Consistency between dynamical and thermodynamical stabilities for perfect fluid in f(R)f(R) theories

We investigate the stability criterions for perfect fluid in $f(R)$ theories which is an important generalization of general relativity. Firstly, using Wald's general variation principle, we recast Seifert's work and obtain the dynamical stability criterion. Then using our generalized thermodynamical criterion, we obtain the concrete expressions of the criterion. We show that the dynamical stability criterion is exactly the same as the thermodynamical stability criterion. This result suggests that there is an inherent connection between the thermodynamics and gravity in $f(R)$ theories. It should be pointed out that using the thermodynamical method to determine the stability for perfect fluid is simpler and more directly than the dynamical method.Comment: 18page

Thermodynamical stability for perfect fluid

According to maximum entropy principle, it has been proved that the gravitational field equations could be derived by the extrema of total entropy for perfect fluid, which implies that thermodynamic relations contain information of gravity. In this manuscript, we obtain a criterion for thermodynamical stability of an adiabatic, self-gravitating perfect fluid system by the second variation of total entropy. We show, for Einstein's gravity with spherical symmetry spacetime, that the criterion is consistent with that for dynamical stability derived by Chandrasekhar and Wald. We also find that the criterion could be applied to cases without spherical symmetry, or under general perturbations. The result further establishes the connection between thermodynamics and gravity.Comment: 10 page

N′-(1-Phenyl­ethyl­idene)isonicotinohydrazide

The title compound, C14H13N3O, was prepared from hypnone and isoniazid. The dihedral angle between the aromatic rings is 12.21 (2)°. In the crystal, N—H⋯O hydrogen bonds link the mol­ecules into chains propagating in [001] and C—H⋯O inter­actions consolidate the packing

LHC Search of New Higgs Boson via Resonant Di-Higgs Production with Decays into 4W

Searching for new Higgs particle beyond the observed light Higgs boson h(125GeV) will unambiguously point to new physics beyond the standard model. We study the resonant production of a CP-even heavy Higgs state $H^0$ in the di-Higgs channel via, $gg\to H^0\to h^0h^0\to WW^*WW^*$, at the LHC Run-2 and the high luminosity LHC (HL-LHC). We analyze two types of the $4W$ decay modes, one with the same-sign di-leptons ($4W\to\ell^\pm\nu\ell^\pm\nu 4q$) and the other with tri-leptons ($4W\to\ell^\pm\nu\ell^\mp\nu\ell^\pm\nu 2q$). We perform a full simulation for the signals and backgrounds, and estimate the discovery potential of the heavy Higgs state at the LHC Run-2 and the HL-LHC, in the context of generical two-Higgs-doublet models (2HDM). We determine the viable parameter space of the 2HDM as allowed by the theoretical constraints and the current experimental limits. We systematically analyze the allowed parameter space of the 2HDM which can be effectively probed by the heavy Higgs searches of the LHC, and further compare this with the viable parameter region under the current theoretical and experimental bounds.Comment: v3: JHEP published version, 34pp, 10 Figs(36 plots) and 9 Tables. Only minor typos fixed, references added. v2: JHEP version. All results and conclusions un-changed, discussions and references added. (This update is much delayed due to author's traveling and flu.

The clinical feature of silent infections of novel coronavirus infection (COVID‐19) in Wenzhou

Here were reported clinical features of silent infected COVID‐19 patients. Our study showed that the prevalence of the silent infection of COVID‐19 is 5.8% (95% CI: 3.4‐9.9%), which is much higher than 1.2% which from the report in China CDC. The silent infection patients were more likely to be young adults, the patients without chronic disease. All of the cases in the presented study was found because they were traced as close contact of confirmed cases. Our study indicated that traced the close contract of confirmed case, long time self‐quarantine, and screening is necessary to prevent the secondary cases in community

Protein kinase C-α signals P115RhoGEF phosphorylation and RhoA activation in TNF-α-induced mouse brain microvascular endothelial cell barrier dysfunction

