Human physiological and metabolic responses to an attempted winter crossing of Antarctica: the effects of prolonged hypobaric hypoxia.

An insufficient supply of oxygen to the tissues (hypoxia), as is experienced upon high-altitude exposure, elicits physiological acclimatization mechanisms alongside metabolic remodeling. Details of the integrative adaptive processes in response to chronic hypobaric hypoxic exposure remain to be sufficiently investigated. In this small applied field study, subjects (n = 5, male, age 28-54 years) undertook a 40 week Antarctica expedition in the winter months, which included 24 weeks residing above 2500 m. Measurements taken pre- and postexpedition revealed alterations to glucose and fatty acid resonances within the serum metabolic profile, a 7.8 (±3.6)% increase in respiratory exchange ratio measured during incremental exercise (area under curve, P > 0.01, mean ± SD) and a 2.1(±0.8) % decrease in fat tissue (P < 0.05) postexpedition. This was accompanied by an 11.6 (±1.9) % increase (P > 0.001) in VO2 max corrected to % lean mass postexpedition. In addition, spine bone mineral density and lung function measures were identified as novel parameters of interest. This study provides, an in-depth characterization of the responses to chronic hypobaric hypoxic exposure in one of the most hostile environments on Earth.

Interleukin-12p70-dependent interferon- gamma production is crucial for resistance in African trypanosomiasis.

African trypanosomiasis encompasses diseases caused by pathogenic trypanosomes, infecting both humans and animals. In the present article, we dissected the possible role of members of the interleukin (IL)-12 family during infection with Trypanosoma brucei brucei and Trypanosoma evansi in mice. IL-12p35(-/-), IL-12p40(-/-), and IL-12p35(-/-)/p40(-/-) mice were susceptible to both pathogens, as was demonstrated by the increased mortality among these mice, compared with wild-type C57BL/6 mice. The different IL-12p70(-/-) mouse strains showed similar mortality kinetics, suggesting that IL-12p70--but not the IL-12p80 homodimer or IL-23--plays a crucial role in survival. Although there were similar plasma levels of immunoglobulin (Ig) M and IgG2a in IL-12-deficient mice and wild-type mice, interferon (IFN)- gamma production, especially during early infection, was severely impaired in all IL-12p70(-/-) mouse strains, demonstrating an IL-12p70-dependent mechanism for IFN- gamma production. Because IFN- gamma receptor-deficient mice (IFN- gamma R(-/-)) were also highly susceptible to both Trypanosoma species, IL-12p70-dependent IFN- gamma production seems to be the important mechanism involved in resistance against both pathogens.