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Organic amines are important solvent and raw material in laboratory and industry, as well as releasing from cigarette smoke. It is significant to detect low-concentration amines for environment and public health. Here we reported that as-synthesized zinc oxide is an effective electrode material of electrochemical sensor for the detection of amines. The characterization results reveal that the ZnO morphologies experienced a change from hexagonal bowl-like microparticles, cones, prisms to nanoparticles by adjusting the reaction time, temperature, solvents and additives. Interestingly, ZnO material possessing hexagonal shapes and different sizes exhibits distinct electrochemical response in various amines solution, suggesting that there is a better dependent relationship between different morphological ZnO and amines detection. Particularly, regular hexagonal ZnO nanotablets exhibit a detectable electrochemical response and selectivity to ammonia, implying it can be serve as electrode material for highly effective detection of organic amines.

Tin dioxide is important gas sensor material and has wide applications in the detection of toxic gases and volatile organic compounds. Here, we synthesized a 3D laminated structural CuO/SnO2 material possessing p-n heterostructures. The morphology and structure were characterized by XRD, SEM, TEM and XPS techniques and the sensing properties were investigated for the detection of triethylamine (TEA). The results indicate that 3D laminated CuO/SnO2 material, assembled by lamellae consisting of ordered nanoparticles, exhibit an enhanced sensing performance compared with SnO2, and notably, CuO/SnO2 with size less than 1 μm has obvious high selectivity in the detection of 100 ppm TEA. Particularly, it has a high response and stability to 1 and 5 ppm TEA (S is 8 and 33), and that is higher than SnO2 material, suggesting 3D laminated CuO/SnO2 is an effective candidate material served as sensor platform to detect low-concentration amines.

In this work, a facile one-step co-exfoliation method has been constructed to prepare the water-processable all-carbon composites (PG/GO) made of pristine graphene (PG) and graphene oxide (GO) using ultrasonic cell disruptor. The microstructure of the PG/GO composites can be conveniently controlled by varying the ultrasonic time and power. The morphology and structure of the PG/GO composites were characterized using UV-visible absorption spectra, atomic force microscopy, scanning electron microscope, and X-ray photoelectron spectroscopy. The application of these PG/GO composites to supercapacitor has been also explored. As a result, the PG/GO composites deliver more excellent electrochemical performance compared with most all-carbon composites reported. The composite synthesized under the optimized experimental condition (PG/GO10:1) exhibits a specific capacitance of 293.6 F g−1 at the scan rate of 10 mV s−1 and 326.3 F g−1 at the current density of 0.5 A g−1, respectively. The cycling stability of these PG/GO composites is quite good. The specific capacitance of PG/GO10:1 increases with increasing the cycle number and even breaks through 126.9% of the initial value after 10,000 cycles at the scan rate of 100 mV s−1.

Two-dimensional (2D) materials possess unique properties and advantages in catalysis, photo/-electronic and sensor devices. Here, we proposed a facile route to synthesize 2D ZnO nanoplates with gri...

Ascl2 has been shown to be involved in tumorigenesis in colorectal cancer (CRC), although its epigenetic regulatory mechanism is largely unknown. Here, we found that methylation of the Ascl2 promoter (bp -1670 ∼ -1139) was significantly increased compared to the other regions of the Ascl2 locus in CRC cells and was associated with elevated Ascl2 mRNA expression. Furthermore, we found that promoter methylation was predictive of CRC patient survival after analyzing DNA methylation data, RNA-Seq data, and clinical data of 410 CRC patient samples from the MethHC database, the MEXPRESS database, and the Cbioportal website. Using the established TET methylcytosine dioxygenase 2 (TET2) knockdown and ectopic TET2 catalytic domain-expression cell models, we performed glucosylated hydroxymethyl-sensitive quatitative PCR (qPCR), real-time PCR, and Western blot assays to further confirm that hypermethylation of the Ascl2 promoter, and elevated Ascl2 expression in CRC cells was partly due to the decreased expression of TET2. Furthermore, BCLAF1 was identified as a TET2 interactor in CRC cells by LC-MS/MS, coimmunoprecipitation, immunofluorescence colocalization, and proximity ligation assays. Subsequently, we found the TET2-BCLAF1 complex bound to multiple elements around CCGG sites at the Ascl2 promoter and further restrained its hypermethylation by inducing its hydroxymethylation using chromatin immunoprecipitation-qPCR and glucosylated hydroxymethyl-qPCR assays. Finally, we demonstrate that TET2-modulated Ascl2-targeted stem gene expression in CRC cells was independent of Wnt signaling. Taken together, our data suggest an additional option for inhibiting Ascl2 expression in CRC cells through TET2-BCLAF1-mediated promoter methylation, Ascl2-dependent self-renewal of CRC progenitor cells, and TET2-BCLAF1-related CRC progression.

