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Aim: Pacific hagfish are exceptionally tolerant to high environmental ammonia (HEA). Here, we elucidated a cellular mechanism that enables hagfish to actively excrete ammonia against steep ammonia gradients expected to be found inside a decomposing whale carcass. Methods: Hagfish were exposed to varying concentrations of HEA in the presence or absence of environmental Na+, while plasma ammonia levels were tracked. 14C‐methylammonium was used as a proxy for NH4+ to measure efflux in whole animals and in isolated gill pouches; the latter allowed us to assess the effects of amiloride specifically on Na+/H+ exchangers (NHEs) in gill cells. Western blotting and immunohistochemistry were utilized to evaluate the abundance and sub‐cellular localization of Rhesus glycoprotein (Rh) channels in the response to HEA. Results: Hagfish actively excreted NH4+ against steep inwardly directed ENH4+ (ΔENH4+ ~ 35 mV) and pNH3 (ΔpNH3 ~ 2000 μtorr) gradients. Active NH4+ excretion and plasma ammonia hypo‐regulation were contingent on the presence of environmental Na+, indicating a Na+/NH4+ exchange mechanism. Active NH4+ excretion across isolated gill pouches was amiloride‐sensitive. Exposure to HEA resulted in decreased abundance of Rh channels in the apical membrane of gill ionocytes. Conclusions: During HEA exposure, hagfish can actively excrete ammonia against a steep concentration gradient using apical NHEs energized by Na+‐K+‐ATPase in gill ionocytes. Additionally, apical Rh channels are removed from the apical membrane, presumably to reduce ammonia loading from the environment. We suggest that this mechanism allows hagfish to maintain tolerable ammonia levels while feeding inside decomposing carrion, allowing them to exploit nutrient‐rich food‐falls. [ABSTRACT FROM AUTHOR]

Background: Little is known about risk factors for anxiety in young children. The current study investigated the value of a set of theoretically derived risk factors to predict symptoms of anxiety in a sample of preschool-aged children. Methods: Mothers ( n = 632) and fathers ( n = 249) completed questionnaires twice, 12 months apart. Measures were selected to assess several risk factors derived from current theory, including parental negative affectivity, child inhibition, parent overprotection, and impact of life events. Results: Even at this young age anxiety across 12 months was moderately to highly stable ( r’s = .75 and .74 based on maternal and paternal report respectively). Over and above this stability, according to maternal report, anxiety at 12 months was significantly predicted by prior maternal overprotection, impact of negative life events, child’s inhibition, and maternal negative affectivity. According to paternal report, anxiety at 12 months was significantly predicted by prior paternal overprotection and impact of negative life events. The models did not differ significantly for girls and boys. Conclusions: The results support theories of the development of anxiety, especially the role of parental and external environmental factors, and point to possible targets for prevention of heightened anxiety in young children. [ABSTRACT FROM AUTHOR]

Aim: Pacific hagfish are exceptionally tolerant to high environmental ammonia (HEA). Here, we elucidated a cellular mechanism that enables hagfish to actively excrete ammonia against steep ammonia gradients expected to be found inside a decomposing whale carcass., Methods: Hagfish were exposed to varying concentrations of HEA in the presence or absence of environmental Na + , while plasma ammonia levels were tracked. 14 C-methylammonium was used as a proxy for NH 4 + to measure efflux in whole animals and in isolated gill pouches; the latter allowed us to assess the effects of amiloride specifically on Na + /H + exchangers (NHEs) in gill cells. Western blotting and immunohistochemistry were utilized to evaluate the abundance and sub-cellular localization of Rhesus glycoprotein (Rh) channels in the response to HEA., Results: Hagfish actively excreted NH 4 + against steep inwardly directed E NH4 + (ΔE NH4 +  ~ 35 mV) and pNH 3 (ΔpNH 3  ~ 2000 μtorr) gradients. Active NH 4 + excretion and plasma ammonia hypo-regulation were contingent on the presence of environmental Na + , indicating a Na + /NH 4 + exchange mechanism. Active NH 4 + excretion across isolated gill pouches was amiloride-sensitive. Exposure to HEA resulted in decreased abundance of Rh channels in the apical membrane of gill ionocytes., Conclusions: During HEA exposure, hagfish can actively excrete ammonia against a steep concentration gradient using apical NHEs energized by Na + -K + -ATPase in gill ionocytes. Additionally, apical Rh channels are removed from the apical membrane, presumably to reduce ammonia loading from the environment. We suggest that this mechanism allows hagfish to maintain tolerable ammonia levels while feeding inside decomposing carrion, allowing them to exploit nutrient-rich food-falls., (© 2022 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.)