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This study provides a rapid and low-energy method for the preparation of nanocomposite hydrogels with excellent mechanical properties and electrical conductivity.

In this study, a simple and rapid method was proposed to prepare conductive composite hydrogels with excellent mechanical properties and pH response.

Deep eutectic solvent (DES) was synthesized from choline chloride (ChCl) and acrylamide (AM), and P(AM-co-MA) hydrogels were prepared by adding different contents of maleic acid (MA) to DES by frontal polymerization.

A deep eutectic solvent (DES) was synthesized from urea (U), acrylamide (AM), and choline chloride (ChCl). ZnO was dispersed in the DES as a filler, and nanocomposite hydrogels (ZnO/P(U-AM-ChCl)) were successfully prepared by frontal polymerization (FP). The hydrogels were verified by Fourier infrared spectroscopy to contain ZnO nanoparticles (ZnO-NPs). The swelling behaviour, conductivity, and antibacterial properties of the ZnO nanocomposite hydrogels were investigated. The results showed that the ZnO/P(U-AM-ChCl) hydrogels had excellent antibacterial properties and exhibited super high inhibition rates of 81.87% and 88.42% against two basic colonies of Gram-negative and Gram-positive bacteria, respectively. The equilibrium swelling of the hydrogels was found to increase significantly from 9.30 to 12.29 with the addition of ZnO, while the ZnO/P(U-AM-ChCl) hydrogel conductivity exhibited good UV sensitivity. This study provides a rapid and low-energy method for the preparation of nanocomposite hydrogels with excellent antibacterial properties.

Broadband sound absorption has consistently been a challenge in designing underwater sound absorption structure (USAS). Most research of USASs achieve broadband sound absorption through structural optimization, which curbs the freedom of designing, and commonly alights it at the expense of increased thickness. In this paper, a method is reported to broaden the frequency band of the USAS by embedding a membrane-type resonator into the cavity, which forming a membrane-type underwater acoustic absorption metamaterial. We demonstrate the mechanism of membrane-type metamaterial by theory, and verify it by simulation and experiment. The experimental results show that the sound absorption coefficient in the frequency range of 2000–10 000 Hz is significantly improved after implanting the membrane-type resonator into the cavity. The average sound absorption coefficient is increased by nearly 17%, and the improvement effect of the sound absorption covers to each frequency point, which is consistent with our expectation. As the case of applying membrane-type metamaterials to the design process of underwater acoustic structures, this research possesses great application potential in acoustic wave communication and device compatibility design technologies.

Context α-Hederin, a potent bioactive compound of Pulsatilla chinensis (Bunge) Regel (Ranunculaceae), has many pharmacological uses, but its effect on cancer cell metabolism is still unclear. Objective To elucidate the role of α-hederin in the glucose metabolism of lung cancer cells. Materials and methods Cell Counting Kit 8 and colony formation assays were employed to assess the antiproliferative effects of α-hederin. Glucose uptake, ATP generation, and lactate production were measured. Glycolysis-related proteins were detected using western blotting, and a sirtuin 6 (SIRT6) inhibitor was used to verify A549 cell proliferation. Sixty male BALB/c nude mice were divided into normal control, 5-FU (25 mg/kg), and α-hederin (5 and 10 mg/kg) groups to assess the antitumor effect for 32 days. Glycolysis-related protein expression was evaluated using immunohistochemical analysis. Results α-Hederin inhibited A549 (IC50 = 13.75 μM), NCI-H460 (IC50 = 17.57 μM), and NCI-H292 (IC50 = 18.04 μM) proliferation; inhibited glucose uptake and ATP generation; and reduced lactate production. Furthermore, α-hederin (10 and 15 μM) markedly inhibited hexokinase 2, glucose transporter 1, pyruvate kinase M2, lactate dehydrogenase A, monocarboxylate transporter, c-Myc, hypoxia-inducible factor-1α, and activated SIRT6 protein expression. Using a SIRT6 inhibitor, we demonstrated that α-hederin inhibits glycolysis by activating SIRT6. A tumour xenograft mouse model of lung cancer confirmed that α-hederin (5 and 10 mg/kg) inhibits lung cancer growth by inhibiting glycolysis in vivo. Discussion and conclusions α-Hederin inhibits A549 cell growth by inhibiting SIRT6-dependent glycolysis. α-Hederin might serve as a potential agent to suppress cancer.

