Multifunctional polyaniline modified calcium alginate aerogel membrane with antibacterial, oil-water separation, dye and heavy metal ions removal properties for complex water purification.

With the rapid development of urbanization, the discharge of industrial wastewater has led to increasingly critical water pollution issues. Additionally, heavy metals, organic dyes, microorganisms and oil pollution often coexist and have persistence and harmfulness. Developing materials that can treat these complex pollutants simultaneously has important practical significance. In this study, a calcium alginate-based aerogel membrane (PANI@CA membrane) was prepared by spraying, polymerization, Ca2+ cross-linking and freeze-drying using aniline and sodium alginate as raw materials. Oil-water emulsion can be separated by PANI@CA membrane only under gravity, and the separation efficiency was as high as 99 %. At the same time, the membrane can effectively intercept or adsorb organic dyes and heavy metal ions. The removal rates of methylene blue and Congo red were above 92 % and 63 % respectively even after ten times of cyclic filtration. The removal rate of Pb2+ was up to 95 %. In addition, PANI@CA membrane shows excellent photothermal conversion ability, and it can effectively kill Staphylococcus aureus under 808 nm laser irradiation. PANI@CA membrane has the advantages of low cost, simple preparation, good stability and high recycling ability, and has potential application prospects in wastewater treatment.

CircMAN1A2 is upregulated by Helicobacter pylori and promotes development of gastric cancer.

Helicobacter pylori (H. pylori) is one of the main causes of gastric cancer. It has been reported that circRNAs play a vital role in the development of multiple types of cancer. However, the role of H. pylori-induced circRNAs in the development of gastric cancer has not been studied. In this study, we found that H. pylori could induce the upregulation of circMAN1A2 in AGS and BGC823 cells independent of CagA. The downregulation of circMAN1A2 could inhibit the proliferation, migration and invasion of gastric cancer cells, and circMAN1A2 could promote the progression of gastric cancer induced by H. pylori by sponging miR-1236-3p to regulate MTA2 expression. Furthermore, circMAN1A2 knockdown inhibited xenograft tumour growth in vivo, and the overexpression of circMAN1A2 was associated with the progression of gastric cancer. Hence, Helicobacter pylori induced circMAN1A2 expression to promote the carcinogenesis of gastric cancer, and circMAN1A2 might be a new potential diagnostic marker and therapeutic target for gastric cancer.

The ATP Level in the mPFC Mediates the Antidepressant Effect of Calorie Restriction.

Food deprivation can rescue obesity and overweight-induced mood disorders, and promote mood performance in normal subjects. Animal studies and clinical research have revealed the antidepressant-like effect of calorie restriction, but little is known about the mechanism of calorie restriction-induced mood modification. Previous studies have found that astrocytes modulate depressive-like behaviors. Inositol 1,4,5-trisphosphate receptor type 2 (IP3R2) is the predominant isoform in mediating astrocyte Ca2+ signals and its genetic knockout mice are widely used to study astrocyte function in vivo. In this study, we showed that deletion of IP3R2 blocked the antidepressant-like effect induced by calorie restriction. In vivo microdialysis experiments demonstrated that calorie restriction induced an increase in ATP level in the medial prefrontal cortex (mPFC) in naïve mice but this effect disappeared in IP3R2-knockout mice, suggesting a role of astrocytic ATP in the calorie restriction-induced antidepressant effect. Further experiments showed that systemic administration and local infusion of ATP into the mPFC induced an antidepressant effect, whereas decreasing ATP by Apyrase in the mPFC blocked calorie restriction-induced antidepressant regulation. Together, these findings support a role for astrocytic ATP in the antidepressant-like effect caused by calorie restriction.

Involvement of P2X2 receptor in the medial prefrontal cortex in ATP modulation of the passive coping response to behavioral challenge.

