Fabrication of CdS-SBA-15 nanomaterials and their photocatalytic activity for degradation of salicylic acid under visible light.

CdS-SBA-15 nanomaterials were synthesized by solvothermal method using cadmium nitrate as cadmium source and thiourea as sulfur source. The properties of as-prepared materials were characterized by means of XRD, FTIR, TEM, XPS, N2 physisorption, UV-Vis DRS and PL spectra, etc. The results show as-synthesized materials have partially ordered mesoporous structure, larger specific surface area, and higher content of CdS and good crystallinity. The combination of SBA-15 and CdS did almost no reduction in the absorption light range of CdS, but greatly increased the photocapacity of the composite. The synergistic effect of CdS and SBA-15 leads to improving the photocatalytic degradation activity of salicylic acid under visible light. When the photocatalyst was 30 mg (0.75 g/L) and the concentration of salicylic acid was 10 mg/L, the maximum degradation efficiency of salicylic acid was 84.93% after 6 h of light. Photocatalytic reaction has a lower activation energy (2.90 kJ/mol), activation enthalpy (3.13 kJ/mol) and activation entropy (-281.00 J/(mol K)). The photocatalytic mechanism study demonstrates that superoxide radicals (O2•-) are the most key active species, e- and h+ have something to do with the photocatalytic reaction, while ·OH has little to do with the photocatalytic reaction. In sum, the protection effect of SBA-15 on CdS nanomaterials makes the composite have a higher photolumination intensity and a higher photocatalytic activity.

Text Prior Guided Scene Text Image Super-resolution.

Scene text image super-resolution (STISR) aims to improve the resolution and visual quality of low-resolution (LR) scene text images, while simultaneously boost the performance of text recognition. However, most of the existing STISR methods regard text images as natural scene images, ignoring the categorical information of text. In this paper, we make an inspiring attempt to embed text recognition prior into STISR model. Specifically, we adopt the predicted character recognition probability sequence as the text prior, which can be obtained conveniently from a text recognition model. The text prior provides categorical guidance to recover high-resolution (HR) text images. On the other hand, the reconstructed HR image can refine the text prior in return. Finally, we present a multi-stage text prior guided super-resolution (TPGSR) framework for STISR. Our experiments on the benchmark TextZoom dataset show that TPGSR can not only effectively improve the visual quality of scene text images, but also significantly improve the text recognition accuracy over existing STISR methods. Our model trained on TextZoom also demonstrates certain generalization capability to the LR images in other datasets.

Unfractionated heparin attenuates endothelial barrier dysfunction via the phosphatidylinositol-3 kinase/serine/threonine kinase/nuclear factor kappa-B pathway.

