Theory of Mixed-State Effect on Quasiparticle Interference in Iron-based Superconductors

Based on a phenomenological model with $s_{\pm}$ or s-wave pairing symmetry, the mixed-state effect on quasiparticle interference in iron-based superconductors is investigated by solving large-scale Bogoliubov-de Gennes equations based on the Chebyshev polynomial expansion. Taking into account the presence of magnetic field, our result for the $s_{\pm}$ pairing is in qualitative agreement with recent scanning tunneling microscopy experiment while for the s-wave pairing, the result is in apparent contradiction with experimental observations, thus excluding the s-wave pairing. Furthermore, we treat the effect of vortices rigorously instead of approximating the vortices as magnetic impurities, thus our results are robust and should be more capable of explaining the experimental data

Analyzing the Dynamics of a Rumor Transmission Model with Incubation

This paper considers a rumor transmission model with incubation that incorporates constant recruitment and has infectious force in the latent period and infected period. By carrying out a global analysis of the model and studying the stability of the rumor-free equilibrium and the rumor-endemic equilibrium, we use the geometric approach for ordinary differential equations which is based on the use of higher-order generalization of Bendixson’s criterion. It shows that either the number of rumor infective individuals tends to zero as time evolves or the rumor persists. We prove that the transcritical bifurcation occurs at R0 crosses the bifurcation threshold R0=1 by projecting the flow onto the extended center manifold. Since the rumor endemic level at the equilibrium is a continuous function of R0, as a consequence for successful eradication of the rumor, one should simply reduce R0 continuously below the threshold value 1. Finally, the obtained results are numerically validated and then discussed from both the mathematical and the sociological perspectives

Inhalation of electronic cigarettes slightly affects lung function and inflammation in mice

Electronic cigarettes have become increasingly popular, but the results of previous studies on electronic cigarette exposure in animals have been equivocal. This study aimed to evaluate the effects of electronic cigarette smoke (ECS) and cigarette smoke (CS) on lung function and pulmonary inflammation in mice to investigate whether electronic cigarettes are safer when compared to cigarettes. 32 specific pathogen-free BALB/c male mice were randomly grouped and exposed to fresh air (control), mint-flavored ECS (ECS1, 6 mg/kg), cheese-flavored ECS (ECS2, 6 mg/kg), and CS (6 mg/kg). After 3 weeks exposure to ECS or CS, we measured lung function (PIF and Penh) and blood oxygen saturation. The levels of TNF-α and IL-6 in the bronchoalveolar lavage fluid (BALF) and serum were measured using ELISA. HE staining was performed to observe the pathological changes in the lung tissues. The levels of IL-6 in BALF and serum, and TNF-α in BALF, were elevated similarly in the ECS and CS groups compared to the control group. Significant elevation was observed in serum TNF-α levels in the CS group. The total count of cells in BALF were increased after ECS1 exposure and CS exposure. PIF and oxygen saturation decreased, and Penh increased markedly in the CS group but not in the ECS groups. Compared with the ECS groups, mice in the CS group had widened lung tissue septa and increased inflammatory cell infiltration. However, we did not detect significant differences between mint-flavored and cheese-flavored e-cigarettes in our study. Overall, our findings suggested that both ECS and CS impair lung function and histopathology while promoting inflammation. In contrast, ECS has a less negative impact than CS

HSD11B1 is upregulated synergistically by IFNγ and TNFα and mediates TSG-6 expression in human UC-MSCs.

Funder: the National Key R&D Program of China [2018YFA0107500], National Natural Science Foundation of China [81530043, 81930085 and 31771260], the Scientific Innovation Project of the Chinese Academy of Sciences [XDA16020403], the Social Development Project of Jiangsu Province [BE2016671], and the State Key Laboratory of Radiation Medicine and Protection, Soochow University [GZN1201804 and GZN1201903].Inflammatory factors such as IFNγ and TNFα could endow mesenchymal stem cells (MSCs) a potent immunomodulatory property, a process called licensing, but the mechanisms are not fully understood. We here found that glucocorticoid-activating enzyme 11β-hydroxysteroid dehydrogenase type 1 (HSD11B1), which converts inactive cortisone to the active cortisol and thereby regulates tissue glucocorticoid (GC) levels, was greatly upregulated by IFNγ and TNFα in human umbilical cord-derived MSCs (UC-MSCs) in a synergistic manner. While IFNγ alone was not able to induce HSD11B1, it could increase the activity of NF-kB and thus augment the upregulation of HSD11B1 by TNFα. Interestingly, the upregulation of HSD11B1 by IFNγ and TNFα also required glucocorticoid receptor. Furthermore, HSD11B1 was shown to be required for the expression of TNF-stimulated gene 6 (TSG-6), an important anti-inflammatory effector molecule of MSCs. Therefore, the inflammatory factors IFNγ and TNFα can promote GC metabolism and thereby drive the expression of anti-inflammatory factor TSG-6 in human UC-MSCs, forming a potential negative feedback loop. These findings help to understand the relationship between inflammation and GC metabolism

