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Flower scent is one of the main ornamental characteristics of herbaceous peony, and the improvement of flower fragrance is a vital objective of herbaceous peony breeding. In this study, 87 herbaceous peony cultivars were divided into three groups (no/light fragrance, medium fragrance, and strong fragrance) based on their sensory evaluation scores, and 16 strong fragrance cultivars and one no fragrance cultivar were selected for subsequent analysis. Sixty-eight volatile components were detected in these 17 cultivars based on solid-phase microextraction (SPME) and gas chromatography/mass spectrometry (GC/MS), and 26 types were identified as important scent components. They were composed of terpenoids, benzenoids/phenylpropanoids, and fatty acid derivatives. According to the content and odor threshold of these main aroma components, the characteristic aroma substances of herbaceous peony were identified, including linalool, geraniol, citronellol, and phenylethyl alcohol (2-PE). The cultivars of strong scented herbaceous peony were divided into three types: rose scent, lily scent, and mixed scent. We explored the possible key genes of characteristic aroma substances in herbaceous peony petals with different odors through the qRT-PCR. The key genes encoding monoterpene biosynthesis were found to be PlDXS2, PlDXR1, PlMDS1, PlHDR1, PlGPPS3, and PlGPPS4. In addition, the linalool synthase (LIS) gene and the geraniol synthase (GES) gene were also found. PlAADC1, PlPAR1, and PlMAO1, related to the biosynthesis of 2-PE were detected, and the synthetic pathway of 2-PE was speculated. In conclusion, these findings revealed that the difference in gene expression of monoterpene and 2-PE synthesis pathway was related to the difference in the fragrance of herbaceous peony. This study explored the releasing pathway of herbaceous peony characteristic aroma substances and provided key genetic resources for fragrance improvement. [ABSTRACT FROM AUTHOR]

Pyrrole-ligated 1,3,4-oxadiazole is a very important pharmacophore which exhibits broad therapeutic effects such as anti-tuberculosis, anti-epileptic, anti-HIV, anti-cancer, anti-inflammatory, antioxidant, and antibacterial activities. A one-pot Maillard reaction between D-Ribose and an L-amino methyl ester in DMSO with oxalic acid at 2.5 atm and 80 °C expeditiously produced pyrrole-2-carbaldehyde platform chemicals in reasonable yields, which were utilized for the synthesis of pyrrole-ligated 1,3,4-oxadiazoles. Benzohydrazide reacted with the formyl group of the pyrrole platforms to provide the corresponding imine intermediates, which underwent I2-mediated oxidative cyclization to the pyrrole-ligated 1,3,4-oxadiazole skeleton. The structure and activity relationship (SAR) of the target compounds with varying alkyl or aryl substituents of the amino acids and electron-withdrawing or electron-donating substituents on the phenyl ring of benzohydrazide were evaluated for antibacterial activity against Escherichia coli, Staphylococcus aureus, and Acinetobacter baumannii as representative Gram(–) and Gram(+) bacteria. Branched alkyl groups from the amino acid showed better antibacterial activities. Absolutely superior activities were observed for 5f-1 with an iodophenol substituent against A. baumannii (MIC < 2 μg/mL), a bacterial pathogen that displays a high resistance to commonly used antibiotics. [ABSTRACT FROM AUTHOR]

Reference 1 Gu L, Sang Y, Nan X. circCYP24A1 facilitates esophageal squamous cell carcinoma progression through binding PKM2 to regulate NF- B-induced CCL5 secretion. Correction: circCYP24A1 facilitates esophageal squamous cell carcinoma progression through binding PKM2 to regulate NF- B-induced CCL5 secretion 6 circCYP24A1 interacts with PKM2 and promotes NF- B pathway-mediated CCL5 secretion in vitro. a Binding of CYP24A1 with PKM2 was idntified by RNA pull-down-western blot analysis. b The co-localization of circCYP24A1 (red) with PKM2 (green) in KYSE30 and TE1 cells was idntified by RNA FISH-immunofluorescence. c Protein levels in ESCC cells with circCYP24A1 overexpression or PKM2 knockdown. d mRNA and protein levels of CCL5 in ESCC cells with circCYP24A1 overexpression or PKM2 knockdown. e The proliferation ability of ESCC cells with circCYP24A1 overexpression or PKM2 knockdown was detected by CCK-8 assays. f The migration and invasion abilities of ESCC cells with circCYP24A1 overexpression or PKM2 knockdown were detected by transwell migration and matrigel invasion assay. [Extracted from the article]

Background: Esophageal squamous cell carcinoma (ESCC) is a common gastrointestinal malignant tumor, while the molecular mechanisms have not been fully elucidated. Multiple circular RNAs have been reported to involve in the onset and progression of malignant tumors through various molecular mechanisms. However, the clinical significance and functional mechanism of most circRNAs involved in the progression of ESCC remains obscure. Methods: RNA-Seq was used to explore potential circRNAs in participated in 5 pairs of ESCC and their corresponding normal esophageal tissues. The up-regulated circCYP24A1 was selected. Fluorescence in situ hybridization was cunducted to verificated the expression and intracellular localization of circCYP24A1 by using the tissue microarray. The Kaplan–Meier method and Cox proportional hazards model was used to examine the potential prognostic value of circCYP24A1 on overall survival of ESCC patients. The biological function were confirmed by gain- and loss-of-function approaches in vivo. mRNA expression profile microarray was proformed to investigate the downstream signaling pathways involved in circCYP24A1. RNA pull-down assay and mass spectrometry were performed to identify the proteins associated with circCYP24A1. Rescue experiments were carried out to identified hypothetical regulatory role of circCYP24A1 on ESCC progression in vivo and in virto. Results: In this study, we identified circCYP24A1 in ESCC tissues by RNA sequencing, which is up-regulated in 114 cases of ESCC tissues and acts as a novel prognosis-related factor. Moreover, circCYP24A1 promoted the ability of proliferation, migration, invasion and clone formation in vitro, as well as tumor growth in vivo. Mechanistically, chemokine (C-Cmotif) ligand 5 (CCL5) is functional downstream mediator for circCYP24A1, which is screened by mRNA microarray. Moreover, circCYP24A1 physically interacts with M2 isoform of pyruvate kinase (PKM2). Rescue experiments showed that PKM2 knockdown partly reverses the promotional effects of circCYP24A1. It was revealed that circCYP24A1 increases secretion of CCL5 through the mechanism mainly by interacting with PKM2, an activator of NF-κB pathway, and thereby accelerate malignant progression of ESCC. Conclusions: Up-regulated circCYP24A1 could activate NF-κB pathway by binding PKM2, which promotes the secretion of CCL5 and accelerate malignant progression of ESCC. Our fndings recommended a novel function for circCYP24A1 as a potential effective biomarker for judging prognosis and a therapeutic target in ESCC. [ABSTRACT FROM AUTHOR]

Objective: Apoptosis plays a major role in the progression of acute respiratory distress syndrome (ARDS) that may involve the interaction of the high mobility group box 1 (HMGB1) protein with the receptor for advanced glycation end products (RAGE). However, the underlying mechanism remains unclear. Thus, we aimed to explore the mechanisms of HMGB1-RAGE axis-induced apoptosis in ARDS. Methods: Blood samples from ARDS patients and healthy volunteers were collected to investigate the correlation between serum HMGB1 levels and the severity of ARDS in patients. Mouse models of ARDS induced by caecal ligation and perforation and A549 cell models established by stimulation with recombinant human HMGB1 (rHMGB1) were designed to explore lung inflammatory injury and apoptosis. Results: Serum HMGB1 levels were significantly increased in ARDS patients compared to controls, and HMGB1 levels in the Severe group and Nonsurvival group were significantly higher than those in the Mild and Moderate group and Survival group. In vivo, compared to sham mice, ARDS mice showed significant lung inflammatory injury and apoptosis as well as upregulation of HMGB1 and RAGE and endoplasmic reticulum stress (ERs) protein expression. All injury was attenuated by treatment with an HMGB1 inhibitor GA, a RAGE blocker FPS-ZM1, and an ERs inhibitor 4-PBA. In vitro, A549 cells challenged with rHMGB1 exhibited significant increases in the levels of proteins in the RNA-like endoplasmic reticulum kinase (PERK)/eukaryotic initiation factor 2alpha (eIF2α)/activating transcription factor 4 (ATF4) pathway and in apoptosis, all of which were significantly inhibited by pre-treatment with lenti-shPERK and an anti-RAGE antibody. Conclusion: The HMGB1-RAGE axis induces apoptotic injury during ARDS, possibly through PERK/eIF2α/ATF4-mediated ERs. [ABSTRACT FROM AUTHOR]

