Biomedical subjects
T Ward
Publications and source records attributed to T Ward.
Development of new instructional materials in the IMC network.
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Development of new instructional materials in the IMC network.
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The RCS Faculty of Dental Surgery celebrates it's 21st anniversary.
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The abstinence violation effect in bulimia nervosa.
Bulimia nervosa often follows a chronic and relapsing course. To understand relapse in this disorder, we highlight cognitive processes underlying the binge/purge cycle. Links are drawn between cognitions, causal perceptions, and the binge/purge cycle in a reformulation of the abstinence violation effect with a special focus on attributions. This reformulation is then applied to the lapse-relapse transition in bulimia nervosa. Finally, theoretical and clinical implications of the reformulation are presented.
Real time confocal laser scanning microscopy: potential applications in space medicine and cell biology.
Photodynamic therapy (PDT), in which tissues may be rendered fatally light-sensitive represents a relatively novel treatment for cancer and other disorders such as cardiovascular disease. It offers significant application to disease control in an isolated environment such as space flight. In studying PDT in the laboratory, low energy lasers such as HeNe lasers are used to activate the photosensitized cellular target. A major problem associated with these studies is that events occurring during actual exposure of the target cells to the system cannot be examined in real time. In this study HeLa cells were photosensitized and photodynamic activation was accomplished using the scanning microbeam from a confocal laser scanning microscope. This form of activation allowed for simultaneous photoactivation and observation and facilitated the recording of events at a microscopic level during photoactivation. Effects of photodynamic activation on the target cells were monitored using the fluorophores rhodamine 123 and ethidium homodimer-1. Potential applications of these forms of analyses to space medicine and cell biology are discussed.
Mammary tumor induction and premature ovarian failure in ApcMin mice are not enhanced by Brca2 deficiency.
Inherited BRCA2 mutations predispose individuals to breast cancer and increase risk at other sites. Recent studies have suggested a role for the APC I1307K allele as a low-penetrance breast cancer susceptibility gene that enhances the phenotypic effects of BRCA1 and BRCA2 mutations. To model the consequences of inheriting mutant alleles of the BRCA2 and APC tumor suppressor genes, we examined tumor outcome in C57BL/6 mice with mutations in the Brca2 and Apc genes. We hypothesized that if the Brca2 and Apc genes were interacting to influence mammary tumor susceptibility, then mammary tumor incidence and/or multiplicity would be altered in mice that had inherited mutations in both genes. Female and male offspring treated with a single IP injection of 50 mg/kg N-ethyl-N-nitrosourea (ENU) at 35 days of age developed mammary adenoacanthomas by 100 days of age. The female Apc-mutant and Brca2/Apc double-mutant progeny had mean mammary tumor multiplicities of 6.7+/-2.8 and 7.2+/-2.7, respectively, compared to wild-type and Brca2-mutant females, which had mean mammary tumor multiplicities of 0.1+/-0.4 and 0.3+/-0.5, respectively. Female ENU-treated Apc-mutant and Brca2/Apc double heterozygotes were also susceptible to premature ovarian failure. Thus, the inheritance of an Apc mutation predisposes ENU-treated female and male mice to mammary tumors and, in the case of female mice, to ovarian failure. These results indicate that mammary tumor development in Apc-mutant mice can progress independently of ovarian hormones. The Apc mutation-driven phenotypes were not modified by mutation of Brca2, perhaps because Brca2 acts in a hormonally dependent pathway of mammary carcinogenesis.
In vivo infection of mice with Coxsackie B4 virus induces long-term functional changes in pancreatic islets with minimal alteration in blood glucose.
The long-term effects of Coxsackie B4 (CB4) infection of mice on pancreatic islet function were investigated. Mice were inoculated with various strains of CB4 virus and 2, 3 and 6 months later islet insulin synthesis and release from isolated islets were measured. Insulin release at basal glucose concentration (2 mmol l-1) was higher in islets from mice inoculated with pancreas-adapted CB4 strains than in control islets or those from mice inoculated with tissue culture-adapted CB4. Thus, two strains of pancreas-adapted virus (P11 and P12) increased basal insulin release by 72% compared with control islets (p less than 0.05) 1 month after inoculation. Another strain (P13) increased insulin release by 421% at 3 months post-inoculation (p less than 0.01) and by 192% at 6 months (p less than 0.05) compared with control islets. The rate of total protein synthesis in islets from P11-inoculated mice 1 month later was 61% lower than in control islets at basal glucose levels (p less than 0.001), and was 25% lower at 20 mmol l-1 glucose (p less than 0.01). There were no significant changes in protein synthesis in islets from infected mice at 3 or 6 months. The abnormal insulin release occurred with minimal changes in random blood glucose concentrations. Histologically the islets were unchanged and there were no detectable islet cell antibodies. These results show that CB4 infection may lead to a persistent metabolic dysfunction in islets with minimal changes in blood glucose levels.
The role of the hospital dentist.
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