Objective: To evaluate the effect of ultrasound interventional injection of cisplatin in the treatment of hepatocellular carcinoma (HCC). Methods: 68 patients with HCC admitted to our hospital from February 2016 to February 2018 were enrolled. According to the different treatment methods, they were divided into a study group and a control group. The control group was treated with hepatic artery embolization chemotherapy (n=34), the study group adopted interventional ultrasound injection of cisplatin (n=34). The clinical treatment effects of the two groups of patients were compared; the liver function and the occurrence of adverse reactions were compared; all patients were followed up for 24 months, and their progressive-free survival (PFS) was also compared. Results: The study group had higher total effective rate compared with the control group (91.18% vs 67.65%) (P

The Wnt signaling pathway controls stem cell identity in the intestinal epithelium and cancer stem cells (CSCs). The transcription factor Ascl2 (Wnt target gene) is fate decider of intestinal cryptic stem cells and colon cancer stem cells. It is unclear how Wnt signaling is translated into Ascl2 expression and keeping the self-renewal of CRC progenitor cells. We showed that the exogenous Ascl2 in colorectal cancer (CRC) cells activated the endogenous Ascl2 expression via a direct autoactivatory loop, including Ascl2 binding to its own promoter and further transcriptional activation. Higher Ascl2 expression in human CRC cancerous tissues led to greater enrichment in Ascl2 immunoprecipitated DNA within the Ascl2 promoter in the CRC cancerous sample than the peri-cancerous mucosa. Ascl2 binding to its own promoter and inducing further transcriptional activation of the Ascl2 gene was predominant in the CD133(+)CD44(+) CRC population. R-spondin1/Wnt activated Ascl2 expression dose-dependently in the CD133(+)CD44(+) CRC population, but not in the CD133(−)CD44(−) CRC population, which was caused by differences in Ascl2 autoregulation under R-spondin1/Wnt activation. R-spondin1/Wnt treatment in the CD133(+)CD44(+) or CRC CD133(−)CD44(−) populations exerted a different pattern of stemness maintenance, which was defined by alterations of the mRNA levels of stemness-associated genes, the protein expression levels (Bmi1, C-myc, Oct-4 and Nanog) and tumorsphere formation. The results indicated that Ascl2 autoregulation formed a transcriptional switch that was enhanced by Wnt signaling in the CD133(+)CD44(+) CRC population, thus conferring their self-renewal.

