Fluctuation theorem for entropy production during effusion of a relativistic ideal gas

The probability distribution of the entropy production for the effusion of a relativistic ideal gas is calculated explicitly. This result is then extended to include particle and anti-particle pair production and annihilation. In both cases, the fluctuation theorem is verified.Comment: 6 pages, no figure

Models of granular ratchets

We study a general model of granular Brownian ratchet consisting of an asymmetric object moving on a line and surrounded by a two-dimensional granular gas, which in turn is coupled to an external random driving force. We discuss the two resulting Boltzmann equations describing the gas and the object in the dilute limit and obtain a closed system for the first few moments of the system velocity distributions. Predictions for the net ratchet drift, the variance of its velocity fluctuations and the transition rates in the Markovian limit, are compared to numerical simulations and a fair agreement is observed.Comment: 15 pages, 4 figures, to be published on Journal of Statistical Mechanics: Theory and Experiment

Fluctuation theorem for the effusion of an ideal gas

The probability distribution of the entropy production for the effusion of an ideal gas between two compartments is calculated explicitly. The fluctuation theorem is verified. The analytic results are in good agreement with numerical data from hard disk molecular dynamics simulations.Comment: 11 pages, 10 figures, 2 table

Powerful ordered collective heat engines

We introduce a class of stochastic engines in which the regime of units operating synchronously can boost the performance. Our approach encompasses a minimal setup composed of $N$ interacting units placed in contact with two thermal baths and subjected to a constant driving worksource. The interplay between unit synchronization and interaction leads to an efficiency at maximum power between the Carnot, $\eta_{c}$, and the Curzon-Ahlborn bound, $\eta_{CA}$. Moreover, these limits can be respectively saturated maximizing the efficiency, and by simultaneous optimization of power and efficiency. We show that the interplay between Ising-like interactions and a collective ordered regime is crucial to operate as a heat engine. The main system features are investigated by means of a linear analysis near equilibrium, and developing an effective discrete-state model that captures the effects of the synchronous phase. The present framework paves the way for the building of promising nonequilibrium thermal machines based on ordered structures.Comment: Improved main text and supplemental material. Some figures and new analysis were performe

Kinetic analysis of a chiral granular motor

We study the properties of a heterogeneous, chiral granular rotor that is capable of performing useful work when immersed in a bath of thermalized particles. The dynamics can be obtained in general from a numerical solution of the Boltzmann-Lorentz equation. We show that a mechanical approach gives the exact mean angular velocity in the limit of an infinitely massive rotor. We examine the dependence of the mean angular velocity on the coefficients of restitution of the two materials composing the motor. We compute the power and efficiency and compare with numerical simulations. We also perform a realistic numerical simulation of a granular rotor which shows that the presence of non uniformity of the bath density within the region where the motor rotates, and that the ratchet effect is slightly weakened, but qualitatively sustained. Finally we discuss the results in connection with recent experiments.Comment: 19 pages, 12 figure

The in vivo endothelial cell translatome is highly heterogeneous across vascular beds

Endothelial cells (ECs) are highly specialized across vascular beds. However, given their interspersed anatomic distribution, comprehensive characterization of the molecular basis for this heterogeneity in vivo has been limited. By applying endothelial-specific translating ribosome affinity purification (EC-TRAP) combined with high-throughput RNA sequencing analysis, we identified pan EC-enriched genes and tissue-specific EC transcripts, which include both established markers and genes previously unappreciated for their presence in ECs. In addition, EC-TRAP limits changes in gene expression after EC isolation and in vitro expansion, as well as rapid vascular bed-specific shifts in EC gene expression profiles as a result of the enzymatic tissue dissociation required to generate single-cell suspensions for fluorescence-activated cell sorting or single-cell RNA sequencing analysis. Comparison of our EC-TRAP with published single-cell RNA sequencing data further demonstrates considerably greater sensitivity of EC-TRAP for the detection of low abundant transcripts. Application of EC-TRAP to examine the in vivo host response to lipopolysaccharide (LPS) revealed the induction of gene expression programs associated with a native defense response, with marked differences across vascular beds. Furthermore, comparative analysis of whole-tissue and TRAP-selected mRNAs identified LPS-induced differences that would not have been detected by whole-tissue analysis alone. Together, these data provide a resource for the analysis of EC-specific gene expression programs across heterogeneous vascular beds under both physiologic and pathologic conditions