BACKGROUND: Vascular endothelial dysfunction is considered a key pathophysiologic process for the development of acute lung injury. In this study, we aimed at investigating the effects of unfractionated heparin (UFH) on the lipopolysaccharide (LPS)-induced changes of vascular endothelial-cadherin (VE-cadherin) and the potential underlying mechanisms. METHODS: Male C57BL/6 J mice were randomized into three groups: vehicle, LPS, and LPS + UFH groups. Intraperitoneal injection of 30 mg/kg LPS was used to induce sepsis. Mice in the LPS + UFH group received subcutaneous injection of 8 U UFH 0.5 h before LPS injection. The lung tissue of the mice was collected for assessing lung injury by measuring the lung wet/dry (W/D) weight ratio and observing histological changes. Human pulmonary microvascular endothelial cells (HPMECs) were cultured and used to analyze the effects of UFH on LPS- or tumor necrosis factor-alpha (TNF-α)-induced vascular hyperpermeability, membrane expression of VE-cadherin, p120-catenin, and phosphorylated myosin light chain (p-MLC), and F-actin remodeling, and on the LPS-induced activation of the phosphatidylinositol-3 kinase (PI3K)/serine/threonine kinase (Akt)/nuclear factor kappa-B (NF-κB) signaling pathway. RESULTS: In vivo, UFH pretreatment significantly attenuated LPS-induced pulmonary histopathological changes (neutrophil infiltration and erythrocyte effusion, alveolus pulmonis collapse, and thicker septum), decreased the lung W/D, and increased protein concentration (LPS vs. LPS + UFH: 0.57 ±â€Š0.04 vs. 0.32 ±â€Š0.04 mg/mL, P = 0.0092), total cell count (LPS vs. LPS + UFH: 9.57 ±â€Š1.23 vs. 3.65 ±â€Š0.78 × 10/mL, P = 0.0155), polymorphonuclear neutrophil percentage (LPS vs. LPS + UFH: 88.05% ±â€Š2.88% vs. 22.20% ±â€Š3.92%, P = 0.0002), and TNF-α (460.33 ±â€Š23.48 vs. 189.33 ±â€Š14.19 pg/mL, P = 0.0006) in the bronchoalveolar lavage fluid. In vitro, UFH pre-treatment prevented the LPS-induced decrease in the membrane expression of VE-cadherin (LPS vs. LPS + UFH: 0.368 ±â€Š0.044 vs. 0.716 ±â€Š0.064, P = 0.0114) and p120-catenin (LPS vs. LPS + UFH: 0.208 ±â€Š0.018 vs. 0.924 ±â€Š0.092, P = 0.0016), and the LPS-induced increase in the expression of p-MLC (LPS vs. LPS + UFH: 0.972 ±â€Š0.092 vs. 0.293 ±â€Š0.025, P = 0.0021). Furthermore, UFH attenuated LPS- and TNF-α-induced hyperpermeability of HPMECs (LPS vs. LPS + UFH: 8.90 ±â€Š0.66 vs. 15.84 ±â€Š1.09 Ω·cm, P = 0.0056; TNF-α vs. TNF-α + UFH: 11.28 ±â€Š0.64 vs. 18.15 ±â€Š0.98 Ω·cm, P = 0.0042) and F-actin remodeling (LPS vs. LPS + UFH: 56.25 ±â€Š1.51 vs. 39.70 ±â€Š1.98, P = 0.0027; TNF-α vs. TNF-α + UFH: 55.42 ±â€Š1.42 vs. 36.51 ±â€Š1.20, P = 0.0005) in vitro. Additionally, UFH decreased the phosphorylation of Akt (LPS vs. LPS + UFH: 0.977 ±â€Š0.081 vs. 0.466 ±â€Š0.035, P = 0.0045) and I kappa B Kinase (IKK) (LPS vs. LPS + UFH: 1.023 ±â€Š0.070 vs. 0.578 ±â€Š0.044, P = 0.0060), and the nuclear translocation of NF-κB (LPS vs. LPS + UFH: 1.003 ±â€Š0.077 vs. 0.503 ±â€Š0.065, P = 0.0078) in HPMECs, which was similar to the effect of the PI3K inhibitor, wortmannin. CONCLUSIONS: The protective effect of UFH against LPS-induced pulmonary endothelial barrier dysfunction involves VE-cadherin stabilization and PI3K/Akt/NF-κB signaling.

Properties of magnetic carbon nanomaterials and application in removal organic dyes.

Magnetic carbon nanomaterials were prepared facilely by one step hydrothermal synthesis method using biologically regenerated glucose as carbon sources and ferric ammonium citrate as iron sources. As-synthesized nanomaterials were characterized by means of SEM, TEM, XRD, N2 adsorption-desorption, VSM and XPS etc. techniques. Results show as-prepared magnetic nanomaterials are sphere particles with aggregation state and magnetic α-Fe particles are enclosed by carbon matrixes. With increase of calcination temperature, the degrees of the sample aggregation decrease, whereas the average particle sizes, BET specific surface areas and saturation magnetizations increase. The carbon with graphite structure has higher adsorption efficiency than that of amorphous carbon for organic dye rhodamine B in water. Whereas the iron with amorphous structure shows higher photocatalytic activity than that of the iron with crystalline structure for the degradation of rhodamine B. And rhodamine B in water can almost be degraded completely through the combination of adsorption and photocatalysis.

An initial differential renal function between 35% and 40% has greater probability of leading to normal after pyeloplasty in patients with unilateral pelvic-ureteric junction obstruction.

