Bitschlangballe1920

Pest species control operations are most effective if every individual in a population is targeted. Yet, individual personality drives variation in animal responses to devices such as traps and baits. Failing to account for differences in behavior during control operations may drive a selective removal, resulting in residual animals with biased expressions of personality. If these biased traits are passed onto offspring, control operations would become increasingly problematic. To test if biased trait expressions in founding populations are passed on to offspring, we quantified personality traits in wild-caught house mice (Mus musculus) and created founder populations selected for biased (high, low) or intermediate expressions of activity. We released the behaviorally biased populations into outdoor yards to breed to the F1 generation and, 10 weeks later, removed the mice and quantified the personality traits of the offspring. Despite the strong personality bias in founder populations, we observed no transgenerational transfer of personality and detected no personality bias in the F1 generation. Our results provide reassuring evidence that a single intensive control operation that selects for survivors with a personality bias is unlikely to lead to a recovering population inherently more difficult to eradicate, at least for house mice.Morphological traits have served generations of biologists as a taxonomic indicator, and have been the main basis for defining and classifying species diversity for centuries. A quantitative integration of behavioural characters, such as vocalizations, in studies on biotic differentiation has arisen more recently, and the relative importance of these different traits in the diversification process remains poorly understood. To provide a framework within which to interpret the evolutionary interplay between morphological and behavioural traits, we generated a draft genome of a cryptic Southeast Asian songbird, the limestone wren-babbler Napothera crispifrons. We resequenced whole genomes of multiple individuals of all three traditional subspecies and of a distinct leucistic population. We demonstrate strong genomic and mitochondrial divergence among all three taxa, pointing to the existence of three species-level lineages. Despite its great phenotypic distinctness, the leucistic population was characterized by shallow genomic differentiation from its neighbour, with only a few localized regions emerging as highly diverged. Quantitative bioacoustic analysis across multiple traits revealed deep differences especially between the two taxa characterized by limited plumage differentiation. Our study demonstrates that differentiation in these furtive songbirds has resulted in a complex mosaic of colour-based and bioacoustic differences among populations. Extreme colour differences can be anchored in few genomic loci and may therefore arise and subside rapidly.In secondary mitral regurgitation, the concept that the mitral valve (MV) is an innocent bystander, has been challenged by many studies in the last decades. The MV is a living structure with intrinsic plasticity that reacts to changes in stretch or in mechanical stress activating biohumoral mechanisms that have, as purpose, the adaptation of the valve to the new environment. If the adaptation is balanced, the leaflets increase both surface and length and the chordae tendineae lengthen the result is a valve with different characteristics, but able to avoid or to limit the regurgitation. However, if the adaptation is unbalanced, the leaflets and the chords do not change their size, but become stiffer and rigid, with moderate or severe regurgitation. These changes are mediated mainly by a cytokine, the transforming growth factor-β (TGF-β), which is able to promote the changes that the MV needs to adapt to a new hemodynamic environment. SBC-115076 in vitro In general, mild TGF-β activation facilitates leaflet growth, excessive TGF-β activation, as after myocardial infarction, results in profibrotic changes in the leaflets, with increased thickness and stiffness. The MV is then a plastic organism, that reacts to the external stimuli, trying to maintain its physiologic integrity. This review has the goal to unveil the secret life of the MV, to understand which stimuli can trigger its plasticity, and to explain why the equation "large heart = moderate/severe mitral regurgitation" and "small heart = no/mild mitral regurgitation" does not work into the clinical practice.This is the first report of successful potassium metal battery anode cycling with an aluminum-based rather than copper-based current collector. Dendrite-free plating/stripping is achieved through improved electrolyte wetting, employing an aluminum-powder-coated aluminum foil "Al@Al," without any modification of the support surface chemistry or electrolyte additives. The reservoir-free Al@Al half-cell is stable at 1000 cycles (1950 h) at 0.5 mA cm-2 , with 98.9% cycling Coulombic efficiency and 0.085 V overpotential. The pre-potassiated cell is stable through a wide current range, including 130 cycles (2600 min) at 3.0 mA cm-2 , with 0.178 V overpotential. Al@Al is fully wetted by a 4 m potassium bis(fluorosulfonyl)imide-dimethoxyethane electrolyte (θCA = 0°), producing a uniform solid electrolyte interphase (SEI) during the initial galvanostatic formation cycles. On planar aluminum foil with a nearly identical surface oxide, the electrolyte wets poorly (θCA = 52°). This correlates with coarse irregular SEI clumps at formation, 3D potassium islands with further SEI coarsening during plating/stripping, possibly dead potassium metal on stripped surfaces, and rapid failure. The electrochemical stability of Al@Al versus planar Al is not related to differences in potassiophilicity (nearly identical) as obtained from thermal wetting experiments. Planar Cu foils are also poorly electrolyte-wetted and become dendritic. The key fundamental takeaway is that the incomplete electrolyte wetting of collectors results in early onset of SEI instability and dendrites.Hand-foot skin reaction (HFSR) is a common side effect caused by several tyrosine kinase inhibitors, including sunitinib. However, the nature of the cornifying factors related to the molecular biological mechanisms underlying HFSR remains poorly understood. We used human keratinocyte models to investigate the key cornifying factors for dermatological and biological abnormalities induced by sunitinib. On the basis of the results of microarray analysis using the three-dimensional (3D) human epidermal model, keratin (KRT)6A, serine protease inhibitor (SERPIN)B1, KRT5, and SERPIN Kazal-type 6 were selected as candidate genes related to HFSR. Sunitinib treatment significantly decreased the expression of SERPINB1 and KRT6A in the immunohistochemical staining of the 3D epidermal model. In PSVK1 cells, but not in normal human epidermal keratinocyte cells, both of which are human normal keratinocyte cell lines, sunitinib decreased the expression of KRT6A with a concomitant decrease in levels of phosphorylated extracellular signal-regulated kinases (ERK)1/2 and phosphorylated p38 mitogen-activated protein kinase (MAPK).