Swellable Array Strategy Based on Designed Flexible Double Hypercross-linked Polymers for Synergistic Adsorption of Toluene and Formaldehyde.

High-capacity adsorption and removal of complex volatile organic compounds (VOCs) from real-world environments is a tough challenge for researchers. Herein, a swellable array adsorption strategy was proposed to realize the synergistic adsorption of toluene and formaldehyde on the flexible double hypercross-linked polymers (FD-HCPs). FD-HCPs exhibited multiple adsorption sites awarded by a hydrophobic benzene ring/pyrrole ring and a hydrophilic hydroxyl structural unit. The array benzene ring, hydroxyl, and pyrrole N sites in FD-HCPs effectively captured toluene and formaldehyde molecules through π-π conjugation and electrostatic interaction and weakened their mutual competitive adsorption. Interestingly, the strong binding force of toluene molecules to the skeleton deformed the pore structure of FD-HCPs and generated new adsorption microenvironments for the other adsorbate. This behavior significantly improved the adsorption capacity of FD-HCPs for toluene and formaldehyde by 20% under multiple VOCs. Moreover, the pyrrole group in FD-HCPs greatly hindered H2O molecule diffusion in the pore, thus efficiently weakening the competitive adsorption of H2O toward VOCs. These fascinating properties enabled FD-HCPs to achieve synergistic adsorption for multicomponent VOC vapor under a highly humid environment and overcame single-species VOC adsorption properties on state-of-the-art porous adsorbents. This work provides the practical feasibility of synergistic adsorption to remove complex VOCs in real-world environments.

Adaptive energy filtering method based on time-domain image sequences for high-accuracy spot target localization.

High-accuracy spot target localization is an essential optical measurement technique in fields such as astronomy and biophysics. Random noise generated during the imaging process limits further improvement of centroiding accuracy. Research for centroiding methods can no longer meet the demand for higher accuracy. This limitation is even more severe for low signal to noise ratio (SNR) imaging measurements. This paper proposes an energy filtering method based on time-domain extended image sequences, which is a typical application such as a star tracker. The energy variations of the spot in continuous sequences are analyzed, and the energy is filtered at pixel level. The filtered pixel response that is closer to real energy is involved in the calculation of the centroid. Adaptive variations of filter parameters for different energy distributions are also realized. Both simulations and laboratory experiments are designed to verify the effectiveness of the approach. The results show that this method can effectively and adaptively filter the spot energy at pixel level and further improve centroiding accuracy.

CMOS imager non-uniformity response correction-based high-accuracy spot target localization.

High-accuracy spot target detection based on a complementary metal-oxide semiconductor (CMOS) image sensor, such as astronomy magnitude, medicine, and astronomy photometrics, needs accurate pixel response. Because pixels have different silicon structures and read outputting, each pixel has non-uniformity response with specific illumination. The flat-field correction of a CMOS image sensor is crucial before image processing. In this work, a flat-field model and correction method based on spot scale areas of CMOS image sensor pixel response are proposed. Compared with traditional full-plane calibration, this method aims at spot areas to fit most selected normal pixels' mean response curve with different light intensities and exposure times, which can guarantee spot imaging areas with higher accurate pixel response. Finally, the accuracy of this flat-field correction method is evaluated by the influence on spot target extraction accuracy. The experimental results indicate that using this flat-field correction method can decrease the non-uniform variance from 7.34 (LSB/10 bit) to 1.91 (LSB/10 bit) (improved by 74.1%) and reduce the noise effect on spot extraction accuracy, which improves it from 0.3453 pixel to 0.0116 pixel (1σ). The proposed approach solves the problem of non-uniform pixel response and improves imaging SNR for high-accuracy spot target localization.

Suppression of stray light based on energy information mining.

The star tracker plays a critical role in precision aerospace missions due to its high accuracy, absolute attitude output, and low power consumption. For an optical sensor, the problem of stray light is always an important research issue. A star energy information mining method for stray light suppression is proposed in this study. The gray-level co-occurrence matrix and k-nearest neighbor algorithm are adopted to identify the types of stray light that enter the optical system. Effective recognition of the stray light types is an important premise for the following steps. Then the parameters are optimized during background estimation. When star spots are extracted, the local differential encoding combined with Levenshtein distance filtering is conducted to eliminate the interference noise spots. The proposed algorithm can achieve accurate star spot extraction even when stray light exists in real night sky observation experiments.

Hydrogen regulates mitochondrial quality to protect glial cells and alleviates sepsis-associated encephalopathy by Nrf2/YY1 complex promoting HO-1 expression.