// Xiaolong Wei 1 , Jun Ye 1 , Yangyang Shang 1 , Haoyuan Chen 1 , Shanxi Liu 1 , Li Liu 1 and Rongquan Wang 1 1 Institute of Gastroenterology of PLA, Southwest Hospital, Third Military Medical University, Chongqing, China Correspondence to: Rongquan Wang, email: rongquanw@hotmail.com Keywords: achaete scute-like 2; Wnt signaling; Hippo signaling; colorectal cancer; progenitor cells Received: June 21, 2017 Accepted: November 08, 2017 Published: November 27, 2017 ABSTRACT Achaete scute-like 2 (Ascl2) is the Wnt signaling target, its regulation by other signaling is undefined. Now we demonstrated that CD133 + /CD44 + cell population from HT-29 or Caco-2 cells exhibited cancer stem cell (CSC) properties with highly expressed Ascl2, which is related to the Hippo signaling pathway. YAP1 interference in CD133 + /CD44 + HT-29 or Caco-2 cells reduced their proliferation, colony-forming ability and tumorsphere formation in vitro and inhibited the ‘stemness’-associated genes and Ascl2 expression. Enforcing YAP1 expression in HT-29 or Caco-2 cells triggered the opposite changes. Ascl2 interference reversed the phenotype of YAP1-enforced expressed HT-29 or Caco-2 cells. Kruppel-like factor 5 (KLF5) protein, not KLF5 mRNA levels, were increased due to YAP1 overexpression which is reported to prevent KLF5 degradation. Co-immunoprecipitation (Co-IP) assays demonstrated that YAP1 bound with KLF5 in HT-29 and Caco-2 cells. Luciferase and chromatin immunoprecipitation (ChIP) assays indicated that both YAP1 and KLF5 bound to the first two loci with GC-boxes in Ascl2 promoter and induced Ascl2 transcription. The decreased Ascl2 transcription by YAP1 interference required an intact KLF5 binding site (GC-box) within Ascl2 promoter, KLF5 knockdown reduced YAP1 binding and Ascl2 luciferase reporter activity upon YAP1 overexpression. Positive correlation among YAP1 and Ascl2 mRNA levels was observed in colorectal cancer (CRC) samples. Thus, our study demonstrated that Ascl2, a fate decider of CRC progenitor cells can be activated by the Hippo signaling pathway in CRC progenitor cells, and ensured their self-renewability.

The attachment of cell-surface carbohydrates to proteins mediated by the amino acids serine or threonine (O-glycan) is involved in tumor metastasis; the roles of O-glycans vary depending on their structure, but the detailed mechanisms by which O-glycans trigger signaling to control tumor metastasis are largely unknown. In this study, we found that the reduced expression of core 3 synthase correlated with metastasis to lymph nodes and distant organs, resulting in poor prognosis for colorectal cancer (CRC) patients. Mechanically, we revealed that mucin-type core 3 O-glycan was synthesized at the membrane-tethered MUC1 N terminus because of core 3 synthase expression in colon cancer cells. This further inhibited the translocation of MUC1-C to the nucleus, initiated p53 gene transcription that was dependent on the inhibition of MUC1-C nucleus translocation, activated p53-mediated miR-200c expression and resulted in mesenchymal-epithelial transition (MET). Inhibition of MUC1 via small interfering RNA (siRNA) in re-expressed core 3 synthase colon cancer cells further inhibited MUC1-C nucleus translocation, increased p53 and miR-200c expression, and enhanced MET. However, inhibition of p53 via siRNA or miR-200c via miR-200c inhibitor in re-expressed core 3 synthase colon cancer cells promoted the epithelial-mesenchymal transition (EMT) in a reversible manner. Core 3 synthase mRNA levels and the p53 mRNA levels or miR-200c levels in the colon cancerous samples were positively correlated. Our findings suggest a novel mechanism linking mucin-type core 3 O-glycan to the EMT-MET plasticity of CRC cells via MUC1/p53/miR-200c-dependent signaling cascade and shed light on therapeutic strategies to treat this malignancy.

An electrochemical sensor was promoted for the rapid and efficient detection of hydrogen peroxide via the ZnO nano/microrods-based (GCE) electrode. The ZnO nano/microrods were controllable prepared by changing zinc precursor under hydrothermal condition and the sensing properties of ZnO materials were studied. The sensing performance was optimized by adjusting ZnO’s morphologies and size. The ZnO nanorods (ZNRs)-based electrode exhibits a notable sensing response toward hydrogen peroxide compared to other modified GCE. More importantly, the developed ZNRs-based sensor possesses high sensitivity of 10.8 μA mM−1 and a detection limit (LOD) of 0.28 μM. Thus, the synthesized ZNRs material is proved to be a potential material for the hydrogen peroxide detection in various fields.

