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BackgroundRobotic-assisted surgery (RAS) with its advantages continues to gain popularity among surgeons. This study analyzed the increased costs of RAS in common surgical procedures using the National Inpatient Sample.MethodsRetrospective analysis of the 2012–2014 Healthcare Cost and Utilization Project-NIS was performed for the following laparoscopic/robotic procedures: cholecystectomy, ventral hernia repair, right and left hemicolectomy, sigmoidectomy, abdominoperineal resection, and total abdominal hysterectomy (TAH). Patients with additional concurrent procedures were excluded. Costs were compared between the laparoscopic procedures and their RAS counterparts. Total costs and charges for cholecystectomy (the most common procedure in the dataset) were compared based on the payer and characteristics of hospital (region, rural/urban, bed size, and ownership).ResultsA total of 91,630 surgeries (87,965 laparoscopic, 3665 robotic) were analyzed. The average cost for the laparoscopic group was $10,227 ± $4986 versus $12,340 ± $5880 for the robotic cases (p < 0.001). The overall and percentage increases for laparoscopic versus robotic for each procedure were as follows: cholecystectomy $9618 versus $10,944 (14%), ventral hernia repair $10,739 versus $13,441 (25%), right colectomy $12,516 versus $15,027 (20%), left colectomy $14,157 versus $17,493 (24%), sigmoidectomy $13,504 versus $16,652 (23%), abdominoperineal resection $17,708 versus $19,605 (11%), and TAH $9368 versus $9923 (6%). Hysterectomy was the only procedure performed primarily using RAS and it was found to have the lowest increase in costs. Increased costs were associated with even higher increases in charges, especially in investor-owned private hospitals.ConclusionRAS is more costly when compared to conventional laparoscopic surgery. Additional costs may be lower in centers that perform a higher volume of RAS. Further analysis of long-term outcomes (including reoperations and readmissions) is needed to better compare the life-long treatment costs for both surgical approaches.

The N-doped bismuth tungstate （BizWOt） photocatalysts with high visible light activity were prepared by the hydrothermal method using urea as a nitrogen source. The as-prepared N-doped Bi2WO6 samoles were characterized by X-ray diffraction, scanning electron microscopy, specific surface area, photocurrent analysis, and UV-Vis diffuse re- flectrance spectroscopy. The photocatalytic activity was evaluated by photocatalytic degradation of rhodamine B （RhB） solution under visible light irradiation. The photocatalytic mechanisms were analyzed by active species trapping experi- ments which revealed that the holes were the main active species of N-doped BizWO6 products in aqueous solution under visible light irradiation, rather than .OH and O-. With the assistance of H202, the photocatalytic activity for degradation of RhB could be further improved because H202 reacted with conduction band electrons to generate more hydroxyl radicals. KEY WORDS：

Glomerular endothelial cell （GEC） injury plays an important role in the early stage of diabetic nephropathy （DN）. Previous studies show that a PKCβ inhibitor is effective for treating DN. In the current study we further explored the effects and molecular mechanisms of PKCI3 inhibitors on GEC apoptosis in DN in streptozotocin-induced diabetic mice in vivo and high glucoseor PMA-treated human renal glomerular endothelial cells （HRGECs） in vitro. In the diabetic mice, hyperglycemia caused aggravated nephropathy and GEC apoptosis accompanied by significantly increased expression of swiprosin-1, a potentally pro-apoptotic protein. Administration of LY333531 （1 mg.kg-1.d-1 for 8 weeks） significantly attenuated both GEC apoptosis and swiprosin-1 upregulation in the diabetic mice. Similar results were observed in high glucoseor PMA-treated HRGECs in vitro. The pro-apoptotic role of swiprosin-1 was further examined using HRGECs treated with lentivirus mediating RNA interference or over-expression and swiprosin-1-knockout mice. Over-expression of swiprosin-1 in HRGECs resulted in increases in apoptosis and in caspase-9, caspase-3 and Bax expression. In contrast, knockdown of swiprosin-1 attenuated high glucoseor PMA-induced HRGECs apoptosis. Furthermore, over-expression of swiprosin-1 promoted interaction between swiprosin-1 and caspase-9 and increased the formation of apoptosomes. In diabetic swiprosin-1-/- mice, the kidney/body weight, urinary albumin, glomerular hypertrophy, mitochondrial apoptotic-associated proteins and GEC apoptosis were significantly attenuated as compared with those in diabetic swiprosin-1＋/＋ mice. These results demonstrate that swiprosin-1 is up-regulated by PKCβ in the early stage of DN, and that PKCβ facilitates GEC apoptosis through the mitochondrial-dependent pathway.

