As a class of porous materials with crystal lattices, metal–organic frameworks (MOFs), featuring outstanding specific surface area, tunable functionality, and versatile structures, have attracted huge attention in the past two decades. Since the first conductive MOF is successfully synthesized in 2009, considerable progress has been achieved for the development of conductive MOFs, allowing their use in diverse applications for electrochemical energy storage. Among those applications, supercapacitors have received great interest because of their high power density, fast charging ability, and excellent cycling stability. Here, the efforts hitherto devoted to the synthesis and design of conductive MOFs and their auspicious capacitive performance are summarized. Using conductive MOFs as a unique platform medium, the electronic and molecular aspects of the energy storage mechanism in supercapacitors with MOF electrodes are discussed, highlighting the advantages and limitations to inspire new ideas for the development of conductive MOFs for supercapacitors.

BackgroundTo evaluate whether PI3K/Akt pathway could effect on apoptosis and its mechanism in nasopharyngeal carcinoma cells.MethodsThe activation of the PI3K/Akt and its effect on CNE-2Z cells in vivo and in vitro was investigated by MTT assay, flow cytometry, western blot, ELISA, terminal deoxyribonucleotide transferase-mediated nick-end labeling assays (TUNEL), and immunohistochemical analyses, using PI3K inhibitor, LY294002.ResultsThe results showed that LY294002 inhibited the phosphorylating of Akt (S473), cell proliferation, and induced apoptosis in CNE-2Z cells. However, our experiment results also demonstrated that apoptosis-induced LY294002 was directly regulated by caspase-9 activation pathway.ConclusionThese data suggested that PI3K inhibitor, LY294002, induced apoptosis by caspase-9 activation pathway and might be as a potentially useful target for therapeutic intervention in nasopharyngeal carcinoma patients.

BackgroundOverexpression of ubiquitin-conjugating enzyme 2C (UBE2C) has been detected in many types of human cancers, and is correlated with tumor malignancy. However, the role of UBE2C in human nasopharyngeal carcinoma (NPC) is unclear. In this study, we investigated the role of aberrant UBE2C expression in the progression of human NPC.MethodsImmunohistochemical analysis was performed to detect UBE2C protein in clinical samples of NPC and benign nasopharyngeal tissues, and the association of UBE2C expression with patient clinicopathological characteristics was analyzed. UBEC2 expression profiles were evaluated in cell lines representing varying differentiated stages of NPC and immortalized nasopharyngeal epithelia NP-69 cells using quantitative RT-PCR, western blotting and fluorescent staining. Furthermore, UBE2C was knocked down using RNA interference in these cell lines and proliferation and cell cycle distribution was investigated.ResultsImmunohistochemical analysis revealed that UBE2C protein expression levels were higher in NPC tissues than in benign nasopharyngeal tissues (P<0.001). Moreover, high UBE2C protein expression was positively correlated with tumor size (P=0.017), lymph node metastasis (P=0.016) and distant metastasis (P=0.015) in NPC patients. In vitro experiments demonstrated that UBE2C expression levels were inversely correlated with the degree of differentiation of NPC cell lines, whereas UBE2C displayed low level of expression in NP-69 cells. Knockdown of UBE2C led to significant arrest at the S and G2/M phases of the cell cycle, and decreased cell proliferation was observed in poorly-differentiated CNE2Z NPC cells and undifferentiated C666-1 cells, but not in well-differentiated CNE1 and immortalized NP-69 cells.ConclusionsOur findings suggest that high expression of UBE2C in human NPC is closely related to tumor malignancy, and may be a potential marker for NPC progression.

Sensitive and stable biomarkers that facilitate depression detection and monitor the antidepressant efficiency are currently unavailable. Thus, the objective is to investigate the potential of DNA methylation and histone modifications of brain-derived neurotrophic factor (BDNF) in monitoring severity and antidepressive effects of acupuncture. The depression rat model was imitated by social isolation and chronic unpredicted mild stress (CUMS). The expression of serum BDNF was detected by enzyme-linked immunosorbent assay (ELISA), the hippocampal BDNF, acetylation levels in histone H3 lysine 9 (acH3K9), and HDAC2 by Western blot, the hippocampal mRNA of BDNF by RT-polymerase chain reaction (PCR). The DNA methylation patterns of the promoter I of BDNF was detected by MS-PCR. We investigated that the expression of BDNF in serum and hippocampus were significantly downregulated compared with controls. The same trend was found in mRNA of BDNF. Notably, acupuncture reversed the downregulation of BDNF in serum and hippocampus and mRNA of BDNF compared with model group. Acupuncture reversed the CUMS-induced downregulation of hippocampal acH3K9. On the contrary, the CUMS-induced upregulation of hippocampal HDAC2 in model group was significantly reversed by acupuncture. Collectively, the antidepressant effect of acupuncture might be mediated by regulating the DNA methylation and histone modifications of BDNF, which may represent novel biomaker for detection of depression and monitoring severity and antidepressive effects.