Circular RNAs (circRNAs) are a type of noncoding RNA, which play a vital role in the occurrence and development of esophageal squamous cell carcinoma (ESCC). While the role of novel circADAMTS6 in ESCC remains unknown. We assessed circADAMTS6 expression in ESCC tissues and cells, and the relationship between circADAMTS6 expression and overall survival of ESCC patients. Functional experiments in vitro and xenograft in vivo assay were applied to explore the functions and mechanisms of circADAMTS6 in ESCC. Results found that up-regulation of circADAMTS6 was associated with poor overall survival and may acted as an independent risk factor for ESCC prognosis. Knockdown of circADAMTS6 significantly inhibited the proliferation, migration and invasion of ESCC cells and growth of xenograft tumors in vivo. Induced AGR2 expression was able to rescue the loss of function induced by si-circADAMTS6 in KYSE150 cell. CircADAMTS6 may acts as oncogene by activating AGR2 and the Hippo signaling pathway coactivator YAP in ESCC. [ABSTRACT FROM AUTHOR]

Background: Earlier meta-analysis has publicized that Radix Astragali (RA) and Radix Angelicae sinensis (RAS) are valuable to pulmonary function and exercise capacity in patients with idiopathic pulmonary fibrosis (IPF). Objectives: The objective of the study was to regulate the pharmacological mechanism of RA and RAS in IPF treatment. Materials and Methods: Microarray datasets for IPF were examined in the Gene Expression Omnibus database and differentially expressed genes (DEGs) were recognized. Active compounds and target genes of RA and RAS were recognized using the Traditional Chinese Medicine Systems Pharmacology platform. The DEGs were combined with the active target genes to construct a medicine-compound-gene network and a protein–protein interaction network using Cytoscape software. Gene ontology function enrichment and Kyoto Encyclopedia of Genes and Genomes pathway enrichment were studied using RGUI. A gene-pathway network was established using Cytoscape and molecular docking was done using AutoDock Tool and AutoDock Vina software. Results: We recognized 1566 DEGs and 40 candidate target genes of RA and RAS acting on IPF. The six key active compounds prophesied were quercetin, kaempferol, stigmasterol, 7-O-methylisomucronulatol, formononetin, and beta-sitosterol. Following network construction and enrichment, the two main pathways were acknowledged, namely the tumor necrosis factor signaling pathway and advanced glycation end (AGE) products receptor for AGE signaling pathway. Preliminary molecular docking to confirm interactions between key compounds and their protein targets in the pathways was carried out. Conclusion: The pharmacological mechanisms of RA and RAS in IPF treatment have been further elucidated, which could show valuable in future studies on their mechanisms of action for the treatment of IPF. [ABSTRACT FROM AUTHOR]

Uterine leiomyosarcoma (uLMS) is a rare but malignant gynaecological tumour with a poor survival outcome. The present study was aimed at identifying the key genes and pathways in the development of uLMS through bioinformatics analysis. To minimize the frequency of false‑positive results of the bioinformatics analysis, 3 microarrays including GSE764, GSE64763 and GSE68312 were downloaded from Gene Expression Omnibus (GEO). Differentially expressed genes (DEGs) were screened out using the online tool GEO2R. Then, Gene Ontology and Kyoto Encyclopaedia of Genes and Genomes pathway enrichment analyses were performed using the Database for Annotation, Visualization and Integrated Discovery. Finally, a protein‑protein interaction (PPI) network of the DEGs was constructed using Cytoscape, and module analysis was conducted using the plug‑in MCODE. A total of 95 DEGs including 21 upregulated genes and 74 downregulated genes were identified. The upregulated DEGs were annotated with ‘DNA metabolic process’, ‘nucleobase‑containing compound biosynthetic process’ and ‘cellular macromolecule biosynthetic process’, while the downregulated DEGs were annotated with ‘cellular response to chemical stimulus’, ‘movement of cell or subcellular component’ and ‘response to inorganic substances’. The results of the PPI network analysis demonstrated that matrix metallopeptidase 9, apolipoprotein E, cyclin E1 and syndecan 1 were the predominant upregulated genes in uLMS. Additionally, the genes in the main module were enriched in ‘proteoglycans in cancer’, ‘p53 signalling pathway’ and ‘extracellular matrix‑receptor interaction’. The key genes and pathways identified in the present study may provide valuable clues for clarifying the molecular mechanism underlying the development of uLMS and demonstrate promise for use as diagnostic markers and therapeutic targets. [ABSTRACT FROM AUTHOR]

Background: MAGE‐A genes belong to the cancer/testis antigens family. The prognostic significance of MAGE‐A expression in the peripheral blood of patients with lung cancer is unknown. Therefore, this study evaluated the expression and possible prognostic significance of MAGE‐A in the peripheral blood of patients with lung cancer. Methods: In this study, we detected MAGE‐A gene expression in the peripheral blood of 150 patients with lung cancer and 30 healthy donors using multiplex semi‐nested PCR and analyzed their correlation with clinicopathological risk factors. Results: MAGE‐A expression was associated with factors indicating poor prognosis. The expression of MAGE‐A and each individual MAGE‐A gene were also associated with low overall survival in patients with lung cancer. Conclusion: The expression of MAGE‐A genes in peripheral blood may act as a poor prognostic marker in patients with lung cancer. [ABSTRACT FROM AUTHOR]

Background and Aims This study aims to investigate the expression pattern of melanoma-associated antigen-A11 (MAGE-A11) in esophageal squamous cell carcinoma (ESCC) specimens and analyze its prognostic significance for ESCC patients. In addition, the purpose of our study was also to explore the biological function of MAGE-A11 in ESCC cells based on DNA microarray. Methods Immunohistochemistry was used to detect the expression of MAGE-A11 in ESCC specimens, and its prognostic significance was analyzed by statistical analysis. DNA microarray and quantitative RT-PCR were used to explore the different expression of MAGE-A11 downstream genes in ESCC cells. Cell invasion assay and MTT assay were used to detect the effect of MAGE-A11 cDNA on the invasion and proliferation of ESCC cells. Results Of the ESCC specimens, 59.3% showed positive MAGE-A11 expression. MAGE-A11 expression in ESCC specimens was positively associated with distant lymph node metastasis. Overall survival of ESCC patients with positive MAGE-A11 expression was shorter than in patients with negative MAGE-A11 expression. Multivariate Cox regression analysis showed MAGE-A11 expression is an independent poor prognostic factor for ESCC patients. Overexpression of MAGE-A11 changed a variety of gene expressions, which was associated with various cell functions such as protein ubiquitination, cell proliferation and apoptosis, tumor invasion and metastasis. Overexpression of MAGE-A11 directly increased the invasion and proliferation of ESCC cells. Conclusions MAGE-A11 is an independent poor prognostic marker for ESCC patients. MAGE-A11 regulates various cell functions and directly increases the invasion and proliferation of ESCC cells. [ABSTRACT FROM AUTHOR]

Oxidative stress is involved in hepatic stellate cells (HSCs) activation and extracellular matrix overproduction. We previously reported the promising effects of dioscin against CCl 4 -induced liver fibrosis, but its effects and mechanisms on BDL- and DMN-induced liver fibrosis remain unknown. The results in the present study indicated that dioscin significantly inhibited HSCs activation and attenuated hepatic fibrosis in rats. Furthermore, dioscin markedly up-regulated the levels of sirtuin 1 (Sirt1), HO-1, GST, GCLC and GCLM via increasing the nuclear translocation of nuclear erythroid factor 2-related factor 2 (Nrf2), which in turn inhibited mitogen-activated protein kinase 14 (p38 MAPK) phosphorylation and reduced the levels of COL1A1, COL3A1, α-SMA and fibronectin. These results were further validated by knockdown of Sirt1 and Nrf2 using siRNAs silencing, and abrogation of p38 MAPK using SB-203580 (a p38 MAPK inhibitor) in HSC-T6 and LX-2 cells. Collectively, our findings confirmed the potent effects of dioscin against liver fibrosis and also provided novel insights into the mechanisms of this compound as a candidate for the prevention of liver fibrosis in the future. [ABSTRACT FROM AUTHOR]

It has been reported that the trimethylation of histone 3 on lysine 27 (H3K27me3) is required for enhancer of zeste homology 2 (EZH2)-mediated repression of various genes essential for tumorigenesis and tumor development. Here, we reported the expression of EZH2 and H3K27me3 in esophageal squamous cell carcinoma (ESCC) specimens was higher than the pericarcinoma esophageal specimens. Their expression was positively associated with the poor prognosis of ESCC patients. EZH2 expression, histological grade and distant lymph node metastasis were all independent factors for poor prognosis of ESCC. In addition, enforced expression of EZH2 in esophageal cancer-derived cells could increase the overall H3K27me3 level. Our results suggested the expression of EZH2 and H3K27me3 could serve as biomarkers in the prediction of ESCC patients’ survival and ESCC metastasis. [ABSTRACT FROM PUBLISHER]

