Regulation Mechanism and Potential Value of Active Substances in Spices in Alcohol-Liver-Intestine Axis Health.

Excessive alcohol intake will aggravate the health risk between the liver and intestine and affect the multi-directional information exchange of metabolites between host cells and microbial communities. Because of the side effects of clinical drugs, people tend to explore the intervention value of natural drugs on diseases. As a flavor substance, spices have been proven to have medicinal value, but they are still rare in treating hepatointestinal diseases caused by alcohol. This paper summarized the metabolic transformation of alcohol in the liver and intestine and summarized the potential value of various perfume active substances in improving liver and intestine diseases caused by alcohol. It is also found that bioactive substances in spices can exert antioxidant activity in the liver and intestine environment and reduce the oxidative stress caused by diseases. These substances can interfere with fatty acid synthesis, promote sugar and lipid metabolism, and reduce liver injury caused by steatosis. They can effectively regulate the balance of intestinal flora, promote the production of SCFAs, and restore the intestinal microenvironment.

Conjugated Linoleic Acid Ameliorates High Fat-Induced Insulin Resistance via Regulating Gut Microbiota-Host Metabolic and Immunomodulatory Interactions.

Interaction between gut microbiota, host immunity and metabolism has been suggested to crucially affect the development of insulin resistance (IR). This study aims to investigate how gut microbiota, inflammatory responses and metabolism in individuals with IR are affected by the supplementation of conjugated linoleic acid (CLA) and how this subsequently affects the pathophysiology of IR by using a high-fat diet-induced IR mouse model. Serum biochemical indices showed that 400 mg/kg body weight of CLA effectively attenuated hyperglycemia, hyperlipidemia, glucose intolerance and IR, while also promoting antioxidant capacities. Histomorphology, gene and protein expression analysis revealed that CLA reduced fat deposition and inflammation, and enhanced fatty acid oxidation, insulin signaling and glucose transport in adipose tissue or liver. Hepatic transcriptome analysis confirmed that CLA inhibited inflammatory signaling pathways and promoted insulin, PI3K-Akt and AMPK signaling pathways, as well as linoleic acid, arachidonic acid, arginine and proline metabolism. Gut microbiome analysis further revealed that these effects were highly associated with the enriched bacteria that showed positive correlation with the production of short-chain fatty acids (SCFAs), as well as the improved SCFAs production simultaneously. This study highlights the therapeutic actions of CLA on ameliorating IR via regulating microbiota-host metabolic and immunomodulatory interactions, which have important implications for IR control.

Fucoidan from Ascophyllum nodosum and Undaria pinnatifida attenuate SARS-CoV-2 infection in vitro and in vivo by suppressing ACE2 and alleviating inflammation.

The global healthcare challenge posed by COVID-19 necessitates the continuous exploration for novel antiviral agents. Fucoidans have demonstrated antiviral activity. However, the underlying structure-activity mechanism responsible for the inhibitory activity of fucoidans from Ascophyllum nodosum (FUCA) and Undaria pinnatifida (FUCU) against SARS-CoV-2 remains unclear. FUCA was characterized as a homopolymer with a backbone structure of repeating (1 â†’ 3) and (1 â†’ 4) linked α-l-fucopyranose residues, whereas FUCU was a heteropolysaccharide composed of Fuc1-3Gal1-6 repeats. Furthermore, FUCA demonstrated significantly higher anti-SARS-CoV-2 activity than FUCU (EC50: 48.66 vs 69.52 µg/mL), suggesting the degree of branching rather than sulfate content affected the antiviral activity. Additionally, FUCA exhibited a dose-dependent inhibitory effect on ACE2, surpassing the inhibitory activity of FUCU. In vitro, both FUCA and FUCU treatments downregulated the expression of pro-inflammatory cytokines (IL-6, IFN-α, IFN-γ, and TNF-α) and anti-inflammatory cytokines (IL-10 and IFN-ß) induced by viral infection. In hamsters, FUCA demonstrated greater effectiveness in attenuating lung and gastrointestinal injury and reducing ACE2 expression, compared to FUCU. Analysis of the 16S rRNA gene sequencing revealed that only FUCU partially alleviated the gut microbiota dysbiosis caused by SARS-CoV-2. Consequently, our study provides a scientific basis for considering fucoidans as poteintial prophylactic food components against SARS-CoV-2.

