Gill T J, Kunz H W, Rapaport F T
Department of Pathology, University of Pittsburgh, School of Medicine, Pennsylvania 15261.
J Surg Res. 1989 Nov;47(5):433-7. doi: 10.1016/0022-4804(89)90097-8.
The genetic control of resistance to a standardized model of severe thermal injury was studied using crosses between a resistant (BUF) and a susceptible (F344) strain of inbred rats; their reciprocal F1 hybrids and all eight possible backcross matings were examined for resistance to the same injury. Males were much more resistant than females, and none of the genes involved in resistance was linked to the major histocompatibility complex; there was also no evidence for a maternal effect upon the resistance of the offspring to thermal injury. The most parsimonious genetic model for host resistance to thermal injury based on the experimental data postulates control of resistance by two autosomal dominant genes and one X-linked recessive gene, with resistance factors being linearly additive.