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Biodiversity and ecosystem functioning (BEF) often correlate positively with BEF studies focusing mostly on plant diversity manipulations. Plant performance is directly and indirectly impacted by soil organisms, but the role of increasing soil biodiversity on plant performance has mainly been tested in an uncontrolled way or with low biodiversity levels. An additional knowledge gap exists on the effect of (interactive) global change drivers – such as drought – on the soil BEF (sBEF) relationship. We here tested sBEF relationships by manipulating microbiome predatory protist diversity (0–30 species) in ambient controls and under abiotic (drought) and biotic stresses (nematode addition dominated by plant parasites). We then used plant (Solanum lycopersicum) biomass as a response in an 8-week greenhouse experiment. We show that the increasing biodiversity effect on plant biomass ranged from positive (up to 23% with biotic stress), to neutral (ambient conditions and with both stresses co-occurring), to negative (up to 39% with abiotic stress). Together, sBEF relationships were context-dependent and often contradicted generally reported positive (s)BEF relationships. Therefore, we propose that positive sBEF claims likely are not the norm and should be evaluated in a context-dependent manner. To better elucidate sBEF relationships, more manipulative studies should be performed under different conditions such as global change drivers and with a range of organismal groups. • SBEF relationships reported were context-dependent, challenging (s)BEF studies. • Protist diversity, though indirectly linked to plants, impacts plant performance. • We show no evidence of functional similarity effects on the sBEF relationship. [ABSTRACT FROM AUTHOR]

Abstract: The recently discovered apolipoprotein A5 (APOA5) gene has been shown to be important in determining plasma triglyceride levels, a major cardiovascular disease risk factor. We searched for possible associations of the APOA5 gene polymorphisms S19W and −1131T>C with coronary heart disease (CHD) in a Chinese population. A total of 483 Chinese CHD patients and 502 control non-CHD subjects were genotyped by polymerase chain reaction–restriction fragment length polymorphism for these 2 single nucleotide polymorphisms. We found that the minor allele 19W was observed only in CHD patients and not in controls, with allelic frequencies of 0.047 and 0.000, respectively (P < .000001), and the minor allele −1131C was significantly higher in CHD patients than in controls (0.391 vs 0.299, P < .0001). These results suggest that both the S19W and −1131T>C variations in the APOA5 gene are associated with the CHD and appear to be 2 genetic risk factors for CHD susceptibility in Chinese. Moreover, we found that triglyceride levels were significantly higher in −1131C carriers than in −1131T subjects of the control group and that high-density–lipoprotein cholesterol was decreased in −1131C carriers among CHD patients. [Copyright &y& Elsevier]

The primary focus of this study was to explore the effects of cyclic AMP response element-binding protein H (CREBH) on the development of nonalcoholic fatty liver disease (NAFLD). CREBH knockout (KO) and wildtype (WT) mice were averagely divided into a methionine and choline-deficient (MCD) or high fat (HF) diet group and respective chow diet (CD) groups. Mice were sacrificed after 4-week treatment for MCD model and 24-week treatment for HF model. Characteristics of nonalcoholic steatohepatitis-related liver fibrosis in KO-MCD/HF group were verified by hepatic histological analyses. Compared with WT-MCD/HF group, levels of plasma ALT and hepatic hydroxyproline increased in KO-MCD/HF group. Significantly higher levels of MCP-1, αSMA, Desmin, COL-1, TIMP-1, TGF-β1, TGF-β2 were found while MMP-9 and FGF21 mRNA levels decreased in KO-MCD/HF group. There was also a distinct difference of mRNA levels of TNFα, CTGF and CCND1 in KO-HF group compared with controls. Protein levels of MCP-1, BAX, αSMA, COL-1, TGF-β1 and SMAD2/3 significantly increased in KO-MCD/HF group and CCND1 was also upregulated in KO-HF group compared to their counterparts. CREBH knockout may primarily regulate the TGF-β1 signaling pathway via TGF-β2 and FGF21 resulting in more severe inflammation and fibrosis in NAFLD. • CREBH deficiency aggravates hepatic fibrosis in NAFLD mouse models. • CREBH deficiency enhances TGF-β signaling pathway. • CREBH deficiency inhibits expression of FGF21. • CREBH can be a potential therapeutic strategy of NAFLD. [ABSTRACT FROM AUTHOR]

