Effect of colchicine injection prior to the initiating phase of two-stage skin carcinogenesis in mice.

Colchicine injected 5, 9 and 24 h respectively before initiation (using s.c. injection of urethane for initiating action and TPA skin applications for promoting action, in female ICR mice) led to a significant increase in skin tumour incidence in the --9-h group, and an increase in percentage malignancy in both the --5- and --9-h groups. These times corresponded to the peak of metaphase arrest by the colchicine. The results are discussed in relation in those of Pound and Withers (1963) and others, who found that mitotic stimulation at the time of urethane initiating action raised the ultimate tumour incidence; and the inference is drawn that initiating action in mouse skin may occur during the M phase, rather than during the G1, S, or G2 phases, as suggested by others

Failure of syngeneic bone marrow cells to protect against MC-induced lymphoma in dba-2 mice.

IT has been shown long ago that shielding the bone marrow (Kaplan and Brown, 1951) or spleen (Lorenz et al., 1953) of mice during exposure to whole-body X-irradiation, or injection of syngeneic bone marrow cells after whole-body irradiation (Kaplan et al., 1953), reduces the incidence of thymic lymphomas resulting from the irradiation. How the effect is brought about has never been satisfactorily explained. There is presumably some essential factor in the normal hematopoietic system which irradiation is able to depress. Whether this inhibitory process affects a specific stage in radiation leukaemogenesis, or whether it is concerned with the leukaemogenic process as such, irrespective of the nature of the leukaemogenic agent, has not so far been fully established. Indirect evidence would suggest, however, that the former (i.e. a specific anti-radiation effect) is the more likely explanation. It is known, for instance, that bone marrow cells of C3H mice, though acceptable to tolerant AKR mice, fail to inhibit the spontaneous development of thymic lymphomas in the latter strain (Miller, 1960). In the case of leukaemogenesis b

Physicians’ Explanatory Models of Pediatric Inflammatory Bowel Disease: A Qualitative Interview Study

Explanatory models are culturally informed representations of illness that convey understandings of the etiology and expected course of disease. Substantial research has explored lay explanatory models, but examining physicians’ clinical explanatory models can also provide insight into patients’ understandings of illness because physicians are a foundational source of authoritative knowledge that shapes lay concepts of illness and disease. This study characterized the explanatory models used by pediatric gastroenterologists when explaining inflammatory bowel disease (IBD) to children. We conducted semi-structured qualitative interviews with 20 pediatric gastroenterologists across the United States about their clinical communication and explanatory models. We identified two primary explanatory models used to describe immune dysregulation in pediatric IBD: the defense and protection model, which characterizes the immune system as an army that erroneously sees the body as “non-self” and attacks it; and the switch model, which conceptualizes treatment as activating a switch that turns off a faulty immune response. We also identified two models used by some physicians to describe inflammation: the scratch and scrape model, which compares IBD inflammation to scratches or scrapes on the skin; and the bonfire model, which compares inflammation to a fire in need of extinguishing. While the use of militaristic metaphors is pervasive in medicine, describing autoimmunity as a battle against the self may lead children to perceive their body as the enemy. This may be compounded by describing the immune system as “confused” while noting its ongoing protective function. Use of these explanatory models may nevertheless improve patient disease-related knowledge