The effects of polychlorinated biphenyls exposure on non-alcoholic fatty liver disease : role of aryl hydrocarbon receptor.

Polychlorinated biphenyls (PCBs) are detectable in serum of 100% of adults in US, and has been associated with fatty liver disease in epidemiological studies. PCBs are classified as either dioxin-like (DL) or non-dioxin-like (NDL) PCB based on their ability to activate the aryl hydrocarbon receptor (AhR). We used exposures that reflect human bioaccumulation patterns, which resembles Aroclor 1260 with a low level of the DL-PCB, PCB 126. Our aim was to determine if this exposure will activate the human and mouse AhR and examine if receptor activation influences these steatotic responses due to PCB exposures. DL-PCBs exposure-induced AhR activation in luciferase assays and induction of AhR target gene expression demonstrated that the Mouse AhR was much more sensitive than human AhR to activation by DL-PCBs. Our PCB mixture reflected this by activating the mouse AhR, but not human AhR in vivo. The ability of PCBs to activate the AhR would be predicted to be WHO toxicity equivalency = rat \u3emouse \u3e\u3ehuman. Mice were exposed to either PCB 126 (20 μg/kg), Aroclor 1260 (20 mg/kg) or both, for 2 weeks. PCB 126 or Aroclor 1260/PCB 126 significantly activated AhR, but only PCB 126 exposure alone induced mild hepatic steatosis. AhR activation suppressed the induction of CAR and PXR targets. More complex patterns of attenuation were observed with genes involved in lipid metabolism. PCB exposures require a hypercaloric diet to transition steatosis to steatohepatitis in murine models. Mice were fed high fat diet and received the same treatments as the 2-week study for 12 weeks. Our PCBs mixture exposure did not induce wasting syndrome, and failed to exacerbate steatosis. In addition, PCB 126 exposure activated AhR. Aroclor 1260 exposure drove hepatic steatosis to steatohepatitis. Either PCB 126 or the Aroclor 1260/PCB 126 mixture protected against high fat diet induced liver injury and liver fibrosis. All PCB exposures affected hepatic lipid metabolism

Efferocytosis in liver diseaseKey points

Summary: The process of dead cell clearance by phagocytic cells, called efferocytosis, prevents inflammatory cell necrosis and promotes resolution and repair. Defective efferocytosis contributes to the progression of numerous diseases in which cell death is prominent, including liver disease. Many gaps remain in our understanding of how hepatic macrophages carry out efferocytosis and how this process goes awry in various types of liver diseases. Thus far, studies have suggested that, upon liver injury, liver-resident Kupffer cells and infiltrating monocyte-derived macrophages clear dead cells, limit inflammation, and, through macrophage reprogramming, repair liver damage. However, in unusual settings, efferocytosis can promote liver disease. In this review, we will focus on efferocytosis in various types of acute and chronic liver diseases, including metabolic dysfunction-associated steatohepatitis. Understanding the mechanisms and consequences of efferocytosis by hepatic macrophages has the potential to shed new light on liver disease pathophysiology and to guide new treatment strategies to prevent disease progression

Lignin-induced Expression of Aspergillus oryzae 5992 Genes using Suppression Subtractive Hybridization

A previous study reported that a novel Aspergillus oryzae strain (CGMCC5992) can synthesize lignin hydrolytic enzymes for lignin degradation from straw. The present work involves the different gene expression of A. oryzae 5992 grown in media using lignin and glucose as carbon sources by suppression subtractive hybridization. Surprisingly, peroxidase was found in up-regulation genes, which is the key enzyme for degrading lignin. This shows that A. oryzae 5992 can secrete peroxidase in the presence of lignin. The functions of up-regulation genes also included gluconeogenesis, repairs, as well as signal and transporter proteins in the cell membrane. In addition, the down-regulation of genes was closely related to the aerobic metabolism of glucose, the fatty acid synthesis of the cell membrane, and the synthesis and utilization of ATP. Therefore, A. oryzae could regulate metabolism using lignin as carbon source, including lignin degradation promotion, glucose metabolism inhibition, and glucose regeneration

Facile and Safe Synthesis of Novel Self-Pored Amine-Functionalized Polystyrene with Nanoscale Bicontinuous Morphology

The chloromethyl-functionalized polystyrene is the most commonly used ammonium cation precursor for making anion exchange resins (AER) and membranes (AEM). However, the chloromethylation of polystyrene or styrene involves highly toxic and carcinogenic raw materials (e.g., chloromethyl ether) and the resultant ammonium cation structural motif is not stable enough in alkaline media. Herein, we present a novel self-pored amine-functionalized polystyrene, which may provide a safe, convenient, and green process to make polystyrene-based AER and AEM. It is realized by hydrolysis of the copolymer obtained via random copolymerization of N-vinylformamide (NVF) with styrene (St). The composition and structure of the NVF-St copolymer could be controlled by monomeric ratio, and the copolymers with high NVF content could form bicontinuous morphology at sub-100 nm levels. Such bicontinuous morphology allows the copolymers to be swollen in water and self-pored by freeze-drying, yielding a large specific surface area. Thus, the copolymer exhibits high adsorption capacity (226 mg/g for bisphenol A). Further, the amine-functionalized polystyrene has all-carbon backbone and hydrophilic/hydrophobic microphase separation morphology. It can be quaternized to produce ammonium cations and would be an excellent precursor for making AEM and AER with good alkaline stability and smooth ion transport channels. Therefore, the present strategy may open a new pathway to develop porous alkaline stable AER and AEM without using metal catalysts, organic pore-forming agents, and carcinogenic raw materials

Scenario Analysis of Natural Gas Consumption in China Based on Wavelet Neural Network Optimized by Particle Swarm Optimization Algorithm

Natural gas consumption has increased with an average annual growth rate of about 10% between 2012 and 2017. Total natural gas consumption accounted for 6.4% of consumed primary energy resources in 2016, up from 5.4% in 2012, making China the world’s third-largest gas user. Therefore, accurately predicting natural gas consumption has become very important for market participants to organize indigenous production, foreign supply contracts and infrastructures in a better way. This paper first presents the main factors affecting China’s natural gas consumption, and then proposes a hybrid forecasting model by combining the particle swarm optimization algorithm and wavelet neural network (PSO-WNN). In PSO-WNN model, the initial weights and wavelet parameters are optimized using PSO algorithm and updated through a dynamic learning rate to improve the training speed, forecasting precision and reduce fluctuation of WNN. The experimental results show the superiority of the proposed model compared with ANN and WNN based models. Then, this study conducts the scenario analysis of the natural gas consumption from 2017 to 2025 in China based on three scenarios, namely low scenario, reference scenario and high scenario, and the results illustrate that the China’s natural gas consumption is going to be 342.70, 358.27, 366.42 million tce (“standard” tons coal equivalent) in 2020, and 407.01, 437.95, 461.38 million tce in 2025 under the low, reference and high scenarios, respectively. Finally, this paper provides some policy suggestions on natural gas exploration and development, infrastructure construction and technical innovations to promote a sustainable development of China’s natural gas industry