Exploring the mechanism of probiotics in enhancing the utilization of chemical components (or polyphenols) of grape seed extract.

Fecal samples from 20 healthy adults were collected for in vitro fermentation experiments to investigate the effects of combined probiotics on the utilization of grape seed extract in humans. After fermenting for 24 h, short-chain fatty acids, metabolites, and gut microbiota composition were analyzed. Short-chain fatty acids in the grape seed extract probiotics group were significantly higher than those in the grape seed extract group. Probiotics significantly enhanced the conversion and utilization of catechins and epicatechins in grape seed extract group and increased the production of 3-hydroxyphenylacetic acid. The 16S rRNA sequencing results revealed that compound probiotics significantly increased the relative abundance of Lacticaseibacillus, HT002, Bifidobacterium, and Lactobacillus and reduced that of Escherichia-Shigella. Our findings showed considerable individual variability in the metabolic utilization of grape seed extract in humans. The consumption of probiotics appears to significantly enhance the utilization.

Fructose corn syrup induces inflammatory injury and obesity by altering gut microbiota and gut microbiota-related arachidonic acid metabolism.

Excessive fructose corn syrup (FCS) intake brings a series of health problems. The aim of the present study was to explore the mechanism of FCS-induced metabolic disorders from the perspective of gut microbiota. Mice were fed for 16 weeks with normal or 30% FCS drinking water. Compared to the control group, FCS caused significantly higher fat deposition, hepatic steatosis, liver and intestinal inflammatory damages (P<.05). FCS increased the abundance of Muribaculaceae in vivo and in vitro, which was positively correlated with the indices of metabolic disorders (P<.05). In vivo and in vitro data indicated that FCS enhanced the microbial function involved in pentose phosphate pathway and arachidonic acid metabolism, metabolomics further demonstrated that FCS led to an increase in prostaglandins (the catabolites of arachidonic acid) (P<.05). Our study confirmed that FCS can directly promote gut microbiota to synthesize inflammatory factor prostaglandins, which provides new insights and directions for the treatment of FCS-induced metabolic disorders and inflammation.

Experimental determination and QSAR analysis of the rate constants for SO5•- reactions with aromatic micropollutants in water.

S(IV)-based systems used for advanced oxidation processes (AOPs) have been constructed for the degradation of organic contaminants via oxysulfur radicals, including SO3•-, SO4•-, and SO5•-. Although SO5•- is proposed as an active species in AOPs processes, research on the reactivity of SO5•- has remained unclear. In this work, 53 target aromatic micropollutants (AMPs), including 13 phenols, 27 amines, and 13 PPCPs were selected to determine the second-order reaction rate constants for SO5•- using the competitive kinetics method, in which the [Formula: see text] values, observed at pH 4 ranged from (2.44 ± 0.00) × 105 M-1 s-1 to (4.41 ± 0.28) × 107 M-1 s-1. Quantitative structure-activity relationship (QSAR) models for the oxidation of AMPs by SO5•- were developed based on 40 [Formula: see text] values of amines and phenols, and their molecular descriptors, using the stepwise multiple linear regression method. This comprehensive model exhibited the excellent goodness-of-fit (Radj2 = 0.802), robustness (QLOO2 = 0.749), and predictability (Qext2 = 0.656), and the one-electron oxidation potential (Eox), energy of the highest occupied molecular orbital energy (EHOMO), and most positive net atomic charge on the carbon atoms (qC+) were considered the most influential descriptors for the comprehensive model, indicating that SO5•- oxidizes pollutants via single electron transfer reaction and exhibits a strong oxidation capacity, especially for pollutants containing electron-donating groups. Moreover, the [Formula: see text] values of 13 PPCPs were predicted using this comprehensive model, which suggested the practical application significance of the QSAR model. This study emphasizes the direct oxidation capacity of SO5•-, which is important to evaluate and simulate AOPs based on S(IV).

