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The objective of our study was to elucidate the possible underlying mechanism for the protective effect of ischaemic preconditioning (IPC) against ischaemia-reperfusion (I/R) injury and to provide new research perspectives of long non-coding RNAs (lncRNAs). In this study, serum and liver tissue samples were collected to measure indexes of liver injury from a mouse liver model in sham, I/R injury and I/R + IPC groups. Furthermore, liver samples from 5 randomly selected mice per group were extracted and subjected to the microarray and subsequent bioinformatics analysis. IPC ameliorated liver damage by lowered liver transaminase levels and pro-inflammatory cytokines. A total of 167 lncRNAs and 108 messenger RNAs (mRNAs) were significantly differentially expressed genes (DEGs) between the I/R + IPC and I/R groups. Gene Ontology (GO) analysis revealed that these genes were mainly related to unfolded proteins, responses to topologically incorrect proteins, responses to temperature stimuli, protein folding and protein refolding. Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway analysis indicated that the DEGs were enriched in the following pathways: protein processing in the endoplasmic reticulum; antigen processing and presentation; and fructose and mannose metabolism. Additionally, the 7 selected DEGs (Hspa1ab, Chka, Clec2h, Mvd, Adra1a, AK085737 and AK088966) were validated in modules of the lncRNA-mRNA weighted coexpression network, which agreed with the qRT–PCR and chip data. And the identified differentially expressed lncRNAs and mRNAs may provide new clues to understand the pivotal pathophysiological mechanism by which IPC alleviates I/R-caused liver damage. • Ischaemic preconditioning (IPC) attenuates the liver IR injury in mice. • The microarray identified markedly differentially expressed mRNAs and lncRNAs. • Functional analysis indicates lncRNAs participate in the effects of IPC. • A key gene cluster involves in IPC-mediated protection. • Some lncRNA-mRNA pairs relate to the protective effect of IPC. [ABSTRACT FROM AUTHOR]

[Display omitted] • A facile co-precipitation method is used to prepare catalysts with particles confined in cheap MOF. After calcination, more catalytic active sites could be exposed, which greatly improves the performance of the catalyst. • Compared with other methods, the co-precipitation method is simple, low-cost, and can better control the metal loading. At the same time, the problem of easy agglomeration of Cu nanoparticles and easy phase separation of Cu and ZnO at high temperature could be alleviated greatly. • The as-prepared Cu/ZnO x /ZrO 2 catalyst shows much better performance for CO 2 hydrogenation to methanol than the commercialized catalyst and catalyst prepared by double solvents method. The ternary Cu/ZnO/Al 2 O 3 catalyst is usually employed for producing methanol from syngas (CO/CO 2 /H 2) or from CO 2 hydrogenation in industry. However, this catalyst often suffers from the aggregation of Cu nanoparticles and the phase separation of Cu and ZnO. In this work, a highly efficient and stable catalyst (Cu/ZnO x /ZrO 2) for CO 2 hydrogenation to methanol is prepared via co-precipitation method with UiO-66 as structural template. Cu/Zn is effectively combined and encapsulated in the channels of UiO-66, which avoids the aggregation of metal particles. The ZrO 2 support derived from UiO-66 enhances the interaction between the support and Cu/Zn, and thus improves the catalytic performance significantly. This catalyst shows a high space–time yield of 216.7 g (MeOH) ·kg (cat) −1·h−1 at 260 °C, 4 MPa and GHSV = 12000 h−1. Furthermore, the catalyst shows good stability over a period of 50 h on stream. The performance of Cu/ZnO x /ZrO 2 is much better than that of commercial catalysts and most of catalysts previously reported. [ABSTRACT FROM AUTHOR]

