Biomedical subjects
H E Thomas
Publications and source records attributed to H E Thomas.
Cholesterol-phospholipid ratio in the prediction of coronary heart disease. The Framingham study.
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Five-year assessment of sputum-positive pulmonary tuberculosis notified in Birmingham in 1957-58.
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EXANTHEMA IN PEAR, AND COPPER DEFICIENCY.
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Beta cell destruction in the development of autoimmune diabetes in the non-obese diabetic (NOD) mouse.
In the non-obese diabetic (NOD) mouse model of Type 1 (insulin-dependent) diabetes, evidence suggests that pancreatic beta cells are destroyed in part by apoptotic mechanisms. The precise mechanisms of beta cell destruction leading to diabetes remain unclear. The NOD mouse has been studied to gain insight into the cellular and molecular mediators of beta cell death, which are discussed in this review. Perforin, secreted by CD8(+) T cells, remains one of the only molecules confirmed to be implicated in beta cell death in the NOD mouse. There are many other molecules, including Fas ligand and cytokines such as interferon-gamma, interleukin-1 and tumor necrosis factor-alpha, which may lead to beta cell destruction either directly or indirectly via regulation of toxic molecules such as nitric oxide. As beta cell death can occur in the absence of perforin, these other factors, in addition to other as yet unidentified factors, may be important in the development of diabetes. Effective protection of NOD mice from beta cell destruction may therefore require inhibition of multiple effector mechanisms.
The beta cell in autoimmune diabetes: many mechanisms and pathways of loss.
Death of pancreatic beta cells is the final step in the pathogenesis of type 1 diabetes before it becomes clinically apparent. Applying recent basic research about how cells die to the clinical problem of diabetes is a current opportunity and challenge. To date, perforin is the only factor definitely implicated in beta-cell killing in the non-obese diabetic (NOD) mouse model, although some perforin-deficient NOD mice develop diabetes. Our results suggest that other factors that cause beta-cell death remain to be identified.
Smoking status and the electrocardiogram: a cross-sectional and longitudinal study.
Previous cross-sectional studies have shown age trends in electrocardiographic wave patterns, including leftward shift in frontal plane axis and decreases in R, S, and T wave amplitudes with age. The effects of smoking on electrocardiographic measurements have also been examined. Findings of several studies vary and include possible smoking-induced changes in T wave amplitude and frontal plane axis measurements. To examine both cross-sectionally and longitudinally the effects of cigarette smoking on electrocardiographic measurements, serial recordings obtained 5 yr apart were taken from 702 healthy male participants of the Normative Aging Study, who were 23-74 yr of age at their first examination. These men were classified as current smokers (at both baseline and follow-up examinations, N = 291), former smokers (men who stopped smoking prior to the baseline examination, N = 203), or never smokers (at any time, N = 208). At baseline, P-R interval duration was shorter in current smokers than in former or never smokers. Longitudinal results indicated that R, S, and T wave amplitudes decreased at greater rates in smokers than in nonsmokers. These findings suggest that changes in the electrocardiogram attributed to aging may be modified by smoking.
Risk factors in coronary heart disease.
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