Prominent Size Effects without a Depolarization Field Observed in Ultrathin Ferroelectric Oxide Membranes

The increasing miniaturization of electronics requires a better understanding of material properties at the nanoscale. Many studies have shown that there is a ferroelectric size limit in oxides, below which the ferroelectricity will be strongly suppressed due to the depolarization field, and whether such a limit still exists in the absence of the depolarization field remains unclear. Here, by applying uniaxial strain, we obtain pure in-plane polarized ferroelectricity in ultrathin SrTiO3 membranes, providing a clean system with high tunability to explore ferroelectric size effects especially the thickness-dependent ferroelectric instability with no depolarization field. Surprisingly, the domain size, ferroelectric transition temperature, and critical strain for room-temperature ferroelectricity all exhibit significant thickness dependence. These results indicate that the stability of ferroelectricity is suppressed (enhanced) by increasing the surface or bulk ratio (strain), which can be explained by considering the thickness-dependent dipole-dipole interactions within the transverse Ising model. Our study provides new insights into ferroelectric size effects and sheds light on the applications of ferroelectric thin films in nanoelectronics

Detailed Comparison of the Pnicogen Bond with Chalcogen, Halogen and Hydrogen Bonds

The characteristics of the pnicogen bond are explored using a variety of quantum chemical techniques. In particular, this interaction is compared with its halogen and chalcogen bond cousins, as well as with the more common H-bond. In general, these bonds are all of comparable strength. More specifically, they are strengthened by the presence of an electronegative substituent on the electron-acceptor atom, and each gains strength as one moves down the appropriate column of the periodic table, for example, from N to P to As. These noncovalent bonds owe their stability to a mixture in nearly equal parts of electrostatic attraction and charge transfer, along with a smaller dispersion component. The charge transfer arises from the overlap between the lone pair of the electron donor and a σ* antibond of the acceptor. The angular characteristics of the equilibrium geometry result primarily from a compromise between electrostatic and induction forces. Angular distortions of the H-bond are typically less energetically demanding than comparable bends of the other noncovalent bonds

Research on Coal and Rock Type Recognition Based on Mechanical Vision

In order to identify different kinds of coal, rock, and gangue, the FPV integrated image transmission camera is used to collect images of 6 types of coal, 8 types of rocks, and 2 types of coal gangue, and the images are processed based on the two-dimensional discrete wavelet transform (2D-DWT) based on the steerable pyramid decomposition (SPD). The maximum likelihood estimation method is used to estimate the parameters, and, the coal and rock types are judged by comparing the similarity of each image. The results show the following: (1) in the eight kinds of rocks, the recognition accuracy of shale and limestone is 90%, that of anorthosite is 95%, and those of other rocks are 100%; (2) the accuracy of comprehensive identification of coal, rock, and gangue is 93%, the comprehensive of coal and gangue is 78%, and the rock classification is 97%; (3) the identification time of 6 types of coal samples, 8 types of rock samples, and 2 types of coal gangue samples are in the range of 2 s∼3 s, which is far less than 10 s, which can meet the requirements of coal and rock identification in terms of recognition speed; and (4) according to 20 groups of data, the range, variance, and standard deviation of the same coal gangue sample meet the accuracy requirements of coal and rock identification. The identification method provides an effective method to improve the efficiency of coal separation, effectively determine the distribution of coal and rock, and timely adjust the cutting height of shearer drum and the operation parameters of various fully mechanized mining equipment, so as to improve the recovery rate of coal resources

Expression of sperm-associated antigen 6 in liver cancer tissue and its clinical significance

