Nilpotent Networks and 4D RG Flows

Starting from a general $\mathcal{N} = 2$ SCFT, we study the network of $\mathcal{N} = 1$ SCFTs obtained from relevant deformations by nilpotent mass parameters. We also study the case of flipper field deformations where the mass parameters are promoted to a chiral superfield, with nilpotent vev. Nilpotent elements of semi-simple algebras admit a partial ordering connected by a corresponding directed graph. We find strong evidence that the resulting fixed points are connected by a similar network of 4D RG flows. To illustrate these general concepts, we also present a full list of nilpotent deformations in the case of explicit $\mathcal{N} = 2$ SCFTs, including the case of a single D3-brane probing a $D$- or $E$-type F-theory 7-brane, and 6D $(G,G)$ conformal matter compactified on a $T^2$, as described by a single M5-brane probing a $D$- or $E$-type singularity. We also observe a number of numerical coincidences of independent interest, including a collection of theories with rational values for their conformal anomalies, as well as a surprisingly nearly constant value for the ratio $a_{\mathrm{IR}} / c_{\mathrm{IR}}$ for the entire network of flows associated with a given UV $\mathcal{N} = 2$ SCFT. The $\texttt{arXiv}$ submission also includes the full dataset of theories which can be accessed with a companion $\texttt{Mathematica}$ script.Comment: v2: 73 pages, 12 figures, clarifications and references adde

Periods of Ehrhart Coefficients of Rational Polytopes

Let P⊂R^n be a polytope whose vertices have rational coordinates. By a seminal result of E. Ehrhart, the number of integer lattice points in the kth dilate of P (k a positive integer) is a quasi-polynomial function of k — that is, a "polynomial" in which the coefficients are themselves periodic functions of k. It is an open problem to determine which quasi-polynomials are the Ehrhart quasi-polynomials of rational polytopes. As partial progress on this problem, we construct families of polytopes in which the periods of the coefficient functions take on various prescribed values

Challenges in Linking Cognition and Survival: A Review

Linking cognitive performance with fitness outcomes, measured using both reproductive and survival metrics, of free-living animals is crucial for understanding the evolution of cognition. Although there is increasing evidence showing a link between cognitive traits and reproductive success metrics, studies specifically exploring the link between cognition and survival are scarce. We first explore which cognitive traits related to survival have been investigated in free-living animals. We also discuss the challenges associated with investigating the links between cognition and survival. We then review studies that specifically consider survival of animals of known cognitive abilities that are either free-living or in captivity and later released into the wild. We found nine studies exploring cognitive traits in wild populations. The relationships between these cognitive traits and survival were equivocal. We found a further nine studies in captive-reared populations trained to predator cues and later released into the wild. Training to recognize predator cues was correlated with increased survival in the majority of studies. Finally, different individual intrinsic characteristics (i.e., age, body condition, personality, sex) showed varied effects between studies. We argue that finding ecologically relevant cognitive traits is crucial for gaining a better understanding of how selection impacts certain cognitive traits, and how these might contribute to an individual's survival. We also suggest possible standardized, easy to implement, cognitive tests that can be used in long-term studies, which would generate large sample sizes, take into account intrinsic characteristics, and provide an opportunity to understand the mechanisms, development and evolution of cognition

Thermal contact resistance between two nanoparticles

We compute the thermal conductance between two nanoparticles in contact based on the Molecular Dynamics technique. The contact is generated by letting both particles stick together under van der Waals attractions. The thermal conductance is derived from the fluctuation-dissipation theorem and the time fluctuations of the exchanged power. We show that the conductance is proportional to the atoms involved in the thermal interaction. In the case of silica, the atomic contribution to the thermal conductance is in the range of 0.5 to 3 nW.K-1. This result fits to theoretical predictions based on characteristic times of the temperature fluctuation. The order of magnitude of the contact conductance is 1 \mu W.K-1 when the cross section ranges from 1 to 10nm2

Cardiomyocyte proliferation, a target for cardiac regeneration

International audienceCardiac diseases, characterized by cardiomyocyte loss, lead to dramatic impairment of cardiac function and ultimately to congestive heart failure. Despite significant advances, conventional treatments do not correct the defects in cardiac muscle cell numbers and the prognosis of congestive heart failure remains poor. The existence, in adult mammalian heart, of low but detectable cardiomyocyte proliferative capacities has shifted the target of regenerative therapy toward new therapeutical strategy. Indeed, the stimulation of terminally differentiated cardiomyocyte proliferation represents the main therapeutic approach for heart regeneration. Increasing evidence demonstrating that the loss of mammalian cardiomyocyte renewal potential shortly after birth causes the loss of regenerative capacities, strongly support the hypothesis that a detailed understanding of the molecular mechanisms controlling fetal and postnatal cardiomyocyte proliferation is essential to identify targets for cardiac regeneration. Here, we will review major developmental mechanisms regulating fetal cardiomyocyte proliferation and will describetheimpactofthedevelopmentalswitch,operatingatbirthanddrivingpostnatalheartmaturation,ontheregulationofadultcardiomyocyteproliferation,all these mechanisms representing potential targets for cardiac repair and regeneration

J021 Regulation of cardiac progenitor cells during development

Cardiac progenitor cells of the second heart field (SHF) contribute to the poles of the elongating embryonic heart. Failure or perturbation of SHF development leads to congenital heart defects. Recent studies have demonstrated the existence, in the postnatal heart, of resident cardiac progenitor cells that specifically express the transcription factor Islet1, a SHF marker, and that have the potential to differentiate into cardiomyocytes, smooth muscle and endothelial cells. Interestingly, several evidences suggest that these residual progenitor cells arise from the SHF.Through analysis of a transgene integration site position effect we have identified the transcriptional repressor Hes1 as a novel regulator of SHF development. Hes1, a target gene of the Notch signaling pathway, is expressed SHF progenitor cells. Analysis of E15.5 Hes1-/- embryos reveals outflow tract alignment defects (ventricular septal defects and overriding aorta). At earlier developmental stages, Hes1-/- embryos display SHF proliferation defects, cardiac neural crest cells reduction and fail to completely extend the outflow tract. Thus these data reveal a role for Hes1, and potentially Notch signaling, in SHF development.Given the importance of Isl1 as a marker of resident progenitor cells in the later heart we are analysing the role of known and novel regulators of the SHF (Hes1, Fgf10 and Tbx1) in the regulation of myocardial progenitor cell fate and in the definition of the critical niche occupied by residual cardiac progenitor cells in the forming and definitive heart.In Fgf10-/- mice, outflow tract alignment occurs normally. However, Fgf10-/- hearts are highly dysmorphic. We thus hypothesize that Fgf10 deletion may affect the proliferative capacities of SHF progenitors in order to maintain the residual progenitor cells pool in the fetal heart. Initial results have revealed that whereas Fgf10-/- hearts undergo heart tube extension normally, proliferation is impaired.Together, our results identify Hes1 as a novel regulator of SHF progenitor cell deployment and reveal a potential role of Fgf10 in regulating cardiac progenitor cell fate and cardiac growth during the fetal period. This study will increase our understanding of the molecular mechanisms governing the maintenance and differentiation of cardiac progenitor cells