P2X2 and P2X3 receptors are widely expressed in both the peripheral nervous system and the central nervous system and have been proven to participate in different peripheral sensory functions, but there are few studies on the involvement of P2X2 and P2X3 receptors in animal behaviors. Here we used P2X2 and P2X3 knockout mice to address this issue. P2X2 knockout mice showed normal motor function, exploratory behavior, anxiety-like behaviors, learning and memory behaviors and passive coping response to behavioral challenge. Nevertheless, the effect of ATP infusion in the medial prefrontal cortex (mPFC) on the passive coping response was blocked by P2X2 but not P2X3 receptor deletion. Additionally, no deficits in a wide variety of behavioral tests were observed in P2X3 knockout mice. These findings demonstrate a role of P2X2 receptor in the mPFC in adenosine-5'-triphosphate modulation of the passive coping response to behavioral challenge and show that the P2X2/P2X3 receptor is dispensable for behaviors.

Knockdown of lncRNAXLOC_001659 inhibits proliferation and invasion of esophageal squamous cell carcinoma cells.

BACKGROUND: Studies have shown that long non-coding RNAs (lncRNAs) play a key role in almost all key physiological and pathological processes, including different types of malignant tumors. Our previous lncRNA microarray results have shown that lncRNA XLOC_001659 is upregulated in esophageal cancer (EC) tissues, with a fold change of 20.9 relative to normal esophageal tissues. But its effect and the molecular biological mechanisms on proliferation and invasion of EC cells remain unclear. AIM: To investigate the effect of lncRNA XLOC_001659 on esophageal squamous cell carcinoma (ESCC) cells and explore the molecular biological mechanisms involved. METHODS: RT-qPCR assay was used to quantify the expression levels of lncRNAXLOC-001659 and miR-490-5p. The proliferative capacity of the cells was determined using CCK8 and colony formation assays, and the effect of lncRNAXLOC-001659 on the invasion of ESCC cells was determined by Transwell assay. Dual-luciferase reporter assay was used to detect the target genes of lncRNAXLOC-001659 and miR-490-5p. RESULTS: The results of RT-qPCR showed that the expression of lncRNAXLOC_001659 was upregulated in ESCC cells. CCK-8 assay showed that knockdown of lncRNAXLOC_001659 significantly inhibited ESCC cell proliferation. Colony formation and Transwell invasion assays showed that knockdown of lncRNAXLOC_001659 or overexpression of miR-490-5p significantly inhibited ESCC cell growth and invasion. Furthermore, lncRNAXLOC_001659 acts as an endogenous sponge by competitively binding to miR-490-5p to downregulate miR-490-5p. Further results confirmed that miR-490-5p targeted PIK3CA, and the recovery of PIK3CA rescued lncRNAXLOC_001659 knockdown or miR-490-5p overexpression-mediated inhibition of cell proliferation and invasion, which suggested the presence of an lncRNAXLOC_001659/miR-490-5p/PIK3CA regulatory axis. CONCLUSION: Knockdown of lncRNA XLOC_001659 inhibits proliferation and invasion of ESCC cells via regulation of miR-490-5p/PIK3CA, suggesting that it may play a role in ESCC tumorigenesis and progression.

Retraction Note to: Effect of miR-451 on the Biological Behavior of the Esophageal Carcinoma Cell Line EC9706.

The Editor-in-Chief has retracted this article [1] because Figure 8 overlaps with Figure 6b of [2] and Figure 6 overlaps with Figure 3 of [3] and Figure 3 of [4].

[Retracted] Effects of cyclin E gene silencing on the proliferation of esophageal cancer cell lines, EC9706, Eca109 and KYSE30.

Subsequently to the publication of this article, an interested reader drew to our attention the fact that the six panels shown in Fig. 6 shared several areas of identity among them. Following an internal investigation, a laboratory technician, who was responsible for editing the pictures, admitted that the data as presented in the figure had been manipulated after having mislaid some of the original data. The corresponding author of the article takes responsibility for this oversight, and therefore the paper is to be retracted from publication. All of the named authors agree to this retraction. We deeply regret that these errors were allowed to remain in the paper, and extend our apologies to the readership of the Journal. [the original article was published in Molecular Medicine Reports 7: 799-804, 2013; DOI: 10.3892/mmr.2013.1280].

Inhibitory effect of α-solanine on esophageal carcinoma in vitro.

