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Among the three pre-treatment materials, Fe3O4@HPMC@DMSA NPs were selected to be the best material and were used to perform MSPE-HPLC-UV.

Accumulating evidence has linked benzo(α)pyrene (BαP) exposure to carcinogenesis with severe damages to reproductive, hematopoietic, hepatic, and renal tissues. Ginger (Zingiber officinale Roscoe) rhizome consumed worldwide as a spice and herbal medicine, exhibits a variety of health benefits including antioxidant, anti-inflammatory, and anti-cancer activities. In the present work, the efficacy of three ginger compounds namely 6-gingerol, zingerone, and curcumin against BαP-induced toxicity in mice was investigated. Kunming Swiss albino male mice were orally gavage with curcumin, 6-gingerol, or zingerone (all at a dose of 100 mg/kg body weight) for two weeks before intraperitoneal injection with benzo(α)pyrene (BαP) at 20 mg/kg body weight. The effect of these ginger compounds on antioxidant and xenobiotic-metabolising enzymes in vivo was investigated. Results showed that pre-treatment with curcumin, 6-gingerol, or zingerone significantly (p < 0.05) increased catalase (CAT) and glutathione peroxidase (GPx) activities in serum and liver of mice, upregulated activities of phase II enzymes (quinone reductase (QR) and glutathione-S-transferase (GST)), and their protein and mRNA levels in liver of mice; but reduced levels of activities, protein, and mRNA of phase I enzymes (CYP1A1 and CYP1A2) as compared to those of BαP-only treatment. Furthermore, these compounds significantly (p < 0.05) stimulated nuclear factor erythroid 2-related factor 2 (Nrf2) protein expression, whilst curcumin suppressed the expression of Kelch-like ECH-associated protein 1 (Keap1) in liver. These results could contribute to our understanding of the potential beneficial effects of consuming ginger as food and/or dietary supplement.

Supplementary Data from Low Glucose–Induced Overexpression of HOXC-AS3 Promotes Metabolic Reprogramming of Breast Cancer

Breast cancer is the most common malignancy in women worldwide. However, the mechanisms underlying breast cancer energy metabolism and progression remain obscure. Cancer cells rapidly adapt to microenvironments with fluctuating nutrient levels. Here, we characterized a long noncoding RNA (lncRNA), HOXC-AS3, which is activated upon glucose deprivation to trigger a nutrient-stress response and a switch in glucose metabolism. Upregulation of HOXC-AS3 in breast cancer was identified by in published microarray and RNA-sequencing datasets, and then confirmed by qRT-PCR in fresh breast cancer tissues. Glucose deprivation induced HOXC-AS3 overexpression in a dose- and time-dependent manner in breast cancer cells. Gain- and loss-of-function experiments in vitro and in vivo showed that HOXC-AS3 triggers energy metabolism reprogramming. ChIRP-mass spectrometry and unique molecular identifier RNA immunoprecipitation and high-throughput sequencing (UMI RIP-seq) identified binding motifs of HOXC-AS3 with SIRT6. HOXC-AS3 selectively antagonized SIRT6-mediated H3K9ac deacetylation of glycolysis-related genes. Moreover, HOXC-AS3 binding to SIRT6 prevented contact inhibition of HIF1α, leading to reprogramming of metabolic pathways. In addition, HOXC-AS3, SP1, and miR-1224–5p formed a positive feedback loop to maintain cancer-promoting signals. Furthermore, administration of anti-HOXC-AS3-motif-RNAs effectively blocked the function of HOXC-AS3, ultimately suppressing breast cancer progression. These results reveal a critical role for HOXC-AS3 in regulating the metabolic reprogramming of breast cancer cells under metabolic stress. Use of an anti-HOXC-AS3-motif RNA mixture may be a promising strategy to suppress breast cancer progression.Significance:HOXC-AS3 is a low glucose–activated long noncoding RNA that triggers metabolic reprogramming in breast cancer cells to adapt to nutrient stress, identifying HOXC-AS3 as a potential therapeutic target for breast cancer treatment.