Sensitization of Glioma Cells to Tamoxifen-Induced Apoptosis by Pl3-Kinase Inhibitor through the GSK-3β/β-Catenin Signaling Pathway

Malignant gliomas represent one of the most aggressive types of cancers and their recurrence is closely linked to acquired therapeutic resistance. A combination of chemotherapy is considered a promising therapeutic model in overcoming therapeutic resistance and enhancing treatment efficacy. Herein, we show by colony formation, Hochest 33342 and TUNEL staining, as well as by flow cytometric analysis, that LY294002, a specific phosphatidylinositide-3-kinase (PI3K) inhibitor, enhanced significantly the sensitization of a traditional cytotoxic chemotherapeutic agent, tamoxifen-induced apoptosis in C6 glioma cells. Activation of PI3K signaling pathway by IGF-1 protected U251 cells from apoptosis induced by combination treatment of LY294002 and tamoxifen. Interference of PI3K signaling pathway by PI3K subunit P85 siRNA enhanced the sensitization of U251 glioma cells to tamoxifen -induced apoptosis. By Western blotting, we found that combination treatment showed lower levels of phosphorylated AktSer473 and GSK-3βSer9 than a single treatment of LY294002. Further, we showed a significant decrease of nuclear β-catenin by combination treatment. In response to the inhibition of β-catenin signaling, mRNA and protein levels of Survivin and the other three antiapoptotic genes Bcl-2, Bcl-xL, and Mcl-1 were significantly decreased by combination treatment. Our results indicated that the synergistic cytotoxic effect of LY294002 and tamoxifen is achieved by the inhibition of GSK-3β/β-catenin signaling pathway

Golgi-associated LC3 lipidation requires V-ATPase in noncanonical autophagy

Autophagy is an evolutionarily conserved catabolic process by which cells degrade intracellular proteins and organelles in the lysosomes. Canonical autophagy requires all autophagy proteins (ATGs), whereas noncanonical autophagy is activated by diverse agents in which some of the essential autophagy proteins are dispensable. How noncanonical autophagy is induced and/or inhibited is still largely unclear. In this study, we demonstrated that AMDE-1, a recently identified chemical that can induce canonical autophagy, was able to elicit noncanonical autophagy that is independent of the ULK1 (unc-51-like kinase 1) complex and the Beclin1 complex. AMDE-1-induced noncanonical autophagy could be specifically suppressed by various V-ATPase (vacuolar-type H(+)-ATPase) inhibitors, but not by disturbance of the lysosome function or the intracellular ion redistribution. Similar findings were applicable to a diverse group of stimuli that can induce noncanonical autophagy in a FIP200-independent manner. AMDE-1-induced LC3 lipidation was colocalized with the Golgi complex, and was inhibited by the disturbance of Golgi complex. The integrity of the Golgi complex was also required for multiple other agents to stimulate noncanonical LC3 lipidation. These results suggest that the Golgi complex may serve as a membrane platform for noncanonical autophagy where V-ATPase is a key player. V-ATPase inhibitors could be useful tools for studying noncanonical autophagy

Paeonol Ameliorates Glucose and Lipid Metabolism in Experimental Diabetes by Activating Akt

Our previous study proved that paeonol (Pae) could lower blood glucose levels of diabetic mice. There are also a few reports of its potential use for diabetes treatment. However, the role of Pae in regulating glucose and lipid metabolism in diabetes remains largely unknown. Considering the critical role of serine/threonine kinase B (Akt) in glucose and lipid metabolism, we explored whether Pae could improve glucose and lipid metabolism disorders via Akt. Here, we found that Pae attenuated fasting blood glucose, glycosylated serum protein, serum cholesterol and triglyceride (TG), hepatic glycogen, cholesterol and TG in diabetic mice. Moreover, Pae enhanced glucokinase (GCK) and low-density lipoprotein receptor (LDLR) protein expressions, and increased the phosphorylation of Akt. In insulin-resistant HepG2 cells, Pae increased glucose uptake and decreased lipid accumulation. What’s more, Pae elevated LDLR and GCK expressions as well as Akt phosphorylation, which was consistent with the in vivo results. Knockdown and inhibition experiments of Akt revealed that Pae regulated LDLR and GCK expressions through activation of Akt. Finally, molecular docking assay indicated the steady hydrogen bond was formed between Pae and Akt2. Experiments above suggested that Pae ameliorated glucose and lipid metabolism disorders and the underlying mechanism was closely related to the activation of Akt