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For large-scale multi-objective evolutionary algorithms (LSMOEAs), obtaining efficient evolutionary directions in an ultrahigh-dimensional decision space to produce high-quality offspring is a major challenge. This study proposes a novel framework called the directed quick search-guided large-scale evolutionary framework (QSLMOF) to address multi-objective optimization problems on a large scale. The framework contains two innovative strategies: the bidirectional vector-based sampling strategy (BDVS) and the quick search-guided directed reproduction strategy (QS-DRS). BDVS is introduced as an approach to swiftly discern promising solutions that can steer the exploration in the large-scale decision space. This is achieved by formulating two distinct types of sampling directions to rapidly reduce the search space and strike a delicate balance between convergence and diversity. In QS-DRS, we introduced the concept of the potential convergence gradient (PCG), incorporating directional information from historical searches and convergence directions indicated byelite solutions in the current population. With this property, inferior solutions can obtain excellent search directions to explore the decision space, which can improve the convergence rate and prevent the search from falling into a local optimum. The proposed large-scale evolutionary framework incorporates an existing environmental selection mechanism. Comprehensive experiments show that the two novel strategies improve the search efficiency and evolutionary quality of LSMOEAs in ultrahigh-dimensional decision spaces. Moreover, the proposed framework outperformed seven state-of-the-art LSMOEAs for nine large-scale multi-objective benchmark problems LSMOP1-LSMOP9 with up to three objectives and 10 000 decision variables. • Our guiding idea is to obtain accurate search directions in large-scale search space. • A sampling method that can obtain promising solutions in reduced space. • A quick search way in original space can provide direction improvement for solutions. • A framework that can make existing MOEAs more competent for large-scale problems. [ABSTRACT FROM AUTHOR]

To study the effects of mineral fulvic acid (FuA) on broiler performance, slaughter performance, blood biochemistry index, antioxidant function, immune performance, and intestinal microflora, 360 Arbor Acres (AA) broiler chickens with similar body weights were randomly divided into 5 groups with 6 replicates in each group and 12 chickens in each replicate in the current study. Chickens in the control group (C) were fed with the basal diet, and chickens in the test groups (I, II, III, and IV) were fed with the diet supplemented with 0.05%, 0.1%, 0.2%, and 0.3% mineral FuA, respectively. The indicators were measured on the hatching day, d 21 and d 35. From the whole experimental period, FuA supplement significantly increased average body weight (ABW) (P < 0.05), average daily gain (ADG) of broilers (P < 0.05), and thymus weight (P < 0.05) in II and IV groups, but bascially reduced the pH value of thigh meat. FuA supplement significantly improved aspartate aminotransferase (AST) activity in the group III on d 35 (P < 0.05) and the serum levels of IgA and IgG on d 21 and d 35 (P < 0.05), but reduced glutathione peroxidase (GSH-Px) level on d 21 (P < 0.05) and malondialdehyde (MDA) level in serum on d 35 (P < 0.05). FuA supplement significantly affected the abundance of Barnesiella, Lachnospiraceae, Alistipes, Lactobacillus , and Christensenellaceae on genus level. Differences between group III and other groups were significant in the genera microflora composition on d 21 and d 35. Functional analysis showed that the cecum microbiota were mainly enriched in carbohydrate metabolism, amino acid metabolism, and energy metabolism. In conclusion, FuA may potentially have significant positive effects on the growth performance and immune function of AA chickens through the modulation of the gut microbiota, and the 0.1% FuA was the best in broiler diet based on the present study. [ABSTRACT FROM AUTHOR]

Retinol saturase (RetSat) is an endoplasmic reticulum-localized oxidoreductase highly expressed in organs involved in lipid metabolism such as white (WAT) and brown adipose tissue (BAT). Cold exposure was shown to increase RETSAT protein in BAT but its relevance for non-shivering thermogenesis, a process with beneficial effects on metabolic health, is unknown. We analyzed the regulation of RetSat expression in white and brown adipocytes and different murine adipose tissue depots upon β-adrenergic stimulation and cold exposure. RetSat function during the differentiation and β-adrenergic stimulation of brown adipocytes was dissected by loss-of-function experiments. Mice with BAT-specific deletion of RetSat were generated and exposed to cold. Gene expression in human WAT was analyzed and the effect of RetSat depletion on adipocyte lipolysis investigated. We show that cold exposure induces RetSat expression in both WAT and BAT of mice via β-adrenergic signaling. In brown adipocytes, RetSat has minor effects on differentiation but is required for maximal thermogenic gene and protein expression upon β-adrenergic stimulation and mitochondrial respiration. In mice, BAT-specific deletion of RetSat impaired acute but not long-term adaptation to cold exposure. RetSat expression in subcutaneous WAT of humans correlates with the expression of genes related to mitochondrial function. Mechanistically, we found that RetSat depletion impaired β-agonist-induced lipolysis, a major regulator of thermogenic gene expression in adipocytes. Thus, RetSat expression is under β-adrenergic control and determines thermogenic capacity of brown adipocytes and acute cold tolerance in mice. Modulating RetSat activity may allow for therapeutic interventions towards pathologies with inadequate metabolic activity. • Adipose RetSat expression is induced by β-adrenergic signaling and cold exposure. • Loss of RetSat in brown adipocytes reduces thermogenic gene expression. • Mice lacking RetSat in BAT have impaired acute cold tolerance. • RetSat depletion in brown and white adipocytes interferes with lipolysis. [ABSTRACT FROM AUTHOR]