In vitro intestinal simulation system on the carbon source utilization characteristics and mechanism of interspecific syntrophic effects of Bifidobacterium longum CECT7894 and Pediococcus pentosaceus CECT8330.

The combination of Bifidobacterium longum and Pediococcus pentosaceus is a clinically effective probiotic formulation for alleviating infantile colic; however, their utilization characteristics and mechanism of action surrounding their combined use of sugar sources remains unclear. Using in vitro simulation technology, this study set up individual and mixed cultures of the two probiotics at unique concentrations, and different types of prebiotics, carbohydrates and polyols were added. Gas and short-chain fatty acid production, substrate utilization, as well as growth of the individual and mixed probiotics were detected at the beginning of fermentation, 24 h, and 48 h. Further, the mechanism of the syntrophic effect of the two probiotics was explored based on their growth characteristics. It was found that neither strain produced gas after 24 h and 48 h of cultivation, but could synergistically utilize fructo oligosaccharides (FOS) when mixed. There was an increasing trend of acetic acid production for B. longum in yeast extract, casitone and fatty acid (YCFA) and FOS medium with increasing of bacterial concentrations at 24 h and 48 h; whereas the trend for P. pentosaceus was less obvious. When bacterial concentrations were >5 billion CFU·g-1, the mixed culture showed significantly lower acetic acid production than B. longum alone. By adding lactic and acetic acids to the YCFA medium and observing P. pentosaceus growth, the results suggested that Pediococcus pentosaceus could use the acetic acid and lactic acid produced by Bifidobacterium longum for growth. When the bacterial concentration was 5 billion CFU·g-1, the acetic acid production of B. longum was significantly higher in the mixed cultures in lactulose, lactose, FOS, galactooligosaccharide, and inulin medium; whereas the reverse was true for culturing in xylitol, carboxymethyl cellulose sodium, and sorbitol medium. Further, the mixed cultures produced significantly more acetic acid than B. longum alone. In summary, through in vitro simulation experiments, the optimal ratio and potential interaction mechanisms between B. longum and P. pentosaceus were revealed here, offers a basis for understanding how the probiotic combinations may improve infant colic symptoms by influencing the gut pH and regulating the gut microbiota mechanisms.

Graphene quantum dots blocking the channel egresses of cytochrome P450 enzyme (CYP3A4) reveals potential toxicity.

Graphene quantum dots (GQDs) have garnered significant attention, particularly in the biomedical domain. However, extensive research reveals a dichotomy concerning the potential toxicity of GQDs, presenting contrasting outcomes. Therefore, a comprehensive understanding of GQD biosafety necessitates a detailed supplementation of their toxicity profile. In this study, employing a molecular dynamics (MD) simulation approach, we systematically investigate the potential toxicity of GQDs on the CYP3A4 enzyme. We construct two distinct simulation systems, wherein a CYP3A4 protein is enveloped by either GQDs or GOQDs (graphene oxide quantum dots). Our results elucidate that GQDs come into direct contact with the bottleneck residues of Channels 2a and 2b of CYP3A4. Furthermore, GQDs entirely cover the exits of Channels 2a and 2b, implying a significant hindrance posed by GQDs to these channels and consequently leading to toxicity towards CYP3A4. In-depth analysis reveals that the adsorption of GQDs to the exits of Channels 2a and 2b is driven by a synergistic interplay of hydrophobic and van der Waals (vdW) interactions. In contrast, GOQDs only partially obstruct Channel 1 of CYP3A4, indicating a weaker influence on CYP3A4 compared to GQDs. Our findings underscore the potential deleterious impact of GQDs on the CYP3A4 enzyme, providing crucial molecular insights into GQD toxicology.

RIT1 regulates mitosis and promotes proliferation by interacting with SMC3 and PDS5 in hepatocellular carcinoma.