A new graphene oxide/pristine graphene/polyaniline (GPP) composite is successfully prepared. Transmission electron microscope, Scanning electron microscope, Raman spectroscopy and X-ray photoelectron spectroscopy were used to characterize the electronic structure and morphology of GPP composites. The specific capacitance of GPP is 1231.8 F g−1 and 598.1 F g−1 in a three-electrode system and a symmetric supercapacitor at 1.0 A g−1. The specific capacitance of GPP maintains about 71.2% and 55.1% after 10000 cycles in the three-electrode and two-electrode systems, respectively.

In this work, a Fe3O4/graphene oxide (GO)/pristine graphene (PG) ternary composite was synthesized successfully by a two-step method: first graphite was added into GO dispersion to get the GO/PG composite, followed by loading Fe3O4 nanoparticles via a co-precipitation method. The structure of Fe3O4/GO/PG was characterized by scanning electron microscopy (SEM) and X-ray photoelectron spectroscopy (XPS). Compared with the Fe3O4/GO binary composite, Fe3O4/GO/PG composite shows more excellent properties. An electrochemical sensor fabricated with Fe3O4/GO/PG was used to detect dopamine (DA). The linear detection ranges of DA is 5-50 μM with detection limits of 3.37 μM.

3D elliptical ZnO microspheres self-assembled from 1D nanowires were synthesized via a facile solvothermal route. Their morphology and structures were characterized by X-ray diffraction, scanning electron microscopy and N2 adsorption-desorption techniques, and the gas-sensing properties were investigated. The results indicate that as-synthesized elliptical wool ball-like ZnO can be controlled by adjusting alkali concentrations and it exhibits enhanced sensitivity and high selectivity to acetone. Notably, the response to 10 and 100 ppm reached 14 and 36 respectively, which are 4 and 1.5 times as much as that of the nanorods-composed ZnO, implying wool ball-like ZnO microstructures can be served as sensor material for acetone detection.

In this work, a new Fe3O4/graphene oxide (GO)/pristine graphene (PG) ternary composite (Fe3O4/GO/PG) was successfully synthesized. The structure of Fe3O4/GO/PG was characterized by transmission electron microscopy (TEM). The TEM result shows that the small PG sheets are attached to the larger GO sheets and the Fe3O4 nanoparticles are anchored on the surface of GO/PG composite. A sensor based on this Fe3O4/GO/PG has been fabricated successfully to detect dopamine (DA) and hydrogen peroxide (H2O2). The linear detection ranges for DA and H2O2 are 0.30–30 μM and 0.50–277 μM, respectively, with detection limits of 0.18 and 0.09 μM.

In this paper, a graphene/nickel-cobalt hydroxide ternary hydrogel (G-Ni-Co) with superior electrochemical performances was prepared by a simple hydrothermal method using Ni(NO3)2·6H2O, Co(NO3)2·6H2O, and graphene oxide as the starting materials. The mass fraction and the pH value of the reaction system were optimized. The prepared G-Ni-Co was assembled into a symmetric supercapacitor and its electrochemical performance was estimated. In a symmetric supercapacitor, the specific capacitance of G-Ni-Co is 551.3 F g-1 at the scan rate of 10 mV s-1 and 646.1 F g-1 at the current density of 0.5 A g-1, respectively. The specific capacitance still retains 70.8% after 5000 cycles at the scan rate of 100 mV s-1. The energy density reaches 108.6 W h kg-1 at a power density of 550.0 W kg-1 and remains 72.4 W h kg-1 at 7600.0 W kg-1, respectively.

