Peroxisomal regulation of redox homeostasis and adipocyte metabolism

Peroxisomes are ubiquitous cellular organelles required for specific pathways of fatty acid oxidation and lipid synthesis, and until recently their functions in adipocytes have not been well appreciated. Importantly, peroxisomes host many oxygen-consumption reactions and play a major role in generation and detoxification of reactive oxygen species (ROS) and reactive nitrogen species (RNS), influencing whole cell redox status. Here, we review recent progress in peroxisomal functions in lipid metabolism as related to ROS/RNS metabolism and discuss the roles of peroxisomal redox homeostasis in adipogenesis and adipocyte metabolism. We provide a framework for understanding redox regulation of peroxisomal functions in adipocytes together with testable hypotheses for developing therapies for obesity and the related metabolic diseases

Overexpression of long non-coding RNA NORAD promotes invasion and migration in malignant melanoma via regulating the MIR-205-EGLN2 pathway.

Growing evidence suggests that long non-coding RNAs NORAD and miR-205 play a significant role in regulating cancer progression and metastasis. In this study, high expression of NORAD was firstly observed in melanoma tissues and human malignant melanoma cell lines, our aim was to study the interaction of them in the process of invasion and migration of malignant melanoma cells. NORAD, miR-205, and EGLN2 mRNA level in MM cells was detected by qRT-PCR. In situ hybridization (ISH) was performed to detect NORAD expression in MM tissues specimens. Effects of NORAD and miR-205 on Prolyl hydroxylase 2 (EGLN2) expression was explored by western blot in MM cells line. Dual-luciferase reporter assay was performed to verify the interaction relationship between NORAD and miR-205, as well as, miR-205 and EGLN2. Transwell assay was conducted to explore the effects of NORAD and miR-205 in vitro. Xenografts in nude mice experiment were used to confirm the role of NORAD and miR-205 in vivo. In vitro, NORAD knockdown significantly inhibited migration and invasion of malignant melanoma cells and elevated the expression of miR-205, there was an interaction between miR-205 and NORAD in the RNA-induced silencing complex. Upregulation of miR-205 induced significant inhibition of migratory and invasive ability compared with the scrambled control. However, downregulating NORAD largely reversed this effect. Furthermore, the regulatory effects of miR-205 on EGLN2 levels and the induction of endoplasmic reticulum stress were reversed by NORAD. In vivo, deletion of miR-205 induced tumor growth in nude mice. NORAD may play critical roles in tumorigenesis and progression of malignant melanoma by regulating of the miR-205-EGLN2 pathway, and may serve as a new therapeutic target

Facile fabrication of lightweight porous FDM-printed polyethylene/graphene nanocomposites with enhanced interfacial strength for electromagnetic interference shielding

In order to shield the massive electromagnetic perturbations and meet the more and more stringent requirement for advanced electronic equipment, development of diverse, lightweight and high-performance electromagnetic interference (EMI) shielding materials is urgent but still challenging. Herein, the facile and green method which combines fused deposition modeling (FDM) 3D printing, ball milling and microwave (MW) irradiation technology was proposed to fabricate exfoliated graphene nanoplatelets (GNPs) incorporated liner low density polyethylene (LLDPE) nanocomposite lightweight parts with porous and complex geometry structure. FDM 3D printing possesses high flexibility for structure design, which can significantly broaden the application of materials in various fields. Benefiting from design of a unique porous lamellar structure, the printed LLDPE/GNPs nanocomposite parts can achieve a prominent EMI shielding effectiveness (SE) of ~32.4 dB (with thickness-normalized specific EMI SE (SSE/t) of 318 dB cm2/g) in the range of 8.2–12.4 GHz. This remarkable characteristic is due to internal multiple reflections and absorption of electromagnetic (EM) waves. In addition, the specific FDM 3D-printed porous parts prepared by our strategy exhibit a relatively higher EMI SE at a lower density than those lightweight EMI shields in literatures. The use of MW irradiation technology improves mechanical properties, especially for the interfacial bonding strength between filaments. More importantly, this strategy is highly favorable for the fabrication of lightweight porous EMI shields with tailorable and optimized shape/structure, which could be expected to be applied in aerospace fields, portable electronic devices, smart devices and so on

microRNA-33a-5p increases radiosensitivity by inhibiting glycolysis in melanoma.

Glycolysis was reported to have a positive correlation with radioresistance. Our previous study found that the miR-33a functioned as a tumor suppressor in malignant melanoma by targeting hypoxia-inducible factor1-alpha (HIF-1α), a gene known to promote glycolysis. However, the role of miR-33a-5p in radiosensitivity remains to be elucidated. We found that miR-33a-5p was downregulated in melanoma tissues and cells. Cell proliferation was downregulated after overexpression of miR-33a-5p in WM451 cells, accompanied by a decreased level of glycolysis. In contrast, cell proliferation was upregulated after inhibition of miR-33a-5p in WM35 cells, accompanied by increased glycolysis. Overexpression of miR-33a-5p enhanced the sensitivity of melanoma cells to X-radiation by MTT assay, while downregulation of miR-33a-5p had the opposite effects. Finally, in vivo experiments with xenografts in nude mice confirmed that high expression of miR-33a-5p in tumor cells increased radiosensitivity via inhibiting glycolysis. In conclusions, miR-33a-5p promotes radiosensitivity by negatively regulating glycolysis in melanoma

Pyrolysis treatment of nonmetal fraction of waste printed circuit boards : Focusing on the fate of bromine

Advanced thermal treatment of electronic waste offers advantages of volume reduction and energy recovery. In this work, the pyrolysis behaviour of nonmetallic fractions of waste printed circuit boards was studied. The fate of a bromine and thermal decomposition pathway of nonmetallic fractions of waste printed circuit boards were further probed. The thermogravimetric analysis showed that the temperatures of maximum mass loss were located at 319°C and 361°C, with mass loss of 29.6% and 50.6%, respectively. The Fourier transform infrared Spectroscopy analysis revealed that the spectra at temperatures of 300°C–400°C were complicated with larger absorbance intensity. The nonmetallic fractions of waste printed circuit boards decomposed drastically and more evolved products were detected in the temperature range of 600°C–1000°C. The gas chromatography–mass spectrometry analysis indicated that various brominated derivates were generated in addition to small molecules, such as CH4, H2O and CO. The release intensity of CH4 and H2O increased with temperature increasing and reached maximum at 600°C–800°C and 400°C–600°C. More bromoethane (C2H5Br) was formed as compared with HBr and methyl bromide (CH3Br). The release intensity of bromopropane (C3H7Br) and bromoacetone (C3H5BrO) were comparable, although smaller than that of bromopropene (C3H5Br). More dibromophenol (C6H4Br2O) was released than that of bromophenol (C6H5BrO) in the thermal treatment. During the thermal process, part of the ether bonds first ruptured forming bisphenol A, propyl alcohol and tetrabromobisphenol A. Then, the tetrabromobisphenol A decomposed into C6H5BrO and HBr, which further reacted with small molecules forming brominated derivates. It implied debromination of raw nonmetallic fractions of waste printed circuit boards or pyrolysis products should be applied for its environmentally sound treating.© 2020 Sage. The article is protected by copyright and reuse is restricted to non-commercial and no derivative uses. Users may also download and save a local copy of an article accessed in an institutional repository for the user's personal reference.fi=vertaisarvioitu|en=peerReviewed