Can changes in body mass and total body water accurately predict hyponatremia after a 161-km running race?

OBJECTIVE: To relate changes in body mass, total body water (TBW), extracellular fluid (ECF), and serum sodium concentration ([Na]) from a 161-km ultramarathon to finish time and incidence of hyponatremia. DESIGN: Observational. SETTING: : The 2008 Rio Del Lago 100-Mile (161-km) Endurance Run in Granite Bay, California. PARTICIPANTS: Forty-five runners. MAIN OUTCOME MEASUREMENTS: Pre-race and post-race body mass, TBW, ECF, and serum [Na]. RESULTS: Body mass and serum [Na] significantly decreased 2% to 3% (P < 0.001) from pre-race to post-race, but TBW and ECF were unchanged. Significant relationships were observed between finish time and percentage change in body mass (r = 0.36; P = 0.01), TBW (r = 0.50; P = 0.007), and ECF (r = 0.61; P = 0.003). No associations were found between post-race serum [Na] and percentage change in body mass (r = -0.04; P = 0.94) or finish time (r = 0.5; P = 0.77). Hyponatremia (serum [Na] < 135 mmol/L) was present among 51.2% of finishers. Logistic regression prediction equation including pre-race TBW and percentage changes in TBW and ECF had an 87.5% concordance with the classification of hyponatremia. CONCLUSIONS: Hyponatremia occurred in over half of the 161-km ultramarathon finishers but was not predicted by change in body mass. The combination of pre-race TBW and percentage changes in TBW and ECF explained 87.5% of the variation in the incidence of hyponatremia. CLINICAL SIGNIFICANCE: Exercise-associated hyponatremia can occur simultaneously with dehydration and cannot be predicted by weight checks at races.

A murine DC-SIGN homologue contributes to early host defense against Mycobacterium tuberculosis.

The C-type lectin dendritic cell-specific intercellular adhesion molecule-3 grabbing nonintegrin (DC-SIGN) mediates the innate immune recognition of microbial carbohydrates. We investigated the function of this molecule in the host response to pathogens in vivo, by generating mouse lines lacking the DC-SIGN homologues SIGNR1, SIGNR3, and SIGNR5. Resistance to Mycobacterium tuberculosis was impaired only in SIGNR3-deficient animals. SIGNR3 was expressed in lung phagocytes during infection, and interacted with M. tuberculosis bacilli and mycobacterial surface glycoconjugates to induce secretion of critical host defense inflammatory cytokines, including tumor necrosis factor (TNF). SIGNR3 signaling was dependent on an intracellular tyrosine-based motif and the tyrosine kinase Syk. Thus, the mouse DC-SIGN homologue SIGNR3 makes a unique contribution to protection of the host against a pulmonary bacterial pathogen.

The macrophage-inducible C-type lectin, mincle, is an essential component of the innate immune response to Candida albicans.

The recognition of carbohydrate moieties by cells of the innate immune system is emerging as an essential element in antifungal immunity, but despite the number and diversity of lectins expressed by innate immune cells, few carbohydrate receptors have been characterized. Mincle, a C-type lectin, is expressed predominantly on macrophages, and is here shown to play a role in macrophage responses to the yeast Candida albicans. After exposure to the yeast in vitro, Mincle localized to the phagocytic cup, but it was not essential for phagocytosis. In the absence of Mincle, production of TNF-alpha by macrophages was reduced, both in vivo and in vitro. In addition, mice lacking Mincle showed a significantly increased susceptibility to systemic candidiasis. Thus, Mincle plays a novel and nonredundant role in the induction of inflammatory signaling in response to C. albicans infection.