Mesoporous hydroxyapatite (HA) was synthesized through gas–liquid chemical precipitation method at ambient temperature without any template. Structure, morphology and pore size distribution of HA were analyzed via X-ray powder diffraction, scanning electron microscopy, transmission electron microscopy, high-resolution electron microscopy and N 2 adsorption/desorption. The chemotherapeutic agent doxorubicin (DOX) was used to investigate the drug adsorption and release behavior of HA. The kinetics of DOX adsorption on HA followed the pseudo-second-order rate expression. Adsorption isotherms at various temperatures were obtained, and the equilibrium data fitted the Langmuir model. The values of thermodynamic parameters (Gibbs free energy, entropy, and enthalpy changes) demonstrated that the adsorption process was spontaneous and endothermic. In vitro pH-responsive (pH = 7.4, 5.8) controlled release was investigated. DOX-loaded HA showed a slow, long-term, and steady release rate. The release rate at pH5.8 was larger than that at pH7.4. Consequently, the as-prepared mesoporous HA has potential applications in controlled drug delivery systems. [ABSTRACT FROM AUTHOR]

In this contribution, we introduced a simple, efficient, and green method of preparing a mesoporous Fe 3 O 4 /hydroxyapatite (HA) composite. The as-prepared material had a large surface area, high pore volume, and good magnetic separability, which made it suitable for targeted drug delivery systems. The chemotherapeutic agent doxorubicin (DOX) was used to investigate the drug release behavior of Fe 3 O 4 /HA composite. The drug release profiles displayed a little burst effect and pH-dependent behavior. The release rate of DOX at pH 5.8 was larger than that at pH 7.4, which could be attributed to DOX protonation in acid medium. In addition, the released DOX concentrations remained at 0.83 and 1.39 μg/ml at pH 7.4 and 5.8, respectively, which indicated slow, steady, and safe release rates. Therefore, the as-prepared Fe 3 O 4 /hydroxyapatite composite could be an efficient platform for targeted anticancer drug delivery. [ABSTRACT FROM AUTHOR]

Abstract: Poly(N-isopropylacrylamide)-b-[poly(ethyl acrylate)-g-poly(2-(diethylamino)ethyl methacrylate)] (PNIPAM-b-(PEA-g-PDEAEMA)) double hydrophilic graft copolymers were employed to prepare stable colloidal gold nanoparticles in situ with controllable size in aqueous media without any external reducing agent. PDEAEMA side chains served as reduction agent and stabilizer and PNIPAM segment acted as a hydrated layer to enhance the stability of gold nanoparticles. These gold nanoparticles showed a remarkable colloidal stability without any observable flocculation or aggregation for at least 2 months and they were characterized by UV–vis, XRD, TEM and AFM in detail. The size of gold nanoparticles can be tuned by adjusting the length of PDEAEMA side chains and the molar ratio of [DEAEMA]/[AuCl4 −]. Both the increasing of the length of PDEAEMA side chains and the decreasing of [DEAEMA]/[AuCl4 −] molar ratio resulted in the fall of size. [Copyright &y& Elsevier]

Abstract: We used HCl and NH3 gases to adjust the pH value of the suspension prepared by mixing the Pb(Ac)2 and K2CrO4 aqueous solutions, and found the structure, morphology and size of the initial precipitates changed at room temperature. In the acid condition, when the ratio of [Pb2+]/[CrO4 2−] was 1:1, 1:5 or 1:10, the initial orthorhombic PbCrO4 precipitates would translate to the monoclinic PbCrO4. And the aspect ratio of the obtained particles increased with a decrease in the ratio of [Pb2+]/[CrO4 2−]. In the basic condition, with the increase in the concentration of the hydroxyl ions, the products converted from the orthorhombic PbCrO4 to the monoclinic Pb2CrO5. The phenomena and results provide the information of the phase formation and transition in the Pb–Cr–O system, and enrich the field of the crystal growth. [Copyright &y& Elsevier]

Abstract: Sm-doped cerium dioxide (SDC) with fcc structure was formed using a gas–liquid chemical co-precipitation process at room temperature. Morphology and structure of the as-prepared samples were characterized using TG, XRD, TEM, HRTEM and SAED techniques. Under our specific experimental conditions, two kinds of 1D nano-structures SDC have been mainly obtained. SDC nanowires are 0.3–1.2μm in lengths and 5–20nm in diameters. SDC nanotubes have outer diameters in 10–40nm with lengths up to 2μm. The as-prepared SDC shows very strong UV absorption ability and the maximum absorption peak redshifts compared with that of SDC nanoparticles. [Copyright &y& Elsevier]

Abstract: PbCrO4 and Pb2CrO5 have been selectively synthesized via a chemical gas–liquid precipitation process by adjusting the pH value. The structure, size and morphology of the as-synthesized products are characterized by X-ray diffraction and transmission electron microscopy. Differences in UV–Vis spectra are related to differences in size and morphology. [Copyright &y& Elsevier]

Abstract: Nanocrystalline CeO2 powders were synthesized by the combustion reactions using citric acid and glycol as fuels and nitrate as an oxidant. The adiabatic flame temperatures in the auto ignition processes of the precursors were calculated theoretically. XRD measurements indicated that the powders produced in the combustion processes were cubic fluorite CeO2 phase. The size and morphology of the particles and extent of agglomeration in the powders were studied using transmission electron microscopy (TEM) and the particle size analyzer respectively. Blue shifts of the absorption peak of the as-prepared powders were observed. [Copyright &y& Elsevier]

Hypoxia inducible factor 1α (HIF1α) plays a critical role in atherosclerosis as demonstrated in endothelial-targeted HIF1α -deficient mice. However, it has not been shown if specific pharmacological inhibitors of HIF1α can be used as potential drugs for atherosclerosis. PX-478 is a selective inhibitor of HIF1α, which was used to reduce cancer and obesity in animal models. Here, we tested whether PX-478 can be used to inhibit atherosclerosis. We first tested PX-478 in human aortic endothelial cells (HAEC) and found that it significantly inhibited expression of HIF1α and its targets, including Collagen I. Next, two independent atherosclerosis models, C57BL/6 mice treated with AAV-PCSK9 and ApoE −/− mice, were used to test the efficacy of PX-478. Both mouse models were fed a Western diet for 3 months with bi-weekly treatment with PX-478 (40 mg/kg) or saline. PX-478 treatment reduced atherosclerotic plaque burden in the aortic trees in both mouse models, while plaque burden in the aortic sinus was reduced in the AAV-PCSK9 mouse model, but not in the ApoE −/− mice. Russell-Movat's Pentachrome and Picrosirius Red staining showed a significant reduction in extracellular matrix remodeling and collagen maturation, respectively, in the PX-478-treated mice. As expected, PX-478 treatment reduced diet-induced weight-gain and abdominal adipocyte hypertrophy. Interestingly, PX-478 reduced plasma LDL cholesterol by 69% and 30% in AAV-PCSK9 and ApoE −/− mice, respectively. To explore the cholesterol-lowering mechanisms, we carried out an RNA sequencing study using the liver tissues from the ApoE −/− mouse study. We found 450 genes upregulated and 381 genes downregulated by PX-478 treatment in the liver. Further, gene ontology analysis showed that PX-478 treatment upregulated fatty acid and lipid catabolic pathways, while downregulating lipid biosynthesis and plasma lipoprotein particle remodeling processes. Of interest, Cfd , Elovl3 , and Insig2 were some of the most downregulated genes by PX-478, and have been implicated in fat storage, fatty acid elongation, and cholesterol metabolism. The downregulation of Cfd, Elovl3, and Insig2 was further validated by qPCR in the liver tissues of ApoE −/− mice treated with PX-478. These results suggest that PX-478 is a potential anti-atherogenic drug, which targets vascular endothelium and hepatic cholesterol pathways. [Display omitted] • We tested the therapeutic efficacy of PX-478, a selective HIF1α inhibitor, in two mouse models of atherosclerosis. • PX-478 inhibited atherosclerosis in both models and it reduced extracellular matrix remodeling and collagen maturation. • Unexpectedly, PX-478 reduced plasma cholesterol levels in both mouse models. • RNA sequencing showed that PX-478 altered more than 800 genes, which regulate fatty acids, lipids, and lipoproteins. • Repurposing PX-478 is a potential anti-atherogenic avenue. [ABSTRACT FROM AUTHOR]