Background: α-hederin an effective component of Pulsatilla chinensis (Bunge) Regel, Studies showed that α-hederin exert many pharmacological activities, However, the effect of α-hederin on metabolism is still unclear. This study aimed to illuminate the role of α-hederin in glucose metabolism in lung cancer cells and investigate the molecular mechanism of α-hederin. Methods: CCK8 and colony formation assays were employed to assess the anti-proliferative effects induced by α-hederin. Glucose uptake, ATP generation, and reduced lactate production were measured using kits, and an A549 tumor xenograft mouse model of lung cancer was used to assess the in vivo antitumor effect of α-hederin (5, 10 mg/kg). Glycolytic-related key enzymes hexokinase 2 (HK2), glucose transporters 1 (GLUT1), pyruvate kinase M2 (PKM2), lactate dehydrogenase A (LDHA), monocarboxylate transporter (MCT4), c-Myc, Hypoxia inducible factor-1α (HIF-1α) and Sirtuin 6 (SIRT6) protein expression were detected by western blotting and immunohistochemical staining and SIRT6 inhibitors was verified in A549 cells. Results: Our results showed that cell proliferation was significantly inhibited by α-hederin in a dose-dependent manner and that α-hederin inhibited glucose uptake and ATP generation and reduced lactate production. Furthermore, α-hederin remarkably inhibited HK2, GLUT1, PKM2, LDHA, MCT4, c-Myc, HIF-1α and activated SIRT6 protein expression. Using inhibitors, we proved that α-hederin inhibits glycolysis by activating SIRT6. Moreover, a tumor xenograft mouse model of lung cancer further confirmed that α-hederin inhibits lung cancer growth via inhibiting glycolysis in vivo. Conclusions: α-hederin inhibits the growth of non-small cell lung cancer A549 cells by inhibiting glycolysis. The mechanism of glycolysis inhibition includes α-hederin activating the expression of the glycolytic related protein SIRT6.

The problem of person re-identification has attracted a lot of attention in the field of machine vision. In practice, the non-overlapping sample images change drastically and the sample size is small, which makes the metric model overfitting phenomenon. In this paper, based on the k-NN and the sample normality property, we propose a resampling linear discriminant analysis (LDA) algorithm to suppress the local constraints caused by small samples, then train it to obtain the person re-identification metric learning model. A semi-supervised LDA algorithm with semi-supervised characteristics is developed by optimizing the inter-class scatter for weighting. A joint distance metric-based approach is also proposed to learn both the Mahalanobis distance and Euclidean distance. The improved algorithm is tested on the VIPeR and CUHK01 datasets, and the results indicate that, despite the change in the total number of training samples, the algorithm in this paper shows high recognition accuracy.

Anemoside B4 (B4) is a compound extracted from Pulsatilla chinensis(P. chinensis). Pharmacological studies have proved that it has certain anti-inflammatory activity. Acute ulcerative colitis (ulcerative colitis) is a non-specific inflammatory disease whose pathogenesis is not completely known, and there is no effective drugs. The purpose of this study was to investigate the protective effect of B4 on ulcerative colitis and its mechanism. In this study, the C57BL/6 mice model of ulcerative colitis was established by DSS [3% (w/v)] and treated with intraperitoneal injection of B4 and oral administration of mesalazine, respectively. During the experiment, the clinical symptoms of the mice were scored by the disease activity index (DAI). Histopathological changes were observed by HE staining. In addition, the effect of LPS on Raw264.7 cells was also studied. In vivo studies showed that B4 could prevent DSS-induced colitis mice from losing weight, shortening colon length and improving pathological changes of colon tissues. B4 significantly reduced levels of inflammatory cytokines IL-1β, IL-6, and TNF-α in colon tissues. In vitro experiments, B4 was almost nontoxic to Raw264.7 cells and could protect the Raw264.7 cells induced by LPS. In terms of mechanism, B4 significantly inhibited the activation of the TLR4 signaling pathway induced by DSS and down-regulate the expression of key proteins in the TLR4/NF-κB/MAPK signaling pathway in Raw264.7 cells induced by LPS. These findings suggest that the inhibition of B4 on ulcerative colitis may be through the TLR4/NF-κB/MAPK pathway. Therefore, B4 may be used as a potential drug for the treatment of ulcerative colitis.