My graduate career has taken me from inquiring about the roles of endosymbionts in sympatric speciation, through genes required for worms to enter into suspended animation, to a mammalian model for treating a variety of hypoxia/ischemia-based disease...
My graduate career has taken me from inquiring about the roles of endosymbionts in sympatric speciation, through genes required for worms to enter into suspended animation, to a mammalian model for treating a variety of hypoxia/ischemia-based diseases. The work described here demonstrates that concepts learned in one model system (worms) can be successfully applied to other systems (mice) and also reveals the possibilities of discovering benefit by studying a phenomenon. Specifically, suspension was previously known to be inducible in worms via a change in their environment (removal of oxygen) and, by analyzing the physiological aspects of mammalian hibernators, altered environments (addition of low levels of H2S) put mice into a hibernation-like suspended state. This suspended state is characterized by a ten-fold drop in metabolic rate, which is followed by a drop in core body temperature to within ∼2°C of the ambient temperature. Not only does H2S induce a suspended state, there is benefit for these mice, compared to their active counterparts, in their ability to survive otherwise lethal hypoxia. Mice pretreated with H 2S can survive over six hours in 5% oxygen (compared to the ∼15 minute survival time for untreated controls) and survival is possible at oxygen tensions as low as 3%. The broad, whole organism approach demonstrated here has provided a potentially broad, widely applicable solution to a variety of medically relevant problems involving insufficient oxygen within the body.