The anti-inflammatory property of polydatin, a natural active ingredient found in the rhizome of Polygonum cuspidatum , has been verified. Although a variety of physiological functions have been uncovered, the protective effects and mechanism of polydatin on LPS-induced acute kidney injury remain unclear. Kidney histological change, MDA content, MPO activity, TNF-α, IL-1β, and IL-6 production were measured in this study. Furthermore, NF-κB and Nrf2 were tested by western blotting. In this study, polydatin not only significantly attenuated serum creatinine and BUN levels, but also remarkably inhibited TNF-α, IL-1β, and IL-6 production, MPO activity, and MDA content. Polydatin significantly inhibited LPS-induced NF-κB activation. Also, polydatin significantly increased Nrf2 and HO-1 expression. Taken together, all the above results indicate that polydatin had protective effects against LPS-induced AKI by blocking inflammatory and oxidative responses. • Polydatin significantly reduced the expression of TNF-α, IL-1β, and IL-6 in kidney tissues, MPO activity, and MDA content. • Polydatin also remarkably inhibited serum creatinine and BUN. • Polydatin significantly inhibited LPS-induced NF-κB activation. • Treatment of polydatin significantly increased the expression of Nrf2 and HO-1. [ABSTRACT FROM AUTHOR]

Objective: To observe the effect of the whole-process care model of the medical union on the improvement of kinesiophobia and bone mineral density in patients with osteoporosis. Methods: In this descriptive study, a convenient sampling method was used to select 148 patients with osteoporosis who visited the hospital from January 2020 to December 2021. Patients aged ≥ 18 years and diagnosed with osteoporosis through quantitative computed tomography (QCT) were included in the study. They were able to cooperate during follow-up and had normal cognitive function. Patients with combined spinal curvature, thoracic deformity, and pulmonary dysfunction, accompanied by severe cardiovascular or limb dysfunction, and those who withdrew midway or participated in other clinical studies were excluded. According to whether to use the whole-process care model of the medical union, they were divided into intervention group and control group, with 74 cases each. The control group used conventional care, and the intervention group used the whole-process care model of the medical association. The occurrence of kinesiophobia between the two groups were compared. The dual-energy X-ray absorption detector is used to measure differences in bone density changes. Results: There was no significant difference between the two groups in the TSK scale score and the incidence of kinesiophobia before intervention (P > 0.05). The TSK scale scores of patients in the intervention group were higher than those in the control group at 3 months and 6 months after operation (P < 0.05). The incidence of kinesiophobia in the intervention group for 3 months and 6 months was significantly lower than that in the control group (P < 0.05). There was no significant difference in bone mineral density between the two groups before and 3 months after intervention (P > 0.05). The bone mineral density of lumbar spine, femoral neck and total hip in the intervention group was significantly higher than that in the control group after 6 months of intervention (P < 0.05). Conclusion: The whole-process care model of the medical association is used for osteoporosis patients, which might reduce the risk of kinesiophobia and improve the bone density of the lumbar spine and total hip in patients. But further promotion and improvement of relevant support systems are needed to achieve comprehensive promotion and maximize clinical benefits in this field. [ABSTRACT FROM AUTHOR]

To evaluate the clinical characteristics and prognostic significance of MAGE-A11 and transcription factors (SP1, TFCP2 and ZEB1) in patients with esophageal squamous cell carcinoma (ESCC). To assess the expression of MAGE-A11 and transcription factors (SP1, TFCP2 and ZEB1) in 121 ESCC samples were respectively detected by immunohistochemical method. The results showed MAGE-A11 and transcription factors (SP1,TFCP2 and ZEB1) expression were associated with some clinical features in patients, such as pathological differentiation, tumor size, clinical stage, lymph node metastasis and distant metastasis. Kaplan-Meier analysis showed that patients with ESCC having high MAGE-A11 and transcription factors (SP1,TFCP2 and ZEB1) expression had a worse prognosis compared to the patients with low expression. Multivariate Cox proportional hazards regression model revealed that MAGE-A11 expression, TFCP2 expression, lymph node metastasis and distant metastasis were independently associated with ESCC patients' survival. High expression of MAGE-A11 and transcription factors (SP1,TFCP2 and ZEB1) in ESCC tissues suggests promoting ESCC progression and poor prognosis, co-expression of MAGE-A11 and transcription factors even worse. [ABSTRACT FROM AUTHOR]

1D porous g-C3N4 nanorods were synthesized using chitosan as a template, offering a large surface area and enhanced visible light absorption. These nanorods exhibited a remarkable 8.3-fold increase in H2 generation rate (26.6 μmol h−1) compared to bulk g-C3N4. [ABSTRACT FROM AUTHOR]

Abstract: Although radiotherapy has been widely applied to treating cervical cancer in the clinic, its therapeutic efficacy is often restricted to the radioresistance of cancer cells. Retinoblastoma protein‐interacting zinc finger gene 1 (RIZ1) has been suggested as a tumour suppressor gene, whereas its role in cervical cancer with or without radiotherapy has been unclear. In this study, two cervical cancer cell lines, HeLa and SiHa cells, stably transfected with RIZ1 overexpression plasmid were subjected to ionizing radiation, and their survival fractions were calculated by assessing their clonogenic abilities. Our results showed that the forced overexpression of RIZ1 significantly reduced the clonogenic survival rates of both HeLa and SiHa cells exposed to ionizing radiation. By analysing the cell apoptotic status, we found that the RIZ1‐overexpressed cervical cancer cells under ionizing radiation were more vulnerable to damage, and more γ‐H2AX foci were found in these cells. Furthermore, the volumes of tumour xenografts formed by the RIZ1‐overexpressed cells in nude mice under ionizing radiation were smaller than those generated by the control cells. There were more morphological changes, apoptosis cells and lower expression of PCNA in RIZ1‐overexpressed tumour tissues of mice after exposure to ionizing radiation. Taken together, our study demonstrates that the overexpression of RIZ1 combined with radiotherapy facilitates apoptosis and DNA damage of cervical cancer cells. [ABSTRACT FROM AUTHOR]

Background As the best characterized CTA family members, melanoma-associated antigens (MAGE) have been reported to express in various malignant tumors. However, the expression pattern of MAGE-A family in gastric cancer (GC) specimens and their prognostic and therapeutic significance for GC patients is still unclear. Materials and methods Tissue microarray − based immunohistochemistry analysis was used to examine the expression of MAGE-A family members (including MAGE-A1, −A2, −A3, −A4, −A6, −A10, and −A12) in 86 cases of GC specimens, 20 cases of the corresponding adjacent normal gastric specimens, and 9 cases of intraepithelial neoplasia specimens. The association between MAGE-A expression and the clinicopathological parameters as well as the 5-year overall survival of GC patients was analyzed. Results 54.7% of GC specimens showed positive MAGE-A expression. In the adjacent normal gastric specimens, MAGE-A was not expressed in the normal surface mucous cells, but expressed in some normal fundic glands. In addition, MAGE-A expression was also detected in intraepithelial neoplasia specimens. In GC specimens, MAGE-A expression was associated with lymph node metastasis, poor differentiation, and high clinical TNM stage. MAGE-A expression was also correlated with the poor 5-year overall survival of GC patients. However, MAGE-A expression is not an independent prognostic factor for GC patients. Conclusions MAGE-A family may be involved in the gastric cancer progression, and their expression could be considered to improve the prognostic evaluation for GC patients. [ABSTRACT FROM AUTHOR]

Esophageal squamous cell carcinoma (ESCC) is a common malignancy with high morbidity and mortality. Although circular RNAs (circRNAs) play important roles in various cancers including ESCC, the role of the circRNA mannosidase alpha class 1A member 2 (circMAN1A2) in ESCC has been rarely studied. This study aimed to explore the role of circMAN1A2 in ESCC. CircMAN1A2 expression in ESCC tissues and cells was evaluated, and the relationship between circMAN1A2 expression and prognosis in patients with ESCC was analyzed. C–C chemokine ligand 5 (CCL5) was found to be a downstream target of circMAN1A2 by analysing the Agilent Microarray. Next, we performed in vitro and in vivo xenotransplantation assays to explore the role of circMAN1A2 in ESCC. We observed that high circMAN1A2 expression is associated with poor prognosis in patients with ESCC. Suppression of circMAN1A2 expression inhibits the proliferation, migration, and invasiveness of ESCC via regulating CCL5. Our results suggest that circMAN1A2 can promote the progression of ESCC by regulating CCL5. Thus, circMAN1A2 might be a novel diagnostic biomarker of ESCC, and targeting circMAN1A2 using inhibitors could be a potential therapeutic strategy to treat ESCC. [Display omitted] • CircMANA2 is highly expressed in ESCC tissues and cells. • Down-regulation of circMAN1A2 inhibits the proliferation, migration and invasiveness of ESCC. • CircMAN1A2 may be a novel diagnostic biomarker and therapeutic target of ESCC. [ABSTRACT FROM AUTHOR]

