A genetic Xenopus laevis tadpole model to study lymphangiogenesis

Lymph vessels control fluid homeostasis, immunity and metastasis. Unraveling the molecular basis of lymphangiogenesis has been hampered by the lack of a small animal model that can be genetically manipulated. Here, we show that Xenopus tadpoles develop lymph vessels from lymphangioblasts or, through transdifferentiation, from venous endothelial cells. Lymphangiography showed that these lymph vessels drain lymph, through the lymph heart, to the venous circulation. Morpholino-mediated knockdown of the lymphangiogenic factor Prox1 caused lymph vessel defects and lymphedema by impairing lymphatic commitment. Knockdown of vascular endothelial growth factor C (VEGF-C) also induced lymph vessel defects and lymphedema, but primarily by affecting migration of lymphatic endothelial cells. Knockdown of VEGF-C also resulted in aberrant blood vessel formation in tadpoles. This tadpole model offers opportunities for the discovery of new regulators of lymphangiogenesis.status: publishe

Is the prevalence of exercise-associated hyponatremia higher in female than in male 100-KM ultra-marathoners?

Purpose. The prevalence of exercise-associated hyponatremia (EAH) has mainly been investigated in male endurance athletes. The aim of the present study was to investigate the prevalence of EAH in female 100-km ultra-marathoners and to compare them to male ultra-runners since females are considered more at risk of EAH. Methods. Changes in body mass, hematocrit, [Na+] and [K+] levels in both plasma and urine, plasma volume, urine specific gravity, and the intake of energy, fluids and electrolytes was determined in 24 male and 19 female 100-km ultra-marathoners. Results. Three male (11%) and one female (5%) ultra-marathoners developed asymptomatic EAH. Body mass decreased, while plasma [Na+], plasma [K+] and hematocrit remained stable in either gender. Plasma volume, urine specific gravity and the potassium-to-sodium ratio in urine increased in either gender. In males, fluid intake was related to running speed (r = 0.50, p = 0.0081), but not to the change in body mass, in post-race plasma [Na+], in the change in hematocrit and in the change in plasma volume. Also in males, the change in hematocrit was related to both the change in plasma [Na+] (r = 0.45, p = 0.0187) and the change in the potassium-to-sodium ratio in urine (r = 0.39, p = 0.044). Sodium intake was neither related to post-race plasma [Na+] nor to the change in plasma volume. Conclusions. The prevalence of EAH was not higher in female compared to male 100-km ultra-marathoners. Plasma volume and plasma [Na+] were maintained and not related to fluid intake, most probably due to an activation of the reninangiotensin-aldosterone-system