• An automated phenotypic parameter measurement method based on RGB-D camera is proposed. • The 2D image segmentation results were applied to 3D point cloud segmentation. • The proposed point cloud segmentation method has high accuracy (accuracy = 98.7 %) and maintains the original point cloud resolution. • Accuracy of plant phenotype measurements and biomass estimation were acceptable. • Non-contact and low-cost measurement for crop cultivation was provided. Traditional phenotypic measurements were destructive, time-consuming and laborious. 3D computer vision technology collects plant information in a non-destructive manner and can work continuously. The purpose of this paper is to measure lettuce multi-phenotypic parameters and estimate biomass by point clouds. The result shows: (1) RGB information improved the segmentation effect of the point cloud. (2) The point cloud segmentation method proposed in this paper has a high accuracy (accuracy = 98.7 %) and keeps high spatial resolution. (3) On the test set, the R 2 of height, diameter, leaf area, fresh weight and dry weight are 0.935, 0.905, 0.969, 0.966 and 0.968, respectively, the cumulative NMSE is as low as 0.069. The Totalscore is 15 % better than the 1st of the online challenge held based on this data set. The results showed that the plant phenotypic extraction method proposed in this paper was accurate and efficient, and could be applied for high-throughput phenotyping. [ABSTRACT FROM AUTHOR]

Lipotoxicity and unresolved oxidative stress are key drivers of metabolic inflammation in nonalcoholic steatohepatitis (NASH). cAMP-response element binding protein H(CREBH) is a liver-specific transcription factor and regulates the glucose and lipid metabolism of NASH. However, its role in mitochondrial oxidative stress and its association with sirtuin 3 (SIRT3), a master regulator of deacetylation for mitochondrial proteins, remains elusive. In this study, AML-12 cells were treated with palmitic acid to imitate the pathological changes of NASH in vitro and 8-week-old male C57BL/6J mice were fed with a high-fat (HF) diet or a methionine-choline-deficient (MCD) diet to build the widely accepted in vivo model of NASH. We found that lipid overload induced mitochondrial oxidative stress and stimulated the expression of CREBH and SIRT3. CREBH overexpression alleviated the mitochondrial oxidative stress. Moreover, CREBH promoted SIRT3 expression, which regulated the deacetylation of manganese superoxide dismutase (MnSOD) and inhibited NOD-Like Receptor Pyrin Domain Containing 3 (Nlrp3) inflammasome activation whereas suppression of SIRT3 damaged the protecting ability of CREBH in mitochondrial oxidative stress. CREBH knockout mice were highly susceptible to HF and MCD diet-induced NASH with more severe oxidative stress. Collectively, our results firstly provided the support that CREBH could serve as a protective factor in the progression of NASH by regulating the acetylation of MnSOD and the activation of Nlrp3 inflammasome through SIRT3. These results suggest that CREBH might be a valuable therapeutic candidate for NASH. [Display omitted] • Lipid overload induced mitochondrial oxidative stress and stimulated the expression of CREBH and SIRT3. • CREBH overexpression promoted SIRT3 expression, regulating MnSOD acetylation and inhibiting Nlrp3 inflammasome activation. • Suppression of SIRT3 damaged the protecting ability of CREBH against mitochondrial oxidative stress in hepatocytes. • This study identifies a novel mechanism of CREBH in the development of NASH, providing a valuable therapeutic candidate for NASH. [ABSTRACT FROM AUTHOR]

It is well established that aboveground-belowground interactions moderate ecosystem functioning. The direct and indirect effects of plants on belowground communities have been explored by many studies; however, few studies have considered how grazing moderate the direction and intensity of these effects. In this study, we explored how grazing by yak moderates the effect of the shrub Dasiphora fruticosa on nematode communities through a short-term shrub removal experiment in a grazed and ungrazed alpine meadow on the Tibetan plateau. We used structural equation modelling (SEM) to assess both the direct effects of D. fruticosa and indirect effects mediated by changes in understorey vegetation composition and edaphic properties, on nematode communities. The presence of D. fruticosa had no significant impact on the abundance of nematodes in the ungrazed meadow. By contrast, D. fruticosa had a strong negative direct effect on nematode abundance, but also a positive indirect effect due to greater grass biomass, in the grazed meadow. The effect of D. fruticosa on nematode community composition was limited, with only a marginally significant direct effect on nematode community composition in the grazed meadow. Instead, nematode community composition was strongly related to soil water content and organic matter content in both grazing treatments, and soil pH in the grazed meadow. Our results indicate that grazing moderate aboveground-belowground linkages through direct and indirect shrub effects on nematode abundance, but have limited effects on nematode community composition. [ABSTRACT FROM AUTHOR]