Background Acceleration of negative respiratory conversion of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in patients with coronavirus disease 2019 (COVID-19) might reduce viral transmission. Nirmatrelvir/ritonavir is a new antiviral agent recently approved for treatment of COVID-19 that has the potential to facilitate negative conversion. Methods A cohort of hospitalized adult patients with mild-to-moderate COVID-19 who had a high risk for progression to severe disease were studied. These patients presented with COVID-19 symptoms between 5 March and 5 April 2022. The time from positive to negative upper respiratory reverse transcription-polymerase chain reaction (RT-PCR) conversion was assessed by Kaplan-Meier plots and Cox proportional hazards regression with the adjustment for patients' baseline demographic and clinical characteristics. Results There were 258 patients treated with nirmatrelvir/ritonavir and 224 nontreated patients who had mild-to-moderate COVID-19. The median (interquartile range) time for patients who converted from positive to negative RT-PCR was 10 days (7–12 days) in patients treated ≤5 days after symptom onset and 17 days (12–21 days) in nontreated patients. The proportions of patients with a negative conversion at day 15 were 89.7% and 42.0% in treated patients and nontreated patients, corresponding to a hazard ratio of 4.33 (95% confidence interval, 3.31–5.65). Adjustment for baseline differences between the groups had little effect on the association. Subgroup analysis on treated patients suggests that time to negative conversion did not vary with the patients' baseline characteristics. Conclusions This cohort study of high-risk patients with mild-to-moderate COVID-19 found an association between nirmatrelvir/ritonavir treatment and accelerated negative RT-PCR respiratory SARS-CoV-2 conversion that might reduce the risk of viral shedding and disease transmission. [ABSTRACT FROM AUTHOR]

Simple Summary: circRNF10 is significantly downregulated in breast cancer (BC) tissues, and its downregulation is associated with a poor prognosis. circRNF10 regulates PTEN expression and the PI3k/Akt/MICA signaling pathway by sponging miR-934. Our findings revealed that circRNF10 functions as a novel anti-oncogene in BC, and overexpression of circRNF10 could enhance the killing efficiency of NK-92MI cells against BC cells. Circular RNA (circRNA), a type of non-coding RNA, has received a great deal of attention with regard to the initiation and progression of tumors. However, the molecular mechanism and function of circRNAs in breast cancer (BC) remain unclear. In the current study, we discovered that hsa_circ_0028899 (also called circRNF10) was significantly reduced in BC tissues, and a higher level of circRNF10 was markedly related to a favorable prognosis. The results of CCK8, colony formation, Transwell, ELISA, and NK cell-mediated cytotoxicity assays indicated that increased circRNF10 expression could significantly repress the proliferation, invasion, and migration of BC cells and enhance the killing efficiency of NK cells against BC cells. According to these biological functions, the possible role and molecular mechanism of circRNF10 in BC cells were further investigated. We used bioinformatics prediction tools to predict circRNF10-bound miRNAs, which were verified by many experimental studies, including FISH, luciferase reporter assays, RIP, and Western blots. These data suggest that circRNF10 serves as a molecular sponge for miR-934 to further regulate PTEN expression and PI3k/Akt/MICA signaling in vitro and tumor growth in vivo. Altogether, these findings reveal that circRNF10 functions as a novel anti-oncogene in BC via sponging miR-934 and suppressing the PI3K/Akt/MICA pathway. [ABSTRACT FROM AUTHOR]

To build radiomics based OS prediction tools for local advanced cervical cancer (LACC) patients treated by concurrent chemoradiotherapy (CCRT) alone or followed by adjuvant chemotherapy (ACT). And, to construct adjuvant chemotherapy decision aid. 83 patients treated by ACT following CCRT and 47 patients treated by CCRT were included in the ACT cohort and non-ACT cohort. Radiomics features extracted from primary tumor area of T2-weighted MRI. Two radiomics models were built for ACT and non-ACT cohort in prediction of 3 years overall survival (OS). Elastic Net Regression was applied to the the ACT cohort, meanwhile least absolute shrinkage and selection operator plus support vector machine was applied to the non-ACT cohort. Cox regression models was used in clinical features selection and OS predicting nomograms building. The two radiomics models predicted the 3 years OS of two cohorts. The receiver operator characteristics analysis was used to evaluate the 3 years OS prediction performance of the two radiomics models. The area under the curve of ACT and non-ACT cohort model were 0.832 and 0.879, respectively. Patients were stratified into low-risk group and high-risk group determined by radiomics models and nomograms, respectively. And, the low-risk group patients present significantly increased OS, progression-free survival, local regional control, and metastasis free survival compare with high-risk group (P < 0.05). Meanwhile the prognosis prediction performance of radiomics model and nomogram is superior to the prognosis prediction performance of Figo stage. The two radiomics model and the two nomograms is a prognosis predictor of LACC patients treated by CCRT alone or followed by ACT. • Radiomics models predicted the prognosis of LACC patients treated by adjuvant chemotherapy following CCRT and CCRT alone. • Radiomics models and nomograms presented better predicting performance compare with Figo stage. • The correlationship between radiomics models, nomograms, clinical features were inconsistent for ACT and non-ACT cohort. [ABSTRACT FROM AUTHOR]

Interaction between tumor cells and tumor microenvironment (TME) is critical to promote tumor progression and metastasis. As the most abundant immune cells in TME, macrophages can be polarized into M2-like tumor-associated macrophages (TAMs) which further promote tumor progression. However, to date, the molecular mechanisms of TAM polarization in TME are still largely unknown. In the present study, we revealed that circular RNA circWWC3 could up-regulate the expression and secretion of IL-4 in breast cancer cells. Enhanced secretion of IL-4 from breast cancer cells could augment the M2-like polarization of macrophages in TME, which further promotes the migration of breast cancer cells. In addition, increased secretion of IL-4 from breast cancer cells could induce the expression PD-L1 in M2 macrophages. Moreover, up-regulated IL-4 also enhanced the expression of PD-L1 in breast cancer cells, which further facilitates breast cancer immune evasion. Though analyzing the expression of circWWC3, IL-4, PD-L1, and CD163 in 140 cases of breast cancer tissues, we found that high expression of circWWC3 was associated with poor overall survival and disease-free survival of breast cancer patients. Breast cancer patients with circWWC3high/PD-L1high breast cancer cells and CD163high macrophages had a poorer overall survival and disease-free survival. Conclusively, circWWC3 might augment breast cancer progression through promoting M2 macrophage polarization and tumor immune escape via regulating the expression and secretion of IL-4. CircWWC3 might be a potential therapeutic target in breast cancer. [ABSTRACT FROM AUTHOR]

[Display omitted] • The interaction between the -Cl functional group and the amino group is detrimental to carbon capture and phase separation. • Calculation of the reaction mechanism of mixed amines with CO 2. • Classical molecular dynamics reveals the effect of functional groups on intermolecular forces. • Analysis of the impact of log P values on the absorption and regenerative performance of absorbents. Biphasic solvents significantly reduce the energy consumption of CO 2 capture processes due to their phase separation behavior. In this investigation, the effects of six absorption accelerators and five phase splitters (alcohols) on the CO 2 absorption, CO 2 desorption and phase separation performance of biphasic solvents were evaluated. In addition to the phase splitter being 3-chloro-1-propanol, the higher the hydrophobicity (log P) of the phase splitter, the better the absorbent phase separation performance. The phase splitting behavior of the absorbent changes the carbon capture environment of the amine, and the new carbon capture environment is not conducive to the reaction between the amine and CO 2 , therefore, a phase splitter with a lower log P can improve the CO 2 loading of the absorbent. The CO 2 desorption performance of the absorbent was significantly enhanced by the presence of more alcohols in the rich phase. Diethylenetriamine (DETA) reacts with CO 2 to produce a product with the largest dipole moment, which is suitable for the phase separation of various mixed amines. Synergistic effects between 2-Aminoethanol (MEA) and DETA are evident, as the partial substitution of DETA with MEA yields no substantial changes in phase separation performance. To better understand the effects of mixed amines and phase splitter on the CO 2 uptake and phase separation behavior of biphasic solvents, the present study carried out density-functional theory (DFT) calculations and molecular dynamics (MD) simulations, to analyse in depth the effects of different functional groups on the intermolecular forces, the CO 2 absorption mechanism and synergistic effects between mixed amines. This study was carried out to analyse in detail the effects of different functional groups on the intermolecular forces, and the mechanism of CO 2 absorption between mixed amines and the synergistic effects. [ABSTRACT FROM AUTHOR]

