Bayesian inference of the crust–core transition density via the neutron-star radius and neutron-skin thickness data

In this work,we perform a Bayesian inference of the crust-core transition density ρ_(t) of neutron stars based on the neutron-star radius and neutron-skin thickness data using a thermodynamical method.Uniform and Gaussian distributions for the ρ_(t) prior were adopted in the Bayesian approach.It has a larger probability of having values higher than 0.1 fm^(−3) for ρ_(t) as the uniform prior and neutron-star radius data were used.This was found to be controlled by the curvature K_(sym) of the nuclear symmetry energy.This phenomenon did not occur if K_(sym) was not extremely negative,namely,K_(sym)>−200 MeV.The value ofρ_(t) obtained was 0.075_(−0.01)^(+0.005) fm^(−3) at a confidence level of 68%when both the neutron-star radius and neutron-skin thickness data were considered.Strong anti-correlations were observed between ρ_(t),slope L,and curvature of the nuclear symmetry energy.The dependence of the three L-K_(sym) correlations predicted in the literature on crust-core density and pressure was quantitatively investigated.The most probable value of 0.08 fm^(−3) for ρ_(t) was obtained from the L-K_(sym) relationship proposed by Holt et al.while larger values were preferred for the other two relationships.

Blocking Posttranslational Core Fucosylation Ameliorates Rat Peritoneal Mesothelial Cell Epithelial-Mesenchymal Transition

Background：Core fucosylation （CF）,catalyzed by α-1,6 fucosyltransferase （Fut8） in mammals,plays an important role in pathological processes through posttranslational modification of key signaling receptor proteins,including transforming growth factor （TGF）-β receptors and platelet-derived growth factor （PDGF） receptors.However,its effect on peritoneal fibrosis is unknown.Here,we investigated its influence on epithelial-mesenchymal transition （EMT） of rat peritoneal mesothelial cells （PMCs） in vitro induced by a high-glucose （HG） culture solution.Methods：Rat PMCs were first cultured in a HG （2.5%） culture solution to observe the CF expression level （fluorescein isothiocyanate-lens culinaris agglutinin）,we next established a knockdown model of rat PMCs in vitro with Fut8 small interfering RNA （siRNA） to observe whether inhibiting CF decreases the messenger RNA （mRNA） expression and protein expression of Fut8 and reverses EMT status.Rat PMCs were randomly divided into control group,mock group （transfected with scrambled siRNA）,Fut8 siRNA group,HG group,HG ＋ mock group,and HG ＋ Fut8 siRNA group.Finally,we examined the activation of TGF-β/Smad2/3 signaling and PDGF/extracellular signal-regulated kinase （ERK） signaling to observe the influence of CF on them.Results：CF,Fut8 mRNA,and protein expression were all significantly upregulated in HG-induced EMT model than those in the control rat PMCs （P 〈 0.05）.Fut8 siRNA successfully blocked CF of TGF-β receptors and PDGF receptors and attenuated the EMT status （E-cadherin and α-SMA and phenotypic changes） in HG-induced rat PMCs.In TGF-β/Smad2/3 signaling,Fut8 siRNA did not suppress the protein expression of TGF-3 receptors and Smad2/3;however,it significantly suppressed the phosphowlation of Smad2/3 （relative expression folds of HG ＋ Fut8 group vs.HG group：7.6 ± 0.4 vs.15.1 ± 0.6,respectively,P 〈 0.05）.In PDGF/ERK signaling,Fut8 siRNA did not suppress the protein expression of PDGF receptors and ERK,but it significantly suppressed the phosphorylation of ERK （relative expression folds of HG ＋ Fut8 group vs.HG group：8.7 ± 0.9 vs.15.6 ± 1.2,respectively,P 〈 0.05）.Blocking CF inactivated the activities of TGF-β and PDGF signaling pathways,and subsequently blocked EMT.Conclusions：These results demonstrate that CF contributes to rat PMC EMT.and that blocking it attenuates EMT.CF regulation is a potential therapeutic target of peritoneal fibrosis.