Aims Baicalin (BA), an active flavonoid compound originating from the herb of Scutellaria baicalensis Georgi , has been previously shown to exert anti-inflammation and anti-oxidant effects in liver diseases. However, the potential role of BA in the regulation of non-alcoholic steatohepatitis (NASH) remains elusive. In this study, we newly explored the hepatoprotective effects of BA in MCD diet-induced NASH by ameliorating hepatic steatosis, inflammation, fibrosis and apoptosis. Main methods NASH was induced in mice fed a methionine and choline-deficient (MCD) diet for 4 weeks. The mice were simultaneously treated with or without BA for 4 weeks. Serum liver functional markers and inflammatory indicators were assessed by biochemical and ELISA methods, respectively. The livers were histologically examined using H&E, Oil Red O and Masson's trichrome staining methods. The qRT-PCR, IHC and Western blotting assays were applied to analyze mechanisms underlying BA protection. Key findings BA treatment significantly attenuated MCD diet-induced hepatic lipid accumulation partly through regulating the expression of SREBP-1c, FASN, PPARα and CPT1a. BA treatment dramatically suppressed MCD diet-induced hepatic inflammation, which was associated with decrease in serum TNF-α, IL-1β and MCP-1 production, macrophage influx and suppression of nuclear factor-κB activation. Additionally, BA was proved to prevent liver fibrosis, which appears to be mediated by inhibition of α-SMA, TGF-β1 and Col1A1. Furthermore, BA markedly inhibited hepatocyte apoptosis and cleaved caspase-3 protein expression in MCD diet-induced mice. Significance These results provide a possible basis of the underlying mechanism for the application of BA in the treatment of NASH. [ABSTRACT FROM AUTHOR]

The ultrafast, reversible, nonvolatile and multistimuli responsive phase change of Ge-Sb-Te (GST) alloy makes it an interesting "smart" material. The optical features of GST undergo significant variation when its state changes between amorphous and crystalline, meaning that they are useful for tuning photonic components. A GST phase change material (PCM) can be efficiently triggered by stimuli such as short optical or electrical pulses, providing versatility in high-performance photonic applications and excellent capability to control light. In this review, we study the fundamentals of GST-tuned photonics and systematically summarise the progress in this area. We then introduce current developments in both GST-metal hybrid metamaterials and GST-based dielectric metamaterials, and investigate the strategy of designing reversibly switchable GST-based photonic devices and their advantages. These devices may have a vast array of potential applications in optical memories, switches, data storage, cloaking, photodetectors, modulators, antennas etc. Finally, the prospect of implementing GST PCM in emerging fields within photonics is considered. [ABSTRACT FROM AUTHOR]

• Scoparone improves hepatic inflammation and autophagy in mice with MCD diet. • Scoparone has an effect on autophag in macrophages, but not hepatocytes. • Scoparone inhibited the up-regulation of p62 transcription by ROS/P38/Nrf2 axis. • Scoparone enhances autophagy flux by promoting autolysosome formation. • Scoparone regulates autophagy by inhibiting PI3K/AKT/mTOR pathway. Scoparone has been shown to ameliorate many forms of liver disease, and several underlying molecular mechanisms involved have been previously revealed. However, the potential role of scoparone in autophagy, which is dysregulated in nonalcoholic fatty liver disease-nonalcoholic steatohepatitis (NAFLD-NASH), has not been evaluated. In the current study, we investigated the effect and potential mechanisms of scoparone in hepatic autophagy in mice with NASH. In vivo, mice were fed a methionine–choline deficient (MCD) diet to establish a NASH model and then subjected to treatment with or without scoparone for 4 weeks. In vitro, scoparone was applied in a hepatocellular lipid overload model in AML12 cells challenged with palmitic acid (PA) and in lipopolysaccharide (LPS)-induced RAW264.7 cells. Scoparone improved impaired autophagy and several key features of NASH in mice fed an MCD diet. In vitro , scoparone had an effect on the autophagy of macrophages but not hepatocytes. In RAW264.7 cells, scoparone reduced the LPS-induced accumulation of autophagosomes and autophagy substrates, the production of reactive oxygen species (ROS) and the inflammatory response. Scoparone inhibited the upregulation of p62 transcription, which is mediated by the ROS/P38/Nrf2 axis. Chloroquine (CQ), an inhibitor of autophagic flux, significantly inhibited scoparone-mediated protection against inflammation. In addition, scoparone suppressed activation of the PI3K/AKT/mTOR pathway, and MHY1485 (an mTOR activator that inhibits autophagy) inhibited the anti-inflammatory effect of scoparone. In LPS-induced macrophages, scoparone regulates autophagy and further suppresses inflammation by inhibiting the ROS/P38/Nrf2 axis and PI3K/AKT/mTOR pathway and enhancing autophagic flux. Scoparone may improve hepatic autophagy and NASH partly through enhancing autophagy in macrophages but not hepatocytes. Scoparone is expected to become a novel therapeutic drug for NASH or diseases associated with dysregulated autophagy in macrophages. [ABSTRACT FROM AUTHOR]