Performance Study of Diamond Powder-Filled Sodium Silicate-Based Thermal Conductive Adhesives.

With the development of miniaturized, highly integrated, and multifunctional electronic devices, the heat flow per unit area has increased dramatically, making heat dissipation a bottleneck in the development of the electronics industry. The purpose of this study is to develop a new inorganic thermal conductive adhesive to overcome the contradiction between the thermal conductivity and mechanical properties of organic thermal conductive adhesives. In this study, an inorganic matrix material, sodium silicate, was used, and diamond powder was modified to become a thermal conductive filler. The influence of the content of diamond powder on the thermal conductive adhesive properties was studied through systematic characterization and testing. In the experiment, diamond powder modified by 3-aminopropyltriethoxysilane coupling agent was selected as the thermal conductive filler and filled into a sodium silicate matrix with a mass fraction of 34% to prepare a series of inorganic thermal conductive adhesives. The thermal conductivity of the diamond powder and its content on the thermal conductivity of the adhesive were studied by testing the thermal conductivity and taking SEM photos. In addition, X-ray diffraction, infrared spectroscopy, and EDS testing were used to analyze the composition of the modified diamond powder surface. Through the study of diamond content, it was found that as the diamond content gradually increases, the adhesive performance of the thermal conductive adhesive first increases and then decreases. The best adhesive performance was achieved when the diamond mass fraction was 60%, with a tensile shear strength of 1.83 MPa. As the diamond content increased, the thermal conductivity of the thermal conductive adhesive first increased and then decreased. The best thermal conductivity was achieved when the diamond mass fraction was 50%, with a thermal conductivity coefficient of 10.32 W/(m·K). The best adhesive performance and thermal conductivity were achieved when the diamond mass fraction was between 50% and 60%. The inorganic thermal conductive adhesive system based on sodium silicate and diamond proposed in this study has outstanding comprehensive performance and is a promising new thermal conductive material that can replace organic thermal conductive adhesives. The results of this study provide new ideas and methods for the development of inorganic thermal conductive adhesives and are expected to promote the application and development of inorganic thermal conductive materials.

Role of metformin in functional endometrial hyperplasia and polycystic ovary syndrome involves the regulation of MEG3/miR­223/GLUT4 and SNHG20/miR­4486/GLUT4 signaling.

Metformin (MET) can effectively treat endometrial hyperplasia (EH), and the expression of glucose transporter type 4 insulin­responsive (GLUT4) is closely associated with the development of EH. The present study aimed to verify the effect of MET in functional EH and polycystic ovary syndrome (PCOS). H&E staining was performed to analyze the severity of EH, and immunohistochemistry was performed to evaluate the expression of GLUT4 in the endometrium of PCOS rats. Reverse transcription­quantitative PCR was used to calculate the expression of long non­coding (lnc)RNA­maternally expressed gene 3 (MEG3), lncRNA­small nucleolar RNA host gene 20 (SNHG20), GLUT4 mRNA, microRNA (miR)­223 and miR­4486. Sequence analysis and luciferase assays were performed to explore the regulatory relationship among certain lncRNAs, miRNAs and target genes. EH in PCOS rats was efficiently inhibited by MET administration. The increased expression of GLUT4 in PCOS rats was attenuated by MET treatment. Moreover, the expression levels of lncRNA­MEG3 and lncRNA­SNHG20 were significantly inhibited in the endometrium of PCOS rats. MET treatment also showed remarkable efficiency in restoring the expression of lncRNA­MEG3 and lncRNA­SNHG20. Meanwhile, the expression levels of miR­223 and miR­4486 were notably elevated in the endometrium of PCOS rats, while MET treatment reduced the expression of miR­223 and miR­4486 in PCOS rats. Furthermore, a luciferase assay confirmed the inhibitory relationship between miR­223 and lncRNA­MEG3/GLUT4 expression, as well as between miR­4486 and lncRNA­SNHG20/GLUT4 expression. GLUT4 knockdown restored the decreased viability of HCC­94 cells induced by overexpression of lncRNA­MEG3. To conclude, MET exhibited a therapeutic effect in the treatment of EH by modulating the lncRNA­MEG3/miR­223/GLUT4 and lncRNA­SNHG20/miR­4486/GLUT4 signaling pathways. This work provides mechanistic insight into the development of EH.

Down-regulation of EDN1 gene expression by circulating miR-206 is associated with risk of preeclampsia.

