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International students are a bridge between Chinese and foreign cultures, but they still face multiple dilemmas in Chinese cultural communication due to different cultural backgrounds and values. In this paper, we utilize the subsumption sorting algorithm to sort the amount of cultural communication of international students’ exchanges, which is dynamically switched by a combination of two methods: back-block forward interpolation and header exchange. The D-S monopolistic competition model is used to construct the theoretical model of international student exchange that affects China’s international cultural communication power. The CES utility function is used to construct China’s international cultural communication network, which calculates the total amount of communication culture of cross-cultural exchanges between international students. In the end, an analysis of 85 international student samples revealed a correlation between international student exchanges and China’s international cultural communication. The results show that the correlation coefficient between international student exchanges and China’s international cultural communication is 0.305 p > 0.05, indicating that international student exchanges have a positive promotion effect on China’s international cultural communication. This study examines the general law of international cultural communication, which is crucial in promoting Chinese culture worldwide.

Oligodendrocytes express low-density lipoprotein receptor (LDLR) to endocytose cholesterol for the maintenance of adulthood myelination. However, the potential role of LDLR in chronic cerebral ischemia-related demyelination remains unclear. We used bilateral carotid artery stenosis (BCAS) to induce sustained cerebral ischemia in mice. This hypoxic-ischemic injury caused a remarkable decrease in oligodendroglial LDLR, with impaired oligodendroglial differentiation and survival. Oligodendroglial cholesterol levels, however, remained unchanged. Mouse miR-344e-3p and the human homolog miR-410-3p, 2 miRNAs directly targeting Ldlr, were identified in experimental and clinical leukoaraiosis and were thus implicated in the LDLR reduction. Lentiviral delivery of LDLR ameliorated demyelination following chronic cerebral ischemia. By contrast, [Ldlr.sup.-/-] mice displayed inadequate myelination in the corpus callosum. [Ldlr.sup.-/-] oligodendrocyte progenitor cells (OPCs) exhibited reduced ability to differentiate and myelinate axons in vitro. Transplantation with [Ldlr.sup.-/-] OPCs could not rescue the BCAS-induced demyelination. Such LDLR-dependent myelin restoration might involve a physical interaction of the Asn-ProVal-Tyr (NPVY) motif with the phosphotyrosine binding domain of Shc, which subsequently activated the MEK/ERK pathway. Together, our findings demonstrate that the aberrant oligodendroglial LDLR in chronic cerebral ischemia impairs myelination through intracellular signal transduction. Preservation of oligodendroglial LDLR may provide a promising approach to treat ischemic demyelination., Introduction Oligodendrocytes, the only cells capable of forming myelin in white matter, are highly sensitive to hypoxic-ischemic injury (1, 2). Damage to oligodendrocytes triggers rapid and profound demyelination, which ultimately [...]

In this study, 46 PM 2.5 samples collected from Nanjing, China were analyzed for total PAH concentration, with 14 samples assessed for PAH inhalation bioaccessibility and dioxin toxicity. The concentration of 19 PAH compounds in PM 2.5 ranged from 4.03 to 102 ng m -3 . When PAH inhalation bioaccessibility was assessed using simulated epithelial lung fluid, mean bioaccessibility values ranged from 3.21% (Benzo(c)fluorene) to 44.2% (Acenaphthylene). Benzo(a)pyrene concentration in 50% of the PM 2.5 samples exceeded the Chinese air quality standard of 2.5 ng m -3 , however, when bioaccessibility was considered, all samples were below the criterion. Similarly, the cancer risk probability for all PM 2.5 samples was >10 -4 incidences on the basis of total PAH concentration, while only 37% of samples posed a risk >10 -4 after incorporation of bioaccessibility. Dioxin toxicity of PM 2.5 -bound PAHs was also investigated by characterizing mRNA expression of cytochrome P450 superfamily members in human lung cells (A549 cell). Compared to total PAH concentration, the use of bioaccessible concentration was better at predicting dioxin toxicity of PM 2.5 -associated PAHs (correlation coefficient R 2  = 0.40-0.83 with p < 0.05). This study indicates that PAH inhalation bioaccessibility is an important consideration when assessing and predicting the risk posed by PM 2.5 particles, which is particularly important for countries with deteriorating air quality., (Copyright © 2018 Elsevier B.V. All rights reserved.)

When brain injury happens, endogenous neural stem cells (NSCs) located in the adult subventricular zone (SVZ) and subgranular zone (SGZ) are attacked by ischemia/reperfusion to undergo cellular apoptosis and death before being induced to migrate to the lesion point and differentiate into mature neural cells for damaged cell replacement. Although promoting antiapoptosis and NSC survival are critical to neuroregeneration, the mechanism has yet been elucidated clearly. Here in this study, we established an in vitro oxygen-glucose deprivation (OGD)/reoxygenation model on NSCs and detected glucose-regulated protein 78 (GRP78) involved in apoptosis, while in the absence of GRP78 by siRNA transfection, OGD/reoxygenation triggered PI3K/Akt, ERK1/2, and NF- κ B/p65 activation, and induced NSC apoptosis was attenuated. Further investigation, respectively, with the inhibitor of PI3K/Akt or ERK1/2 demonstrated a blockage on GRP78 upregulation, while the inhibition of NF- κ B rarely affected GRP78 induction by OGD/reoxygenation. The results indicated the bidirectional regulations of GRP78-PI3K/Akt and GRP78-ERK1/2 and the one-way signalling transduction through GRP78 to NF- κ B/p65 on NSC survival from OGD/reoxygenation. In conclusion, we found that GRP78 mediated the signalling cross talk through PI3K/Akt, ERK1/2, and NF- κ B/p65, which leads to antiapoptosis and NSC survival from ischemic stroke. Our finding gives a new evidence of GRP78 in NSCs as well as a new piece of signalling mechanism elucidation to NSC survival from ischemic stroke.

Stem cell survival after transplantation determines the efficiency of stem cell treatment, which develops as a novel potential therapy for several central nervous system (CNS) diseases in recent decades. The engrafted stem cells face the damage of oxidative stress, inflammation, and immune response at the lesion point in host. Among the damaging pathologies, oxidative stress directs stem cells to apoptosis and even death through several signalling pathways and DNA damage. However, the in-detail mechanism of stem cell survival from oxidative stress has not been revealed clearly. Here, in this study, we used hydrogen peroxide (H 2 O 2 ) to induce the oxidative damage on neural stem cells (NSCs). The damage was in consequence demonstrated involving the activation of heat shock protein 90 (HSP90) and NF- κ B/p65 signalling pathways. Further application of the pharmacological inhibitors, respectively, targeting at each signalling indicated an upper-stream role of HSP90 upon NF- κ B/p65 on NSCs survival. Preinhibition of HSP90 with the specific inhibitor displayed a significant protection on NSCs against oxidative stress. In conclusion, inhibition of HSP90 would attenuate NF- κ B/p65 activation by oxidative induction and promote NSCs survival from oxidative damage. The HSP90/NF- κ B mechanism provides a new evidence on rescuing NSCs from oxidative stress and also promotes the stem cell application on CNS pathologies.