Breast cancer is the most common malignancy in women worldwide. However, the mechanisms underlying breast cancer energy metabolism and progression remain obscure. Cancer cells rapidly adapt to microenvironments with fluctuating nutrient levels. Here, we characterized a long noncoding RNA (lncRNA), HOXC-AS3, which is activated upon glucose deprivation to trigger a nutrient-stress response and a switch in glucose metabolism. Upregulation of HOXC-AS3 in breast cancer was identified by in published microarray and RNA-sequencing datasets, and then confirmed by qRT-PCR in fresh breast cancer tissues. Glucose deprivation induced HOXC-AS3 overexpression in a dose- and time-dependent manner in breast cancer cells. Gain- and loss-of-function experiments in vitro and in vivo showed that HOXC-AS3 triggers energy metabolism reprogramming. ChIRP-mass spectrometry and unique molecular identifier RNA immunoprecipitation and high-throughput sequencing (UMI RIP-seq) identified binding motifs of HOXC-AS3 with SIRT6. HOXC-AS3 selectively antagonized SIRT6-mediated H3K9ac deacetylation of glycolysis-related genes. Moreover, HOXC-AS3 binding to SIRT6 prevented contact inhibition of HIF1α, leading to reprogramming of metabolic pathways. In addition, HOXC-AS3, SP1, and miR-1224–5p formed a positive feedback loop to maintain cancer-promoting signals. Furthermore, administration of anti-HOXC-AS3-motif-RNAs effectively blocked the function of HOXC-AS3, ultimately suppressing breast cancer progression. These results reveal a critical role for HOXC-AS3 in regulating the metabolic reprogramming of breast cancer cells under metabolic stress. Use of an anti-HOXC-AS3-motif RNA mixture may be a promising strategy to suppress breast cancer progression. Significance: HOXC-AS3 is a low glucose–activated long noncoding RNA that triggers metabolic reprogramming in breast cancer cells to adapt to nutrient stress, identifying HOXC-AS3 as a potential therapeutic target for breast cancer treatment.

Introduction Demyelination causes neurological deficits involving visual, motor, sensory symptoms. Deregulation of several enzymes has been identified in demyelination, which holds potential for the development of treatment strategies for demyelination. However, the specific effect of methionine sulfoxide reductase A (MsrA) on demyelination remains unclear. Hence, this study aims to explore the effect of MsrA on oxidative stress and inflammatory response of microglia in demyelination. Methods Initially, we established a mouse model with demyelination induced by cuprizone and a cell model provoked by lipopolysaccharide (LPS). The expression of MsrA in wild-type (WT) and MsrA-knockout (MsrA-/-) mice were determined by RT-qPCR and Western blot analysis. In order to further explore the function of MsrA on inflammatory response, and oxidative stress in demyelination, we detected the expression of microglia marker Iba1, inflammatory factors TNF-α and IL-1β and intracellular reactive oxygen species (ROS), superoxide dismutase (SOD) activity, as well as expression of the NOX2-MAPKs/NF-κB signaling pathway-related genes in MsrA-/- mice and LPS-induced microglia following different treatments. Results MsrA expression was downregulated in MsrA-/- mice. MsrA silencing was shown to produce severely injured motor coordination, increased expressions of Iba1, TNF-α, IL-1β, ROS and NOX2, and extent of ERK, p38, IκBα, and p65 phosphorylation, but reduced SOD activity. Conjointly, our study suggests that Tat-MsrA fusion protein can prevent the cellular inflammatory response and subsequent demyelination through negative regulation of the NOX2-MAPKs/NF-κB signaling pathway. Conclusion Our data provide a profound insight on the role of endogenous antioxidative defense systems such as MsrA in controlling microglial function.

