La Cueva de El Sidrón (Piloña Asturias)

Estado de las excavaciones y estudios en la Cueva de El Sidrón (PIloña, Asturias)

Extension and Dynamics of the Andes inferred from the 2016 Parina (Huarichancara) Earthquake

The M w 6.1 2016 Parina earthquake led to extension of the south Peruvian Andes along a normal fault with evidence of Holocene slip. We use InSAR, seismology and field mapping to determine a source model for this event and show that extension at Parina is oriented NE-SW, which is parallel to the shortening direction in the adjacent sub-Andean lowlands. In addition, we use earthquake source models and GPS data to demonstrate that shortening within the sub-Andes is parallel to topographic gradients. Both observations imply that forces resulting from spatial variations in gravitational potential energy are important in controlling the geometry of the deformation in the Andes. We calculate 9 the horizontal forces per unit length acting between the Andes and South America due to these potential energy contrasts to be 4 − 8 × 10 12 N per metre along-strike of the mountain range. Normal faulting at Parina implies that the Andes in south Peru have reached the maximum elevation that can be supported by the forces transmitted across the adjacent foreland, which requires that the foreland faults have an effective coefficient of friction <0.2. Additionally, the onset of extension in parts of the central Andes following orogen-wide compression in the late Miocene suggests there has been a change in the force balance within the mountains. We propose that shortening on weak detachment faults within the Andean foreland since ∼5-9 Ma reduced the shear tractions acting along the base of the upper crust in the eastern Andes, leading to extension in the highest parts of the range

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field

Perlecan is required for FGF-2 signaling in the neural stem cell niche

In the adult subventricular zone (neurogenic niche), neural stem cells double-positive for two markers of subsets of neural stem cells in the adult central nervous system, glial fibrillary acidic protein and CD133, lie in proximity to fractones and to blood vessel basement membranes, which contain the heparan sulfate proteoglycan perlecan. Here, we demonstrate that perlecan deficiency reduces the number of both GFAP/CD133-positive neural stem cells in the subventricular zone and new neurons integrating into the olfactory bulb. We also show that FGF-2 treatment induces the expression of cyclin D2 through the activation of the Akt and Erk1/2 pathways and promotes neurosphere formation in vitro. However, in the absence of perlecan, FGF-2 fails to promote neurosphere formation. These results suggest that perlecan is a component of the neurogenic niche that regulates FGF-2 signaling and acts by promoting neural stem cell self-renewal and neurogenesis