To study the correlation between circulating microRNA-206 (miR-206) levels and endothelin-1 (ET-1) levels, and to explore its association with preeclampsia (PE) risk.Reverse transcription-PCR (RT-PCT) was used to compare the plasma miR-206 levels in 200 PE patients and 200 healthy controls. The correlation between miR-206 and ET-1 levels in plasma of PE patients was analyzed by Pearson analysis. MiR-206 was transfected into human umbilical vein endothelial cells cells and ET-1 expression was analyzed by enzyme-linked immunosorbent assay.RT-PCR results showed that plasma miR-206 levels in PE patients were significantly higher than those in the control group (P < .01). The results of receiver operating characteristic curve analysis showed that the area under the curve of plasma miR-206 level in the diagnosis of PE was 0.94 (95% confidence interval: 0.92-0.96). Plasma ET-1 levels in PE patients were significantly lower than those in the control group by enzyme-linked immunosorbent assay (P < .01). The area under the curve of plasma ET-1 level in the diagnosis of PE was 0.92 (95% confidence interval: 0.90-0.95). The level of miR-206 in plasma was negative correlated with ET-1 level (r = -0.37, P < .01). The expression level of ET-1 was significantly decreased in human umbilical vein endothelial cells cells transfected with miR-206.miR-206 can down-regulate the expression of EDN1 gene, which may be related to the increased risk of preeclampsia.

Retinal Vascular Network Topology Reconstruction and Artery/Vein Classification via Dominant Set Clustering.

The estimation of vascular network topology in complex networks is important in understanding the relationship between vascular changes and a wide spectrum of diseases. Automatic classification of the retinal vascular trees into arteries and veins is of direct assistance to the ophthalmologist in terms of diagnosis and treatment of eye disease. However, it is challenging due to their projective ambiguity and subtle changes in appearance, contrast, and geometry in the imaging process. In this paper, we propose a novel method that is capable of making the artery/vein (A/V) distinction in retinal color fundus images based on vascular network topological properties. To this end, we adapt the concept of dominant set clustering and formalize the retinal blood vessel topology estimation and the A/V classification as a pairwise clustering problem. The graph is constructed through image segmentation, skeletonization, and identification of significant nodes. The edge weight is defined as the inverse Euclidean distance between its two end points in the feature space of intensity, orientation, curvature, diameter, and entropy. The reconstructed vascular network is classified into arteries and veins based on their intensity and morphology. The proposed approach has been applied to five public databases, namely INSPIRE, IOSTAR, VICAVR, DRIVE, and WIDE, and achieved high accuracies of 95.1%, 94.2%, 93.8%, 91.1%, and 91.0%, respectively. Furthermore, we have made manual annotations of the blood vessel topologies for INSPIRE, IOSTAR, VICAVR, and DRIVE datasets, and these annotations are released for public access so as to facilitate researchers in the community.

B7-H3 Induces Ovarian Cancer Drugs Resistance Through An PI3K/AKT/BCL-2 Signaling Pathway.

PURPOSE: This study was aimed to investigate the underlying mechanism of B7-H3 induced ovarian cancer proliferation and drugs resistance. MATERIALS AND METHODS: We compared the expression of B7-H3 in ovarian tumor tissues from high-malignant or low-malignant patients by immunohistochemistry. We established B7-H3 overexpression and knockout ovarian cells by CRISPR-Cas9 technology and examined the expression of the PI3K/AKT/BCL-2 signals in tumor cells by Western blot or immunofluorescence. We detected the B7-H3 overexpression ovarian cancer cells drugs resistance by CCK8 cell proliferation analysis and Annexin V/PI staining. Tumor-bearing mice were used to investigate the anticancer effects of PI3K/AKT inhibitors in combination with B7-H3 neutralizing antibodies. RESULTS: Enhanced expression of B7-H3 was observed in ovarian tumor tissues from high-malignant patients compared to those from low-malignant patients. Notably, B7-H3 overexpression caused enhanced cells proliferation and chemo-resistance in vitro and in vivo through the activation of PI3K/AKT signaling pathways and up-regulation of BCL-2 protein. Combination of chemotherapeutic agents and B7-H3 neutralizing antibodies efficiently reverses the drugs resistance induced by B7-H3, resulting in improved anticancer effects in ovarian cancer. CONCLUSION: B7-H3 expression induces the activation the PI3K/AKT signaling pathway and up-regulates BCL-2 in protein level, resulting in the sustained growth and chemo-resistance in ovarian cancer. Blockade of B7-H3 signals efficiently reverses the chemo-resistance, which provides an innovative target in ovarian cancer treatment.