BACKGROUND: Sepsis-associated encephalopathy (SAE) is a complication of the central nervous system in patients with sepsis. Currently, no effective treatment for sepsis is available. Hydrogen plays a protective role in different diseases; however, the detailed mechanism of hydrogen-treated disease remains unclear. The purpose of this study was to investigate the effect of hydrogen on SAE in vitro and in vivo and the mechanism of hydrogen in mitochondrial dynamics and its function in astrocytes and microglia stimulated by lipopolysaccharides (LPSs). METHODS: Animal models of SAE were generated by cecal ligation and puncture, and the SAE model was established by in vitro LPS stimulation. MTT, lactate dehydrogenase (LDH), reactive oxygen species (ROS), heme oxygenase-1 (HO-1) activity, mitochondrial membrane potential (MMP), and cell apoptosis assays were used to determine the effect of hydrogen on astrocytes and microglia stimulated by LPSs. The relationships between nuclear factor erythroid 2-related factor 2 (Nrf2), YY1, and HO-1 were examined by chromatin immunoprecipitation and co-immunoprecipitation. Mitochondrial homeostasis-related proteins in LPS-stimulated glial cells and brain tissues of SAE mice were detected by western blotting. The effects of hydrogen treatment in the SAE mouse model were investigated using Morris water maze and Y-maze analyses. RESULTS: After performing experiments with different concentrations of LPSs in vitro, we selected 1000 ng/ml for subsequent experiments. Hydrogen attenuated the increase in ROS, LDH, and apoptosis and promoted decreases in cell activity and MMP, further promoting an increase in HO-1 expression induced by LPSs in astrocytes and microglia. Moreover, hydrogen further promoted the expression of Nrf2, HO-1, PGC-1α, TFAM, PARKIN, and PINK1, inhibited LPS-induced OPA1 and MFN2 expression in astrocytes and microglia, and downregulated the expression of DRP1 after LPS induction. Intriguingly, hydrogen treatment enhanced the binding between Nrf2 and YY1. However, silencing Nrf2 or YY1 abolished the protective effects of hydrogen on cell activity, LDH, ROS, and MMP; apoptosis; and regulation of Nrf2, HO-1, PGC-1α, TFAM, OPA1, DRP1, MFN2, PARKIN, and PINK1 in microglia. Finally, hydrogen treatment improved the results of behavioral detection, apoptosis, Nrf2, HO-1, PGC-1α, TFAM, OPA1, DRP1, MFN2, PARKIN, PINK1, and cytokines in SAE in vivo. CONCLUSIONS: Hydrogen improved cell injury and mitochondrial quality, which were associated with HO-1 expression promoted by the Nrf2/YY1 complex in vitro. Thus, hydrogen treatment may represent a novel therapeutic method for treating SAE.

Accelerating the Fe(III)/Fe(II) cycle via enhanced electronic effect in NH2-MIL-88B(Fe)/TPB-DMTP-COF composite for boosting photo-Fenton degradation of sulfamerazine.

In the photo-Fenton reactions, fast recombination of photoinduced electrons and holes in Fe-based metal-organic frameworks (Fe-MOFs) slows Fe(III)/Fe(II) cycle, which remains big challenge that significantly retards the overall process. Herein, NH2-MIL-88B(Fe) (NM88) was modified with 3,5-diaminobenzoic acid (DB) and TPB-DMTP-COF (COF-OMe) to in situ construct NM88(DB)0.85/COF-OMe composite that could strongly harvest the visible light for photo-Fenton degradation of sulfamerazine (SMR). With the addition of DB, electron-donating effect of NM88 was strengthened, which then promoted amino groups to react with aldehyde groups (Schiff-base), and thus highly facilitated the interfacial contact between NM88 and COF-OMe. Such modifications increased the degradation rate constants for NM88(DB)0.85/COF-OMe to 15.1 and 17.3 times that of NM88 and COF-OMe respectively with good reusability. Moreover, the catalyst exhibited 32-170 times higher degradation kinetics in comparison to other reported catalysts. Results showed that due to the Schiff-base reaction between NM88(DB) and COF-OMe, electron density on Fe(III) was decreased; and the photogenerated electrons of COF-OMe moved to NM88(DB) to reduce Fe(III), thus resulting in the generation of highly active Fe(II) and ·OH species. Furthermore, the main reactive species were determined to be ·OH and ·O2- by trapping experiments, and a possible mechanism of the degradation system followed Z-scheme charge transfer.

Corrigendum: CircAFF1 aggravates vascular endothelial cell dysfunction mediated by miR-516b/SAV1/YAP1 axis.

[This corrects the article DOI: 10.3389/fphys.2020.00899.].

Downregulation of circFASTKD1 ameliorates myocardial infarction by promoting angiogenesis.

Circular RNAs (circRNAs), a novel class of endogenous long non-coding RNAs, have attracted considerable attention due to their closed continuous loop structure and potential clinical value. In this study, we investigated the function of circFASTKD1 in vascular endothelial cells. CircFASTKD1 bound directly to miR-106a and relieved its inhibition of Large Tumor Suppressor Kinases 1 and 2, thereby suppressing the Yes-Associated Protein signaling pathway. Under both normal and hypoxic conditions, the ectopic expression of circFASTKD1 reduced the viability, migration, mobility and tube formation of vascular endothelial cells, whereas the downregulation of circFASTKD1 induced angiogenesis by promoting these processes. Moreover, downregulation of circFASTKD1 in mice improved cardiac function and repair after myocardial infarction. These findings indicate that circFASTKD1 is a potent inhibitor of angiogenesis after myocardial infarction and that silencing circFASTKD1 exerts therapeutic effects during hypoxia by stimulating angiogenesis in vitro and in vivo.

circAFF1 Aggravates Vascular Endothelial Cell Dysfunction Mediated by miR-516b/SAV1/YAP1 Axis.

Pathological vascular endothelial damage caused by hypoxia is the basis of many vascular-related diseases. However, the role of circular RNA in hypoxic vascular injury is still poorly understood. Here, we found that hypoxia induced AFF1 circular RNA (circAFF1) can activate the SAV1/YAP1 and lead to the dysfunction of vascular endothelial cells. In HUV-EC-C and HBEC-5i cells, circAFF1 was upregulated under CoCl2 induced hypoxic conditions. The abnormal expression of circAFF1 inhibited the proliferation, tube formation, migration of vascular endothelial cells. The effect of circAFF1 is achieved by the adsorption of miR-516b to release SAV1, which in turn causes the phosphorylation of YAP1. Moreover, we found that the upregulation of circAFF1 in 235 Patients with subarachnoid hemorrhage. Taken together, we clarify the role of circAFF1/miR-516b/SAV1/YAP1 axis in vascular endothelial dysfunction and its potential early diagnostic value of disease caused by hypoxia injury in blood vessels.