Modified three-level techniques of retroperitoneal laparoscopic procedures to treat adrenal lesions for patients with BMI ≥ 25 Kg/m2.

Objective: To evaluate the modified Zhang's 'three-level' technique of retroperitoneal laparoscopic adrenalectomy (RLA) to treat adrenal lesions for patients with BMI of 25-30 Kg/m2. Methods: A retrospective analysis was performed in all patients with BMI of 25-30 Kg/m2 in our hospital from January 2014 to December 2019. Those who underwent laparoscopic adrenal surgery were divided into two groups on the basis of the technique used: the Zhang's technique (the ZT group) and the modified technique (the MT group). Results: Herein, 170 operations were included (ZT, 91 patients; MT, 79 patients). RLA was successfully performed in all of them. Compared with the ZT group patients, the MT group patients showed shorter operation time (p = 0.007), lesser intraoperative blood loss (p = 0.023), shorter operation time, earlier postoperative diet recovery (p < 0.001), shorter postoperative drainage time (p < 0.001) and shorter postoperative hospitalization period (p = 0.001). It was also worth noting that the unplanned total adrenalectomy rate was significantly less in the MT group than in the ZT group (0% vs. 10.8%, p = 0.020). There was no significant difference in the complications between the two groups (3.3% vs. 2.5%, p = 0.567). Conclusions: We found that MT was a beneficial retroperitoneal laparoscopic treatment for adrenal lesions in patients who had a BMI of 25-30 Kg/m2. It may provide a reference for the treatment of adrenal surgical diseases in such patients.

A Gas Sensing Channel Composited with Pristine and Oxygen Plasma-Treated Graphene.

Oxygen plasma treatment has been reported as an effective way of improving the response of graphene gas sensors. In this work, a gas sensor based on a composite graphene channel with a layer of pristine graphene (G) at the bottom and an oxygen plasma-treated graphene (OP-G) as a covering layer was reported. The OP-G on top provided oxygen functional groups and serves as the gas molecule grippers, while the as-grown graphene beneath serves as a fast carrier transport path. Thus, the composite channel (OP-G/G) demonstrated significantly improved response in NH3 gas sensing tests compared with the pristine G channel. Moreover, the OP-G/G channel showed faster response and recovering process than the OP-G channel. Since this kind of composite channel is fabricated from chemical vapor deposited graphene and patterned with standard photolithography, the device dimension was much smaller than a gas sensor fabricated from reduced graphene oxide and it is favorable for the integration of a large number of sensing units.

Long non-­coding RNA SNHG16 functions as a tumor activator by sponging miR­373­3p to regulate the TGF­ß­R2/SMAD pathway in prostate cancer.

Long non­coding RNAs (lncRNAs) are involved in the pathogenesis of prostate cancer (PCa) as competitive endogenous RNA. The present study aimed to investigate the molecular mech--anisms of lncRNA small nucleolar RNA host gene 16 (SNHG16) in the proliferation and metastasis of PCa cells. Cancer tissues and adjacent normal tissues were collected from 80 patients with PCa who did not receive any treatment. Reverse transcription­quantitative PCR analysis was performed to detect the expression levels of SNHG16, hsa­microRNA (miRNA/miR)­373­3p and transforming growth factor­ß receptor type 2 (TGF­ß­R2), and Spearman's correlation coefficient analysis was performed to assess the correlations between these molecules. Furthermore, the effects of SNHG16 knockdown and overexpression on the biological functions of DU­145 PCa cells and TGF­ß­R2/SMAD signaling were analyzed. The dual­luciferase reporter assay was performed to assess the associations between SNHG16 and miR­373­3p, and TGF­ß­R2 and miR­373­3p, the effects of which were verified via rescue experiments. The results demonstrated that the expression levels of SNHG16 and TGF­ß­R2 were significantly upregulated in PCa tissues, whereas miR­373­3p expression was significantly downregulated (P<0.001). In addition, negative correlations were observed between SNHG16 and miR­373­3p (rho, ­0.631) and miR­373­3p and TGF­ß­R2 (rho, ­0.516). Overexpression of SNHG16 significantly promoted the proliferation, migration and invasion of PCa cells (P<0.05), and significantly increased the protein expression levels of TGF­ß­R2, phosphorylated (p)­SMAD2, p­SMAD3, c­Myc and E2F4 (P<0.001). Notably, the results revealed that miR­373­3p is a target of SNHG16, and miR­373­3p knockdown rescued short hairpin (sh)­SNHG16­suppressed cellular functions by promoting TGF­ß­R2/SMAD signaling. The results also revealed that miR­373­3p targets TGF­ß­R2. Notably, transfection with miR­373­3p inhibitor rescued sh­TGF­ß­R2­suppressed cell proliferation and migration. Taken together, the results of the present study suggest that SNHG16 promotes the proliferation and migration of PCa cells by targeting the miR­373­3p/TGF­ß­R2/SMAD axis.