[Display omitted] • The solubilizer increased the concentration of PMDETA dissolved in MEA/DMSO. • There is no significant difference in solvent effect between different types of solubilizers when small amounts of solubilizer are added. • The organic solvent DMSO significantly reduced the heat of vaporization and sensible heat in the rich phase. • Mechanism of the MEA+COO− deprotonation reaction revealed on a molecular scale. Nonaqueous biphasic solvent has remarkable energy-saving potential. The weak force between N, N, N′, N″, N‴-pentamethyldiethylenetriamine (PMDETA) and Dimethyl sulfoxide (DMSO) contributes to facilitating the separation between DMSO and PMDETA, thereby enabling efficient liquid–liquid phase separation. Nevertheless, the weak interactions of PMDETA with other solvent molecules pose considerable challenges in the formulation of fresh homogeneous phase solutions. This study proposes a strategy to enhance PMDETA dissolution by introducing a solubilizer into a hybrid phase splitter, thereby increasing the concentration of PMDETA in the solvent. With the addition of a small quantity of solubilizer, the absorption, regeneration, and phase separation performance among the absorbents are comparable. The phase separation performance is influenced by the number of hydrogen bonds formed by the solubilizer, and the concentration of solubilizer in the lower phase is dependent on its hydrophobicity. Characterization using 13C NMR and FT-IR indicates that CO 2 products primarily exist in the form of MEACOO−/MEAH+. Through DFT and molecular dynamics simulations, the impact of the solvent environment surrounding Ethanolamine (MEA) on the MEA+COO− deprotonation reaction is analyzed. While PMDETA offers a more favorable proton acceptance energy compared to MEA, the limited opportunities for PMDETA to come into contact with MEA molecules may be the primary hindrance to its participation in the reaction. Significantly lower corrosivity and regeneration energy requirements for non-aqueous biphasic solvents compared to 30 wt% MEA make them ideal candidates for energy-efficient, low-corrosivity CO 2 capture. [ABSTRACT FROM AUTHOR]

[Display omitted] • Synthesizing multi-metal composite shell materials for the catalytic oxidation of toluene. • Detailed Density Functional Theory (DFT) calculations to determine the adsorption energy. • Revealing the mechanism of toluene oxidation catalyzed by CoNiCu-LDO. Amidst the increasing concerns regarding the emission of volatile organic compounds (VOCs), the pressing task at hand is the development of effective and environmentally benign technologies for catalytic VOC reduction. In the context of this research endeavor, the distinct attributes of zeolite imidazoline framework (ZIF-67), known for its high yield, absence of deleterious by-products, and rapid synthesis, are harnessed. In pursuit of this goal, a series of ZIF-67-derived layered double oxides (LDO) multimetallic composite shell materials for toluene combustion were successfully synthesized: CoNi-LDO and CoNiM-LDO (M = Ce, Cu, Mn and Fe).The experimental results show that due to the uniform dispersion of Co, Ni, and Cu atoms within the CoNiCu-LDO catalyst, the prevalence of oxygen vacancies, a significant specific surface area, and robust interactions among these constituents, a synergistic formation involving O v - Cu2+ - O 2 - Co3+ - O 2 - Ni3+ emerges, the CoNiCu-LDO exhibits an excellent catalytic efficiency. Furthermore, through Density Functional Theory (DFT), the adsorption energies and the projected density of states (PDOS) for toluene, O 2 , H 2 O, and SO 2 on the catalysts have been meticulously computed. Ultimately, the intricate mechanism underpinning the catalytic oxidation of toluene on CoNiCu-LDO has been unveiled through in situ Diffuse Reflectance Infrared Fourier Transform Spectroscopy (DRIFTS). [ABSTRACT FROM AUTHOR]

The geometric, electronic, optical properties, thermodynamic stability, and work function of Li-doped g-C 3 N 4 monolayer were investigated by the first-principles calculation. It was found that the Li atoms were preferentially substituted the open-hollow sites of g-C 3 N 4 . Interestingly, the “odd” number of Li doped g-C 3 N 4 showed metallic properties, while the “even” number of Li atoms widened the band gap of g-C 3 N 4 . The HOMO and LUMO distributions reveal that the active sites located at edge N and C atoms for both pristine and the Li-doped g-C 3 N 4 . In addition, thermodynamic analysis showed that the doped Li atoms reduced the thermodynamic stability of g-C 3 N 4 monolayer sheets. [ABSTRACT FROM AUTHOR]

Carbon defects in graphitic carbon nitride (g-CN) can modulate the electronic structure for efficient separation of electron–hole pairs, and thereby potentially enhance the photocatalytic H2 generation. However, the mechanism on the separation of electrons and holes in C defect-modified g-CN still remains unclear. Here we report an autogenic ammonia gas route via in-situ urea decomposition to create carbon defects in g-CN for realizing increased photocatalytic H2 generation rate of 36.62 µmol h−1 under visible light exposure, which is 10 times higher than that of g-CN obtained in the absence of autogenic ammonia gas (~ 3.63 µmol h−1). Illustrated by the density functional theory calculations, the C defects can not only reduce the band gap for increased light harvesting, but also delocalize the π electrons in valence band (VB) and conduction band (CB) for efficient charge transfer. Such delocalization of π electrons facilitates the efficient separation of electrons in LUMO and holes in HOMO, then promoting the photocatalytic H2 generation. Therefore, the creation of C defects can be used as an effective route to delocalize the π electrons in g-CN for efficient photocatalytic H2 generation. [ABSTRACT FROM AUTHOR]

[Display omitted] • A novel nonaqueous biphasic solvent TMEDA/MEA/DMSO is proposed. • The mechanisms of absorption and phase separation during CO 2 absorption are elucidated. • TMEDA/MEA/DMSO nonaqueous two-phase absorbent is a low corrosivity biphasic solvent. • Compared to the conventional 30 wt% MEA water-based absorbent, there is a 40 % reduction in regeneration energy. In order to ameliorate the issues of corrosion and high regeneration energy associated with traditional biphasic solvents, a nonaqueous biphasic solvent has been proposed as a potential alternative. This study introduces Tetramethylethylenediamine (TMEDA) as a phase splitter within the Ethanolamine (MEA)/Dimethyl sulfoxide (DMSO) system, resulting in a novel nonaqueous biphasic solvent, TMEDA/MEA/DMSO. Compared with other screened phase splitters, the appropriate polar size and intermolecular interaction force of TMEDA are the key factors that make it comply with the screening of nonaqueous biphasic solvent. When the mass ratio of TMEDA/MEA/DMSO is maintained at 3:3:4, the CO 2 loading attains 0.54 mol (CO 2)/mol (MEA), with the rich phase comprising 75 % of the total. 13C NMR and FT-IR characteristics showed that the absorbent product is mainly in the form of MEACOO−/MEAH+. Absorption and phase separation mechanisms of absorbent elucidated by DFT calculations and molecular dynamics simulations. The limited opportunity for TMEDA to interact with MEA molecules emerges as the primary reason for its reduced involvement in the reaction, with the inclusion of TMEDA intensifying the aggregation of MEACOO−/MEAH+ and triggering phase transition. In comparison to a 30 wt% MEA water-based absorbent, TMEDA/MEA/DMSO exhibits a 40 % reduction in regeneration energy (estimate) and possesses energy-saving attributes, rendering it a promising candidate for CO 2 capture. [ABSTRACT FROM AUTHOR]

• The mechanism of SO 2 adsorption, sulfation, and migration on different catalysts is summarized. • The regeneration methods of sulfur-poisoned catalysts are compared. • Anti-sulfur poisoning modification methods for diverse catalysts are discussed. • Future research directions on the SO 2 resistance of VOCs catalysts are proposed. Emissions of volatile organic compounds (VOCs) cause serious hazards to human health and environmental quality and have become the main focus of air pollution control in many countries and around the world. Catalytic oxidation is widely used to control emissions of VOCs, and the catalysts are the core of catalytic oxidation technology. The presence of trace sulfur species in the actual waste gas inevitably causes toxicity to the catalysts. This phenomenon affects the removal efficiency of VOCs and significantly increases the operating cost, limiting the application of catalytic oxidation technology. This paper first discusses the effect of sulfur dioxide on VOCs oxidation catalysts. The detailed processes of SO 2 adsorption, migration, and conversion on catalysts are summarized. The regeneration methods of sulfur poisoning catalysts are discussed, and various methods for the development of anti-sulfur poisoning catalysts, such as element doping and acidification, are summarized. Finally, the effects of some process parameters on catalyst sulfur poisoning in practical industrial applications are concluded. It provides a reference value for future anti-sulfur poisoning strategies, mechanism analysis, and practical industrial applications of VOCs oxidation catalysts. [ABSTRACT FROM AUTHOR]