BACKGROUND: As a small G protein of Ras family, Ras-like-without-CAAX-1 (RIT1) plays a critical role in various tumors. Our previous study has demonstrated the involvement of RIT1 in promoting malignant progression of hepatocellular carcinoma (HCC). However, its underlying mechanism remains unclear. METHODS: Gene set enrichment analysis (GSEA) was conducted in the TCGA LIHC cohort to investigate the underlying biological mechanism of RIT1. Live cell imaging, immunofluorescence (IF) and flow cytometry assays were used to verify biological function of RIT1 in HCC mitosis. Subcutaneous xenografting of human HCC cells in BALB/c nude mice was utilized to assess tumor proliferation in vivo. RNA-seq, co-immunoprecipitation (Co-IP), mass spectrometry analyses, western blot and IF assays were employed to elucidate the mechanisms by which RIT1 regulates mitosis and promotes proliferation in HCC. RESULTS: Our findings demonstrate that RIT1 plays a crucial role in regulating mitosis in HCC. Knockdown of RIT1 disrupts cell division, leading to G2/M phase arrest, mitotic catastrophe, and apoptosis in HCC cells. SMC3 is found to interact with RIT1 and knockdown of SMC3 attenuates the proliferative effects mediated by RIT1 both in vitro and in vivo. Mechanistically, RIT1 protects and maintains SMC3 acetylation by binding to SMC3 and PDS5 during mitosis, thereby promoting rapid cell division and proliferation in HCC. Notably, we have observed an upregulation of SMC3 expression in HCC tissues, which is associated with poor patient survival and promotion of HCC cell proliferation. Furthermore, there is a significant positive correlation between the expression levels of RIT1, SMC3, and PDS5. Importantly, HCC patients with high expression of both RIT1 and SMC3 exhibit worse prognosis compared to those with high RIT1 but low SMC3 expression. CONCLUSIONS: Our findings underscore the crucial role of RIT1 in regulating mitosis in HCC and further demonstrate its potential as a promising therapeutic target for HCC treatment.

Syntaxin-6 promotes the progression of hepatocellular carcinoma and alters its sensitivity to chemotherapies by activating the USF2/LC3B axis.

Syntaxin-6 (STX6), a protein of the syntaxin family, is located in the trans-Golgi network and is involved in a variety of intracellular membrane transport events. STX6 is overexpressed in different human malignant tumors. However, little is known about its exact function and molecular mechanism in hepatocellular carcinoma (HCC). In this study, we found that the expression of STX6 was significantly increased in HCC tissues and was associated with poor survival. Gain- and loss-of-function experiments showed that STX6 promotes cell proliferation and metastasis of HCC cells both in vitro and in vivo. Mechanistically, STX6 was negatively regulated by the upstream stimulatory factor 2 (USF2). In addition, STX6 facilitates the association of autophagosomes with lysosomes. Importantly, we demonstrated that STX6 overexpression, despite enhanced resistance to lenvatinib, sensitizes HCC cells to the autophagy activator rapamycin. This study revealed that, under the control of USF2, STX6 accelerates the degradation of microtubule-associated protein 1 light chain 3 beta (LC3) by promoting autophagic flux, ultimately promoting HCC progression. Collectively, we suggest that the USF2-STX6-LC3B axis is a potential therapeutic target in liver cancer.

The combination of metagenome and metabolome to compare the differential effects and mechanisms of fructose and sucrose on the metabolic disorders and gut microbiota in vitro and in vivo.

