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Biomedical subjects

D Keast

Publications and source records attributed to D Keast.

131 records · Page 8Linked to original sources
PubMedDate not supplied

Low-tar and high-tar cigarettes.

Mice were exposed for 7 to 8 minutes on weekdays to fresh smoke from high-tar (HT) or low-tar (LT) cigarettes for varying periods of up to 36 weeks. Mice exposed to HT cigarettes exhibited more marked alterations in humoral immune responsiveness, hematological profiles, and pulmonary pathologic findings than those exposed to LT cigarettes. However, cell-mediated immune responsiveness to both bacterial and tumor-specific antigens was depressed similarly in animals exposed to HT or LT cigarettes. Furthermore, the growth rates of subcutaneously established tumors were enhanced similarly in the two groups, with respect to those in control animals.

Animals↗
PubMedDate not supplied

Effects of chronic tobacco smoke exposure on immune responses in aged mice.

Balb/c mice were exposed to fresh smoke, equivalent to 30 high-tar filtered cigarettes/day, for 83 wk or less. After groups of mice were subjected to 56, 64, 72, and 80 wk of tobacco smoke (TS) exposure, serum antibody responses to both T-dependent and T-independent antigens, numbers of plaque-forming cells, spleen cell and lymph node PHA responses, and systemic clearance of normal and opsonised antigen were investigated. Aged TS-exposed mice showed some deterioration of immune responsiveness with age, but results varied; in extreme old age the immunological responsiveness of TS-exposed mice was similar to that of age-matched controls. In addition, groups of mice inoculated with fibrosarcoma cells after 78 wk TS-exposure did not show significantly greater susceptibility to the early development of pulmonary metastases.

Aging↗
PubMedDate not supplied

The role of tobacco smoke, iron ore mine dusts, viruses, and chemicals in experimental cancer.

Assessment of long-term studies on the carcinogenic potential of certain environmental agents has indicated that all of the following appear to activate and/or promote the inherent tumors of the host strains of the animals used irrespective of the extent of additional immunological modulation accompanying the agents: tobacco smoke inhalation, the implantation and inhalation of the respirable fraction of iron ore mine dusts, acute neonatal reovirus 3 infection, urethane, and tobacco smoke inhalation following urethane treatment. It is proposed that these environmental agents function at the onc-gene level as promoters/activators rather than carcinogens, and that this now requires an understanding of the means by which certain environmental agents function at the onc-gene level.

Adenoma↗