Aim： To develop a novel 3D-QSAR approach for study of the epidermal growth factor receptor tyrosine kinase （EGFR TK） and its inhibi- tors. Methods： One hundred thirty nine EGFR TK inhibitors were classified into 3 clusters. Ensemble docking of these inhibitors with 19 EGFR TK crystal structures was performed. Three protein structures that showed the best recognition of each cluster were selected based on the docking results. Then, a novel QSAR （ensemble-QSAR） building method was developed based on the ligand conforma- tions determined by the corresponding protein structures. Results： Compared with the 3D-QSAR model, in which the ligand conformations were determined by a single protein structure, ensemble-QSAR exhibited higher R2 （0.87） and Q2 （0.78） values and thus appeared to be a more reliable and better predictive model. Ensemble-QSAR was also able to more accurately describe the interactions between the target and the ligands. Conclusion： The novel ensemble-QSAR model built in this study outperforms the traditional 3D-QSAR model in rationality, and provides a good example of selecting suitable protein structures for docking prediction and for building structure-based QSAR using available protein structures.

Resveratrol （RSV）, a phytoalexin, has shown to prevent endothelial dysfunction and reduce diabetic vascular complications and the risk of cardiovascular diseases. The aim of this study was to investigate the signaling mechanisms underlying the protecting effects of RSV against endothelial dysfunction during hyperglycemia in vitro and in vivo. Human umbilical vein endothelial cells （HUVECs） were treated with RSV, and then exposed to high glucose （HG, 30 mmol/L）. Akt-Ser473 phosphorylation, eNOS-Ser1177 phosphorylation, and PTEN protein levels in the cells were detected using Western blot. For in vivo studies, WT and Akt-/- mice were fed a normal diet containing RSV （400 mg.kg-1.d-1） for 2 weeks, then followed by injection of STZ to induce hyperglycemia （300 mg/dL）. Endothelial function was evaluated using aortic rings by assessing ACh-induced vasorelaxation. RSV （5-20 pmol/L） dose-dependently increased AKt-Ser473 phosphorylation, accompanied by increased eNOS-Ser1177 phosphorylation in HUVECs; these effects were more prominent under HG stimulation. Transfection with Akt siRNA abolished RSV-enhanced eNOS phosphorylation and NO release. Furthermore, RSV （5-20 pmol/L） dose-dependently decreased the levels of PTEN, which was significantly increased under HG stimulation, and PTEN overexpression abolished RSV-stimulated Akt phosphorylation in HG-treated HUVECs. Moreover, RSV dramatically increased 26S proteasome activity, which induced degradation of PTEN. In in vivo studies, pretreatment with RSV significantly increased Akt and eNOS phosphorylation in aortic tissues and ACh-induced vasorelaxation, and improved diabetes-induced endothelial dysfunction in wild-type mice but not in Akt-/- mice. RSV attenuates endothelial function during hyperglycemia via activating proteasome-dependent degradation of PTEN, which increases Akt phosphorylation, and consequentially upregulation of eNOS-derived NO production.

Room temperature ionic liquids （RTILs） with dispersed carbon pieces exhibit distinctive physiochemical properties. To ex- plore the molecular mechanism, RTILs/carbon pieces mixture was investigated by molecular dynamics （MD） simulation in this work. Rigid and flexible carbon pieces in the form of graphene with different thicknesses and carbon nanotubes in different sizes were dispersed in a representative RTIL 1-butyl-3-methyl-imidazolium dicyanamide （[Bmim][DCA]）. This study demonstrated that the diffusion coefficients of RTILs in the presence of flexible carbons are similar to those of bulk RTILs at varying temperatures, which is in contrast to the decreased diffusion of RTILs in the presence of rigid carbons. In addition, in- terfacial ion number density at rigid carbon surfaces was higher than that at flexible ones, which is correlated with the accessi- ble external surface area of carbon pieces. The life time of cation-anion pair in the presence of carbon pieces also exhibited a dependence on carbon flexibility. RTILs with dispersed rigid carbon pieces showed longer ion pair life time than those with flexible ones, in consistence with the observation in diffusion coefficients. This work highlights the necessity of including the carbon flexibility when performing MD simulation of RTILs in the presence of dispersed carbon pieces in order to obtain the reliable dynamical and interfacial structural properties.