Background The treatment of papillary thyroid microcarcinoma (PTMC) patients is controversial, as PTMC is often found incidentally and its prognosis is quite good. Because lymph node metastasis (LNM) is one of the main predictors of recurrence and impacts the survival rate of PTMC patients, this study aims to retrospectively identify the clinical factors that increase the risk of LNM and/or recurrence and can then be used to separate clinically unfavorable PTMCs from the rest and to help guide their treatment accordingly. Methods Clinical and pathologic data were collected from 3607 patients diagnosed with PTMC at Shanghai Renji Hospital between 2005 and 2015. Univariate and multivariate analyses were performed to identify the clinical predictors of LNM and survival rates were calculated by using the Kaplan–Meier method. Results Our univariate and multivariate analyses show that age of <45 y ( P < 0.01), gender of male ( P < 0.01), tumor diameter >0.7 cm ( P < 0.01), and multifocality ( P < 0.01) significantly increase the risk of central LNM. However, clinical factors, such as LNM, age, gender, multifocality, and operation range, do not affect the 10-y disease-free survival rate ( P > 0.05). Conclusions Clinical factors, such as gender of male, age of <45 y, multifocality, and tumor size >0.7 cm, suggest a higher risk of LNM; however, they do not affect PTMC patients’ 10-y disease-free survival rate. We recommend ipsilateral lobectomy to PTMC patients. For PTMC patients with higher LNM risk, preoperative central and lateral cervical lymph node imaging examination should be emphasized, and lymph node dissection is recommended. The range of dissection should be determined based on the imaging results. [ABSTRACT FROM AUTHOR]

Salicylic acid (SA) is an important signalling molecule that is synthesized by plants and induces the expression of resistance genes. The SA pathway is typically activated by DNA viruses as well as RNA viruses. Here, we demonstrated that heper-component protease (HC-Pro) encoded by tobacco vein banding mosaic virus (TVBMV) decreases in DNA methylation at the promoters of the regulators ACD6 and NPR1 in the SA pathway. We found that the overexpression of HC-Pro increases the expression of components in the SA pathway in plants. The results revealed that HC-Pro interferes in DNA methylation and activates the SA pathway in the HC-Pro transgenic plants and TVBMV-infected plants. We further found that the accumulation of siRNAs derived from the promoter repeats of ACD6 and NPR1 is greatly reduced in the HC-Pro plants. Our results suggested that HC-Pro-mediated interference with DNA methylation is likely caused by a reduction in accumulation of siRNAs. [ABSTRACT FROM AUTHOR]

Recently, the carbodiimide-mediated coupling method has attracted the attention of some scholars in the food field for its safety and high efficiency. In this study, the carbodiimide method was utilized to assemble zein–polyphenol conjugates innovatively. The covalent insertion of polyphenols to zein was confirmed by the increase of molecular weight and the reduction of nucleophilic groups. Chlorogenic acid (CGA) as well as Gallic acid (GA) were selected as polyphenol models, and the total phenolic content of zein–CGA conjugate and zein–GA conjugate reached 71 mg/g and 43 mg/g, individually. Afterwards, the structural and chemical characteristics between zein–polyphenol conjugates and physical mixtures were compared. Scanning electron microscopy (SEM) indicated that zein–polyphenol conjugates formed regularly shaped spheres with small particle sizes. Compared with control zein and physical mixtures, zein–polyphenol conjugates demonstrated better solubility and dispersibility, higher thermal stability as well as lower surface hydrophobicity. In terms of antioxidant capacity, zein–GA conjugate showed higher scavenging abilities of ABTS and DPPH free radicals than zein–CGA conjugate. The present research developed a new approach to fabricating zein–polyphenol conjugates that can be applied in the food industry as functional additives or materials for delivery systems. • Zein–polyphenol conjugates had high polyphenol contents and grafting efficiencies. • The properties of zein were affected by reaction types and polyphenol structures. • The conjugation of polyphenols greatly improved the antioxidant potential of zein. • The conjugates showed better solubility and thermal stability than physical mixtures. [ABSTRACT FROM AUTHOR]

Elemental doping has been proven to be an effective strategy for increasing the catalytic activity and structural stability of Fenton catalysts. Therefore, this work reports that Mn-doped FeS 2 /Fe 2 O 3 (Mn 3 O 4 –FeS 2 /Fe 2 O 3) has excellent catalytic performance for the degradation of Orange II under simulated solar energy. Degradation experiment results showed that the sample with a manganese-iron molar ratio of 1:2 exhibited higher activity than others. The degradation rate of 20 mg/L OII reached 99.0% in 18 min under the conditions of 0.3 g/L Mn 3 O 4 –FeS 2 /Fe 2 O 3 , 5 mM H 2 O 2 and pH = 2.8. In addition to, the Mn 3 O 4 –FeS 2 /Fe 2 O 3 catalyst shows good reusability for Orange II and high activity for other dyes (MB, MG, Rh B and MO) under optimal conditions. Degradation mechanism study indicated that the heterogeneous Fenton reaction was promoted by retarding the recombination of photogenerated charge carriers and accelerating the cycle between Fe3+/Mn2+ and Fe2+/Mn3+, which improved photo-Fenton-like catalytic performance, resulting in the enhanced degradation of organic pollutant. Finally, a possible degradation pathway was proposed according to the results of liquid chromatography-mass spectrometry (LC-MS). In short, the catalyst has potential application value in wastewater treatment. • The degradation of Orange II by Mn 3 O 4 –FeS 2 /Fe 2 O 3 attained to 99.0% in 18 min. • Both.•OH and •O 2 − played important roles in the degradation process. • The photo-Fenton-like catalytic performance of the Mn 3 O 4 –FeS 2 /Fe 2 O 3 catalyst was enhanced. • The catalyst maintained excellent reusability for Orange II and high activity for other dyes. [ABSTRACT FROM AUTHOR]