PURPOSE: We compared the outcomes in patients who were <1 year old and had hydronephrosis with SFU grade 3-4 PUJ obstruction to observe the potential recovery of renal morphology and DRF after successful pyeloplasty. METHODS: All children younger than 1 year old with SFU grade 3-4 PUJ obstruction from January 2013 to June 2015 were retrospectively analyzed. A total of 92 children were grouped according to their DRF value at pyeloplasty as follows: DRF from 30 to ≤35% (group I) and DRF from 35 to ≤40% (group II). We evaluated changes in anteroposterior diameter and differential renal function using ultrasound and diuretic renography. Outcomes were compared using Student t test. RESULTS: Group I comprised 45 patients, and group II included 47 patients. No significant difference was observed in the initial APD, final APD and the improvement of APD after pyeloplasty between two groups. Significant differences were observed between the initial and final DRF values in both groups. The difference in DRF improvement after pyeloplasty between groups I and II was significant. The DRF improved to a normal stage significantly more frequently in group II (21/47; 44.7%) than in group I (13/45; 28.9%). CONCLUSION: The improvement in DRF after pyeloplasty was significant for patients with an initial DRF from 30 to ≤35%. However, patients with an initial DRF from 35 to ≤40% had a greater probability of achieving normal renal function. Patients with severely impaired initial renal function had a marginal probability of achieving a normal value.

Protective effects of heparin on endothelial cells in sepsis.

OBJECTIVE: This study aims to observe the protective effects of heparin on endothelial cells in sepsis and explore the involved signal pathway regulated by heparin. Methods Human vascular endothelial cells were treated by TNFα in vitro to simulate the inflammatory environment when sepsis occurred. They were intervened by heparin and the expression levels of soluble thrombomodulin (sTM) and serum activated protein C (APC) were detected by ELISA, the regulatory mechanism of heparin improving vascular endothelial cells injury induced by TNFα was detected by Western Blotting method, the methylation of histone in the gene promoter region of endothelial nitric oxide synthase (eNOS) and monocyte chemotactic protein-1 (MCP-1) were detected using chromatin immunoprecipitation method. Results Heparin could inhibit the secretion of sTM and APC protein and the expression of MCP-1 gene which involved in NF-κB signal pathway. Conclusions Heparin could protect vascular endothelial cells from injury induced by TNFα and sepsis, the mechanisms were related with the effects of heparin on the histone methylation of promoter region and the regulation of heparin on the MAPK and NF-κB signal pathways. These results provide a theoretical basis for the application of heparin in the prevention and treatment of vascular disease related with sepsis.

miR-205 regulates A549 cells proliferation by targeting PTEN.

miR-205 is an epithelial-specific miRNA and has been shown to orchestrate some cellular processes such as epithelial mesenchymal transition (EMT) and differentiation fate of stem cells in mammary gland. miR-205 play a part of a tumor suppressor in human cancers. However, the role of miR-205 in lung cancer is unclear. In this study, we detected the expression level of miR-205 in 46 cases clinical lung cancer specimens and adjacent normal tissues by stem-loop RT-PCR. We found that the expression of miR-205 was significantly increased in lung cancer specimens compared to adjacent normal tissues (P < 0.01). Furthermore, we observed the expressions of PTEN protein and mRNA in lung cancer tissues and adjacent normal tissues by methods of western blot and Real time PCR respectively. We found that the expressions of PTEN protein and mRNA was significantly decreased in lung cancer specimens compared to adjacent normal tissues. And then, we found there is a negative relationship between the expression of miR-205 and PTEN mRNA in lung cancer by analyzed. To validate whether PTEN was direct targets of miR-205, a dual-luciferase reporter assay was employed, the result showed that PTEN is a target gene of MiR-205. In subsequent experiments, we examined the expressions of PTEN protein and mRNA after transfection of miR-205 mimics or inhibitor into A549 cells, and A549 cell proliferation was measured by CCK-8 tests. We found that the expression of PTEN protein and mRNA in A549 cells were significantly down-regulated or up-regulated after miR-205 mimics and miR-205 inhibitors transfected into, and miR-205 could inhibits A549 cells proliferation. These results indicate that miR-205 might inhibitor the proliferation of A549 cells by regulating the expression of PTEN.