In this study, we examined the impacts of complete and partial substitution of DEEA with physical solvents (n-butanol) on the performance of AEEA/H 2 O absorption, regeneration, and phase separation. The higher hydrophobicity (log P) of n-butanol, as a phase splitter, expedites the separation process from the AEEA-CO 2 product. Through additional refinement of the mass ratio between n-butanol and DEEA, it was observed that substituting a small portion of DEEA with n-butanol had negligible impact on the absorption capacity and enrichment of the enriched phase. However, it significantly reduced the phase separation time between the two solvent phases. Furthermore, an increase in n-butanol concentration can enhance cyclic loading. On the other hand, it reduces the production of AEEACOO−/DEEAH+, which is more stable compared with AEEACOO−/AEEAH+. Molecular dynamics simulations revealed that n-butanol can modulate the reduction of water molecules surrounding AEEA, creating a lower water molecule environment, which improves the absorption rate of the absorbent in the pre-absorption phase. The addition of a low concentration of n-butanol improves the initial absorption rate, phase separation performance, circulation capacity, and further reduces the regeneration energy of the absorption solution without compromising the CO 2 loading and regeneration energy. [Display omitted] • The influence of hybrid phase separators on the absorption and regenerative performance of absorbents was investigated. • The effects of various potential reaction pathways and solvent effects on AEEA/DEEA were computed. • Classical molecular dynamics revealed diverse carbon capture environments for AEEA. • Optimization of phase separation performance and regenerative energy for DEEA/AEEA/H 2 O using n-butanol. [ABSTRACT FROM AUTHOR]

The facile synthesis of mesoporous polymeric carbon nitride (PCN) can enlarge the surface area and provide mass transport channels, which thus potentially boosts its photocatalytic H 2 generation. However, the formation of mesopores in PCN are mainly relying on the hard and soft templates with tedious operations, and it remains a grand challenge in preparing mesoporous PCN without the assistance of templates. Herein we report on an ascorbic acid-assisted hydrothermal route to effectively create the mesoporous in bulk PCN. The mesopores thus formed a typical IV isotherm with an H3 hysteresis loop, and have a pore size distribution of ∼3.8 nm. Moreover, the crystallinity of mesoporous PCN was improved with ascorbic acid-assisted hydrothermal treatment. Meanwhile, ascorbic acid can be converted to carbon materials under hydrothermal conditions. As a result, an increased photocatalytic H 2 generation was realized under visible light exposure. The highest H 2 generation rate is up to 26.8 μmol h−1 for Pt/CN-A10%, near 10 times higher than that of Pt/PCN (2.7 μmol h−1). This work highlights the effectiveness of organic acid-assisted hydrothermal treatment for synthesizing mesoporous PCN for increased photocatalytic performance. [Display omitted] • Ascorbic acid-assisted hydrothermal treatment creates mesoporous polymeric carbon nitride. • The mesopores can form a typical IV isotherm with an H3 hysteresis loop. • The crystallinity is improved after ascorbic acid-assisted hydrothermal treatment. • The highest H 2 generation rate is near 10 times higher than that of bulk PCN. [ABSTRACT FROM AUTHOR]

ZEB1 is an important transcription factor that plays a critical role in TGF-β-induced epithelial-mesenchymal transition (EMT) and tumor metastasis. However, the mechanisms by which ZEB1 regulates metastasis in esophageal squamous cell carcinoma (ESCC) remain largely unknown. Here, we identified a novel circular RNA, circ-DOCK5, the biogenesis of which is directly regulated by ZEB1 and ZEB1-repressed RNA-binding protein eIF4A3. Tissue microarray analysis identified circ-DOCK5 to be downregulated in ESCC tissues, and its downregulation correlated with poor prognosis. Moreover, circ-DOCK5 increased the stability of miR-627-3p by functioning as a "reservoir" for miR-627-3p to partially reverse the ZEB1-enhanced migration and invasion in ESCC. MiR-627-3p inhibited the expression of TGFB2 and the secretion of TGF-β, which further resulted in downregulation of ZEB1 and suppression of TGF-β-induced EMT. In vivo experiments showed that ZEB1 promoted metastasis in ESCC by regulating expression of circ-DOCK5. Therefore, the present study revealed that ZEB1-mediated downregulation of circ-DOCK5 facilitates metastasis in ESCC by forming a positive feedback loop with TGF-β by altering the miR-627-3p/TGFB2 signaling. Targeting this signaling pathway may help suppress progression in ESCC. [ABSTRACT FROM AUTHOR]

Idiopathic pulmonary fibrosis (IPF) is a chronic and progressive scarring disease with unknown etiology. The evidence of a pathogenic role for transforming growth factor‐beta (TGF‐β) in the development and progression of IPF is overwhelming. In the present study, we investigated the role of interleukin‐22 (IL‐22) in the pathogenesis of IPF by regulating the TGF‐β pathway. We measured parameters and tissue samples from a clinical cohort of IPF. IL‐22R knock out (IL‐22RA1−/−) and IL‐22 supplementation mouse models were used to determine if IL‐22 is protective in vivo. For the mechanistic study, we tested A549, primary mouse type II alveolar epithelial cell, human embryonic lung fibroblast, and primary fibroblast for their responses to IL‐22 and/or TGF‐β1. In a clinical cohort, the expression level of IL‐22 in the peripheral blood and lung tissues of IPF patients was lower than healthy controls, and the lower IL‐22 expression was associated with poorer pulmonary function. IL‐22R−/− mice demonstrated exacerbated inflammation and fibrosis. Reciprocally, IL‐22 augmentation by intranasal instillation of recombinant IL‐22 repressed inflammation and fibrotic phenotype. In vitro, IL‐22 treatment repressed TGF‐β1 induced gene markers representing epithelial‐mesenchymal‐transition and fibroblast‐myofibroblast‐transition, likely via the inhibition of TGF‐β receptor expression and subsequent Smad2/3 activation. IL‐22 appears to be protective against pulmonary fibrosis by inhibiting TGF‐β1 signaling, and IL‐22 augmentation may be a promising approach to treat IPF. [ABSTRACT FROM AUTHOR]

The determination of biomarkers in the blood specific for lung adenocarcinoma (LUAD) and lung squamous cell carcinoma (LUSC) is crucial for the selection of effective treatment strategies and the prediction of prognosis. The purpose of the present study was to analyze the differentially expressed genes (DEGs) in LUSC and LUAD from The Cancer Genome Atlas (TCGA) database. In order to identify the potential biomarkers for non-small cell lung cancer (NSCLC) for clinical diagnosis, bioinformatics was used to analyze the DEGs of two subtypes of NSCLC, LUAD and LUSC. Exosomes were isolated from the serum of patients with LUAD or LUSC and identified using transmission electron microscopy, nanoparticle tracking analysis and western blot analysis. A total of four differential exosomal mRNAs were selected for validation with serum samples from 70 patients with NSCLC via reverse transcription-quantitative polymerase chain reaction. Receiver operating characteristic curves were established to evaluate the clinical diagnostic value of four DEGs for patients with LUAD and LUSC. The analysis based on TCGA data revealed the DEGs in LUSC and LUAD: A total of 1,619 genes were differentially expressed in patients with LUSC and LUAD. DEGs analyzed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses revealed that inflammation-related signaling pathways, such as complement pathways, and multiple autoimmune diseases, such as systemic lupus erythematosus and asthma were mainly enriched in LUAD. The cell cycle, Hippo signaling pathway, Rap1 signaling pathway and Wnt signaling pathway were the main signaling pathways enriched in LUSC. The combination of tumor protein P63 (TP63), keratin 5 (KRT5), CEA cell adhesion molecule 6 (CEACAM6) and surfactant protein B (SFTPB) improved the specificity and sensitivity in the diagnosis of different lung cancer subtypes. Exosomal TP63, KRT5, CEACAM6 and SFTPB mRNAs can thus be used as biomarkers to differentiate between LUSC and LUAD, and may provide a novel strategy for their differential diagnosis and treatment. [ABSTRACT FROM AUTHOR]