Sucrose and fructose are the most commonly used sweeteners in the modern food industry, but there are few comparative studies on the mechanisms by which fructose and sucrose affect host health. The aim of the present study was to explain the different effects of fructose and sucrose on host metabolism from the perspective of gut microbiota. Mice were fed for 16 weeks with normal drinking water (CON), 30% fructose drinking water (CF) and 30% sucrose drinking water (SUC). Compared with fructose treatment, sucrose caused significantly higher weight gain, epididymal fat deposition, hepatic steatosis, and jejunum histological injury. Sucrose increased the abundance of LPS-producing bacteria which was positively correlated with obesity traits, while fructose increased the abundance of Lactobacillus. An in vitro fermentation experiment also showed that fructose increased the abundance of Lactobacillus, while sucrose increased the abundance of Klebsiella and Escherichia. In addition, combined with microbial functional analysis and metabolomics data, fructose led to the enhancement of carbohydrate metabolism and TCA cycle capacity, and increased the production of glutamate. The cross-cooperation network greatly influenced the microbiota (Klebsiella, Lactobacillus), metabolites (glutamate, fructose 1,6-biosphosphate, citric acid), and genes encoding enzymes (pyruvate kinase, 6-phosphofructokinase 1, fructokinase, lactate dehydrogenase, aconitate hydratase, isocitrate dehydrogenase 3), suggesting that they may be the key differential factors in the process of fructose and sucrose catabolism. Therefore, the changes in gut microbiome mediated by fructose and sucrose are important reasons for their differential effects on host health and metabolism.

Drug Repurposing Flubendazole to Suppress Tumorigenicity via PCSK9-dependent Inhibition and Potentiate Lenvatinib Therapy for Hepatocellular Carcinoma.

Hepatocellular carcinoma (HCC) is one of the most lethal malignant cancers across the world. It has a poor prognosis and lacks effective therapies, especially for patients with advanced-stage cancer, indicating an urgent need for new therapies and novel therapeutic targets. Here, by screening the U.S. Food and Drug Administration drug library against HCC cell lines, we identified that flubendazole, a traditional anthelmintic drug, could prominently suppress HCC cells in vivo and in vitro. RNA sequence analysis and cellular thermal shift assays showed that flubendazole reduced the expression of PCSK9 protein by direct targeting. The increased expression of PCSK9 in HCC tissues was demonstrated to be correlated with poor prognosis, and the inhibitory ability of flubendazole was selectively dependent on PCSK9 expression. PCSK9 knockdown abolished the antitumor effects of flubendazole in HCC. Mechanistically, flubendazole inhibited the Hedgehog signaling pathway induced by PCSK9, resulting in the downregulation of smoothened (SMO) and GLI Family Zinc Finger 1 (Gli1). Moreover, combining flubendazole with lenvatinib was found more effective than administering lenvatinib only for HCC treatment in vivo and in vitro. These findings reveal the therapeutic potential of flubendazole against HCC and provide clues on new repurposed drugs and targets for cancer treatment.

Promoted wet peroxide oxidation of chlorinated volatile organic compounds catalyzed by FeOCl supported on macro-microporous biomass-derived activated carbon.

Chlorinated volatile organic compounds (CVOCs) are a recalcitrant class of air pollutants, and the strongly oxidizing reactive oxygen species (ROS) generated in advanced oxidation processes (AOPs) are promising to degrade them. In this study, a FeOCl-loaded biomass-derived activated carbon (BAC) has been used as an adsorbent for accumulating CVOCs and catalyst for activating H2O2 to construct a wet scrubber for the removal of airborne CVOCs. In addition to well-developed micropores, the BAC has macropores mimicking those of biostructures, which allows CVOCs to diffuse easily to its adsorption sites and catalytic sites. Probe experiments have revealed HO• to be the dominant ROS in the FeOCl/BAC + H2O2 system. The wet scrubber performs well at pH 3 and H2O2 concentrations as low as a few mM. It is capable of removing over 90% of dichloroethane, trichloroethylene, dichloromethane and chlorobenzene from air. By applying pulsed dosing or continuous dosing to replenish H2O2 to maintain its appropriate concentration, the system achieves good long-term efficiency. A dichloroethane degradation pathway is proposed based on the analysis of intermediates. This work may provide inspiration for the design of catalyst exploiting the inherent structure of biomass for catalytic wet oxidation of CVOCs or other contaminants.

Basic psychological needs satisfaction of stroke patients: a qualitative study.