Highly rigid and versatile functionality of DNA tetrahedron nanostructures is often used in biosensing systems as a potential detection technique. In this work, a signal on-off fluorescence sensor based on the self-assembly DNA tetrahedron was developed for the rapid simultaneous detection of ochratoxin A (OTA) and aflatoxin B1 (AFB1). The fluorophore labeled DNA tetrahedron as probe was successfully synthesized via a simple denaturing annealing, the distance between fluorophore and quencher was regulated according to the change of hairpin structure on the tetrahedron. The fluorescence intensity of Cy3 decreased significantly in the presence of OTA, while the fluorescence intensity of Cy5 kept almost unchanged. And the fluorescence intensity of Cy5 decreased significantly in the presence of AFB1, while the fluorescence intensity of Cy3 kept almost unchanged. In the present of OTA and AFB1, the fluorescence intensity of Cy3 and Cy5 showed decreased significantly simultaneously, indicating the fluorescence sensor can be applied to simultaneous detect OTA and AFB1. Hence, the quantitative analysis of OTA and AFB1 was performed indirectly by the fluorescence intensity changes. The limits of detection (LOD) are as low as 0.005 ng/mL for OTA and 0.01 ng/mL for AFB1. In addition, the novel DNA tetrahedron-based fluorescence sensor possessed a universal applicability, which could be well applied in corn and wine.

Purpose: KIF26B is a member of the kinesin superfamily that is up-regulated in various tumors, including breast cancer (BC), which can promote tumor progression. This study aimed to investigate the potential function of KIF26B in BC, and the underlying mechanisms, focusing mainly on cell proliferation. Methods: KIF26B expression was examined in BC tissue samples obtained from 99 patients. We performed MTS, EdU and flow cytometry assays to detect cell proliferation, and western blotting to measure the expression of cell cycle-related proteins in MDA-MB-231 and MDA-MB-468 cells following KIF26B knockdown. Promoter analysis was used to study the upstream regulatory mechanism of KIF26B. Results：KIF26B was upregulated in BC tissue samples. High expression of KIF26B was associated with clinicopathological parameters, such as positive lymph node metastasis, higher tumor grade and high proliferative index in BC tissue. Furthermore, knockdown of KIF26B expression inhibited MDA-MB-231 and MDA-MB-468 cell proliferation, arresting cells in the G1 phase of the cell cycle in vitro. Similarly, KIF26B silencing decreased the expression levels of Wnt, β-catenin and cell cycle-related proteins such as c-Myc, cyclin D1 and cyclin-dependent kinase 4, whilst increasing the expression of p27. Moreover, ELK1 could bind to the core promoter region of KIF26B and activate its transcription. Conclusion: KIF26B acts as an oncogene in BC that can promote development of BC by regulating multiple proteins involved in the cell cycle. ELK1 activates KIF26B transcription.

Objective The aim of this study was to investigate the role of KIF26A in breast cancer. Method qRT-PCR and immunohistochemistry were conducted to explore KIF26A expression and functional contribution to breast cancer development. MTS, EDU, colony formation assays, and flow cytometry analysis were conducted to assess cell proliferation characteristics and cell cycle progression. A series of 5′-flanking region deletion plasmids and mutating the binding site, with the luciferase reporter assay, were used to identify the core promotor region of KIF26A. The prediction by software and construction of the transcriptional factor plasmids were used to identify the transcriptional factor. Chromatin immunoprecipitation assay could demonstrate transcriptional factor directly binding to the KIF26A promoter. Human Genome Oligo Microarray Assay and gene ontology (GO) and pathway analyses were used to predict the downstream pathway. Results Our results showed that in breast cancer tissues, elevated KIF26A expression was significantly correlated with lymph node metastasis. KIF26A could promote proliferation and G0/G1 phase cell cycle progression in breast cancer cells. The core promoter region of the human KIF26A gene was located upstream of the transcription start site at position −395 to −385. The transcriptional factor E2F1 was shown to activate KIF26A expression. Furthermore, KIF26A was shown to inhibit the expression of p21, then activate CDK–RB–E2Fs pathway. The elevated E2F1 can activate the cell cycle progression and the KIF26A expression, forming feedback loop. Conclusions The present study demonstrated that KIF26A, directly upregulated by E2F1, promoted cell proliferation and cell cycle progression via CDK–RB–E2Fs feedback loop in breast cancer.