• A facile hydrogen-bond-breaking route can awaken n → π* electronic transition in g-C 3 N 4. • The n → π* electronic transition extends the light absorption edge of g-C 3 N 4 to over 510 nm. • Such n → π* electronic transition contributes to increased photocatalytic H 2 generation. Achieving the excitation of lone pairs (n → π*) in graphitic carbon nitride (g-C 3 N 4) can not only extend visible light absorption range, but also increase the amount of catalytically active π electrons, thereby leading to enhanced photocatalytic hydrogen (H 2) generation. However, awakening n → π* electronic transition in g-C 3 N 4 is highly challenging. Here we report on activating n → π* electronic transition by breaking hydrogen bonds in g-C 3 N 4 through a post thermal annealing process. The g-C 3 N 4 thus obtained shows greatly increased photocatalytic H 2 generation under visible light irradiation. Under optimal conditions, the highest H 2 generation rate reached 33.3 μmol·h−1, which is 25 times higher than that of pristine g-C 3 N 4 without n → π* electronic transition (1.3 μmol·h−1). Moreover, the longest wavelength that can photoexcite g-C 3 N 4 to generate H 2 is 510 nm, nearly a 50 nm red shift to the absorption edge of pristine g-C 3 N 4 (~460 nm). This work demonstrates a great potential of utilizing n → π* electronic transition to increase the photocatalytic performance of g-C 3 N 4 via breaking hydrogen bonds. [ABSTRACT FROM AUTHOR]

Asthma is defined as a heterogeneous disease, usually characterized by chronic airway inflammation. Long noncoding RNAs (lncRNAs) play important roles in various biological processes. To know more about the relationships between lncRNAs and asthma, gene microarray analysis was performed to screen differentially expressed lncRNAs between the lung tissue of ovalbumin (OVA) mice and control mice. Further studies showed that downregulating differentially expressed lncRNA-AK149641 by adeno-associated virus 6 (AAV6) in OVA mice inhibited airway inflammation, with improved airway compliance and resistance, diminished infiltration of inflammatory cells, as well as less secretions of mucus, tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6). Moreover, the activity of nuclear factor-kappa B (NF-κB) in the lung tissue was reduced after downregulating lncRNA-AK149641. In conclusion, we proposed that downregulation of lncRNA-AK149641 attenuated the airway inflammatory response in an OVA-induced asthma mouse model, probably in association with modulation of the NF-κB signaling pathway. [ABSTRACT FROM AUTHOR]

Introduction: This study aimed to investigate the mechanism of action of cordyceps polysaccharide on rat acute liver failure (ALF).Material and Methods: Sixty rats were randomly divided into five groups: a normal group, a model group without cordyceps polysaccharide and groups with cordyceps polysaccharide in three different doses (5, 10 and 20 mg/ml). Serum alanine aminotransferase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), and total bilirubin (TBIL) contents were measured for assessing liver function. Hematoxylin and eosin (HE) staining was used for observing liver pathology. Apoptosis was detected through the method of terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining. Protein expression levels of caspase-1, interleukin-18 (IL-18), IL-10, vascular endothelial growth factor (VEGF), and stromal cell-derived factor-1α (SDF-1α) in liver tissue were detected by Western blot. Proliferating cell nuclear antigen (PCNA) and signal regulatory protein-α1 (SIRPα1) contents were measured by PCR.Results: The rat ALF model was established with D-galactosamine induced by lipopolysaccharide (LPS). After modelling, tissue HE staining showed typical manifestation of acute liver injury that emerged in the rat ALF model. The liver failure group showed higher levels of serum ALT and AST, as well as hepatocyte apoptosis, than the groups treated with cordyceps polysaccharide. Cordyceps polysaccharide can effectively suppress the protein expression of caspase-1, IL-18, and IL-10, while simultaneously increasing the protein expression of VEGF and SDF-1α, as well as the mRNA expression of PCNA and SIRPα1.Conclusions: Cordyceps polysaccharide can alleviate the immune response and inflammatory injury in ALF by regulating the balance of pro-inflammatory and anti-inflammatory factors and reducing the apoptosis. [ABSTRACT FROM AUTHOR]

Background: Concurrent chemoradiotherapy is the common first-line treatment for patients with advanced cervical cancer. However, radioresistance remains a major clinical challenge, which results in recurrence and poor survival. Many studies have shown the potential of Delta-like Ligand 4 (DLL4) as a novel prognostic biomarker and therapeutic target in many solid tumors. Previously, we have found that high DLL4 expression in tumor cells may predict the pelvic lymph node metastasis and poor prognosis in patients with cervical cancer. In our present study, we further studied the effects of DLL4 on the biological behavior and radiosensitivity of cervical cancer cells. Methods: The expression of DLL4 and epithelial–mesenchymal transition (EMT) phenotype markers in cervical cancer cell lines or tissues were detected using Western blotting, and the expression of DLL4 mRNA in cervical cancer cell lines or tissues was detected using Quantitative real-time PCR. The effect of DLL4 on cell proliferation, migration, and radiosensitivity was evaluated using the CCK8 assay, flow cytometry, Transwell assays for cell invasion and migration, and Immunofluorescence staining in vitro. Results: The expression of DLL4 in radiotherapy-resistant SiHa cells was significantly higher than that in radiotherapy-sensitive Me-180 cells. Furthermore, downregulation of DLL4 enhanced the radiosensitivity of SiHa and Caski cells via the inhibition of cell proliferation, promotion of radiation-induced apoptosis, and inhibition of the DNA damage repair. Moreover, downregulation of DLL4 inhibited the EMT and reduced the proliferation, invasion, and migration ability in SiHa and Caski cells. Consistent with the DLL4 expression in the cell lines, the expression of DLL4 in the tissues of the radioresistant group was also higher than that of the radiosensitive group. Conclusions: Downregulation of DLL4 inhibited the progression and increased the radiosensitivity in cervical cancer cells by reversing EMT. These results indicated the promising prospect of DLL4 against the radioresistance and metastasis of cervical cancer and its potential as a predictive biomarker for radiosensitivity and prognosis in patients with cervical cancer patients receiving concurrent chemoradiotherapy (cCRT). [ABSTRACT FROM AUTHOR]

Cancer testis antigens (CTAs) are promising targets for T cell-based immunotherapy and studies have shown that certain CT genes are epigenetically depressed in cancer cells through DNA demethylation. Melanoma-associated antigen A11 (MAGE-A11) is a CTA that is frequently expressed in esophageal cancer and is correlated with a poor esophageal cancer prognosis. Consequently, MAGE-A11 is a potential immunotherapy target. In this study, we evaluated MAGE-A11 expression in esophageal cancer cells and found that it was downregulated in several tumor cell lines, which restricted the effect of immunotherapy. Additionally, the specific recognition and lytic potential of cytotoxic T lymphocytes (CTLs) derived from the MAGE-A11 was determined. Specific CTLs could kill esophageal cancer cells expressing MAGE-A11 but rarely lysed MAGE-A11-negative tumor cells. Therefore, induction of MAGE-A11 expression is critical for CTLs recognition and lysis of esophageal cancer cells. Treatment with the DNA methyltransferase inhibitor 5-aza-2′-deoxycytidine increased MAGE-A11 expression in esophageal cancer cells and subsequently enhanced the cytotoxicity of MAGE-A11-specific CD8+T cells against cancer cell lines. Furthermore, we found that PD-L1 expression in esophageal cancer cells affected the antitumor function of CTLs. programmed death-1 (PD-1)/PD-L1 blockade could increase the specific CTL-induced lysis of HLA-A2+/MAGE-A11+ tumor cell lines treated with 5-aza-2′-deoxycytidine. These findings indicate that the treatment of tumor cells with the DNA methyltransferase inhibitor 5-aza-2′-deoxycytidine augments MAGE-A11 expression in esophageal cancer cells. The combination of epigenetic modulation by 5-aza-2′-deoxycytidine and PD-1/PD-L1 blockade may be useful for T cell-based immunotherapy against esophageal cancer. [ABSTRACT FROM AUTHOR]

Surface engineering is of great importance to rationally change the catalyst's surface structure and provide insights into the surface reactivity when developing high-efficiency and earth-abundant catalysts for electrocatalytic water splitting. Herein, nitrogen-doped carbon (NC) nanoparticle-decorated MoS2 is successfully constructed via a surface carbonization strategy simply by sintering MoS2 microspheres and dicyandiamide (DCDA), which generates tiny NC nanoparticles on the MoS2 surface. The presence of NC nanoparticles on MoS2 not only facilitates the charge transfer and reaction kinetics but also promotes the hydrogen adsorption during the electrocatalytic hydrogen evolution reaction (HER) process, thereby endowing the catalyst with a much lower overpotential and a higher current density in comparison to pristine MoS2. This work indicates that the surface carbonization strategy provides a promising way for designing highly active electrocatalysts in terms of surface structure engineering. [ABSTRACT FROM AUTHOR]