α-solanine, a bioactive component and one of the major steroidal glycoalkaloids in potatoes, has been observed to inhibit growth and induce apoptosis in cancer cells. However, the antitumor efficacy of α-solanine on esophageal carcinoma has yet to be fully elucidated. In the present study, the antitumor efficacy of α-solanine against human esophageal carcinoma cells was investigated. It was determined that α-solanine inhibited the growth and proliferation of human esophageal EC9706 and Eca109 cancer cells in a dose-dependent manner, as well as the cell migration and invasion. In addition, the apoptotic rate was increased in the cancer cells treated with α-solanine in a dose-dependent manner, compared with that of the control group (P<0.05). The expression levels of tumor metastasis-related proteins, including matrix metalloproteinase (MMP)-2 and MMP-9, were reduced in the cells treated with α-solanine, as compared with the control group. Conversely, significantly higher expression levels of E-cadherin were detected in the α-solanine-treated groups, as compared with the control group (P<0.05). Therefore, the current results provide a novel insight into the anti-tumor mechanism of α-solanine, and suggest that α-solanine is a potential agent for the prevention and treatment of esophageal carcinoma.

MiR-451 inhibits proliferation of esophageal carcinoma cell line EC9706 by targeting CDKN2D and MAP3K1.

AIM: To investigate the underlying molecular mechanisms of miR-451 to inhibit proliferation of esophageal carcinoma cell line EC9706. METHODS: Assays for cell growth, apoptosis and invasion were used to evaluate the effects of miR-451 expression on EC cells. Luciferase reporter and Western blot assays were used to test whether cyclin-dependent kinase inhibitor 2D (CDKN2D) and MAP3K1 act as major targets of miR-451. RESULTS: The results showed that CDKN2D and MAP3K1 are direct targets of miR-451. CDKN2D and MAP3K1 overexpression reversed the effect of miR-451. MiR-451 inhibited the proliferation of EC9706 by targeting CDKN2D and MAP3K1. CONCLUSION: These findings suggest that miR-451 might be a novel prognostic biomarker and a potential target for the treatment of esophageal squamous cell carcinoma in the future.

Anti-idiotypic nanobody-phage based real-time immuno-PCR for detection of hepatocarcinogen aflatoxin in grains and feedstuffs.

Aflatoxins are a group of extremely toxic small molecules that have been involved in human hepatic and extrahepatic carcinogenesis as causative agents. Herein, we developed a real-time immuno polymerase chain reaction (IPCR) assay for the accurately quantitative detection of aflatoxins in agri-products base on a M13 phage containing aflatoxin anti-idiotypic nanobody and its encoding DNA which was used to design the specific primers. The limit of detection (LOD) of the assay is 0.02 ng/mL, which exhibits a 4-fold improvement over traditional phage ELISA. The developed method was successfully validated with the samples of corn, rice, peanut, and feedstuff, which are major aflatoxin-contaminated agri-products. And the recoveries were from 77.05 to 122.16%. For further validation, the developed assay was also compared with a reference HPLC method for the analysis of aflatoxins in corn and peanuts, and concordant results (R(2) = 0.991) were obtained. In this context, this study provides a novel opportunity to analyze aflatoxins in agri-products.

[Effect of medicines for activating blood and reinforcing Qi on angiogenesis in infarcted myocardium edge area of acute myocardial infarction model in rats].

