NF-kappa B targeting by dehydroxymethylepoxyquinomicin (DHMEQ) in nasopharyngeal carcinoma (NPC) / NF-KB targeting by dehydroxymethylepoxyquinomicin (DHMEQ) in nasopharyngeal carcinoma (NPC) / 抗癌葯物DHMEQ在鼻咽癌中標靶NF-кB腫瘤治療 / Kang ai yao wu DHMEQ zai bi yan ai zhong biao ba NF-кB zhong liu zhi liao

January 2008 (has links)
Wong, Ho Ting. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2008. / Includes bibliographical references (leaves 66-77). / Abstracts in English and Chinese. / Acknowledgement --- p.i / List of abbreviations --- p.ii / List of tables and figures --- p.iv / Abstract in English --- p.vi / Abstract in Chinese --- p.viii / Table of content --- p.x / Chapter Chapter 1 --- Literature review / Chapter 1.1 --- Nasopharyngeal carcinoma (NPC) and treatments --- p.1 / Chapter 1.2 --- EBV and NF-kB signaling in NPC / Chapter 1.2.1 --- Role of EBV and NF-kB in NPC --- p.2 / Chapter 1.2.2 --- NF-kB signaling in cancer --- p.4 / Chapter 1.2.3 --- NF-kB activation in NPC --- p.7 / Chapter 1.2.3.1 --- NF-kB activation by LMP1 --- p.8 / Chapter 1.2.3.2 --- NF-kB and LMP2A --- p.10 / Chapter 1.2.3.3 --- NF-kB activation by non-viral factors --- p.10 / Chapter 1.2.4 --- NF-kB target genes in NPC --- p.11 / Chapter 1.3 --- NF-kB targeting / Chapter 1.3.1 --- NF-kB targeting agents --- p.14 / Chapter 1.3.2 --- "DHMEQ, a novel blocker of NF-kB Transactivation" --- p.15 / Chapter Chapter 2 --- Aim of study and Research plan --- p.18 / Chapter Chapter 3 --- Materials and Methods / Chapter 3.1 --- Cell lines and Reagents --- p.20 / Chapter 3.2 --- Cell viability assay --- p.21 / Chapter 3.3 --- Cell apoptosis detection / Chapter 3.3.1 --- PARP cleavage --- p.22 / Chapter 3.3.2 --- DNA fragmentation --- p.22 / Chapter 3.4 --- Cell cycle analysis --- p.22 / Chapter 3.5 --- Transwell migration or Matrigel invasion assay --- p.23 / Chapter 3.6 --- Soft agar colony formation assay --- p.24 / Chapter 3.7 --- Drug treatment for western blotting --- p.25 / Chapter 3.8 --- "Protein extraction and quantification, SDS-PAGE and western blotting" / Chapter 3.8.1 --- Protein extraction and quantification --- p.25 / Chapter 3.8.2 --- SDS-PAGE and western blotting --- p.26 / Chapter 3.9 --- Fractionation --- p.28 / Chapter 3.10 --- NF-kB transcriptional activity assay / Chapter 3.10.1 --- Construction of NF-kB reporter system --- p.29 / Chapter 3.10.2 --- Luciferase assay --- p.29 / Chapter 3.11 --- Statistical Analysis --- p.30 / Chapter Chapter 4 --- Results / Chapter 4.1 --- Anti-tumor activity of DHMEQ in NPC / Chapter 4.1.1 --- Growth inhibition in NPC cell lines --- p.31 / Chapter 4.1.2 --- Apoptotic induction in NPC cell lines --- p.35 / Chapter 4.1.3 --- Cell cycle arrest in NPC cell lines --- p.38 / Chapter 4.1.4 --- Inhibition of migration and invasive behavior of NPC cell lines --- p.38 / Chapter 4.1.5 --- Abrogation of soft agar colony formation ability of NPC cell lines --- p.43 / Chapter 4.2 --- Mechanistic study of DHMEQ in NPC / Chapter 4.2.1 --- Blockade of p65 nuclear translocation --- p.48 / Chapter 4.2.2 --- Attenuation of NF-kB transcriptional activity --- p.48 / Chapter 4.2.3 --- Downregulation of NF-kB target genes --- p.53 / Chapter Chapter 5 --- Discussion --- p.54 / Chapter Chapter 6 --- Summary --- p.60 / Chapter Chapter 7 --- Future Study --- p.63 / Reference List --- p.66 / Appendix / Chapter Appendix 1 --- Construction of NF-kb report plasm id --- p.78 / Chapter Appendix 2 --- Wound healing assay --- p.86 / Chapter Appendix 3 --- Reverse-phase protein Array --- p.88
4

Positron emission tomography of extra-striatal dopamine release

Gravel, Paul. January 2008 (has links)
Altered dopamine (DA) neurotransmission is implicated in neurological and psychiatric disorders. Positron Emission Tomography (PET) imaging of DA release has mainly been restricted to striatal areas, rich in D2/D 3 receptors, owing to the moderate affinity of the radioligands used. To measure extra-striatal DA release, where D2/D3 receptor concentrations are much smaller, an approach using a high affinity radioligand, such as [18F]Fallypride, is required. The aim of the present study was to investigate in healthy volunteers the suitability of [ 18F]Fallypride to measure variations in D2/D3 receptor occupancy, as a function of amphetamine-induced DA release, in extra-striatal regions. Six healthy male volunteers underwent two 18F-Fallypride PET sessions, following the double-blind oral administration of 0.3 mg/kg of d-amphetamine (Dexedrine) or placebo (lactose), counter-balanced for order. Following amphetamine administration, D2/D3 receptor occupancy of 18F-Fallypride was significantly reduced in striatum, but also in extra-striatal regions, including substantia nigra, amygdala, thalamus, hippocampus, and cortical areas.
5

Positron emission tomography of extra-striatal dopamine release

Gravel, Paul January 2008 (has links)
No description available.
6

Imatinib radiosensitizes bladder cancer by targeting homologous recombination

Qiao, B., Kerr, M., Groselj, B., Teo, M.T., Knowles, M.A., Bristow, R.G., Phillips, Roger M., Kiltie, A.E. January 2013 (has links)
Radiotherapy is a major treatment modality used to treat muscle-invasive bladder cancer, with patient outcomes similar to surgery. However, radioresistance is a significant factor in treatment failure. Cell-free extracts of muscle-invasive bladder tumors are defective in nonhomologous end-joining (NHEJ), and this phenotype may be used clinically by combining radiotherapy with a radiosensitizing drug that targets homologous recombination, thereby sparing normal tissues with intact NHEJ. The response of the homologous recombination protein RAD51 to radiation is inhibited by the small-molecule tyrosine kinase inhibitor imatinib. Stable RT112 bladder cancer Ku knockdown (Ku80KD) cells were generated using short hairpin RNA technology to mimic the invasive tumor phenotype and also RAD51 knockdown (RAD51KD) cells to show imatinib's pathway selectivity. Ku80KD, RAD51KD, nonsilencing vector control, and parental RT112 cells were treated with radiation in combination with either imatinib or lapatinib, which inhibits NHEJ and cell survival assessed by clonogenic assay. Drug doses were chosen at approximately IC40 and IC10 (nontoxic) levels. Imatinib radiosensitized Ku80KD cells to a greater extent than RAD51KD or RT112 cells. In contrast, lapatinib radiosensitized RAD51KD and RT112 cells but not Ku80KD cells. Taken together, our findings suggest a new application for imatinib in concurrent use with radiotherapy to treat muscle-invasive bladder cancer. Cancer Res; 73(5); 1611-20. (c)2012 AACR.

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