Individuals with type 2 diabetes mellitus frequently display heightened levels of palmitic acid (PA) in their serum, which may lead to β-cell damage. The involvement of ferroptosis, a form of oxidative cell death in lipotoxic β-cell injury remains uncertain. Here, we have shown that PA induces intracellular lipid peroxidation, increases intracellular Fe2+ content and decreases intracellular glutathione peroxidase 4 (GPX4) expression. Furthermore, PA causes distinct changes in pancreatic islets and INS-1 cells, such as mitochondrial atrophy and increased membrane density. Furthermore, the presence of the ferroptosis inhibitor has a significant mitigating effect on PA-induced β-cell damage. Mechanistically, PA increased ceramide content and c-Jun N-terminal kinase (JNK) phosphorylation. The ceramide synthase inhibitor effectively attenuated PA-induced β-cell damage and GPX4/Fe2+ abnormalities, while inhibiting JNK phosphorylation. Additionally, the JNK inhibitor SP600125 improved PA-induced cell damage. In conclusion, by promoting ceramide synthesis, PA inhibited GPX4 expression and increased intracellular Fe2+ to induce β-cell ferroptosis. Moreover, JNK may be a downstream mechanism of ceramide-triggered lipotoxic ferroptosis in β-cells. • Ferroptosis is implicated in the lipotoxic damage of β cells. • Palmitic acid induces ferroptosis in β-cell through the GPX4/Fe2+ pathway. • Ceramide plays a crucial role in the induction of ferroptosis in lipotoxic β cells. • JNK is involved in lipotoxic β-cell ferroptosis. [ABSTRACT FROM AUTHOR]

In this paper, we described an integrated modularized microfluidic system that contained two distinct functional modules, one for nucleic acids (NA) extraction and the other for digital PCR (dPCR), allowing for detecting the bovine DNA in ovine tissue. [ABSTRACT FROM AUTHOR]

Objectives Upregulated expression of CC chemokine receptor (CCR)3 was observed in osteoarthritis (OA) cartilage and chondrocytes, but expression of CCR3 on synovial tissue of OA remains unknown. Fibroblast-like synoviocyte (FLS) invasion in synovium appears one of the features of OA, but expression and function of CCR3 on FLS remain uninvestigated. We therefore explored them in the present study. Methods Enzymatically dispersed synovial tissue cells were analyzed by flowcytometry. Primary cultured FLS isolated from OA synovium were challenged and the expression of CCR3, eotaxin-1 and matrix metalloproteinase (MMP)-9 was determined by quantitative real-time PCR (qPCR) and ELISA. Results Approximately 4.5% dispersed OA synovial tissue cells are CCR3+ cells. Among them, 58.4% cells are CD90+CD14−CD3− cells (representing FLS) and 36.7% are CD8+ cells, indicating that FLS are major population of CCR3+ cells in the synovial tissue. Levels of eotaxin-1 and MMP-9 in OA synovial fluid (SF) were greater than that in OA plasma and in healthy control (HC) plasma. Eotaxin-1 induced up to 5.8 and 7.2-fold increases in the expression of MMP-9 mRNA and protein, respectively following 12 h incubation with FLS, which was inhibited by antagonist of CCR3 SB328437 and an inhibitor of ERK U0126, indicating that action of eotaxin-1 on FLS seemed via CCR3 and ERK signaling pathway. IL-1β and TNF-α was found to elicit release of eotaxin-1 from OA FLS. Conclusion FLS via eotaxin-1 and its receptor CCR3 plays an important role in the pathogenesis of OA, which strengthen the concept that OA is likely an inflammation related disease. [ABSTRACT FROM AUTHOR]