// Yangyang Shang 1,* , Qiong Pan 1,* , Lei Chen 1,* , Jun Ye 1 , Xiaoli Zhong 1 , Xiaohuan Li 1 , Linkuan Meng 1 , Jin Guo 1 , Yin Tian 1 , Yonghong He 1 , Wensheng Chen 1 , Zhihong Peng 1 and Rongquan Wang 1 1 Department of Gastroenterology, Southwest Hospital, Third Military Medical University, Chongqing, P. R. China * These authors have contributed equally to this study Correspondence to: Zhihong Peng , email: // Rongquan Wang, email: // Keywords : Achaete scute-like 2, CDX2, transcriptional regulation, colorectal carcinoma, differentiation Received : March 26, 2015 Accepted : August 13, 2015 Published : August 17, 2015 Abstract The role of Achaete scute-like 2 (Ascl2) in colorectal cancer (CRC) cell differentiation is unknown. LS174T, HT-29 and Caco-2 cells have high Ascl2 expression, while Lovo and SW480 cells have low Ascl2 expression. LS174T and HT-29 cells with Ascl2 knockdown were transfected with caudal type homeobox 2 (CDX2) promoter constructs and used for luciferase assays and chromatin immunoprecipitation (ChIP) assays. Ascl2 knockdown promoted differentiation of CRC cells into a goblet cell phenotype, as determined by increased expression of MUC2, TFF3, and CDX2. Ascl2 knockdown activated CDX2 expression through a transcriptional mechanism via direct binding of Ascl2 to the proximal E-box of the CDX2 promoter. Ascl2 over-expression in Lovo and SW480 cells inhibited a goblet cell phenotype, as determined by reduced CDX2 and MUC2 expression. Inverse correlations between Ascl2 and CDX2, and Ascl2 and MUC2 mRNA levels, as well as Ascl2 and CDX2 protein levels were observed in CRC cancerous samples. This study demonstrates CDX2 repression by Ascl2 and highlights a role for Ascl2 in CRC cell differentiation. These findings suggest that the Ascl2/CDX2 axis may serve as a potential therapeutic target in colorectal cancer.

This paper presents a new analytical solution to study the interplay between flowing pressure and production rate for horizontal wells completed within stimulated reservoir volumes (SRV) in tight gas reservoirs. Field practice has shown that all fracturing stages are not effective in production; this has been explained through varying fracture intensity inside and outside of SRVs along the well (fully fractured zone, partially activated zone and non-activated zone). Despite the existing solutions, the novelty of this model is in integrated approach to consider fracturing stages with different fracture intensity, consistent with observations in the field. In addition, the presented model considers wellbore storage effects, stress-dependent and non-Darcy flows considering threshold pressure gradient. Implementing the Laplace transform technique, our multi-linear analytical solution is obtained from the diffusivity equation. We validate the analytic solution with field data; our results are consistent with the field observation. A sensitivity analysis is conducted to study impacts of fracture intensity, threshold pressure gradient, compaction, and size of the stimulated reservoir volume (SRV) on appearance of different flow patterns and ultimate well productivity. Our results suggest a relation between SRV aspect ratio and occurrence of various flow patterns when fracture intensity is changing along the well. In practice, this septa-linear flow model is simple, practical and time-efficient for the transient pressure analysis and production prediction. Furthermore, this work is one step forward to make the analytic solutions more realistic by incorporating different fracture intensity of each fracturing stage.

This article is the first investigation on the fracture network heterogeneity flow for multiple fractured horizontal wells in unconventional reservoirs. Currently, most modeling approaches for multiple fractured horizontal wells are based on flow in several distinct scales (matrix/fracture), in which the network of fractures is assumed to be connected and equivalent to a homogeneous medium of Euclidean geometry. To account for more detailed description of unconventional reservoir, fractal permeability and porosity relationship was introduced to represent reservoir heterogeneity. Fractal flow in a dual-continuum porous medium is taken into consideration to establish a model of hydraulically fractured horizontal wells. The coupled fractal-based tri-linear diffusivity equation helps illuminate the reservoir performance and improve the pressure transient analysis. A tri-linear flow mathematical model is used to represent the flow in hydraulic fractures, in the formation between the fractures, and in the formation away from the hydraulic fractures. To solve the equations at different regions, we prescribe the proper boundary conditions and use Laplace transformation and numerical inversion from the Laplace domain to the time domain. The new semi-analytical solutions were validated via numerical simulations. The type curve of fractal pressure transient behavior was thoroughly examined; which were found to be primarily dependent on the value of the fractal parameters chosen. The proposed model could be used to diagnose the flow regime and interpret the pressure response more accurately for shale/tight oil reservoirs.