Long noncoding RNAs (lncRNAs) were demonstrated to play important roles in gene regulation and cancer progression. However, the functional roles of lncRNAs and the detailed mechanisms underlying gastric cancer (GC) progression remain largely unclear. Here, we identified a novel cancer-related lncRNA, termed lncRNA GCMA (Gastric Cancer metastasis-associated lncRNA), which was upregulated in GC tissues with lymph node metastasis (LNM) compared with tissues without LNM. High expression of GCMA was significantly associated with poor prognosis of patients with GC. Luciferase assays, bioinformatics analyses and chromatin immunoprecipitation (ChIP) assays indicated that SP1 transcription factor directly bound to the GCMA promoter region and activated its transcription. Functionally, upregulation of GCMA dramatically promoted GC cells proliferation, migration and invasion in vitro, whereas knockdown of GCMA elicited the opposite function. Consistently, stable knockdown of GCMA inhibited tumor proliferation, invasion and metastasis in vivo. Mechanistically, by using bioinformatics analyses, RNA binding protein immunoprecipitation (RIP) assays, luciferase assays and western-blot assays, GCMA was demonstrated to function as a competing endogenous RNA (ceRNA) via competitively absorbing miR-124 and miR-34a to upregulate slug and snail, thereby induced epithelial-mesenchymal transition (EMT) and GC cell metastasis in vitro and in vivo. Collectively, these results demonstrate that GCMA functions as an oncogenic lncRNA that may serve as a potential prognostic biomarker for GC and shed new lights on targeted therapy of GC in the future.

Two helical Eu(III) metal-organic frameworks, namely, {[Eu(L)(DMF)(H2O)]·0.5DMF}n (1) and [Eu(L)(DEF)(H2O)]n (2) (H3L=3,5-bis(2-carboxylphenoxy)benzoic acid, DMF=N,N-dimethylformamide, DEF=N,N-diethylformamide), have been solvothermally synthesized in different solvents, respectively. Both complexes possess helical structures through the connectivity of Eu atoms and phenolic-oxygen containing branches of the flexible multicarboxylate ligand. Based on different helices, these two complexes exhibited hexagonal and tetragonal channels, respectively. Both complexes possess (3,6)-connected (4.62)2(42.610.83) topology but with different long Schlafli symbol. The solvent plays an important role in the formation of the final frameworks. Both complexes can sensitively and selectively detect nitrobenzene and Cu2+ ions.

Two 2-D Zn(II) compounds, namely, [Zn(HL1)(bpy)]n (1) and {[Zn(HL2)(bpe)]·0.5bpe}n (2) (H3L1 = 5-(2′-carboxyl phenoxy)isophtalic acid, H3L2 = 1,3-bis(2-carboxylphenoxy)benzoic acid, bpy = 4,4′-bipyridine, bpe = 4,4′-vinylenedipyridine), have been solvothermally synthesized from two flexible phenolic carboxylic acid ligands. Both compounds exhibit 2-D layered structures with 4-conneted 44 and 3- connected 63 topology, respectively. PXRD indicated that these compounds were stable in the basic conditions with pH range of 7–11 and their fluorescence intensities are strongly correlated with the pH value. The protonated carboxylic groups may have influences on the resulting fluorescence intensities. The possible proton transfer mechanism was discussed for such pH sensors in details through FTIR and ICP measurements. In addition, the analytical efficiency and accuracy in practical applications of these sensors were performed on the real lake water.

Two cobalt(ii) compounds, namely, {[Co(HL)(bpy)(H2O)2]·DMF}n (1), and {[Co(HL)(bpe)]·0.5bpe}n (2) (H3L = 1,3-bis(2-carboxylphenoxy)benzoic acid, bpy = 4,4'-bipyridine, bpe = 4,4'-vinylenedipyridine), have been synthesized using cobalt(ii) transition metal salt with phenolic carboxylic acid and different N-donor ligands. The compounds were fully characterized by elemental analysis, infrared spectroscopy (IR), single crystal X-ray diffraction analysis, and thermogravimetric analysis (TGA). Both compounds exhibit 2-D (4,4)-sql networks but with a wavelike and a double layered arrangement, respectively. Remarkably, these two compounds not only exhibit field-induced single-ion relaxation magnetization but also exceptional catalytic activities of benzylic C-H oxidation (conv. 90.3-99%; sele. 98.1-99%).