OBJECTIVE: To study the effect of medicines for activating blood and reinforcing Qi on the number of new micro-vessels and the protein expressions of VEGF and bFGF in the infarcted myocardium edge area of acute myocardial infarction (AMI) model in rats. METHOD: The AMI model of rats was established. After the successful model establishment, rats were randomly divided into the sham-operated group, the model group, the Danshen-Huangqi (1 : 2) group, the Danshen-Huangqi (1 : 1) group, the Chuanxiong-Huangqi (1 : 2) group, the Danshen group, the Chuanxiong group, the Chishao group and the Shexiang Baoxin pill group, with five rats in each group. Rats in each medicated group were orally administered with drugs as per 13.5 g x kg(-1) x d(-1) once everyday for three weeks. The immunohistochemical SP method was adopted to detect the expression of vWF in myocardial tissues, and count the number of micro-vessels (MVC). The protein expression of VEGF and bFGF in myocardial tissues were determined by Western blot. RESULT: The new micro-vessels stained by vWF factor could be found in the infarcted myocardium edge area of the sham-operated group, the model group and all of medicated groups. The sham-operated group show unobvious new micro-vessels in myocardial tissues. A small amount of new micro-vessels could be seen in the infarcted myocardium edge area of the model group. Whereas a larger number of micro-vessels could be seen in the infarcted myocardium edge area of all of medicated groups. The differences between the sham-operated group and the model group had statistical significance (P < 0.05). The differences between each medicated group and the model group had statistical significance as well (P < 0.05 or P < 0.01). The lowest protein expression of VEGF and bFGF was found in myocardium of the sham-operated group, with the statistical significance compared with the model group (P < 0.05). Compared with the model group, each medicated group showed significant increase in the protein expression of VEGF and bFGF, with the statistical significance between them (P < 0.05 or P < 0.01). CONCLUSION: The Danshen group, the Chuanxiong group, the Chishao group, the Danshen-Huangqi (1 : 2) group, the Danshen-Huangqi (1 : 1) group and the Chuanxiong-Huangqi (1 : 2) group show the effect in promoting angiogenesis. Their mechanism for promoting angiogenesis may be related to the improvement of the protein expressions of VEGF and bFGF, so as to increase the contents of VEGF and bFGF and promote the angiogenesis of new vessels.

Resveratrol inhibits the growth of gastric cancer by inducing G1 phase arrest and senescence in a Sirt1-dependent manner.

Resveratrol, a naturally occurring polyphenolic compound, has been reported to exert anticancer activity by affecting diverse molecular targets. In this study, we examined the effects and the underlying mechanisms of resveratrol on gastric cancer. We found that resveratrol inhibited the proliferation of gastric cancer cells in a dose-dependent manner. At the concentration of 25 and 50 µM, resveratrol inhibited the cell viability and diminished the clonogenic potential of gastric cancer cells. Resveratrol treatment arrested gastric cancer cells in the G1 phase and led to senescence instead of apoptosis. Regulators of the cell cycle and senescence pathways, including cyclin D1, cyclin-dependent kinase (CDK4 and 6), p21 and p16, were dysregulated by resveratrol treatment. The inhibitory effects of resveratrol on gastric cancer were also verified in vivo using a nude mice xenograft model. Resveratrol (40 mg/kg/d) exerted inhibitory activities on gastric cancer development and significantly decreased the fractions of Ki67-positive cells in the tumor specimens from the nude mice. After resveratrol treatment, the induction of senescence and the changes in the expression of the regulators involved in the cell cycle and senescence pathways were similar to what we observed in vitro. However, the depletion of Sirtuin (Sirt)1 reversed the above-described effects of resveratrol both in vitro and in vivo. Our data suggest that resveratrol inhibits gastric cancer in a Sirt1-dependent manner and provide detailed evidence for the possibility of applying resveratrol in gastric cancer prevention and therapy.

JMJD2B promotes epithelial-mesenchymal transition by cooperating with ß-catenin and enhances gastric cancer metastasis.

PURPOSE: This study investigated the role of histone demethylase Jumonji domain-containing protein 2B (JMJD2B) in promoting epithelial-mesenchymal transition (EMT) and underlying molecular mechanisms in the progression of gastric cancer. EXPERIMENTAL DESIGN: The induction of EMT by JMJD2B in gastric cancer cells and its underlying mechanisms were examined by a series of assays. In vivo and in vitro assays were performed to clarify invasive potential of JMJD2B in gastric cancer cells. The expression dynamics of JMJD2B were detected using immunohistochemistry in 101 cases of primary gastric cancer tissues. RESULTS: Inhibition of JMJD2B by specific siRNA suppresses EMT of gastric cancer cells, whereas ectopic expression of JMJD2B induces EMT. Importantly, JMJD2B is physically associated with ß-catenin and enhances its nuclear localization and transcriptional activity. JMJD2B, together with ß-catenin, binds to the promoter of the ß-catenin target gene vimentin to increase its transcription by inducing H3K9 demethylation locally. JMJD2B inhibition attenuates migration and invasion of gastric cancer cells in vitro and metastasis in vivo. The expression of JMJD2B was positively correlated with tumor size (P = 0.017), differentiation status (P = 0.002), tumor invasion (P = 0.045), lymph node metastasis (P = 0.000), distant metastasis (P = 0.024), and tumor-node-metastasis (TNM) stage (P = 0.002) in patients with gastric cancer. CONCLUSIONS: The data reveal a novel function of JMJD2B in promoting EMT and gastric cancer invasion and metastasis, implicating JMJD2B as a potential target for reversing EMT and intervention of the progression of gastric cancer.

