Tin dioxide decorated on Ni-encapsulated nitrogen-doped carbon nanotubes for anodic electrolysis and persulfate activation to degrade cephalexin: Mineralization and degradation pathway.

In this study, bamboo-shaped carbon nanotubes exhibiting high nitrogen content and Ni encapsulation (Ni@NCNT) were effectively synthesized by a simple pyrolysis method. The catalytic peroxydisulfate activation for cephalexin (CPX) degradation was investigated using the prepared material. SnO2 was further decorated and fabricated on the anode material (SnO2/Ni@NCNT) for electrochemical degradation of CPX in an aqueous solution. Transmission electron microscopy, X-ray diffraction, and X-ray photoelectron spectroscopy indicated that the SnO2 nanoparticles were uniformly distributed on the surface of Ni@NCNT. Electrochemical characterization employing cyclic voltammetry and linear sweep voltammetry demonstrated that SnO2/Ni@NCNT displayed higher oxygen evolution potential and electrocatalytic activity than Ni@NCNT. Mineralization of CPX in wastewater was performed using electrolysis coupled with persulfate oxidation. The analysis revealed a synergistic strengthening effect. The electropersulfate oxidation resulted in higher total organic carbon (TOC) removal (70.3%) than the sum of electrooxidation (48.1%) and persulfate oxidation (9.2%) toward CPX. This phenomenon might result from the regeneration of sulfate radicals (SO4•-) on the anode and complementary oxidation by SO4•- and OH. Persulfate oxidation alone was shown to result in low TOC removal, although CPX was mostly degraded. Additionally, the CPX degradation pathway involving electropersulfate oxidation was proposed and it is indicated that CPX molecules were completed decomposed by the examination of short chain acids, mineralized ions, and ecotoxicity evolution indicated that the antibiotic was completely degraded. This study provides a new approach for the design and preparation of novel electrode materials and electrochemical degradation facilities for the removal of pollutants via persulfate activation.

Berberine inhibits proliferation and apoptosis of vascular smooth muscle cells induced by mechanical stretch via the PDI/ERS and MAPK pathways.

AIMS: We recently demonstrated that mechanical stretch increases the proliferation and apoptosis of vascular smooth muscle cells (VSMCs) by activating the protein disulfide isomerase (PDI) redox system, thus accelerating atherosclerotic lesion formation in the transplanted vein. At present, there are no efficient intervention measures to prevent this phenomenon. Berberine inhibits pathological vascular remodeling caused by hypertension, but the underlying mechanism is controversial. Herein, we investigate the role of berberine and the underlying mechanism of its effects on mechanical stretch-induced VSMC proliferation and apoptosis. MAIN METHODS: Mouse VSMCs cultivated on flexible membranes were pretreated for 1 h with one of the following substances: berberine, PDI inhibitor bacitracin, MAPK inhibitors, or ERS inhibitor 4-PBA. VSMCs were then subjected to mechanical stretch. Immunofluorescence and western blot were used to detect proliferation and apoptosis, as well as to analyze signaling pathways in VSMCs. KEY FINDINGS: Our results showed that berberine inhibits the PDI-endoplasmic reticulum stress system, thereby attenuating the simultaneous increase of VSMC proliferation and apoptosis in response to mechanical stretch. Interestingly, MAPK inhibitors PD98059, SP600125, and SB202190 significantly reduced the activation of ERS signaling cascades, and their combination with berberine had additive effects. The ERS inhibitor 4-PBA reduced PDI activation and ERS signaling, but not MAPK phosphorylation. Moreover, caspase-3 and caspase-12 were downregulated by berberine. SIGNIFICANCE: These results illustrate a novel mechanism of action of berberine that has practical implications. Our data provide important insights for the prevention and treatment of vascular remodeling and diseases caused by mechanical stretching during hypertension.

Carbon migration and metagenomic characteristics during anaerobic digestion of rice straw.

BACKGROUND: Considerable interest has been expressed in the development of anaerobic digestion (AD) of straw to solve the environmental problems caused by the dumping and burning of straw and to generate clean energy. However, the poor biodegradability of straw and the low efficiency of energy generation achieved during its AD are problematic. Studying the parameter changes involved in the process of AD is helpful for clarifying its micro-mechanisms and providing a theoretical basis for improving its efficiency. Currently, most research into process parameters has focused on gas production, methane content, pH, and volatile fatty acid (VFA) content; limited research has focused on carbon migration and functional gene changes during the AD of straw. RESULTS: Carbon migration and changes in metagenomic characteristics during the AD of rice straw (RS) were investigated. Accumulated biogas production was 388.43 mL/g VS. Carbon in RS was consumed, and the amount of carbon decreased from 76.28 to 36.83 g (conversion rate 51.72%). The degree of hydrolysis rapidly increased during the first 5 days, and a large amount of carbon accumulated in the liquid phase before migrating into the gas phase. By the end of AD, the amount of carbon in the liquid and gas phases was 2.67 and 36.78 g, respectively. According to our metagenomic analysis, at the module level, the abundance of M00357, M00567, M00356, and M00563 (the modules related to the generation of methane) during AD were 51.23-65.43%, 13.96-26.88%, 16.44-22.98%, and 0.83-2.40%, respectively. Methyl-CoM, 5-methyl-5,6,7,8-tetrahydromethanopterin, and Acetyl-CoA were important intermediates. CONCLUSIONS: Carbon was enriched in the liquid phase for the first 5 days and then gradually consumed, and most of the carbon was transferred to the gas phase by the end of AD. In this study, AD proceeded mainly via aceticlastic methanogenesis, which was indicated to be a dominant pathway in methane metabolism. Batch AD could be divided into three stages, including initiation (days 1-5), adaptation (days 6-20), and stabilization (days 21-50), according to biogas production performance, carbon migration, and metagenomic characteristics during AD.