There is a worldwide consensus that renewable energy sources, such as wind power, will play an essential role in the global low-carbon energy transition. However, most quantifications of the CO 2 emissions of wind power systems ignored the indirect footprints induced by supply chains. Thus, this study developed input–output (IO)-based hybrid life-cycle assessment (LCA) models based on China's 2007, 2012, and 2017 economic benchmark data to quantify the economy-wide greenhouse gas (GHG) footprint of China's wind power sector. Moreover, the key sectors driving the footprint variation were identified, and the footprint structure was analyzed via the production layer decomposition method. The study results confirm the decarbonization of the wind power sector in China, with a decrease in the GHG footprint from 52.27 g CO 2 e/kWh in 2007 to 21.23 g CO 2 e/kWh in 2017. This 59.38% GHG footprint reduction was mainly driven by the electricity and heat sector. Most of wind power's GHG footprint (more than 84%) was derived from upstream industries, highlighting the necessity of supply chain analysis in the governance of the wind power industry. • We developed IO-based hybrid LCA model for comprehensive and specific CO 2 footprint accounting. • The decarbonization of China's wind power sector during 2007 to 2017 was quantified. • The evolving trend and driving factors of the CO 2 footprint were identified. • Supply chain governance is indispensable for the decarbonization of China's wind power sector. [ABSTRACT FROM AUTHOR]

Non-alcoholic steatohepatitis (NASH) is emerging as a serious liver disorder characterized by hepatic steatosis and liver inflammation. Nicotinamide adenine dinucleotide (NAD+) and NAD+-dependent deacetylase, SIRT1, play important roles in lipid metabolism in non-alcoholic fatty liver disease (NAFLD). However, their effects on liver inflammation and homeostasis of bile acids (BAs), the extensively proved pathophysiological actors in NASH, have not been fully understood. NASH animal model was induced by a methionine-choline-deficient (MCD) diet in C57BL/6J mice and intraperitoneally injected with NAD+ precursor, an agonist of upstream rate-limiting enzyme NAMPT or downstream SIRT1, or their vehicle solvents. Free fatty acid (FFA) was applied to HepG2 cells to construct the cell model. Induction of NAMPT/NAD+/SIRT1 axis could remarkably alleviate the aggravated inflammation in the liver of NASH mice, accompanied by decreased levels of total BAs throughout the enterohepatic system and a switch of BA synthesis from the classic pathway to the alternative pathway, resulting in less production of pro-inflammatory 12-OH BAs. The expressions of key enzymes including cyp7a1 , cyp8b1 , cyp27a1 and cyp7b1 in BA synthesis were significantly modulated after NAMPT/NAD+/SIRT1 axis induction in both animal and cell models. The levels of pro-inflammatory cytokines in liver were significantly negatively correlated with the intermediates in NAD+ metabolism, which may also be related to their regulation on BA homeostasis. Our results indicated that induction of NAMPT/NAD+/SIRT1 axis may be a potential therapeutic strategy for NASH or its complications related with BAs. [Display omitted] • Induction of NAMPT/NAD+/SIRT1 axis alleviates liver inflammation in NASH mice. • Total BAs and pro-inflammatory 12-OH BAs decreased after NAMPT/NAD+/SIRT1 induction. • A switch of BAs from the classic to alternative pathway occurred in NASH mice. • NAMPT/NAD+/SIRT1 directly influenced the key enzymes of BAs in HepG2 cell model. [ABSTRACT FROM AUTHOR]

This work describes an eco-friendly approach for the green formulation of Ag nanoparticles by Allium ampeloprasum extract, without using any toxic reducing and capping agents. The morphology, structure, and physicochemical properties were characterized by several analytical techniques such as fourier transformed infrared spectroscopy (FT-IR), field emission scanning electron microscopy (FESEM), transmission electron microscopy (TEM), energy dispersive X-ray spectroscopy (EDS), X-ray diffraction (XRD), and Ultraviolet–visible spectroscopy (UV–Vis). The nanoparticles were explored biologically in the anticancer assays. Exposure of the nanoparticles samples to non-small-cell lung cancer cells resulted in cell death, which was mostly due to necrosis but slightly due to late apoptosis. The viability of malignant cell lines reduced dose-dependently in the presence of nanoparticles. The IC50 of nanoparticles were 301, 266, 255, and 250 µg/mL against EKVX, HOP-62, A549 and NCI-H460 cancer cell lines, respectively. The green-synthesized nanoparticles induced cell death, suggesting anticancer prospects that may offer new insight into the development of an anticancer nanomedicine. [ABSTRACT FROM AUTHOR]

