On the causes and consequences of the free-roaming dog problem in southern Chile.

Free-roaming dogs are an important concern for public health, livestock production and the environment. Human behaviors-such as allowing pets to roam, abandoning dogs, or feeding stray animals-could influence free-roaming dog abundance and the frequency of occurrence of dog-caused problems. Here we aim to determine patterns of free-roaming dog abundance in urban and rural areas, to reveal spatial variation in human behaviors underlying the free-roaming dog problem, and to test for associations between free-roaming dog abundance and related problems. We conducted our study in Chile, where dogs are a major environmental issue. In Chile, as in many other Global South countries, many people leave their dogs to roam, partly due to norms and to lax enforcement of dog control laws. To address our objectives, we counted dogs in 213 transects in urban and rural areas to model dog abundance using N-mixture models. Then we conducted interviews in 553 properties around the transects to determine people's dog management, their behavior towards free-roaming dogs and the prevalence of dog-caused problems. Dog abundance was higher in transects where a higher number of owned dogs was allowed to roam, as well as in lower-income neighborhoods (based on property tax valuation). Meanwhile, rural citizens were more likely to let their dogs' roam. Dog abandonment was reported more frequently in lower-income urban neighborhoods and rural areas. Not surprisingly, we found that several problems-such as dog bites-were more frequent where we detected more free-roaming dogs. Our results highlight that the owned dog population is a central component of the free-roaming dog problem, and that human behavior is the key driver underlying the problem. Dog management programs should promote responsible dog-ownership, with a strong message focused on keeping dogs inside properties and preventing abandonment.

On the relationship between baseline corticosterone levels and annual survival of the thorn-tailed rayadito.

Baseline concentrations of glucocorticoids (i.e., cortisol and/or corticosterone) can moderately increase with the degree of energy demands that an individual faces. This could be a mechanism based on which glucocorticods (GCs) can mediate life history trade-offs, and therefore fitness. The 'cort-fitness hypothesis' predicts a negative relationship between GCs and fitness, meanwhile the 'cort-adaptation hypothesis' predicts the opposite pattern. Field studies on the relation between baseline GCs and survival rate have shown mixed results, supporting both positive and negative effect. These ambiguous results could be partially consequence of the short time frame in that most of the studies are carried on. In this study, we tested the predictions of the 'cort-fitness hypothesis' and 'cort-adaptation hypothesis' by using long-term data (eight-year of capture-mark-recapture) of Thorn-tailed Rayadito (Aphrastura spinicauda) in two populations at different latitudes. We assessed whether survival varied as a function of Cort levels and whether it varied in a linear (positive: 'cort-adaptation hypothesis' or negative: 'cort-fitness hypothesis') or curvilinear way. The two populations in our study had different baseline Cort levels, then we evaluated whether the association between baseline Cort and survival probability varied between them. In the high latitude population (i.e., lower baseline Cort levels), we observed a marginally quadratic relationship that is consistent with the cort-fitness hypothesis. In contrast, in the low altitude population we did not find this relation. Our findings suggests that the association between baseline Cort and survival probability is context-dependent, and highlights the importance of comparing different populations and the use of long-term data.

Mechanical stretch induces myelin protein loss in oligodendrocytes by activating Erk1/2 in a calcium-dependent manner.

Myelin loss in the brain is a common occurrence in traumatic brain injury (TBI) that results from impact-induced acceleration forces to the head. Fast and abrupt head motions, either resulting from violent blows and/or jolts, cause rapid stretching of the brain tissue, and the long axons within the white matter tracts are especially vulnerable to such mechanical strain. Recent studies have shown that mechanotransduction plays an important role in regulating oligodendrocyte progenitors cell differentiation into oligodendrocytes. However, little is known about the impact of mechanical strain on mature oligodendrocytes and the stability of their associated myelin sheaths. We used an in vitro cellular stretch device to address these questions, as well as characterize a mechanotransduction mechanism that mediates oligodendrocyte responses. Mechanical stretch caused a transient and reversible myelin protein loss in oligodendrocytes. Cell death was not observed. Myelin protein loss was accompanied by an increase in intracellular Ca2+ and Erk1/2 activation. Chelating Ca2+ or inhibiting Erk1/2 activation was sufficient to block the stretch-induced loss of myelin protein. Further biochemical analyses revealed that the stretch-induced myelin protein loss was mediated by the release of Ca2+ from the endoplasmic reticulum (ER) and subsequent Ca2+ -dependent activation of Erk1/2. Altogether, our findings characterize an Erk1/2-dependent mechanotransduction mechanism in mature oligodendrocytes that de-stabilizes the myelination program.