BACKGROUND: Previous studies have shown that the satisfaction of basic psychological needs is related to psychological well-being. Improving satisfaction will increase personal well-being, promote positive health outcomes, and improve disease recovery. However, no research has focused on the basic psychological needs of stroke patients. Therefore, this study aims to determine the basic psychological needs experience, satisfaction, and its influencing factors of stroke patients. METHODS: 12 males and 6 females in the non-acute phase with stroke were recruited in the Department of Neurology, Nanfang Hospital. The individual, semi-structured interviews were conducted in a separate room. The data were imported to Nvivo 12 and analyzed using the directed content analysis approach. RESULTS: Three main themes consisting of 9 sub-themes were derived from the analysis. These three main themes focused on the needs for autonomy, competence, and relatedness of stroke patients. CONCLUSION: Participants have different degrees of satisfaction of their basic psychological needs, which may be related to their family environment, work environment, stroke symptoms, or other factors. Stroke symptoms can significantly reduce the patients' needs for autonomy and competence. However, the stroke seems to increase the patients' satisfaction of the need for relatedness.

AKR1C3 suppresses ferroptosis in hepatocellular carcinoma through regulation of YAP/SLC7A11 signaling pathway.

AKR1C3 is frequently overexpressed and it is a validated therapeutic target in various tumors including hepatocellular carcinoma (HCC). Our previous study showed that AKR1C3 facilitated HCC proliferation and metastasis by forming a positive feedback loop of AKR1C3-NF-κB-STAT3. Ferroptosis is a form of iron-dependent cell death driven by iron-dependent accumulation of lipid reactive oxygen species and plays an important role in tumor suppression. However, little is known about the role of AKR1C3 in ferroptosis susceptibility. In this study, we found that knockdown of AKR1C3 potently enhanced the sensitivity of HCC cells to ferroptosis inducers both in vitro and in vivo. Overexpression of AKR1C3 protected against ferroptosis in HCC cells. Mechanistically, AKR1C3 regulated ferroptosis through YAP/SLC7A11 signaling in HCC. AKR1C3 knockdown led to a decrease in YAP nuclear translocation, resulted in the inhibition of cystine transporter SLC7A11, and a subsequent increase in the intracellular levels of ferrous iron and ultimately ferroptosis. Moreover, we found that the combination of AKR1C3 and SLC7A11 was a strong predictor of poor prognosis in HCC. Collectively, these findings identify a novel role of AKR1C3 in ferroptosis, and highlighting a candidate therapeutic target to potentially improve the effect of ferroptosis-based antitumor therapy.

Novel lignans from Zanthoxylum nitidum and antiproliferation activity of sesaminone in osimertinib-resistant non-small cell lung cancer cells.

Seven previously undescribed tetrahydrofuran lignans with different configurations and unusual isopentenyl substitutions, nitidumlignans D-J (corresponding to compounds 1, 2, 4, 6, 7, 9 and 10), along with 14 known lignans, were isolated from Zanthoxylum nitidum. Notably, compound 4 is an uncommon naturally occurring furan-core lignan derived from tetrahydrofuran aromatization. The antiproliferation activity of the isolated compounds (1-21) was determined in various human cancer cell lines. The structure-activity study revealed that the steric positioning and chirality of the lignans exert important effects on their activity and selectivity. In particular, compound 3 (sesaminone) exhibited potent antiproliferative activity in cancer cells, including acquired osimertinib-resistant non-small-cell lung cancer (HCC827-osi) cells. Compound 3 also inhibited colony formation and induced the apoptotic death of HCC827-osi cells. The underlying molecular mechanisms revealed that 3 downregulated the activation of the c-Met/JAK1/STAT3 and PI3K/AKT/mTOR signaling pathways in the HCC827-osi cells. In addition, the combination of 3 and osimertinib exhibited synergistic effects on the antiproliferative activity against HCC827-osi cells. Overall, these findings inform the structure elucidation of novel lignans isolated from Z. nitidum, and sesaminone was identified as a potential compound for exerting antiproliferative effects on osimertinib-resistant lung cancer cells.

Rumen microbiota-host transcriptome interaction mediates the protective effects of trans-10, cis-12 CLA on facilitating weaning transition of lambs.

