Global evolution and dispersal of protoplanetary disks (PPDs) is governed by disk angular momentum transport and mass-loss processes. Recent numerical studies suggest that angular momentum transport in the inner region of PPDs is largely driven by magnetized disk wind, yet the wind mass-loss rate remains unconstrained. On the other hand, disk mass loss has conventionally been attributed to photoevaporation, where external heating on the disk surface drives a thermal wind. We unify the two scenarios by developing a 1D model of magnetized disk winds with a simple treatment of thermodynamics as a proxy for external heating. The wind properties largely depend on 1) the magnetic field strength at the wind base, characterized by the poloidal Alfvén speed v Ap , 2) the sound speed c s near the wind base, and 3) how rapidly poloidal field lines diverge (achieve R −2 scaling). When v Ap ≫ c s , corotation is enforced near the wind base, resulting in centrifugal acceleration. Otherwise, the wind is accelerated mainly by the pressure of the toroidal magnetic field. In both cases, the dominant role played by magnetic forces likely yields wind outflow rates that well exceed purely hydrodynamical mechanisms. For typical PPD accretion-rate and wind-launching conditions, we expect v Ap to be comparable to c s at the wind base. The resulting wind is heavily loaded, with total wind mass loss rate likely reaching a considerable fraction of wind-driven accretion rate. Implications for modeling global disk evolution and planet formation are also discussed.

Tumour‐associated macrophage (TAM) is an important component in tumour microenvironment. Generally, TAM exhibits the function of M2‐like macrophage, which was closely related to angiogenesis and tumour progression. Dioscin, a natural steroidal saponin, has shown its powerful anti‐tumour activity recently. However, the mechanism of dioscin involved in immune regulation is still obscure. Here, we observed dioscin induced macrophage M2‐to‐M1 phenotype transition in vitro and inhibited IL‐10 secretion. Meanwhile, the phagocytosis of macrophages was enhanced. In subcutaneous lung tumour models, dioscin inhibited the augmentation of M2 macrophage populations. Furthermore, dioscin down‐regulated STAT3 and JNK signalling pathways in macrophages in vitro. In BMDMs, activating JNK and inhibiting STAT3 induce macrophages to M1 polarization while inhibiting JNK and activating STAT3 to M2 polarization. Additionally, condition mediums from dioscin‐pre‐treated macrophages inhibited the migration of 3LL cells and the tube‐formation capacity of HUVECs. What's more, dioscin‐mediated macrophage polarization inhibited the in vivo metastasis of 3LL cells. In conclusion, dioscin may act as a new anti‐tumour agent by inhibiting TAMs via JNK and STAT3 pathways in lung cancer.

We use the hydrodynamical galaxy formation simulations from the Illustris suite to study the origin and properties of galaxy velocity bias, i.e., the difference between the velocity distributions of galaxies and dark matter inside halos. We find that galaxy velocity bias is a decreasing function of the ratio of galaxy stellar mass to host halo mass. In general, central galaxies are not at rest with respect to dark matter halos or the core of halos, with a velocity dispersion above 0.04 times that of the dark matter. The central galaxy velocity bias is found to be mostly caused by the close interactions between the central and satellite galaxies. For satellite galaxies, the velocity bias is related to their dynamical and tidal evolution history after being accreted onto the host halos. It depends on the time after the accretion and their distances from the halo centers, with massive satellites generally moving more slowly than the dark matter. The results are in broad agreements with those inferred from modeling small-scale redshift-space galaxy clustering data, and the study can help improve models of redshift-space galaxy clustering.

In this paper we calculate the radio burst signals from three kinds of structures of superconducting cosmic strings. By taking into account the observational factors including scattering and relativistic effects, we derive the event rate of radio bursts as a function of redshift with the theoretical parameters Gμ and I of superconducting strings. Our analyses show that cusps and kinks may have noticeable contributions to the event rate and in most cases cusps would dominate the contribution, while the kink-kink collisions tend to have secondary effects. By fitting theoretical predictions with the normalized data of fast radio bursts, we for the first time constrain the parameter space of superconducting strings and report that the parameter space of Gμ ∼ [10 −14 , 10 −12 ] and I ∼ [10 −1 , 10 2 ] GeV fit the observation well although the statistic significance is low due to the lack of observational data. Moreover, we derive two types of best fittings, with one being dominated by cusps with a redshift z = 1.3, and the other dominated by kinks at the range of the maximal event rate.

Lung squamous cell carcinoma (SCC) is one of the deadliest cancers both in China and worldwide. To date, the efficacy of lung SCC treatments is limited. Recent studies have elucidated the powerful anti-tumour role of dioscin in different human cancers. Here, our study aims to investigate the effect of dioscin on lung SCC and its underlying mechanism. First, we found that dioscin not only inhibited cell proliferation and cell migration and induced cell apoptosis in lung SCC cells but also suppressed tumour growth in tumour-bearing mice. Furthermore, we noted that the accumulation of intracellular reactive oxygen species (ROS) was triggered by dioscin in lung SCC cells, leading to the phosphorylation of HSP27 through p38-MAPK and consequent cell apoptosis. The activation of p38-MAPK/HSP27 induced by the p38-MAPK activator Anisomycin enhanced the apoptosis of lung SCC cells, while the ROS inhibitor N-acetyl-L-cysteine (NAC) and the p38-MAPK inhibitor SB203580 both attenuated dioscin-mediated cell apoptosis. Moreover, NAC suppressed the activation of p38-MAPK/HSP27 that induced by dioscin. In conclusion, these results confirm that dioscin facilitates ROS-induced apoptosis via the p38-MAPK/HSP27-mediated pathway in lung SCC.

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The interaction of immune cells and cytokines in the tumor microenvironment affects the development and prognosis of tumors with an unclear potential regulatory mechanism. Recent studies have elucidated the protumor role of Th22 cells and its lineage-specific cytokine IL-22 in different human cancers. The present study is aimed at investigating the biological effect of Th22 cells/IL-22 and its molecular mechanism in the pathogenesis process of non-small-cell lung cancer (NSCLC). It was initially found that Th22 cells were enriched in the peripheral blood of NSCLC patients. The level of Th22 cells in peripheral blood mononuclear cells (PBMCs) was positively correlated with the TNM stage, lymph node metastasis, and clinical tumor biomarkers. Furthermore, IL-22 not only antagonized the apoptosis inducing and cell cycle arresting effect by chemotherapy and molecular targeted drugs on NSCLC cell lines but also promoted tumor cell proliferation and tumor tissue growth. Moreover, IL-22 activated the JAK-STAT3/MAPK/AKT signaling pathway, both in vitro and in vivo. Conclusively, the present results confirm that Th22 cells/IL-22 may serve as a negative immune regulator in lung cancer.

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