Sex differences in stress and immune responses during confinement in Antarctica.

Background: Antarctica challenges human explorers by its extreme environment. The effects of these unique conditions on the human physiology need to be understood to best mitigate health problems in Antarctic expedition crews. Moreover, Antarctica is an adequate Earth-bound analogue for long-term space missions.

Modulations of Neuroendocrine Stress Responses During Confinement in Antarctica and the Role of Hypobaric Hypoxia.

The Antarctic continent is an environment of extreme conditions. Only few research stations exist that are occupied throughout the year. The German station Neumayer III and the French-Italian Concordia station are such research platforms and human outposts.

Stimulation of human neutrophils, monocytes, and platelets by modified C-reactive protein (CRP) expressing a neoantigenic specificity.

C-reactive protein (CRP) can be structurally modified by heat, acid, or urea-chelation to express a neoantigen designated by us as neo-CRP. This antigen is also expressed on the in vitro primary protein translation products of both human and rabbit CRP. Unmodified CRP and CRP complexed with pneumococcal C-polysaccharide (CPS) do not express neo-CRP.

Influence of tuftsin-like synthetic peptides derived from C-reactive protein (CRP) on platelet behaviour.

C-reactive protein (CRP) is an acute-phase reactant that modifies platelet function differently, depending upon its physiochemical state. Aggregated and ligand-complexed forms of CRP initiate the activation of platelets, whereas naturally occurring CRP peptides inhibit platelet activation. The present study documents neutral proteases of the polymorphonuclear leucocyte (PMN) to cleave CRP into reaction products with the potential to inhibit platelet activation, and explore the structure-function relationships involved in the regulation of platelet activation by CRP using synthetic CRP peptides.

Platelet response to aggregated C-reactive protein: fibrinogen-dependent and independent signals.

Fibrinogen augmented gel-filtered platelet (GFP) aggregation only during an intermediate level of platelet activation stimulated by aggregated C-reactive protein (CRP) (AggCRP), implying that a mechanism to utilize fibrinogen is not operative or does not require an exogenous source of fibrinogen at near-maximal or threshold levels of platelet activation. By contrast, inclusion of the tetrapeptide fibrinogen antagonist, Arg-Gly-Asp-Ser(RGDS), inhibited both intermediate and near-maximal, but not threshold, levels of platelet activation stimulated by AggCRP. These data suggest that AggCRP initially stimulates platelets independent of fibrinogen but, in so doing, activates a fibrinogen-dependent mechanism(s) capable of augmenting the overall extent of platelet stimulation.