Developing alternatives to antibiotics for prevention of gastrointestinal dysbiosis in early-weaning farmed animals is urgently needed. This study was to explore the potential effects of trans-10, cis-12 conjugated linoleic acid (CLA) on maintaining ruminal homeostasis of young ruminants during the weaning transition period. Thirty neonatal lambs were selected (6 lambs per group) and euthanized for rumen microbial and epithelial analysis. The lambs were weaned at 28 d and experienced the following 5 treatments: euthanized on d 28 as the pre-weaning control (CON0), fed starter feed for 5 (CON5) or 21 (CON21) d, fed starter feed with 1% of CLA supplemented for 5 (CLA5) or 21 (CLA21) d. Results showed that the average daily weight gain and dry matter intake were significantly higher in CLA5 than CON5 group. As compared with the CON5 and CON21 group, the relative abundances of volatile fatty acid (VFA) producing bacteria including Bacteroides, Treponema, Parabacteroides and Anaerovibrio, as well as the concentrations of acetate, butyrate and total VFA were significantly increased in CLA5 and CLA21 group, respectively. Integrating microbial profiling and epithelial transcriptome results showed that 7 downregulated inflammatory signaling-related host genes IL2RA, CXCL9, CD4, CCR4, LTB, SPP1, and BCL2A1 with CLA supplementation were significantly negatively correlated with both VFA concentration and VFA producing bacteria, while 3 (GPX2, SLC27A2 and ALDH3A1) and 2 (GSTM3 and GSTA1) upregulated metabolism-related genes, significantly positively correlated with either VFA concentration or VFA producing bacteria, respectively. To confirm the effects of CLA on epithelial signal transduction, in vitro experiment was further conducted by treating rumen epithelial cells without or with IL-17A + TNF-α for 12 h after pretreatment of 100 µM CLA or not (6 replicates per treatment). The results demonstrated the anti-inflammatory effect of CLA via suppressing the protein expression of NF-кB p-p65/p65 with the activation of peroxisome proliferator-activated receptor gamma (PPARγ). In conclusion, CLA supplementation enhanced the ruminal microbiota-driven transcriptional regulation in healthy rumen epithelial development via rumen VFA production, and CLA may therefore serve as an alternative way to alleviate early-weaning stress and improve physiological and metabolic conditions of young ruminants.

Insight into the effect of natural organic matter on the photooxidation of arsenite induced by colloidal ferric hydroxides in water.

Surface complexation of arsenite (As(III)) on colloidal ferric hydroxide (CFH) plays an important role not only in the adsorptive immobilization of As(III) but also in the subsequent oxidation of As(III) to arsenate (As(V)) through light-induced ligand-to-metal charge transfer (LMCT) in water at near-neutral pH. However, the effects of natural organic matter (NOM), especially humic substances (HSs) and low molecular weight carboxylic acids (CAs), on the photochemistry of the CFH-As(III) system have not been sufficiently understood. In this work, the inhibition of photooxidation of As(III) in terms of the observed apparent rate constant (kobs) by six HSs (below 16 mg L-1) and seven CAs (below 2.5 mM) has been observed in water containing 66 µM Fe(III) and 5 µM As(III) at pH 7 under simulated solar irradiation consisting of UVA (λmax 365 nm) and UVB (λmax 313 nm) lights. Total inhibition factors (T) have been determined from the combined effect of light-screening factor (S) and competitive complexation factor (C), wherein both S and C varied with NOM concentration. S was obtained by determining the absorbance of NOM, and C was obtained by fitting modified Langmuir or Freundlich models to the amount of As(III) desorbed from CFH upon the addition of NOM. Statistical analysis between the experimental Texp and the calculated one according to Tcal = S × C showed that the Freundlich model (RMSE for HS 0.1609 and for CA 0.1771) was better than the Langmuir model and was statistically robust (QLOO2= 0.691 > 0.5). This work provided an estimation method for the effects of NOM on As(III) photooxidation in the presence of CFH as well as a deeper understanding of the transformation of arsenic species in sunlit water.