Ascl2, a basic helix-loop-helix transcription factor, is a downstream target of WNT signaling that controls the fate of intestinal cryptic stem cells and colon cancer progenitor cells. However, its involvement in colon cancer and downstream molecular events is largely undefined; in particular, the mechanism by which Ascl2 regulates the plasticity of epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET) programs in colon cancer cells remains unknown. In this study, we systematically demonstrate that Ascl2 loss of function in colon cancer cells promotes MET by derepressing the expression of microRNA (miR)-200s (i.e. miR-200b, miR-200a, miR-429, miR-200c, and miR-141) and further activating their expression through a transcriptional mechanism that involves direct binding to the most proximal E-box (E-box2) in the miR-200b-a-429 promoter. Activation of miR-200s due to Ascl2 deficiency led to the inhibition of ZEB1/2 expression and the alteration of epithelial and mesenchymal features. Transfection of miR-200b, miR-200a, and miR-429 inhibitors into Ascl2-deficient colon cancer cells promoted the epithelial-mesenchymal transition in a reversible manner. Transfection of miR-200a or miR-429 inhibitors into Ascl2-deficient colon cancer cells increased cellular proliferation and migration. Ascl2 mRNA levels and the miR-200a, miR-200b, miR-200c, miR-141, or miR-429 levels in the colon cancerous samples were inversely correlated. These results provide the first evidence of a link between Ascl2 and miR-200s in the regulation of EMT-MET plasticity in colon cancer.

We have reported that Achaete scute-like 2 (Ascl2) transcriptionally repressed miR-200 family members and affected the epithelial-mesenchymal transition (EMT)-mesenchymal-epithelial transition (MET) plasticity in colorectal cancer (CRC) cells. However, little is known about the regulation of the Ascl2/miR-200 axis. Here, we found that hypoxia inducible factor-1α (HIF-1α) mRNA levels were positively correlated with Ascl2 mRNA levels and inversely correlated with miR-200b in CRC samples. Mechanistically, we showed that Ascl2 was a downstream target of HIF-1α and had a critical role in the EMT phenotype induced by hypoxia or HIF-1α over-expression. Hypoxia or HIF-1α over-expression activated Ascl2 expression in CRC cells in a direct transcriptional mechanism via binding with the hypoxia-response element (HRE) at the proximal Ascl2 promoter. HIF-1α-induced Ascl2 expression repressed miR-200b expression to induce EMT occurrence. Furthermore, we found HIF-1α was a direct target of miR-200b. MiR-200b bound with the 3′-UTR of HIF-1α in CRC cells. HIF-1α/Ascl2/miR-200b regulatory feedback circuit modulated the EMT-MET plasticity of CRC cells. Our results confirmed a novel HIF-1α/Ascl2/miR-200b regulatory feedback circuit in modulating EMT-MET plasticity of CRC cells, which could serve as a possible therapeutic target.

Nanog is an important embryonic stem cell (ESC) gene that does not function as a classical oncogene, but needs to cooperate with other molecules to potentiate tumorigenic activity. The question addressed by the present study was whether a miRNA link exists between Nanog and epithelial-mesenchymal transition (EMT)-mesenchymal-epithelial transition (MET) plasticity. Here, we found that Nanog mRNA expression level was inversely correlated with miR-200c and miR-200b expression levels in colon cancer cell lines and human colorectal cancer tissues. Forced Nanog expression in low-Nanog colon cancer cells inhibited miR-200c and miR-200b expression, and interfered Nanog expression in high-Nanog colon cancer cells promoted miR-200c and miR-200b expression. Furthermore, we confirmed that Nanog directly repressed transcription of the miR-200c and miR-200b genes, and miR-200c and miR-200b mediated Nanog-induced EMT occurrence. Luciferase and ChIP assays determined that Nanog bound directly to the potential Nanog binding sites in the miR-200c and miR-200b promoters and repressed their transcription. In conclusion, our findings suggest that Nanog modulates EMT-MET plasticity by regulating miR-200 clusters via a direct transcriptional mechanism, and the Nanog-miR-200 axis may be a good therapeutic target for CRC control.

