Despite recognition of the deleterious effects of passive smoking, quantitative information on the intake of environmental tobacco smoke is still lacking. Cotinine is the major metabolite of nicotine found in the urine. We have examined the relationship between urinary cotinine excretion in 472 nonsmokers and the smokiness of their environment. The urinary cotinine levels of nonsmokers who lived with smokers were higher than those of nonsmokers who did not, increasing with the combined daily cigarette consumption of smokers in the family. The urinary cotinine values of nonsmokers who worked with smokers were also higher than those of nonsmokers who did not, increasing with the number of smokers in the workroom. The presence of smokers in both the home and the workplace also increased the cotinine levels. Urban nonsmokers had more cotinine in their urine than rural nonsmokers. We conclude that the deleterious effects of passive smoking may occur in proportion to the exposure of nonsmokers to smokers in the home, the workplace, and the community.
A direct binding study of radioligand [3H]dihydroalprenolol (DHA), a potent beta-adrenergic antagonist, was performed on the particulate fractions of four adrenocortical adenomas (three cortisol-producing adenomas and one aldosterone-producing adenoma) and normal adrenal tissues. The effect of epinephrine on cortisol production was also evaluated in vitro from the cultured tumor cells from one cortisol-producing adenoma. Saturable binding of [3H]DHA to the tumor membranes was observed in two of three cortisol-producing adenomas, but not in the aldosterone-producing adenoma or in normal adrenal tissues. Scatchard analysis of equilibrium binding of [3H]DHA revealed a single class of binding sites on the tumor membranes; the apparent dissociation constant (Kd) was 1 nM in each, and the numbers of binding sites were 108 and 45 fmol/mg protein, respectively. Competition by adrenergic agents with [3H]DHA for binding sites on the membranes from one cortisol-producing adenoma revealed that (+/-)propranolol, a beta-adrenergic antagonist, was about 350-fold more potent than phentolamine, an alpha-adrenergic antagonist, suggesting the beta-adrenergic nature of receptor sites. In addition, stereospecificity was demonstrated by about 1000-fold greater affinity of (-)alprenolol than to (+)alprenolol, both of which are stereoisomers of the beta-adrenergic antagonist. Furthermore, production of cortisol from the cultured tumor cells prepared from the same adenoma was significantly stimulated by epinephrine in addition to ACTH. These data indicate that ectopic beta-adrenergic receptor sites are present in some human adrenocortical tumors which may be functionally related to the activation of adenylate cyclase by catecholamines other than ACTH in those tumors, as previously demonstrated. The mechanism by which such altered cellular membrane characteristics occur in association with neoplastic alteration of the endocrine tissues remains unanswered.
Human epidermal growth factor (hEGF), which stimulates the growth of a variety of cells in culture, has recently been isolated from human urine. In the present study, we identified significant amounts of immunoreactive (IR) hEGF (mean +/- SE, 2.3 +/- 0.09 ng/ml; n = 3) in human pancreatic juice. The IR-hEGF materials were immunologically indistinguishable from standard hEGF, although they were only 5% as active in receptor binding to human placental membrane as in RIA. Gel exclusion chromatography of the pancreatic juice under neutral and acidic conditions revealed three distinct IR-hEGF components with different molecular sizes. Incubation of 125I-labeled hEGF with either the pancreatic juice or the high molecular weight component(s) yielded no aggregation or degradation products. These data suggest that fully immunoreactive but much less bioactive hEGF-like substances which are heterogeneous in size are secreted into human pancreatic juice. Their tissue(s) of origin and physiological functions, if any, remain to be elucidated.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.