Generalized q-rung orthopair fuzzy interactive Hamacher power average and Heronian means for MADM.

In this paper, we establish a novel q-rung orthopair fuzzy (q-ROF) multi-attribute decision making (MADM) model on the basis of the proposed q-ROF interactive Hamacher weighted adjustable power average (q-ROFIHWAPA) and q-ROF interactive Hamacher weighted coordinated Heronian means (HMs), which (1) can reflect the correlations among multiple attributes; (2) weakens the impacts of the extreme evaluation values more reasonably; (3) considers the interactions between the membership degree (MD) and non-membership degree (N-MD) of different q-ROF numbers (q-ROFNs); (4) has the characteristic of generality (It can generate different methods by different operations). Firstly, the q-ROF interactive Hamacher operations, improved score function and new q-ROF entropy (q-ROFE) formula, which are the necessary raw materials for the implementation of MADM, are presented. Secondly, we introduce the adjustable power average (APA) and its weight form (WAPA) to remedy the deficiencies of the classical power averages (PAs). Afterwards we extend the WAPA to q-ROF circumstance and propose the q-ROF interactive Hamacher WAPA (q-ROFIHWAPA), and its basic properties are analyzed. Further, the entropy weight fitting method is presented to determine the parameter carried by the q-ROFIHWAPA. Thirdly, inspired by the evolutionary process of Bonferroni means (BMs), we define the weighted coordinated HM (WCHM) and weighted geometric coordinated HM (WGCHM) based on the traditional HMs, respectively, which eliminate the redundancy of the dual generalized weighted BM (DGWBM) and dual generalized weighted Bonferroni geometric mean (DGWBGM), i.e., the case of τ 1 > τ 2 > ⋯ > τ n . Then we develop the q-ROF interactive Hamacher WCHM (q-ROFIHWCHM) and q-ROF interactive Hamacher WGCHM (q-ROFIHWGCHM) by combining them with the q-ROF interactive Hamacher operations, and the common properties and special cases are also investigated. Finally, we create a MADM algorithm relied on the q-ROFIHWAPA and q-ROFIHWCHM (resp. q-ROFIHWGCHM), and a practical example is introduced to illustrate the effectiveness and superiority of the proposed method.

Quantitative structure-activity relationship for the photooxidation of aromatic micro-pollutants induced by graphene oxide in water.

The photocatalytic degradation behavior of aromatic micro-pollutants (AMPs) exhibits complexity and uncertainty, which mainly depends on the properties of different substituents on benzene. And with similar catalytic reaction substrates, the reaction rate constant could reveal the influence of different characteristics of molecular structure in a specific system. Therefore, the photooxidation pseudo first-order kinetic rate constants (kobs) of 30 AMPs were experimentally determined in Photo-GO system. A quantitative structure-activity relationship (QSAR) model for predicting the photooxidation reaction of AMPs has been developed by stepwise multiple linear regression (MLR) method, based on the lg kobs and representative molecule descriptors (20 in total) including physicochemical, quantum chemical and electrostatic descriptors. Afterwards, Radj2, QLOO2, and Qext2 were calculated as 0.870, 0.841, and 0.732 respectively, which exhibited the excellent goodness-of-fit, robustness, and predictability of the QSAR model, indicating its great prediction ability for photooxidation behavior of AMPs. Meanwhile, during the photooxidation process of AMPs with GO, the model revealed that the one-electron oxidation potential (Eox), molecular dipole moment (µ), and number of hydrogen bond donors (#HD) were the most important molecular structural parameters, which showed that the single electron transfer pathway and adsorption were as the significant steps. Additionally, the Hammett correlation showed that photooxidation of AMPs in Photo-GO system is of typical electrophilic reactions, which demonstrated that the electron-donating substituents could promote the photooxidation of AMPs. The QSAR model was constructed and evaluated to perform the prediction of AMPs reaction kinetics, which provided a guidance for the study of the mechanism and selective oxidation of AOPs photooxidation system based on GO.