Struck by lightning -- the effects upon the men and the ships of HM Navy.
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Biomedical subjects
Publications and source records attributed to H Cannell.
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Volunteer subjects received 50 mg of lignocaine solution as a maxillary infiltration injection, one one occasion as 1% solution and on another as 5% solution. The plasma levels of lignocaine were measured over a two-hour period and similar concentrations were achieved from both solutions, although the larger volumes of the more dilute solution gave slightly higher results, probably reaching toxic levels in one case. The injection of the higher concentration did not produce particularly high plasma levels of lignocaine.
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The literature on Lipomata and intra-oral Lipomata is reviewed and a series of 24 cases presented. In this series the mean age of presentation of the male patients was 53.8 years, whereas that of females was 63.1 years 33.3% of the tumours occurred on the inner aspect of the checks and of these 8 cases, six were males. Of the eight lesions occurring the floor of the mouth and retromolar areas, all but one occurred in females. Evidence is presented to support to the claim that intra-oral lipomata are indeed common benign neoplasms.
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In this study the impact of epidermal growth factor (EGF) on chemosensitivity and susceptibility to lymphokine-activated killer (LAK) cytolysis on six cell lines (one super expressing EGFr i.e. HN5, three high expressing i.e. Hep2, KB and MCF-7 and two low expressing i.e. Fen and HN15) was investigated using the tetrazolium salt reduction assay (MTT) as measured by optical density (OD). Hep2, KB, MCF-7 and Fen lines showed a dose-related inhibition to cisplatin (from 19% to 80%). Treatment of EGFr positive cell lines, Hep2, KB and MCF-7 but not EGFr negative Fen by EGF prior to exposure to cisplatin inhibited the cells by between 10-15% (p<0.05). Exposure of HN5 line to EGF (0.1 ng/ml) prior to LAK assay, led to a decrease in tumour killing (13%, p<0.05). However, at 0.01 ng/ml the pre-treatment enhanced tumour sensitivity. These data indicated that pre-exposure of tumour cells to EGF altered their response to cisplatin and LAK killing and this depended on the degree of EGFr expression. These data may prove helpful for pre-selection of patients for an appropriate therapy.
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