<p>Abstract</p> <p>Background</p> <p>Tumor necrosis factor-<b>α </b>(TNF-<b>α</b>), a proinflammatory cytokine, is capable of activating the small GTPase RhoA, which in turn contributes to endothelial barrier dysfunction. However, the underlying signaling mechanisms remained undefined. Therefore, we aimed to determine the role of protein kinase C (PKC) isozymes in the mechanism of RhoA activation and in signaling TNF-<b>α</b>-induced mouse brain microvascular endothelial cell (BMEC) barrier dysfunction.</p> <p>Methods</p> <p>Bend.3 cells, an immortalized mouse brain endothelial cell line, were exposed to TNF-<b>α </b>(10 ng/mL). RhoA activity was assessed by pull down assay. PKC-<b>α </b>activity was measured using enzyme assasy. BMEC barrier function was measured by transendothelial electrical resistance (TER). p115RhoGEF phosphorylation was detected by autoradiography followed by western blotting. F-actin organization was observed by rhodamine-phalloidin staining. Both pharmacological inhibitors and knockdown approaches were employed to investigate the role of PKC and p115RhoGEF in TNF-<b>α</b>-induced RhoA activation and BMEC permeability.</p> <p>Results</p> <p>We observed that TNF-<b>α </b>induces a rapid phosphorylation of p115RhoGEF, activation of PKC and RhoA in BMECs. Inhibition of conventional PKC by Gö6976 mitigated the TNF-<b>α</b>-induced p115RhoGEF phosphorylation and RhoA activation. Subsequently, we found that these events are regulated by PKC-<b>α </b>rather than PKC-β by using shRNA. In addition, P115-shRNA and n19RhoA (dominant negative mutant of RhoA) transfections had no effect on mediating TNF-<b>α</b>-induced PKC-<b>α </b>activation. These data suggest that PKC-<b>α </b>but not PKC-β acts as an upstream regulator of p115RhoGEF phosphorylation and RhoA activation in response to TNF-<b>α</b>. Moreover, depletion of PKC-<b>α</b>, of p115RhoGEF, and inhibition of RhoA activation also prevented TNF-<b>α</b>-induced stress fiber formation and a decrease in TER.</p> <p>Conclusions</p> <p>Taken together, our results show that PKC-<b>α </b>phosphorylation of p115RhoGEF mediates TNF-<b>α </b>signaling to RhoA, and that this plays a critical role in signaling F-actin rearrangement and barrier dysfunction in BMECs.</p

Peripheral Leukocytapheresis Attenuates Acute Lung Injury Induced by Lipopolysaccharide In Vivo

The mortality of acute lung injury and acute respiratory distress syndrome (ALI/ARDS) remains high and efforts for prevention and treatments have shown little improvement over the past decades. The present study investigated the efficacy and mechanism of leukocytapheresis (LCAP) to partially eliminate peripheral neutrophils and attenuate lipopolysaccharide (LPS)-induced lung injury in dogs. A total of 24 healthy male mongrel dogs were enrolled and randomly divided into LPS, LCAP and LCAP-sham groups. All animals were injected with LPS to induce endotoxemia. The serum levels of leucocytes, neutrophil elastase, arterial blood gas, nuclear factor-kappa B (NF-κB) subunit p65 in lung tissues were measured. The histopathology and parenchyma apoptosis of lung tissues were examined. We found that 7, 3, and 7 animals in the LPS, LCAP, and sham-LCAP groups, respectively, developed ALI 36 h after LPS infusion. The levels of NF-κB p65 in lung tissue, neutrophils and elastase in blood, decreased significantly following LCAP. LCAP also alleviated apoptosis, and NF-κB p65 in lung tissues. Collectively, our results show that partial removal of leucocytes from peripheral blood decreases elastase level in serum. This, in turn, attenuates lung injuries and may potentially decrease the incidence of ALI