The myogenic regulatory factors (MRFs) and myocyte enhancer factor 2 (MEF2) transcription factors have been extensively studied as key transcription factors that regulate myogenic gene expression. However, few reports on the molecular mechanism that modulates chromatin remodeling during skeletal muscle differentiation are available. We reported here that the expression of the H3-K9 methyltransferase Suv39h1 was decreased during myoblast differentiation. Ectopic expression of Suv39h1 could inhibit myoblast differentiation, increasing H3-K9 methylation levels, whereas knockdown of Suv39h1 stimulated myoblast differentiation. Furthermore, Suv39h1 interacted with MEF2C directly and inhibited MEF2 transcription activity in a dose-dependent manner. Together, our studies revealed a molecular mechanism wherein Suv39h1 modulated myogenic gene expression and activation during skeletal muscle differentiation.

As a kind of new carbon materials, graphene has excellent performances such as superior conductivity, high specific surface area (2675 m2 g−1), and high cycle life. But graphene sheets are easily restacked by van der Waals interactions during the processes of preparation, storage, and application of them, which can loss ultrahigh specific surface area. The restacking of graphene sheets could be prevented by constructing graphene hydrogel (GH) or graphene composite. In this work, GH was prepared by a one-step hydrothermal synthesis reaction and glucose is used as a reducing agent, while graphene oxide/polyaniline (GP) composites was prepared by coating polyaniline on GO through in situ chemical polymerization of aniline. Then an asymmetric supercapacitor (GH//GP) was further assembled, where GH and GP are the positive and negative electrodes, respectively. The electrochemical properties of GH, GP, and GH//GP are studied using voltammetry and galvanostatic charge/discharge. The consequences indicate that the energy density of GH//GP reaches 5.6 W h kg−1 at power density of 226.5 W kg−1 and 3.1 W h kg−1 at energy density of 8446.2 W kg−1.

Background How host cell glycosylation affects EPEC or EHEC O157:H7 invasion is unclear. This study investigated whether and how O-glycans were involved in EPEC or EHEC O157:H7 invasion into HT-29 cells. Results Lectin histochemical staining confirmed stronger staining with PNA, which labeled Galβ1, 3 GalNAc (core 1 structure) in HT-29-Gal-OBN and C2GnT2-sh2/HT-29 cells, compared with control cells. EPEC or EHEC O157:H7 invasion into HT-29 and its derived cells was based on the intracellular presence of GFP-labeled bacteria. The differentiation of HT-29 cells led to a reduction in EPEC internalization compared with HT-29 cells (p

The roles of host glycosylation in interactions with EPEC and EHEC O157:H7 are largely unclear; this study examined whether O-glycans are involved in EPEC and EHEC O157:H7 adherence to HT-29 cells. Bacterial adherence to the cultured cells was determined using the direct co-staining of adherent bacteria and host cells, the adherent bacteria plating, and/or the direct fluorescent observation of the adherent GFP-labeled bacteria. A comparison of the adherence of EPEC and EHEC O157:H7 to HT-29-Gal and HT-29 cells indicated that the differentiation of HT-29 cells led to a reduction in the adherence of EPEC and EHEC O157:H7. EPEC and EHEC O157:H7 adhesion decreased after the abrogation of O-glycan biosynthesis mediated by benzyl-α-GalNAc treatment. Core 2 O-glycan-deficient HT-29 cells induced by C2GnT2 knockdown had a significant reduction in EPEC and EHEC O157:H7 adhesion in C2GnT2-sh2/HT-29 cells compared with HT-29 and shRNA-Ctr/HT-29 cells. MUC2 expression in benzyl-α-GalNAc-treated HT-29 cells was significantly reduced but unchanged in C2GnT2-deficient HT-29 cells. EPEC or EHEC O157:H7 infection in C2GnT2-deficient HT-29 cells deteriorated the epithelial barrier function. The occludin expression in the shRNA-Ctr/HT-29 and C2GnT2-sh2/HT-29 cells after infection with EPEC or EHEC O157:H7 was pyknic and discontinuous at the cell surface compared with its continuous distribution of control cells. These data indicate that EPEC and EHEC O157:H7 adherence to HT-29 cells is related to mucin-type core 2 O-glycan. This study provides the concepts toward the design of carbohydrate-dependent inhibition of EPEC and EHEC O157:H7 adhesion to human intestinal epithelial cells.