The gut microbiota colonizing the gastrointestinal tract, is an indispensable "invisible organ" that affects multiple aspects of human health. The gut microbial community has been assumed to be an important stimulus to the immune homeostasis and development, and increasing data support the role of the gut microbiota-immunity axis in autoimmune diseases. Host's immune system requires recognition tools to communicate with the gut microbial evolutionary partners. Among these microbial perceptions, T cells enable the widest spectrum of gut microbial recognition resolution. Specific gut microbiota direct the induction and differentiation of Th17 cells in intestine. However, the detailed links between the gut microbiota and Th17 cells have not been well established. In this review, we describe the generation and characterization of Th17 cells. Notably, we discuss the induction and differentiation of Th17 cells by the gut microbiota and their metabolites, as well as recent advances in our understanding of interactions between Th17 cells and the gut microbiota in human diseases. In addition, we provide the emerging evidences in support of interventions targeting the gut microbes/Th17 cells in human diseases. [Display omitted] ● Th17 cells are clinically correlated with the gut microbiota in human diseases. ● The gut microbiota and their metabolites trigger the induction and differentiation of Th17 cells. ● The gut microbiota can interact with Th17 cells in human diseases. ● The interactions between the gut microbiota and Th17 cells provide opportunities to improve human diseases. [ABSTRACT FROM AUTHOR]

The toxicity effects of chiral pesticides on living organisms have attracted an increasing public attention. This study aims to investigate the toxicity effect and mechanism of hexaconazole (HEX) to human breast cancer cell (MCF-7) at enantiomer levels. HEX exposure obviously inhibited cells activities in a dose-dependent manner. Under the conditions of VIP >1 and p < 0.05, a total of 255 and 177 differential metabolites (DMs), 17 and 15 amino acid- and lipid-related metabolic pathways were disturbed after (+)-HEX and (−)-HEX exposure, respectively. HEX exposure may affect cell membrane function, signal transduction, and cell differentiation. We further investigated the mechanism of enantioselective differences by using molecular docking which showed that CYP17A1 was the main enzyme that leading to endocrine disrupting effects with the binding energy of −6.30 and −6.08 kcal/mol compared to CYP19A1 enzyme which were −5.81 and −5.93 kcal/mol for (+)-HEX and (−)-HEX, respectively. The docking results explained the reasons why (+)-HEX achieved higher cytotoxicity and induced more seriously metabolic profiles than its antipode. These findings could provide a new insight to understand the enantioselective cytotoxicity effect and mechanism of HEX and will be conducive to assessing its risk to human health at enantiomer levels. [Display omitted] • Enantioselective toxicity effect to MCF-7 cells by hexaconazole had been observed. • Hexaconazole exposure significantly affect the metabolic profiles of MCF-7. • Hexaconazole mainly affect lipid- and amino acid-related metabolites and pathways. • (+)-hexaconazole achieved higher cytotoxicity effect to MCF-7 cells than its antipode. [ABSTRACT FROM AUTHOR]

[Display omitted] • Rosemary acid (RA) and ultrasonic (US) have synergistic effect on delaying lipid oxidation of fish during storage. • The inhibitory mechanism of RA and US on endogenous LOX in Large yellow croaker was studied in vitro. • The effects of RA alone and in the presence of US on LOX were evaluated by multi-spectroscopic methods. • Hydrogen bonding and hydrophobic interaction are the main driving forces of bonding. Lipid oxidation will lead to the deterioration of flavor, color and texture of aquatic products with high fatty acid content. The mechanism of ultrasound (US) combined with rosmarinic acid (RA) on lipid oxidation and endogenous enzyme activities of large yellow croaker during cold-storage (4 ℃) was investigated. The result showed that the US and RA have synergistic effects in delaying lipid oxidation and inhibiting endogenous lipase and lipoxygenase (LOX) activities related to oxidation. The inhibition of LOX activity by RA was dose-dependent, and US showed a negative effect on the inhibition of enzyme activity in the presence of low concentration RA. Moreover, RA changes the enzyme structure through static fluorescence quenching and interaction with enzyme molecules. Hydrogen bonding and hydrophobic interaction are the main interaction forces between RA and LOX. This study could provide basic mechanism of US treatment cooperating with polyphenols to inhibit lipid oxidation during food preservation. [ABSTRACT FROM AUTHOR]