Accumulating evidence demonstrates that acupuncture and electroacupuncture (EA) can exert a neuroprotective role for cerebral ischemia, but their precise mechanism remains largely unknown. Therefore, in this study, the effects of EA stimulation on cerebral ischemia reperfusion and its neuroprotective mechanisms were investigated. A rat model of middle cerebral artery occlusion (MCAO) was developed, and EA stimulation (2Hz, 1mA) at Baihui and Siguan acupoints was applied 30min after MCAO and then once daily for 7 consecutive days. The results indicated that EA stimulation significantly reduced the cerebral infarct area and neurological deficit scores, decreased the number of apoptotic cells, up-regulated Bcl-2 protein expression, and down-regulated Bax protein expression. EA stimulation resulted in a significant increase of proliferative cells in the cerebral tissues. Additionally, EA stimulation significantly down-regulated the expression levels of matrix metalloproteinase -9 (MMP-9) mRNA and protein, and simultaneously up-regulated the expression levels of tissue inhibitor of metalloproteinases-1 (TIMP-1) mRNA and protein, which resulted in an imbalance of MMP-9/TIMP-1expression, although it did not significantly change MMP-2 and TIMP-2 expression. These findings indicate that EA stimulation at Baihui and Siguan acupoints exerts a neuroprotective role against cerebral ischemia-reperfusion injury, which is probably associated with the inhibition of apoptosis and altering the balance of MMP-9/TIMP-1 expression.

Two types of lanthanide coordination polymers, namely, [Ln(PA)(NO3)(DMA)3] n (Ln=Gd (1), Dy (2), Eu (3), Tb (4)) (type I), and {[Ln2(PA)3(DMF)4]·2DMF} (Ln=Eu (5), Tb (6)) (type II) (PA=Pamoic acid, DMA=dimethylacetamide, DMF=N,N-dimethylformamide), have been synthesized by the reaction of Ln(NO3)3·6H2O with pamoic acid through layer diffusion method. These complexes were characterized by single crystal X-ray diffraction, infrared spectroscopy (IR), thermogravimetric analysis (TGA), fluorescence and magnetic measurements. Solvents and lanthanide atoms in the reaction play an important role in controlling different structures. Type I demonstrated 1-D linear chain structure connected by Ln atoms and PA ligands. Type II exhibited non-interpenetrating 3-D 6-connected 43612 nets based on binuclear [Ln2(CO2)6(DMF)4] cores. Magnetic properties of complexes 1–4 were investigated in details. Complex 1 shows significant magnetocaloric effect with–ΔSm=20.37 J kg–1 K–1 at 3.0 K and 7 T. Complex 2 exhibits slow relaxation of the magnetization. Complexes 3–6 exhibit both ligand- and metal-centered fluorescent properties. Complex 6 demonstrates fluorescent sensing of DMF and Cu2+ ion.

Rapid Salmonella detection using Recombinase Aided Amplification was established. The reaction completes in 20 min at 39°C and can be performed with a portable device. Once further improved, this method should be a great choice for monitoring contamination, such as foodborne Salmonella or for similar purposes.

The aesthetic appreciation of vocal music in China is embodied in many aspects, and has different perspectives. National Science and explore the needs of China's national vocal music art aesthetic appreciation based on the China promote diversified development of vocal music, and has formed Chinese characteristics of the vocal training system has important value. How China's national vocal music art in the new period, new and better world cultural patterns in maintaining ethnic characteristics, and better international has become an important task in front of vocal workers in china. A vocal art to go international, the first premise is to maintain and strengthen their nationality, their nationality is more cosmopolitan, the nation is the world, it is the truth. We must carefully protect, inherit and develop our national vocal music's origin and irreplaceable, so as to make it truly international. Nationality is the premise and basis of vocal art in China to the international, and international development can make our national vocal music art has stronger artistic vitality, in order to make the sustainable development of our national vocal music art real. Only in this way can we continue to develop and progress, and then we can show the charm of Chinese national art to the world with vocal music art, and show our national spirit to the world.

