Atmospheric tides and their consequences on the rotational dynamics of terrestrial planets

Atmospheric tides can have a strong impact on the rotational dynamics of planets. They are of most importance for terrestrial planets located in the habitable zone of their host star, where their competition with solid tides is likely to drive the body towards non-synchronized rotation states of equilibrium, as observed in the case of Venus. Contrary to other planetary layers, the atmosphere is sensitive to both gravitational and thermal forcings, through a complex dynamical coupling involving the effects of Coriolis acceleration and characteristics of the atmospheric structure. These key physics are usually not taken into account in modelings used to compute the evolution of planetary systems, where tides are described with parametrised prescriptions. In this work, we present a new ab initio modeling of atmospheric tides adapting the theory of the Earth's atmospheric tides (Chapman & Lindzen 1970) to other terrestrial planets. We derive analytic expressions of the tidal torque, as a function of the tidal frequency and parameters characterizing the internal structure (e.g. the Brunt-V\"ais\"al\"a frequency, the radiative frequency, the pressure heigh scale). We show that stratification plays a key role, the tidal torque being strong in the case of convective atmospheres (i.e. with a neutral stratification) and weak in case of atmosphere convectively stable. In a second step, the model is used to determine the non-synchronized rotation states of equilibrium of Venus-like planets as functions of the physical parameters of the system. These results are detailed in Auclair-Desrotour et al. (2017a) and Auclair-Desrotour et al. (2017b).Comment: Proceedings for Astro Fluid conference in memory of Jean-Paul Zahn (Paris, June 2016), 9 pages, 5 figure

TGFb2 involved in the effect of miR-599 in VSMCs.

<p>(A) The protein expression of TGFb2 was measured by western blot. (B) Overexpression of TGFb2 promoted miR-599-induced inhibition of VSMCs proliferation. (C) Ectopic expression of TGFb2 promoted the expression of type I collagen, in miR-599 overexpressing VSMCs. (D) The mRNA expression of type V collagen in VSMCs was measure by qRT-PCR. (E) The mRNA expression of proteoglycan in VSMCs was measure by qRT-PCR. *p<0.05, **p<0.01 and ***p<0.001.</p

Bayesian Diagnostics of Hidden Markov Structural Equation Models with Missing Data

<p>Cocaine is a type of drug that functions to increase the availability of the neurotransmitter dopamine in the brain. However, cocaine dependence or abuse is highly related to an increased risk of psychiatric disorders and deficits in cognitive performance, attention, and decision-making abilities. Given the chronic and persistent features of drug addiction, the progression of abstaining from cocaine often evolves across several states, such as addiction to, moderate dependence on, and swearing off cocaine. Hidden Markov models (HMMs) are well suited to the characterization of longitudinal data in terms of a set of unobservable states, and have increasingly been used to uncover the dynamic heterogeneity in progressive diseases or activities. However, the existence of outliers or influential points may misidentify the hidden states and distort the associated inference. In this study, we develop a Bayesian local influence procedure for HMMs with latent variables in the presence of missing data. The proposed model enables us to investigate the dynamic heterogeneity of multivariate longitudinal data, reveal how the interrelationships among latent variables change from one state to another, and simultaneously conduct statistical diagnosis for the given data, model assumptions, and prior inputs. We apply the proposed procedure to analyze a dataset collected by the UCLA center for advancing longitudinal drug abuse research. Several outliers or influential points that seriously influence estimation results are identified and removed. The proposed procedure also discovers the effects of treatment and individuals’ psychological problems on cocaine use behavior and delineates their dynamic changes across the cocaine-addiction states.</p

miR-599 suppressed VSMCs migration.

<p>Overexpression of miR-599 suppressed VSMCs migration. ***p<0.001.</p

miR-599 suppressed VSMCs proliferation.

<p>(A) The expression of miR-599 was measured by qRT-PCR. (B) CCK-8 analysis showed that overexpression of miR-599 suppressed VSMCs proliferation. (C) The mRNA expression of PCNA in VSMCs was measure by qRT-PCR. (D) The protein expression of PCNA in VSMCs was measure by western blot. (E) The mRNA expression of ki-67 in VSMCs was measure by qRT-PCR. (F) The protein expression of ki-67 in VSMCs was measure by western blot.*p<0.05 and ***p<0.001.</p

miR-599 is inhibited by PDGF-bb in VSMCs.