ObjectiveTo investigate the expression of sperm-associated antigen 6 (Spag6) in liver cancer tissue and its association with the clinicopathological features and prognosis of liver cancer patients, as well as the effect of Spag6 on the proliferation and migration of HCCLM3 hepatoma cells. MethodsClinical samples were collected from 102 liver cancer patients who were treated in Xiangya Hospital of Central South University from August 2006 to November 2009, and Western blot was used to measure the expression of Spag6 in hepatoma cells, normal liver tissue, tumor tissue, and corresponding adjacent tissue. Immunohistochemistry was used to measure the expression of Spag6 in 102 liver cancer tissue samples, and according to the immunohistochemical scoring criteria, the patients were divided into high Spag6 expression group and low Spag6 expression group. Lentivirus-mediated RNA interference technique was used to silence Spag6 expression in HCCLM3 cells; Western blot was used to analyze silencing effect, wound-healing assay was used to investigate the effect of Spag6 gene silencing on the migration of HCCLM3 cells, and colony formation assay was performed to observe the effect of Spag6 gene silencing on the proliferation of HCCLM3 cells. The chi-square test was used to investigate the association between Spag6 expression and clinicopathological features of liver cancer patients, and the Kaplan-Meier survival analysis and log-rank test were used to analyze the association between Spag6 expression and the prognosis of liver cancer patients. ResultsHepatoma cells and liver cancer tissue had significantly higher expression of Spag6 than the normal LO2 cells and normal liver tissue. Immunohistochemistry showed that the expression rate of Spag6 was 58.8% (60/102) in liver cancer tissue samples and 12.7% (13/102) in adjacent tissue samples (χ2=47123,P＜0.001). According to the results of the chi-square test, Spag6 expression was associated with the number of tumor nodules, presence or absence of capsule, vascular invasion, and Edmondson-Steiner classification (χ2=8.360, 6.761, 4.344, and 7.172, P=0.004, 0.009, 0.037, and 0.007). Further analysis showed that the high Spag6 expression group had significantly lower 1-, 3-, and 5-year survival rates than the low Spag6 expression group (71.5% vs 905%,437% vs 688%, 197% vs 487%, χ2=11.228, P=0.001). Cell assays showed significant reductions in the proliferation and migration of HCCLM3 cells after Spag6 gene silencing (both P＜0.01). ConclusionSpag6 is highly expressed in hepatoma cells and liver cancer tissue, and its high expression is associated with poor clinicopathological features and postoperative survival of liver cancer. Spag6 can promote the proliferation and migration of hepatoma cells, suggesting that Spag6 may be involved in the development and progression of liver cancer. Therefore, it can be used as a reference index for predicting the prognosis of liver cancer patients and a potential target for liver cancer treatment

Lentiviral CRISPR/Cas9 nickase vector mediated BIRC5 editing inhibits epithelial to mesenchymal transition in ovarian cancer cells

BIRC5 encodes the protein survivin, a member of the inhibitor of apoptosis family. Survivin is highly expressed in a variety of cancers but has very low expression in the corresponding normal tissues, and its expression is often associated with tumor metastasis and chemoresistance. We report that survivin was highly expressed in ovarian cancer and strongly correlated with patient overall poor survival. For the first time, we provide experimental evidence that survivin is involved in epithelial to mesenchymal transition (EMT) in ovarian cancer cells. Lentiviral CRISPR/Cas9 nickase vector mediated BIRC5 gene editing led to the inhibition of EMT by upregulating epithelial cell marker, cytokeratin 7 and downregulating mesenchymal markers: snail2, β-catenin, and vimentin in both ovarian cancer SKOV3 and OVCAR3 cells. Consistent with this molecular approach, pharmacological treatment of ovarian cancer cells using a small molecule survivin inhibitor, YM155 also inhibited EMT in these ovarian cancer cell lines. Overexpression of BIRC5 promoted EMT in SKOV3 cells. Using molecular or pharmacological approaches, we found that cell proliferation, migration, and invasion were significantly inhibited following BIRC5 disruption in both cell lines. Inhibition of BIRC5 expression also sensitized cell responses to paclitaxel treatment. Moreover, loss of BIRC5 expression attenuated TGFβ signaling in both SKOV3 and OVCAR3 cells. Collectively, our studies demonstrated that disruption of BIRC5 expression inhibited EMT by attenuating the TGFβ pathway in ovarian cancer cells