Myozenin-1 (Myoz1) gene-encoded calsarcin-2 protein was expressed exclusively in fast-twitch muscles. Peroxisome proliferator-activated receptor γ2 (PPAR-γ2) is a key regulator of adipocyte differentiation, fatty acid uptake and storage in mammals. In this study, transgenic (TG) mice were generated by injecting linearized DNA that contained mouse creatine kinase M-type enhancer, Myoz1 core promoter, swine PPAR-γ2 (sPPAR-γ2) and SV40 polyadenylation sequences into pronuclei of fertilized FVB/NJ mouse embryos using microinjection technology. Then, the TG mice were used to identify whether swine Myoz1 (sMyoz1) promoter could upregulate sPPAR-γ2 expression in skeletal muscle in a TG mouse model. The results showed that the sMyoz1 promoter indeed upregulated sPPAR-γ2 expression on both the RNA and protein levels. The target genes of PPAR-γ in fat formation pathways, such as fatty acid-binding protein 4 (FABP4) and lipoprotein lipase (LPL), were also overexpressed on the RNA level. Meanwhile, the level of skeletal muscle triacylglycerol in TG mice was increased (P < 0.05), and the result of Oil Red-O staining in the skeletal muscle sections also showed that the number of lipid droplets was significantly increased in TG mice compared to wild-type mice, which might improve the intramuscular fat (IMF) content. For pork, the quality was mostly influenced by the IMF; the identification of swine muscle-specific promoter, sMyoz1, could further serve to develop transgenic pigs with higher intramuscular fat contents and improve pork quality.

Sarcoendoplasmic reticulum Ca2+-ATPase 1 (SERCA1) as a Ca2+ release channel plays a key role in the relaxation of skeletal muscle through pumping cytosolic Ca2+ into the SR (sarcoplasmic reticulum). In this study, a novel single nucleotide polymorphism (SNP) in exon 8 (C > T) was detected by tetra-primer ARMS-PCR and the tissue expression pattern of SERCA1 was analyzed in eleven tissues. A model of primary skeletal muscle cells in vitro exposed to dexamethasone (DEX, a synthetic corticosteroid) was also employed to determine whether stress hormones cause an increase in intracellular Ca2+ concentration that is associated with alteration in SERCA1 and in turn subsequently affect meat quality. The results showed that the CC genotype has lower content intramuscular fat and higher water than pig carrying the genotype CT and CC. In addition, the additive effects were both significantly (P < 0.05) and allele T seemed to be associate with increase in intramuscular fat, while decrease in water content. Accompanied with previous studies, the high abundance of porcine SERCA1 was found in skeletal muscle tissue. DEX markedly down-regulated the expression of SERCA1, leading to Ca2+ overload. Furthermore, the imbalance of Ca2+ homeostasis up-regulated the transcription level of Calpain1. Taken together, we demonstrated a novel mechanism that the changes in expression of SERCA1 potential disturb the normal Ca2+ channel as well as the balance of Ca2+ homeostasis and which in turn finally activated Ca2+-dependent proteases such as Calpain1 which could affect meat quality.