NANOG regulates the proliferation of PCSCs via the TGF-ß1/SMAD pathway.

PURPOSE: In prostate cancer, castration resistance is a factor that frequently leads to death in individuals with this disease. Recent studies have suggested that prostate cancer stem cells (PCSCs) are pivotal regulators in the establishment of castration resistance. The nanog homeobox (NANOG) and the transforming growth factor (TGF)-ß1/drosophila mothers against decapentaplegic protein (SMAD) signaling pathways are involved in several cancer stem cells but are not involved in PCSCs. The purpose of this study is to investigate the effect of NANOG on the proliferation of PCSCs regulated by the TGF-ß1/SMAD signaling pathway. METHODS: In this study, we used flow cytometry to isolate CD44+/CD133+/NANOG+ PCSCs from DU145 prostate cancer cells. Then we used short hairpin RNA to silence NANOG and observed the biological behavior and the TGF-ß1/SMAD signal of PCSCs. RESULTS: NANOG decreased PCSC proliferation, increased apoptosis, and blocked cell cycling at G0/G1. Furthermore, reduction in the TGF-ß1, p15, and p-SMAD2 expression was observed. CONCLUSION: These findings suggest that NANOG positively regulates the growth of PCSCs through the TGF-ß1/SMAD signaling pathway.

Photoinduced Hysteresis of Graphene Field-Effect Transistors Due to Hydrogen-Complexed Defects in Silicon Dioxide.

Photoinduced hysteresis (PIH) of graphene field-effect transistors (G-FETs) has attracted attention because of its potential in developing photoelectronic or nonvolatile memory devices. In this work, we focused on the role of SiO2 dielectric layer on PIH, where G-FETs have only a SiO2 dielectric layer. Adsorbates are effectively removed before the PIH test. The effects of laser wavelength, laser power density, and temperature on the PIH are systematically investigated. The PIH is significantly enhanced by increasing the hydrogen flow in a hydrogen-atmosphere device thermal annealing. This strongly suggests proton-related defects that play a key role. The pure electronic process for PIH is further ruled out by the significant dependence of the doping rate on the temperature. A mechanism of PIH based on proton generation after hole trapping at [O3≡Si-H] is proposed. The proposed mechanism is well-supported by our experimental data: (1) the observed threshold photon energy for PIH is between 2.76 and 2.34 eV, which is close to the energy barrier for [O3≡Si-H], releasing a proton. (2) No obvious carrier mobility degradation after the PIH process suggests that the bulk defects in SiO2 are the major contributors rather than graphene/SiO2 interface defects. (3) The dependence of the doping rate on the temperature and the laser power density matches a theoretical model based on the random hopping of H+. The results in this work are also valuable for the study of degradation of other oxide dielectric materials in various field-effect transistors.

Cancer cell membrane-cloaked mesoporous silica nanoparticles with a pH-sensitive gatekeeper for cancer treatment.

Nanoparticular drug delivery system (NDDS) has great potential for enhancing the efficacy of traditional chemotherapeutic drugs. However, it is still a great challenge to fabricate a biocompatible NDDS with simple structure capable of optimizing therapeutic efficacy, such as high tumor accumulation, suitable drug release profile (e.g. no premature drug leakage in normal physiological conditions while having a rapid release in cancer cells), low immunogenicity, as well as good biocompatibility. In this work, a simple core/shell structured nanoparticle was fabricated for prostate cancer treatment, in which a mesoporous silica nanoparticle core was applied as a container to high-efficiently encapsulate drugs (doxorubicin, DOX), CaCO3 interlayer was designed to act as sheddable pH-sensitive gatekeepers for controlling drug release, and cancer cell membrane wrapped outlayer could improve the colloid stability and tumor accumulation capacity. In vitro cell experiments demonstrated that the as-prepared nanovehicles (denoted as DOX/MSN@CaCO3@CM) could be efficiently uptaken by LNCaP-AI prostate cancer cells and even exhibited a better anti-tumor efficiency than free DOX. In addition, Live/Dead cell detection and apoptosis experiment demonstrated that MSN/DOX@CaCO3@CM could effectively induce apoptosis-related death in prostate cancer cells. In vivo antitumor results demonstrated that DOX/MSN@CaCO3@CM administration could remarkably suppress the tumor growth. Compared with other tedious approaches to optimize the therapeutic efficacy, this study provides an effective drug targeting system only using naturally biomaterials for the treatment of prostate cancer, which might have great potential in clinic usage.