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Formin-like 3 (FMNL3) plays a crucial role in cytoskeletal mediation and is potentially a biomarker for cell migration; however, its role in cancer metastasis remains unknown. In this study, we found elevated FMNL3 protein expression in clinical nasopharyngeal carcinoma (NPC) tissues. FMNL3 expression positively correlated to the clinical stage, T (tumour), N (lymph node metastasis) and M (distant metastasis) classification of NPC patients. Moreover, FMNL3 positively correlated to Vimentin expression and negatively correlated to E-cadherin expression in clinical NPC samples. In vitro experiments showed that FMNL3 expression was inversely related to NPC cell differentiation status. Overexpression of FMNL3 led to epithelial-to-mesenchymal transition (EMT) in well differentiated CNE1 cells. TGF-β1-treated poorly differentiated CNE2 cells showed changes in EMT accompanied by enhanced FMNL3 expression and cell migration. On the contrary, knockdown of FMNL3 partially attenuated the TGF-β1-promoted CNE2 cell migration, together with associated changes in EMT markers. Finally, knockdown of FMNL3 also weakened EMT in tumours in xenographs. Our study indicates for the first time that TGF-β1/FMNL3 signalling may be a novel mechanism mediating EMT in NPC, which is closely associated with NPC metastasis.

Posttraumatic growth (PTG) may exist in trauma survivors, especially adolescents, whereas rumination is a typical cognitive characteristic among traumatized individuals. However, there were mixed relationships between rumination (intrusive rumination, deliberate rumination) and PTG. The study aimed to increase understanding of the relationships between them by investigating the role of social support among adolescents after the Yancheng tornado. Four hundred forty-three middle school students in the core area of the tornado were administered a revised social support scale based on Furman and Buhrmester's Network of Relationships Inventory, Event-Related Rumination Inventory, and Posttraumatic Growth Inventory. Results showed a nonsignificant relationship between intrusive rumination and PTG, whereas a positive relationship was found between deliberate rumination and PTG. Moreover, social support did not moderate the relationship between intrusive rumination and PTG, but it significantly mediated the relationship between deliberate rumination and PTG. Clinical implications on trauma intervention and limitations as well as future research directions were discussed.

In the present study, we evaluated the role of phosphatidylinositol-3 OH kinase/protein kinase B (PI3K/Akt) signaling on changes to epithelial-to-mesenchymal reverting transition (EMrT) in nasopharyngeal carcinoma (NPC). Protein expression levels of p-Akt (Ser473), and the epithelial‑to-mesenchymal transition (EMT) markers E-cadherin, vimentin, α smooth muscle actin (α-SMA), were examined in clinical samples from 130 cases of undifferentiated non-keratinizing NPC, and 20 cases of benign nasopharyngitis. The relationship between protein expression levels and the statue of NPC lymph node metastasis was analyzed. The poorly‑differentiated NPC cell line CNE2Z was treated with various concentrations of the PI3K inhibitor, LY294002, and western blotting and quantitative polymerase chain reaction assays were used to analyze the activation of PI3K/Akt signaling and expression of E-cadherin, vimentin and α-SMA. The ability of cellular migration and invasion was assessed using Transwell assays. The in vivo effects of LY294002 on metastasis and expression of EMT markers in CNE2Z cells was evaluated using tumor xenograft experiments. The expression levels of p-Akt (Ser473) in NPC samples were higher than those in nasopharyngitis. There were reduced levels of membrane E-cadherin protein expression, and increased cytosol vimentin and α-SMA expression levels in NPC samples compared with those in nasopharyngitis samples. High expression levels of p-Akt (Ser473), vimentin, and α-SMA, and low expression levels of E-cadherin were positively associated with lymph node metastasis of NPC cells. Treating CNE2Z cells with LY294002 inhibited p-Akt (Ser473), vimentin and α-SMA expression but upregulated E-cadherin expression, leading to significantly attenuated cell invasion and migration. Administration of mice with LY294002 resulted in upregulation of membrane E-cadherin, and downregulation of vimentin and α-SMA in CNE2Z xenografts, with reduced pulmonary metastasis. Our findings suggest that inhibiting the PI3K/Akt pathway using LY294002 attenuated NPC metastasis via induction of EMrT.