53 research outputs found
Innovation in Pain Management
No full textThe transcript of a Witness Seminar held by the Wellcome Trust Centre for the History of Medicine at UCL, London, on 12 December 2002.First published by the Wellcome Trust Centre for the History of Medicine at UCL, 2004.©The Trustee of the Wellcome Trust, London, 2004.All volumes are freely available online at: www.history.qmul.ac.uk/research/modbiomed/wellcome_witnesses/.Annotated and edited transcript of a Witness Seminar held on 12 December 2002. Introduction by Dr Christina Faull; edited interview with Professor Patrick Wall.Annotated and edited transcript of a Witness Seminar held on 12 December 2002. Introduction by Dr Christina Faull; edited interview with Professor Patrick Wall.Annotated and edited transcript of a Witness Seminar held on 12 December 2002. Introduction by Dr Christina Faull; edited interview with Professor Patrick Wall.Annotated and edited transcript of a Witness Seminar held on 12 December 2002. Introduction by Dr Christina Faull; edited interview with Professor Patrick Wall.Annotated and edited transcript of a Witness Seminar held on 12 December 2002. Introduction by Dr Christina Faull; edited interview with Professor Patrick Wall.Annotated and edited transcript of a Witness Seminar held on 12 December 2002. Introduction by Dr Christina Faull; edited interview with Professor Patrick Wall.Unrelieved pain caused by cancer is experienced by more than 5 million people worldwide, and over the past 50 years has been accepted as unnecessary by both clinicians and politicians. Major innovations in the understanding of pain and our ability to treat it have been made. This Witness Seminar, chaired by Professor David Clark, describes the development of pain clinics, the introduction of the hospice in Britain, and global implementation of innovative technologies for cancer pain relief and advances in research during the latter part of the twentieth century. International health planners argue that the outstanding challenge is to put this knowledge into practice in healthcare settings around the world, often where resources are limited. Reynolds L A, Tansey E M. (eds) (2004) Innovation in pain management, Wellcome Witnesses to Twentieth Century Medicine, vol. 21. London: The Wellcome Trust Centre for the History of Medicine at UCL.The Wellcome Trust Centre for the History of Medicine at University College London is funded by the Wellcome Trust,which is a registered charity, no. 210183
Measurement of DNA Damage in Individual Cells Using the Single Cell Gel Electrophoresis (Comet) Assay
No full textMeasurement of DNA Interstrand Crosslinking in Individual Cells Using the Single Cell Gel Electrophoresis (Comet) Assay
No full text
Pharmacological and Biochemical Determinants of the Antitumour Activity of the Indoloquinone EO9
No full textMeasurement of Drug-Induced DNA Interstrand Crosslinking Using the Single-Cell Gel Electrophoresis (Comet) Assay
No full textSynthesis and biological evaluation of novel pyrrolo[2,1-c][1,4]benzodiazepine prodrugs for use in antibody-directed enzyme prodrug therapy
No full textTime-dependent cytotoxicity induced by SJG-136 (NSC 694501):influence of the rate of interstrand cross-link formation on DNA damage signaling
No full textSJG-136 is a new pyrrolobenzodiazepine dimer inducing time-dependent cytotoxicity. HCT 116 cells were exposed to 50 nmol/L of SJG-136 for 1 hour or 1 nmol/L of SJG-136 for 24 hours to achieve similar levels of interstrand cross-links (ICL). The short exposure led to a rapid formation of ICLs (1 hour), early H2AX foci formation (4 hours), prominent S phase arrest, and greater phosphorylation of Nbs1 (on serine 343) and Chk1 (on serine 317) than a 24-hour exposure. The prolonged exposure at low concentrations of SJG-136 induced a gradual formation of ICLs (up to 24 hours) which was associated with a limited S phase arrest and delayed Nbs1 phosphorylation. Prolonged exposure was also associated with a reduced phosphorylation of p53 on serines 15 and 20, a limited and delayed phosphorylation on serine 392, and a less prominent increase in p21 levels. These data suggest that the 24-hour exposure to a low concentration of SJG-136 led to delayed and reduced DNA damage signaling compared with a higher concentration of SJG-136 for 1 hour, resulting in greater cytotoxicity and contributing to the time-dependent cytotoxic effect of SJG-136
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