Brownian motion exhibiting absolute negative mobility

We consider a single Brownian particle in a spatially symmetric, periodic system far from thermal equilibrium. This setup can be readily realized experimentally. Upon application of an external static force F, the average particle velocity is negative for F>0 and positive for F<0 (absolute negative mobility).Comment: 4 pages, 3 figures, to be published in PR

Cytokine-mediated degradation of the transcription factor ERG impacts the pulmonary vascular response to systemic inflammatory challenge

BACKGROUND: During infectious diseases, proinflammatory cytokines transiently destabilize interactions between adjacent vascular endothelial cells (ECs) to facilitate the passage of immune molecules and cells into tissues. However, in the lung, the resulting vascular hyperpermeability can lead to organ dysfunction. Previous work identified the transcription factor ERG (erythroblast transformation-specific-related gene) as a master regulator of endothelial homeostasis. Here we investigate whether the sensitivity of pulmonary blood vessels to cytokine-induced destabilization is due to organotypic mechanisms affecting the ability of endothelial ERG to protect lung ECs from inflammatory injury. METHODS: Cytokine-dependent ubiquitination and proteasomal degradation of ERG were analyzed in cultured HUVECs (human umbilical vein ECs). Systemic administration of TNFα (tumor necrosis factor alpha) or the bacterial cell wall component lipopolysaccharide was used to cause a widespread inflammatory challenge in mice; ERG protein levels were assessed by immunoprecipitation, immunoblot, and immunofluorescence. Murine Erg deletion was genetically induced in ECs (Ergfl/fl;Cdh5[PAC]-CreERT2), and multiple organs were analyzed by histology, immunostaining, and electron microscopy. RESULTS: In vitro, TNFα promoted the ubiquitination and degradation of ERG in HUVECs, which was blocked by the proteasomal inhibitor MG132. In vivo, systemic administration of TNFα or lipopolysaccharide resulted in a rapid and substantial degradation of ERG within lung ECs but not ECs of the retina, heart, liver, or kidney. Pulmonary ERG was also downregulated in a murine model of influenza infection. Ergfl/fl;Cdh5(PAC)-CreERT2 mice spontaneously recapitulated aspects of inflammatory challenges, including lung-predominant vascular hyperpermeability, immune cell recruitment, and fibrosis. These phenotypes were associated with a lung-specific decrease in the expression of Tek-a gene target of ERG previously implicated in maintaining pulmonary vascular stability during inflammation. CONCLUSIONS: Collectively, our data highlight a unique role for ERG in pulmonary vascular function. We propose that cytokine-induced ERG degradation and subsequent transcriptional changes in lung ECs play critical roles in the destabilization of pulmonary blood vessels during infectious diseases

Differential roles of factors IX and XI in murine placenta and hemostasis under conditions of low tissue factor

The intrinsic tenase complex (FIXa-FVIIIa) of the intrinsic coagulation pathway and, to a lesser extent, thrombin-mediated activation of FXI, are necessary to amplify tissue factor (TF)-FVIIa-initiated thrombin generation. In this study, we determined the contribution of murine FIX and FXI to TF-dependent thrombin generation in vitro. We further investigated TF-dependent FIX activation in mice and the contribution of this pathway to hemostasis. Thrombin generation was decreased in FIX- but not in FXI-deficient mouse plasma. Furthermore, injection of TF increased levels of FIXa-antithrombin complexes in both wildtype and FXI-/- mice. Genetic studies were used to determine the effect of complete deficiencies of either FIX or FXI on the survival of mice expressing low levels of TF. Low-TF; FIX2/y male mice were born at the expected frequency, but none survived to wean. In contrast, low-TF;FXI-/- mice were generated at the expected frequency at wean and had a 6-month survival equivalent to that of low-TF mice. Surprisingly, a deficiency of FXI, but not FIX, exacerbated the size of blood pools in low-TF placentas and led to acute hemorrhage and death of some pregnant dams. Our data indicate that FIX, but not FXI, is essential for survival of low-TF mice after birth. This finding suggests that TF-FVIIa-mediated activation of FIX plays a critical role in murine hemostasis. In contrast, FXI deficiency, but not FIX deficiency, exacerbated blood pooling in low-TF placentas, indicating a tissue-specific requirement for FXI in the murine placenta under conditions of low TF