<p>(A) PDGF-bb can induce VSMCs proliferation at time-dependently. (B) PDGF-bb can induce VSMCs proliferation at dose-dependently. (C) The expression of miR-599 was measured by qRT-PCR. (D) The expression of miR-599 was measured by qRT-PCR. *p<0.05, **p<0.01 and ***p<0.001.</p

TGFb2 is a direct target of miR-599 in VSMCs.

<p>(A) There is a potential seed sequence of miR-599 in the 3’UTR of TGFb2. (B) miR-599 inhibited the luciferase activity in the TGFb2 with wild-type 3’UTR, whereas, luciferase activity was not drop in the mutant binding sites 3’UTR of TGFb2. (C) Overexpression of miR-599 suppressed the protein expression of TGFb2. ***p<0.001.</p

miR-599 inhibited matrix gene expression in VSMCs.

<p>(A) Overexpression of miR-599 suppressed the type I collagen mRNA expression. (B) The protein expression of type I collagen in VSMCs was measure by western blot. (C) Overexpression of miR-599 suppressed the type V collagen mRNA expression. (D) The protein expression of type V collagen in VSMCs was measure by western blot. (E) Overexpression of miR-599 suppressed the proteoglycan mRNA expression. (D) The protein expression of proteoglycan in VSMCs was measure by western blot.</p

Ab Initio Values of the Gas Transport Properties of Hydrogen Isotopologues and Helium–Hydrogen Mixtures at Low Density

We employed the classical kinetic theory to calculate transport properties as a function of temperature for hydrogen isotopologues and helium–hydrogen mixtures. The viscosity, thermal conductivity, diffusion coefficient, and thermal diffusion factor were computed at low density and over a wide temperature range from 298 to 2000 K. The calculation utilized the spherically symmetric versions of the latest ab initio potentials for the interactions of the like and unlike gas molecules. The computed values are generally consistent with the limited experimental data for HD, ⁴He–H₂, ⁴He–D₂, ⁴He–HD, ³He–H₂, ³He–D₂, H₂–HD, and D₂–HD. Our results provide reliable transport property data for the considered species at temperatures where experimental information is absent

Image_1_Real-world landscape transition of death causes in the immunotherapy era for metastatic non-small cell lung cancer.jpeg

BackgroundWith approval of anti-PD-1/PD-L1, metastatic non-small cell lung cancer (NSCLC) has entered the era of immunotherapy. Since immune-related adverse events (irAEs) occur commonly in patients receiving anti-PD-1/PD-L1, the landscape of death causes may have changed in metastatic NSCLC. We aim to compare patterns of death causes in metastatic NSCLC between the pre-immunotherapy and immunotherapy era to identify the consequent landscape transition of death causes.MethodsIn this cohort study, 298,485 patients with metastatic NSCLC diagnosed between 2000 and 2018 were identified from the Surveillance, Epidemiology, and End Results Program. Unsupervised clustering with Bayesian inference method was performed for all patients’ death causes, which separated them into two death patterns: the pre-immunotherapy era group and the immunotherapy era group. Relative risk (RR) of each death cause between two groups was estimated using Poisson regression. Reduced death risk as survival time was calculated with locally weighted scatterplot smooth (Lowess) regression.ResultsTwo patterns of death causes were identified by unsupervised clustering for all patients. Thus, we separated them into two groups, the immunotherapy era (2015-2017, N=40,172) and the pre-immunotherapy era (2000-2011, N=166,321), in consideration of obscure availability to immunotherapy for patients diagnosed in 2012-2014, when the follow-up cutoff was set as three years. Although all-cause death risk had reduced (29.2%, 13.7% and 27.8% for death risks of lung cancer, non-cancer and other cancers), non-cancer deaths in the immunotherapy era (N=2,100, 5.2%; RR=1.155, 95%CI: 1.101-1.211, PConclusionsThe real-world landscape of death causes has changed in metastatic NSCLC when entering the immunotherapy era, and the increased non-cancer diseases may contribute to the changes that may be associated with commonly occurring irAEs.</p