Lentiviral Vector Mediated Claudin1 Silencing Inhibits Epithelial to Mesenchymal Transition in Breast Cancer Cells

Breast cancer has a high incidence and mortality rate worldwide. Several viral vectors including lentiviral, adenoviral and adeno-associated viral vectors have been used in gene therapy for various forms of human cancer, and have shown promising effects in controlling tumor development. Claudin1 (CLDN1) is a member of the tetraspan transmembrane protein family that plays a major role in tight junctions and is associated with tumor metastasis. However, the role of CLDN1 in breast cancer is largely unexplored. In this study, we tested the therapeutic potential of silencing CLDN1 expression in two breast cancer (MDA-MB-231 and MCF7) cell lines using lentiviral vector mediated RNA interference. We found that a CLDN1 short hairpin (shRNA) construct efficiently silenced CLDN1 expression in both breast cancer cell lines, and CLDN1 knockdown resulted in reduced cell proliferation, survival, migration and invasion. Furthermore, silencing CLDN1 inhibited epithelial to mesenchymal transition (EMT) by upregulating the epithelial cell marker, E-cadherin, and downregulating mesenchymal markers, smooth muscle cell alpha-actin (SMA) and Snai2. Our data demonstrated that lentiviral vector mediated CLDN1 RNA interference has great potential in breast cancer gene therapy by inhibiting EMT and controlling tumor cell growth

KLF4 Promotes Angiogenesis by Activating VEGF Signaling in Human Retinal Microvascular Endothelial Cells

<div><p>The transcription factor Krüppel-like factor 4 (KLF4) has been implicated in regulating cell proliferation, migration and differentiation in a variety of human cells and is one of four factors required for the induction of pluripotent stem cell reprogramming. However, its role has not been addressed in ocular neovascular diseases. This study investigated the role of KLF4 in angiogenesis and underlying molecular mechanisms in human retinal microvascular endothelial cells (HRMECs). The functional role of KLF4 in HRMECs was determined following lentiviral vector mediated inducible expression and shRNA knockdown of KLF4. Inducible expression of KLF4 promotes cell proliferation, migration and tube formation. In contrast, silencing KLF4 inhibits cell proliferation, migration, tube formation and induces apoptosis in HRMECs. KLF4 promotes angiogenesis by transcriptionally activating VEGF expression, thus activating the VEGF signaling pathway in HRMECs.</p></div

KLF4 promotes VEGF-induced tube formation and enhances angiogenesis in vivo.

<p><b>A.B.</b> Tube formation assays were performed in KLF4 expressing and knockdown HRMECs, respectively. The angiogenic effect of KLF4 on VEGF induced tube formation was determined by counting nodes and sprouts of tube-like structures from at least three different fields of three independent experiments and normalized to vehicle treated control cells. Significance was compared between KLF4 expressing and control cells with or without VEGF treatment (*p<0.05, **p<0.01, ***p<0.001). Images were presented from one representative experiment. C. Sections of plugs were stained using CD31 antibody and microvessels were counted from 4 sections of each plug and averaged from total 3 plugs. Significance of CD31 positive vessels were compared between sections of KLF4 expressing and control plugs (*p<0.05).</p

KLF4 promotes VEGF induced cell proliferation.

<p><b>A, B.</b> Cell proliferation was examined at different time points in KLF4 expressing and knocking down HRMECs. Cells were treated with VEGF or vehicle (Veh) following 24h serum-free media culture before measuring cell proliferation using a MTT assay. Significance was observed between KLF4 expressing and control cells with or without VEGF induction. <b>C</b>. Cell apoptosis was examined using ELISA from HRMECs transduced with lentiviral KLF4shRNA1, 2 and Scramble controls. <b>D.</b> One representative Western blot was shown on the active caspase3 expression at indicated time points in KLF4 knockdown and control cells following 12h serum starvation. Significance was compared between KLF4 knockdown and control cells at the indicated time points. Data are presented as mean ±S.E. from 3 independent experiments, (*p<0.05, **p<0.01).</p