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Polyacrylonitrile pre-oxidized fiber（PANOF）is an emerging flame retardant material with low cost and high performance，showing a promising application potential as thermal protection materials in the aerospace field.Pretreated PANOF（t-PANOF）was obtained by the process of oil removing with acetone and surface modification using silane coupling agent KH570 in turn.Scanning electron microscopy（SEM），Fourier transform infrared spectroscopy（FT-IR）and X-ray photoelectron spectroscopy（XPS）were employed to figure out the changes of morphology and chemical structure of the fibers before and after pretreatment and their interfacial properties with silicone rubber（SR）.Effects of t-PANOF on the mechanical and thermal performances of SR were further investigated. With the presence of ceramic forming agent（CFA），the ablation responsive behaviors of CFA/t-PANOF/SR ternary composites were researched as well.The results show that the level of interfacial adhesion between fibers and rubber is significantly enhanced contributed from the pretreatment of PANOF，and the tensile strength of the composites is improved accordingly.However，with the increasing content of t-PANOF，the comprehensive mechanical properties of t-PANOF/SR composites show the trend that increase first and then decrease，indicating that the optimal dosage of the fibers is 5 to 10 phr.t-PANOF skeleton helps to not only enhance the dimensional stability of SR in high temperature and oxygen-rich environment，but also improve the ablation performance of CFA/t-PANOF/SR composites.The antioxidation ceramic layer with fiber skeleton as the main structure is formed on the surface of CFA/t-PANOF/SR composites under the high temperature aerobic gas with the heat flux density of 2 MW/m2，the corresponding linear and mass ablation rate are only 0.02 mm/s and 0.02 g/s respectively，which is expected to be utilized as an ablation material to satisfy the demands of the new generation of aerospace vehicles.

High-cholesterol diet (HCD) and fine particulate matter (PM2.5) are related to stroke. However, little is known about the combined effects of stroke, especially for females. This study investigated the brain injuries in Apolipoprotein E−/− (ApoE−/−) female mice exposed to HCD plus PM2.5 for 6 months. The protein levels of the genes related to stroke and the blood–brain barrier (BBB) in different groups of mice were measured. The molecular regulation mechanisms were explored. The results showed that HCD and PM2.5 co-exposure altered brain–body weight ratio, behavior, brain pathology, and inflammatory markers in mice relative to exposure to HCD or PM2.5 alone. Co-exposure significantly changed the expressions of HIF-1α and the key genes in its signaling pathway in the brains of mice compared to the single exposure. It suggests that the HIF-1α pathway exerts an important regulatory role in brain injury and behavioral abnormality in female mice after 6-month exposure to HCD plus PM2.5, which are potential mechanisms for HCD and PM2.5-triggering stroke in female individuals. [ABSTRACT FROM AUTHOR]

The atmosphere's fine particulate matter (PM2.5) can enter the liver through the circulatory system, leading to hepatic inflammation and fibrosis. As a non-flavonoid polyphenolic compound, resveratrol (RES) has anti-oxidant, anti-inflammatory and hepatoprotective effects, but the molecular mechanisms of liver fibrosis induced by PM2.5 exposure are still limited. In this study, we established an in vitro cell model to investigate the intervention effect of RES with different concentrations (5 and 20 μmol/mL) on mouse hepatic stellate cells (mHSCs) injury induced by PM2.5 (100 μg/mL). We determined the cell viability in mHSCs after treatment with PM2.5 or/and RES for 24 h. We investigated the intracellular oxidative stress by detecting the changes in reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) and lactate dehydrogenase (LDH) levels. We also measured the protein expressions of fibrosis-related genes (α-SMA, Collagen I and Collagen III) and key genes (SIRT1, NF-κB, NLRP3, Cleaved-Caspase1, IL-1β) in the NLRP3 pathway in mHSCs exposed to PM2.5 with or without RES. The results showed that (1) PM2.5 has cytotoxic effects on mHSCs, whereas RES (5 μmol/L and 20 μmol/L) inhibited PM2.5-induced cytotoxicity and LDH leakage; (2) RES effectively reduces ROS and MDA production caused by PM2.5 while concurrently enhancing SOD levels, thereby improving cellular anti-oxidant capacity; (3) the expression of α-SMA, Collagen I and Collagen III were notably downregulated in the PM2.5 plus RES treatment group compared to the PM2.5-exposed group; (4) RES significantly increased SIRT1 expression and decreased the expression of NF-κB, NLRP3, Cleaved-Caspase1 and IL-1β in mHSCs exposure to PM2.5 compared to the PM2.5 group. These results demonstrate that RES can up-regulate SIRT1 and mitigate PM2.5-induced fibrosis by suppressing oxidative stress in mHSCs and the SIRT1/NF–κB/NLRP3 pathway activated by PM2.5. [ABSTRACT FROM AUTHOR]

This paper aims to investigate the impact of CQ on type 2 inflammatory response in MC903-induced AD mice. Methods: An AD mouse model was established via MC903 induction. After CQ treatment, AD mice were intraperitoneally injected with polyinosinic: polycyclic acid [poly (I:C)] or Nigericin. Dermatitis severity was scored, and the thickness of the left ear was measured. The pathological changes in mouse skin tissues were observed by H&E staining. The number of mast cells was counted via TB staining. The content of peripheral blood T-helper 2 (Th2) cells and levels of immunoglobulin E (IgE), thymic stromal-derived lymphopoietin (TSLP), interleukin (IL)-4, IL-13, interferon (IFN)-γ, IL-1β, and IL-18 were assessed by flow cytometry and ELISA. The levels of toll-like receptor 3 (TLR3), NLRP3, ASC, and cleaved caspase-1 proteins in skin tissues were determined by Western blot. Results: CQ treatment abated dermatitis severity and left ear thickness in AD mice, alleviated skin damage, reduced mast cell number, diminished IgE, TSLP, IL-4, and IL-13 levels, and peripheral blood Th2 cell content, with no significant changes in IFN-γ level. CQ alleviated type 2 inflammatory response in AD mice by inhibiting the activation of TLR3. CQ suppressed NLRP3 inflammasome activation. Activating TLR3/NLRP3 annulled CQ-mediated alleviation on type 2 inflammatory response in AD mice. Conclusion: CQ alleviated type 2 inflammatory response in AD mice by inhibiting TLR3 activation and NLRP3 inflammasome activation. [ABSTRACT FROM AUTHOR]

Phosphorus is an element essential to sustaining life, and its compounds are widely involved in the biogeochemical cycles on Earth. Although a handful of phosphorus-bearing species, e.g. PO, have thus far been detected in diatomic form in circumstellar envelopes, their formation processes are still poorly understood. In this study, we examine the structure and spectroscopy of the [Si, O, P] system. Based on high-level ab initio electronic structure calculations with the MRCI + Q and CCSD(T) methods, four isomers could be formed and the most stable form predicted to be bent at all theoretical levels. The doublet and quartet potential energy surfaces (PESs) of P(2D)/P(4S) + SiO(1Σ) reactions are explored, and the spectroscopic parameters of the key isomers involved in the reaction are calculated. The present study highlights the possibility of PO formation via photodissociation of bent-SiOP. The results are expected to aid in the spectroscopic detection of these triatomic phosphorous-bearing species and provide insights into similar reactions of isoelectronic systems. [ABSTRACT FROM AUTHOR]