MiR-21 down-regulation suppresses cell growth, invasion and induces cell apoptosis by targeting FASL, TIMP3, and RECK genes in esophageal carcinoma.

BACKGROUND: miR-21 is overexpressed in esophageal squamous cell carcinoma (ESCC) and is thought to be correlated with the development of the cancer. The target gene of miR-21 including FASL, TIMP3 and RECK is revealed by researchers. miR-21 may be involved in the tumorgenesis of ESCC by targeting FASL, TIMP3 and RECK. AIMS: The purpose of this study was to explore the mechanism of miR-21 in the development of ESCC. METHODS: miR-21 expression in ESCC and the matched non-malignant adjacent tissues (NMATs) was examined by qRT-PCR. Cell growth, cell apoptosis and cell invasion ability of EC9706 and EC-1 cells was examined after the cells were transfected with miR-21 inhibitor. The potential target genes of miR-21 including FASL, TIMP3 and RECK were examined by western blot and Luciferase reporter assay. RESULTS: miR-21 expression was increased significantly in ESCC tissues compared with NMAT. miR-21 down-regulation inhibits cell growth, cell invasion and induces cells to apoptosis. FASL, TIMP3 and RECK are direct targets of miR-21. CONCLUSIONS: miR-21 down-regulation inhibits cell growth, invasion and induces cells to apoptosis by targeting FASL, TIMP3 and RECK genes.

Effects of cyclin E gene silencing on the proliferation of esophageal cancer cell lines, EC9706, Eca109 and KYSE30.

In order to observe the effects of cyclin E gene silencing by small interfering RNA (siRNA) on the growth, proliferation, invasion and apoptosis of esophageal cancer cell lines, including EC9706, Eca109 and KYSE30, siRNA vectors targeting cyclin E gene were constructed and then transfected into the EC9706, Eca109 and KYSE30 human esophageal cancer cell lines. Cyclin E mRNA and protein expression were determined by RT-PCR and western blotting. Cell proliferation and clonality were detected using a CCK-8 test and soft agar colony formation assay. Cell cycle distribution, apoptosis and invasion of EC9706, Eca109 and KYSE30 cells were evaluated with flow cytometry and a transwell culture system. After siRNA vectors targeting the cyclin E gene were transfected into EC9706, Eca109 and KYSE30 cell lines, compared with blank and negative control groups, the expression of cyclin E mRNA and protein (P<0.01), colony-forming units and the number of cells penetrating the transwell membrane (P<0.05) were significantly decreased, the cells in the S and G2/M phase were reduced, the cells in the G0/G1 phase were increased and the apoptosis rate was increased (P<0.01) in the experimental groups. Cyclin E gene silencing effectively inhibits growth, proliferation and invasion of esophageal cancer cells.

Effect of miR-451 on the biological behavior of the esophageal carcinoma cell line EC9706.

BACKGROUND: MicroRNAs play important roles in coordinating a variety of cellular processes. Abnormal expression of miRNAs has been linked to several cancers. However, the functional role of miR-451 in esophageal squamous cell carcinoma remains unclear. AIMS: The present study explored the effects of miR-451 on the biological behavior of the esophageal carcinoma cell line EC9706. METHODS: Synthetic miR-451 mimics were transfected into EC9706 cells using Lipofectamine™ 2000. The expression of miR-451 was analyzed by RT-PCR and the expressions of Bcl-2, AKT and phosphorylated AKT were analyzed by Western blotting. The MTT assay, soft agar colony formation assay, transwell assay and FACS were used to assess the effect of miR-451 on EC9706 cell proliferation, invasion, metastasis and apoptosis. Tumor growth was assessed by subcutaneous inoculation of cells into BALB/c nude mice. RESULTS: In comparison to the controls, a significant increase in the expression of miR-451 was associated with significantly decreased expressions of Bcl-2, AKT and p-AKT, and a significant increase in the apoptosis rate. The number of cell clones was significantly decreased by miR-451 expression, which also caused the inhibition of cell proliferation. The average number of cells penetrating the matrigel was significantly lower than the controls. Injection of miR-451 inhibited tumor growth in a xenograft model. CONCLUSIONS: Upregulated expression of miR-451 induced apoptosis and suppressed cell proliferation, invasion and metastasis in the esophageal carcinoma cell line EC9706. In addition, injection of miR-451 inhibited tumor growth in a xenograft model of esophageal cancer.