To compare serum levels of chemerin in type 2 diabetes mellitus (T2DM) with or without retinopathy, and to investigate the relationship between serum chemerin levels and diabetes retinopathy.A total of 60 T2DM patients and 20 healthy subjects (control group) were enrolled in this study. Of the T2DM patients, 15 had proliferative diabetic retinopathy (PDR group), 20 had non-proliferative retinopathy (NPDR group) and 25 had no retinopathy (T2DM group). Their serum samples were collected for testing the levels of chemerin, vascular endothelial growth factor (VEGF), C-reactive protein (CRP) and so on. The values were analyzed to compare the differences among the groups. Simple linear regression analysis and multiple stepwise linear regression analysis were used to determine the correlations between variables and chemerin. Trend chi-square was used to determine the correlations between chemerin and the severity of diabetic retinopathy (DR).Chemerin levels in group PDR, NPDR and no DR were 147.56 ± 35.98 μg/l, 128.09 ± 16.33 μg/l and 113.19 ± 19.89 μg/l, with the significant difference across the three groups (p 0.05). But there was no difference between control group (109.55 ± 20.98 μg/l) and T2DM group. Simple linear regression show that serum chemerin was correlated with duration of diabetes, body mass index (BMI), serum triglycerides, total-cholesterol, CRP and VEGF, and not correlated with age, systolic and diastolic blood pressure in T2DM patients. Stepwise regression analysis showed that BMI, CRP and VEGF were significantly associated with serum chemerin (p = 0.006, p = 0.011 and p = 0.036, respectively). In addition, the more severity of DR as the chemerin levels increased (χ(2) = 16.07, p 0.001).Serum levels of chemerin were significantly increased in the NPDR and PDR group. Elevated serum level of chemerin and its positive correlation with BMI, CRP and VEGF suggested that chemerin was associated with obesity, inflammation and neovascularization and might be involved in the development of DR.

From a methyl-substituted thieno[2,3-b]thiophene dicarboxylate, three types of three-dimensional (3-D) microporous lanthanide-based metal-organic frameworks, {[Ln(DMTDC)1.5(H2O)2]·DEF}n (type I, Ln = Eu 1, Tb 2), {[Ln(DMTDC)1.5(H2O)2]·0.5DMF·0.5H2O}n (type II, Ln = Gd 3, Dy 4, Er 5), and {[Ln4(DMTDC)6(DMF)2]·0.5DMF·1.5H2O}n (type III, Ln = Er 6) (H2DMTDC = 3,4-dimethylthieno[2,3-b]thiophene-2,5-dicarboxylic acid, DEF = N,N'-diethylformamide, DMF = N,N'-dimethylformamide), have been solventhermally synthesized. Types I and II are isostructural, which exhibit 1-D triangular channels constructed by double-stranded rod-shaped {Ln(CO2)2}n chains. Type III demonstrates an intriguing framework with triple-stranded rod-shaped {Ln(CO2)3}n chains arranged along the (1,1,0) and (1,-1,0) axes and possesses two kinds of triangular channels along two axes, respectively. Immobilization of the Lewis basic sites of thiophene groups induced gas adsorption and sensing properties into these microporous frameworks. Complexes 5(Er) and 6(Er) display moderate adsorption properties toward N2 and CO2, and the Qst of CO2 are as high as 36.3 and 34.8 kJ mol(-1), respectively. Complexes 1(Eu) and 2(Tb) exhibit sensing properties toward nitrobenzene, acetone, and the Cu(2+) ion in both DMF and aqueous solution. Complex 3(Gd) shows a significant magnetocaloric effect with ΔSm = 24.3 J·kg(-1)·K(-1) at 3.0 K and 7 T. Complex 4(Dy) exhibits slow magnetic relaxation with the energy barrier Δ/kB of 48.29 K.