Social and individual features affecting natal dispersal in the colonial Lesser Kestrel

Causes of natal dispersal were studied in an isolated population of the migratory, facultatively colonial Lesser Kestrel (Falco naumanni) in northeastern Spain. During a seven-year study, we gathered information on natal dispersal of 751 individuals and on 24 explanatory variables that evaluated individual traits, conspecific cues in terms of colony size, and different ecological and populational features. We examined separately whether or not individuals changed colonies and how far they moved. Dispersal from the natal colony was high (83%), and dispersers covered a median distance of 7225 m (range 112-136 500 m). The probability of natal dispersal decreased with the size of the natal colony and with the distance to the nearest colony, but not with the distance to unoccupied buildings, in the year of recruitment. Moreover, the shorter the distance to the nearest colony, the shorter the distances that individuals dispersed, particularly to large colonies (>10 pairs). These results support the conspecific attraction hypothesis. Accordingly, the probability of recruiting in the natal colony increased with the proportion of philopatric adults, although beyond a threshold individuals were prevented from recruiting by the more dominant adults in a despotic way. The timing of arrival from the wintering grounds was positively related to the probability of colony change, especially in males. To the extent that this variable is related to the phenotypic quality of individuals, it reinforces the idea that natal dispersal is shaped by intraspecific competition in crowded colonies. Males showed lower frequencies of colony change and dispersed shorter distances than did females, as explained by the different role of the sexes in nest acquisition and defense. Our results indicate that natal dispersal is an evolutionarily labile trait simultaneously influenced by ecological, social, and individual features both within and between populations.Peer Reviewe

Familial atrial fibrillation mutation M1875T-SCN5A increases early sodium current and dampens the effect of flecainide

Aims Atrial fibrillation (AF) is the most common cardiac arrhythmia. Pathogenic variants in genes encoding ion channels are associated with familial AF. The point mutation M1875T in the SCN5A gene, which encodes the α-subunit of the cardiac sodium channel Nav1.5, has been associated with increased atrial excitability and familial AF in patients. Methods and results We designed a new murine model carrying the Scn5a-M1875T mutation enabling us to study the effects of the Nav1.5 mutation in detail in vivo and in vitro using patch clamp and microelectrode recording of atrial cardiomyocytes, optical mapping, electrocardiogram, echocardiography, gravimetry, histology, and biochemistry. Atrial cardiomyocytes from newly generated adult Scn5a-M1875T+/− mice showed a selective increase in the early (peak) cardiac sodium current, larger action potential amplitude, and a faster peak upstroke velocity. Conduction slowing caused by the sodium channel blocker flecainide was less pronounced in Scn5a-M1875T+/− compared to wildtype atria. Overt hypertrophy or heart failure in Scn5a-M1875T+/− mice could be excluded. Conclusion The Scn5a-M1875T point mutation causes gain-of-function of the cardiac sodium channel. Our results suggest increased atrial peak sodium current as a potential trigger for increased atrial excitability

Stupendous, Miserable City: Pasolini\u27s Rome, \u3cem\u3eby John David Rhodes\u3c/em\u3e

Stupendous, Miserable City: Pasolini’s Rome. John David Rhodes. Minneapolis: University of Minnesota Press, 2007. 240 pages. $60.00 (cloth)$20.00 (paper

Load-reducing therapy prevents development of arrhythmogenic right ventricular cardiomyopathy in plakoglobin-deficient mice

ObjectivesWe used a murine model of arrhythmogenic right ventricular cardiomyopathy (ARVC) to test whether reducing ventricular load prevents or slows development of this cardiomyopathy.BackgroundAt present, no therapy exists to slow progression of ARVC. Genetically conferred dysfunction of the mechanical cell–cell connections, often associated with reduced expression of plakoglobin, is thought to cause ARVC.MethodsLittermate pairs of heterozygous plakoglobin-deficient mice (plako+/–) and wild-type (WT) littermates underwent 7 weeks of endurance training (daily swimming). Mice were randomized to blinded load-reducing therapy (furosemide and nitrates) or placebo.ResultsTherapy prevented training-induced right ventricular (RV) enlargement in plako+/– mice (RV volume: untreated plako+/– 136 ± 5 μl; treated plako+/– 78 ± 5 μl; WT 81 ± 5 μl; p < 0.01 for untreated vs. WT and untreated vs. treated; mean ± SEM). In isolated, Langendorff-perfused hearts, ventricular tachycardias (VTs) were more often induced in untreated plako+/– hearts (15 of 25), than in treated plako+/– hearts (5 of 19) or in WT hearts (6 of 21, both p < 0.05). Epicardial mapping of the RV identified macro–re-entry as the mechanism of ventricular tachycardia. The RV longitudinal conduction velocity was reduced in untreated but not in treated plako+/– mice (p < 0.01 for untreated vs. WT and untreated vs. treated). Myocardial concentration of phosphorylated connexin43 was lower in plako+/– hearts with VTs compared with hearts without VTs and was reduced in untreated plako+/– compared with WT (both p < 0.05). Plako+/– hearts showed reduced myocardial plakoglobin concentration, whereas β-catenin and N-cadherin concentration was not changed.ConclusionsLoad-reducing therapy prevents training-induced development of ARVC in plako+/– mice