In order to quantitatively estimate the volume and property transports between the South China Sea and Indonesian Seas via the Karimata Strait, two trawi-resistant bottom mounts, with ADCPs embedded, were deployed in the strait to measure the velocity profile as part of the South China Sea-Indonesian Seas trans- port/exchange （SITE） program. A pair of surface and bottom acoustic modems was employed to transfer the measured velocity without recovering the mooring. The advantage and problems of the instruments in this field work are reported and discussed. The field observations confirm the existence of the South Chi- na Sea branch of Indonesian throughflow via the Karimata Strait with a stronger southward flow in boreal winter and weaker southward bottom flow in boreal summer, beneath the upper layer northward （reversal） flow. The estimate of the averaged volume, heat and freshwater transports from December 2007 to March 2008 （winter） is （-2.7±1.1）×10^6 m^3/s, （-0.30±0.11） PW, 2008 （summer） is （1.2±0.6）×10^6 m^3/s, （0.14±0.03） PW, （-0.18±0.07） × 106 m3/s and from May to September （0.12±0.04）×10^6 m^3/s and for the entire record from December 2007 to October 2008 is （-0.5±1.9）×10^6 m^3/s, （-0.05±0.22） PW, （-0.01±0.15）×10^6 m^3/s （nega- tive/positive represents southward/northward transport）, respectively. The existence of southward bottom flow in boreal summer implies that the downward sea surface slope from north to south as found by Fang et al. （2010） for winter is a year-round phenomenon.

Long noncoding RNAs（lncRNAs）play important roles in human diseases including vascular disease.Given the large number of lncRNAs,however,whether the majority of them are associated with vascular disease remains unknown.For this purpose,here we present a genomic location based bioinformatics method to predict the lncRNAs associated with vascular disease.We applied the presented method to globally screen the human lncRNAs potentially involved in vascular disease.As a result,we predicted 3043 putative vascular disease associated lncRNAs.To test the accuracy of the method,we selected 10 lncRNAs predicted to be implicated in proliferation and migration of vascular smooth muscle cells（VSMCs）for further experimental validation.The results confirmed that eight of the 10 lncRNAs（80%）are validated.This result suggests that the presented method has a reliable prediction performance.Finally,the presented bioinformatics method and the predicted vascular disease associated lncRNAs together may provide helps for not only better understanding of the roles of lncRNAs in vascular disease but also the identification of novel molecules for the diagnosis and therapy of vascular disease.

The PTEN tumor suppressor is a lipid phosphatase that has a central role in regulating the phosphatidylinositol-3- kinase （PI3K） signal transduction cascade. Nevertheless, the mechanism by which the PTEN activity is regulated in cells needs further elucidation. Although previous studies have shown that ubiquitination of PTEN can modulate its stability and subcellular localization, the role of ubiquitination in the most critical aspect of PTEN function, its phos- phatase activity, has not been fully addressed. Here, we identify a novel E3 ubiquitin ligase of PTEN, Ret finger pro- tein （RFP）, that is able to promote atypical polyubiquitinations of PTEN. These ubiquitinations do not lead to PTEN instability or relocalization, but rather significantly inhibit PTEN phosphatase activity and therefore modulate its ability to regulate the PI3K signal transduction cascade. Indeed, RFP overexpression relieves PTEN-mediated inhibi- tory effects on AKT activation; in contrast, RNAi-mediated knockdown of endogenous RFP enhances the ability of PTEN to suppress AKT activation. Moreover, RFP-mediated ubiquitination of PTEN inhibits PTEN-dependent ac- tivation of TRAIL expression and also suppresses its ability to induce apoptosis. Our findings demonstrate a crucial role of RFP-mediated ubiquitination in controlling PTEN activity.