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Two-dimensional metal-organic frameworks and nanoflowers of the MoS2 form a composite structure as an electrode material for high-performance supercapacitor application. MoS2 expands in the accordion-type Ni-MOF layers, and -S- joins the two materials to form a Ni-MOF coating MoS2 composite structure. The composite material MoS2@Ni-MOF combines the structural characteristics of the Ni-MOF and MoS2, and effectively improves the electrochemical performance. The basic skeleton structure of the MoS2@Ni-MOF material remains unchanged, showing a remarkable specific capacitance of 1590.24 F·g−1 at a current density of 1.0 A·g−1 and an excellent cycle stability (retention rate of 87.97% after 20,000 cycles at current of 5.0 A·g−1). Due to the special composite structure of MoS2@Ni-MOF, the as-assembled MoS2@Ni-MOF//AC assymmetric supercapacitor (ASC) device exhibits a maximum energy density of 72.93 Wh·kg−1 at a power density of 375 W·Kg−1. These excellent electrochemical properties indicate that the MoS2@Ni-MOF has potential applications in energy storage devices.

Background In recent years, codeine-containing cough syrups (CCS) have been reported as substances of abuse, especially in adolescents. Chronic CCS abuse can induce physical and psychological dependence. However, the potential brain impairment caused by chronic CCS abuse has not been reported previously. The present study was designed to determine if the striatal dopamine transporter (DAT) levels measured by 99m Tc-TRODAT-1 single photon emission computed tomography (SPECT) brain scans were altered in CCS-dependent subjects and to explore the CCS-caused brain impairment. Methods SPECT brain scans were acquired on 22 CCS-dependent subjects and 27 healthy age matched controls. The volume ( V ) and weight ( W ) of bilateral corpus striatum as well as the 99m Tc-TRODAT-1 uptake ratio of corpus striatum/the whole brain (Ra) were calculated using mathematical models. Results It was displayed that DAT availability of striatum was significantly decreased and the V , W and Ra were greatly reduced in the CCS-dependent group compared to controls (for each comparison p Conclusion Taken together, these results suggest that chronic CCS abuse may cause serious damage to the brain and the neuroimaging findings further illustrate the mechanism of CCS dependence.

Objective Today, more and more evidence suggests that Foxk proteins (Foxk1 and Foxk2) work as transcriptional repressors in different kinds of cancer, but whether Foxk1 has a role in mediating tumorigenesis in breast cancer, the evidence is rare. Methods MCF-7 cells transfected with shFoxk1 displayed a mesenchymal morphology and reduced the expression of E-cadherin, and increased the expression of N-cadherin. Transwell invasion assay and living imaging assay show that the overexpression of Foxk1 could inhibit metastasis in vitro and in vivo. Ribonucleic acid sequencing revealed that the knockdown of Foxk1 resulted in the up-regulation of different oncogenes, which was implicated in metastasis and tumor angiopoiesis. Quantitative chromatin immunoprecipitation, chromatin immunoprecipitation and Luciferase reporter assays suggested that Foxk1 could bind to the promoter of epithelial-mesenchymal transition inducer Twist and vascular endothelial growth factor, VEGF. Mass Spectrometry, co-immunoprecipitation assays and glutathione-S-transferase pull-down assay detected that Foxk1 was physically associated with Ten-eleven translocation 1, TET1, in vivo and in vitro. Results We reported that the mean expression level of Foxk1 in breast cancer was significantly lower than the adjacent noncarcinoma tissue. The higher Foxk1 expression was associated with better prognosis. Endothelial tube formation assays indicated that Foxk1 might regulate breast cancer angiogenesis through transcriptional repression of vascular endothelial growth factor. Furthermore, in vivo magnetic resonance imaging revealed the overexpression of Foxk1 could enhance the detection of the tumors. Further, a strong negative correlation was observed between Foxk1 and Twsit or between Foxk1 and vascular endothelial growth factor, and the higher Foxk1 expression is correlated with better over all survivals and better relapse-free survivals. Conclusions Together, our data indicated the function of Foxk1 as a tumor suppressor in facilitating angiogenesis and metastasis in breast cancer.

In this study, we aimed to explore the potential of dual-energy computed tomography (DECT) in evaluating liver fat; we also compared the diagnostic performance of DECT, T1-weighted dual-echo magnetic resonance (MR) imaging, and 1H-MR spectroscopy (1H-MRS) in assessing hepatic steatosis in a fatty liver rat model. Fat (water) concentration measurements by DECT spectral imaging, MR findings, and 1H-MRS measurements of hepatic fat showed similar correlations with the histopathologic results. Furthermore, a good correlation was observed between the fat (water) concentration and 1H-MRS measurements (r = 0.800 and P less than 0.001). The discriminant accuracies of the fat (water) concentration, MR findings, and 1H-MRS measurements were 66.7, 64, and 56 percent, respectively. Therefore, we conclude that the findings of DECT spectral CT imaging are strongly correlated with histopathologic findings in cases of steatosis; in addition, DECT can allow rapid, accurate evaluations of hepatic steatosis that are as effective as those obtained using T1-weighted dual-echo MR imaging and 1H-MRS.

In recent years, internet addiction disorder (IAD) has become more prevalent worldwide and the recognition of its devastating impact on the users and society has rapidly increased. However, the neurobiological mechanism of IAD has not bee fully expressed. The present study was designed to determine if the striatal dopamine transporter (DAT) levels measured byT99mc-TRODAT-1 single photon emission computed tomography (SPECT) brain scans were altered in individuals with IAD. SPECT brain scans were acquired on 5 male IAD subjects and 9 healthy age-matched controls. The volume (V) and weight (W) of bilateral corpus striatum as well as theT99mc-TRODAT-1 uptake ratio of corpus striatum/the whole brain (Ra) were calculated using mathematical models. It was displayed that DAT expression level of striatum was significantly decreased and theV,W, and Ra were greatly reduced in the individuals with IAD compared to controls. Taken together, these results suggest that IAD may cause serious damages to the brain and the neuroimaging findings further illustrate IAD is associated with dysfunctions in the dopaminergic brain systems. Our findings also support the claim that IAD may share similar neurobiological abnormalities with other addictive disorders.