[Investigation of SLC26A4 mutations associated with inner ear malformations].

OBJECTIVE: To study the molecular pathogenesis of SLC26A4 mutations associated with inner ear malformations including large vestibular aqueduct syndrome (LVAS), Mondini dysplasia and inner ear malformations but not accompanied with LVAS. METHOD: DNA sample and clinical material were obtained from 14 sporadic LVAS probands, six Mondini dysplasia probands and seven inner ear malformations excluding IVAS probands. SLC26A4 gene mutation was analyzed by direct sequencing for its 20 coding exons. GJB2 gene and also mt12SrRNA were analyzed by direct sequencing. RESULT: In 14 cases of LVAS, two mutations were detected in 12 patients (85.7%, either homozygous or compound heterozygous mutations), and one mutation was found in two patients (14.3%). In six cases of Mondini dysplasia, two mutations were detected in all of patients (100%). No mutation could be found in the seven cases of other inner ear abnormalities not accompanied with LVAS. No pathogenic mutation was detected in all of these 27 probands in GJB2 gene and mt12SrRNA 1555/1494T. CONCLUSION: We have shown that LVAS and Mondini dysplasia closely correlate with SLC26A4 gene. No mutation was detected in seven probands of inner ear malformations not accompanied with LVAS. We should study the molecular pathogenesis of this disease in depth.

Histone demethylase JMJD2B is required for tumor cell proliferation and survival and is overexpressed in gastric cancer.

Epigenetic alterations such as aberrant expression of histone-modifying enzymes have been implicated in tumorigenesis. Jumonji domain containing 2B (JMJD2B) is a newly identified histone demethylase that regulates chromatin structure or gene expression by removing methyl residues from trimethylated lysine 9 on histone H3. Recent observations have shown oncogenic activity of JMJD2B. We explored the functional role of JMJD2B in cancer cell proliferation, survival and tumorigenesis, and determined its expression profile in gastric cancer. Knocking down JMJD2B expression by small interfering RNA (siRNA) in gastric and other cancer cells inhibited cell proliferation and/or induced apoptosis and elevated the expression of p53 and p21(CIP1) proteins. The enhanced p53 expression resulted from activation of the DNA damage response pathway. JMJD2B knockdown markedly suppressed xenograft tumor growth in vivo in mice. Moreover, JMJD2B expression was increased in primary gastric-cancer tissues of humans. Thus, JMJD2B is required for sustained proliferation and survival of tumor cells in vitro and in vivo, and its aberrant expression may contribute to the pathogenesis of gastric cancer.

[Effects of CD74 gene on IFNγR gene expression in MG TEC].

AIM: To study the effects of CD74 gene on IFN-γR expression in myasthenia gravis thymic epithelial cell(TEC). METHODS: PCMV-CD74 transiently transfect to primary cultured TEC mediated with lipofectamine, the result of transfection and some autoimmune related genes such as IFN-γR were detected by real-time RT-PCR. RESULTS: Real-time quantitative RT-PCR results show that the mRNA expression level of IL-4R, IL-32, IFN-γR, ECGF1, HLA-A, HLA-DR increased significantly, with the high express ion of CD74 gene in thymic epithelial cells. CONCLUSION: CD74 gene over-expression in TEC can increase IFN-γR mRNA expression.

Rhabdomyoma of the orbit.

The authors describe a rare case of orbital rhabdomyoma in a 3-year-old girl who presented with progressive proptosis of the left eye. An axial computed tomographic scan of the left orbit demonstrated an irregular retrobulbar mass. The tumor was resected locally from the lateral wall of the orbit and the resected specimens were diagnosed as orbital rhabdomyoma. The authors review the literature and discuss the diagnostic implications and treatment strategies.