Protein disulfide isomerase-mediated apoptosis and proliferation of vascular smooth muscle cells induced by mechanical stress and advanced glycosylation end products result in diabetic mouse vein graft atherosclerosis.

Protein disulfide isomerase (PDI) involves cell survival and death. Whether PDI mediates mechanical stretch stress (SS) and/or advanced glycosylation end products (AGEs) -triggered simultaneous increases in proliferation and apoptosis of vascular smooth muscle cells (VSMCs) is unknown. Here, we hypothesized that different expression levels of PDI trigger completely opposite cell fates among the different VSMC subtypes. Mouse veins were grafted into carotid arteries of non-diabetic and diabetic mice for 8 weeks; the grafted veins underwent simultaneous increases in proliferation and apoptosis, which triggered vein graft arterializations in non-diabetic or atherosclerosis in diabetic mice. A higher rate of proliferation and apoptosis was seen in the diabetic group. SS and/or AGEs stimulated the quiescent cultured VSMCs, resulting in simultaneous increases in proliferation and apoptosis; they could induce increased PDI activation and expression. Both in vivo and in vitro, the proliferating VSMCs indicated weak co-expression of PDI and SM-α-actin while apoptotic or dead cells showed strong co-expression of both. Either SS or AGEs rapidly upregulated the expression of PDI, NOX1 and ROS, and their combination had synergistic effects. Inhibiting PDI simultaneously suppressed the proliferation and apoptosis of VSMCs, while inhibition of SM-α-actin with cytochalasin D led to increased apoptosis and cleaved caspases-3 but had no effect on proliferation. In conclusion, different expression levels of PDI in VSMCs induced by SS and/or AGEs triggered a simultaneous increase in proliferation and apoptosis, accelerated vein graft arterializations or atherosclerosis, leading us to propose PDI as a novel target for the treatment of vascular remodeling and diseases.

Simultaneous Increases in Proliferation and Apoptosis of Vascular Smooth Muscle Cells Accelerate Diabetic Mouse Venous Atherosclerosis.

AIMS: This study was designed to demonstrate simultaneous increases in proliferation and apoptosis of vascular smooth muscle cells (VSMCs) leading to accelerated vein graft remodeling and to explore the underlying mechanisms. METHODS: Vein grafts were performed in non-diabetic and diabetic mice. The cultured quiescent VSMCs were subjected to mechanical stretch stress (SS) and/or advanced glycosylation end products (AGEs). Harvested vein grafts and treated VSMCs were used to detect cell proliferation, apoptosis, mitogen-activated protein kinases (MAPKs) activation and SM-α-actin expression. RESULTS: Significantly thicker vessel walls and greater increases in proliferation and apoptosis were observed in diabetic vein grafts than those in non-diabetic. Both SS and AGEs were found to induce different activation of three members of MAPKs and simultaneous increases in proliferation and apoptosis of VSMCs, and combined treatment with both had a synergistic effect. VSMCs with strong SM-α-actin expression represented more activated JNKs or p38MAPK, and cell apoptosis, while the cells with weak SM-α-actin expression demonstrated preferential activation of ERKs and cell proliferation. In contrast, inhibition of MAPKs signals triggered significant decreases in VSMC proliferation, and apoptosis. Treatment of the cells with RNA interference of receptor of AGEs (RAGE) also resulted in significant decreases in both proliferation and apoptosis. CONCLUSIONS: Increased pressure-induced SS triggers simultaneous increases in proliferation and apoptosis of VSMCs in the vein grafts leading to vein arterializations, which can be synergistically accelerated by high glucose-induced AGEs resulting in vein graft atherosclerosis. Either SS or AGEs and their combination induce simultaneous increases in proliferation and apoptosis of VSMCs via different activation of three members of MAPKs resulting from different VSMC subtypes classified by SM-α-actin expression levels.

RAGE mediates accelerated diabetic vein graft atherosclerosis induced by combined mechanical stress and AGEs via synergistic ERK activation.

AIMS/HYPOTHESIS: Diabetes with hypertension rapidly accelerates vascular disease, but the underlying mechanism remains unclear. We evaluated the hypothesis that the receptor of advanced glycation end products (RAGE) might mediate combined signals initiated by diabetes-related AGEs and hypertension-induced mechanical stress as a common molecular sensor. METHODS: In vivo surgical vein grafts created by grafting vena cava segments from C57BL/6J mice into the common carotid arteries of streptozotocin (STZ)-treated and untreated isogenic mice for 4 and 8 weeks were analyzed using morphometric and immunohistochemical techniques. In vitro quiescent mouse vascular smooth muscle cells (VSMCs) with either knockdown or overexpression of RAGE were subjected to cyclic stretching with or without AGEs. Extracellular signal-regulated kinase (ERK) phosphorylation and Ki-67 expression were investigated. RESULTS: Significant increases in neointimal formation, AGE deposition, Ki-67 expression, and RAGE were observed in the vein grafts of STZ-induced diabetic mice. The highest levels of ERK phosphorylation and Ki-67 expression in VSMCs were induced by simultaneous stretch stress and AGE exposure. The synergistic activation of ERKs and Ki-67 in VSMCs was significantly inhibited by siRNA-RAGE treatment and enhanced by over-expression of RAGE. CONCLUSION: RAGE may mediate synergistically increased ERK activation and VSMC proliferation induced by mechanical stretching with and without AGEs. It may serve as a common molecular bridge between the two, accelerating vascular remodeling. This study provides potential drug targets and novel therapeutic strategies for the treatment of vascular diseases resulting from diabetes with hypertension.