Fabrication of a high-quality, small blaze angle grating for visible short-wave infrared hyperspectral cameras.

This study outlines the development of a low line density, small blaze angle grating, optimized for a visible to short-wave infrared hyperspectral camera. An analysis of grating specifications was conducted to meet the precise requirements of this application, particularly focusing on the stringent tolerance limits for the blaze angle. A specialized ruling tool adjustment device was designed to adhere to these exacting blaze angle tolerances. The grating groove shape was examined using atomic force microscopy (AFM), and the theoretical diffraction efficiency of the grating was calculated based on these observations. Additionally, laser-based methods were employed to measure the actual diffraction efficiency of the grating, while interferometry was used to assess the grating's diffraction wavefront. The test results demonstrate our capability to fabricate high-quality gratings with a low line density and small blaze angles that are suitable for advanced hyperspectral imaging applications.

Mechanical protein polycystin-1 directly regulates osteoclastogenesis and bone resorption.

Mechanical loading is required for bone homeostasis, but the underlying mechanism is still unclear. Our previous studies revealed that the mechanical protein polycystin-1 (PC1, encoded by Pkd1) is critical for bone formation. However, the role of PC1 in bone resorption is unknown. Here, we found that PC1 directly regulates osteoclastogenesis and bone resorption. The conditional deletion of Pkd1 in the osteoclast lineage resulted in a reduced number of osteoclasts, decreased bone resorption, and increased bone mass. A cohort study of 32,500 patients further revealed that autosomal dominant polycystic kidney disease, which is mainly caused by loss-of-function mutation of the PKD1 gene, is associated with a lower risk of hip fracture than those with other chronic kidney diseases. Moreover, mice with osteoclast-specific knockout of Pkd1 showed complete resistance to unloading-induced bone loss. A mechanistic study revealed that PC1 facilitated TAZ nuclear translocation via the C-terminal tail-TAZ complex and that conditional deletion of Taz in the osteoclast lineage resulted in reduced osteoclastogenesis and increased bone mass. Pharmacological regulation of the PC1-TAZ axis alleviated unloading- and estrogen deficiency- induced bone loss. Thus, the PC1-TAZ axis may be a potential therapeutic target for osteoclast-related osteoporosis.

Combination of S1-N-Terminal and S1-C-Terminal Domain Antigens Targeting Double Receptor-Binding Domains Bolsters Protective Immunity of a Nanoparticle Vaccine against Porcine Epidemic Diarrhea Virus.

Variants of coronavirus porcine epidemic diarrhea virus (PEDV) frequently emerge, causing an incomplete match between the vaccine and variant strains, which affects vaccine efficacy. Designing vaccines with rapidly replaceable antigens and high efficacy is a promising strategy for the prevention of infection with PEDV variant strains. In our study, three different types of self-assembled nanoparticles (nps) targeting receptor-binding N-terminal domain (NTD) and C-terminal domain (CTD) of S1 protein, named NTDnps, CTDnps, and NTD/CTDnps, were constructed and evaluated as vaccine candidates against PEDV. NTDnps and CTDnps vaccines mediated significantly higher neutralizing antibody (NAb) titers than NTD and CTD recombinant proteins in mice. The NTD/CTDnps in varying ratios elicited significantly higher NAb titers when compared with NTDnps and CTDnps alone. The NTD/CTDnps (3:1) elicited NAb with titers up to 92.92% of those induced by the commercial vaccine. Piglets immunized with NTD/CTDnps (3:1) achieved a passive immune protection rate of 83.33% of that induced by the commercial vaccine. NTD/CTDnps (3:1) enhanced the capacity of mononuclear macrophages and dendritic cells to take up and present antigens by activating major histocompatibility complex I and II molecules to stimulate humoral and cellular immunity. These data reveal that a combination of S1-NTD and S1-CTD antigens targeting double receptor-binding domains strengthens the protective immunity of nanoparticle vaccines against PEDV. Our findings will provide a promising vaccine candidate against PEDV.

Broadband nonlinear modulation of incoherent light using a transparent optoelectronic neuron array.

Nonlinear optical processing of ambient natural light is highly desired for computational imaging and sensing. Strong optical nonlinear response under weak broadband incoherent light is essential for this purpose. By merging 2D transparent phototransistors (TPTs) with liquid crystal (LC) modulators, we create an optoelectronic neuron array that allows self-amplitude modulation of spatially incoherent light, achieving a large nonlinear contrast over a broad spectrum at orders-of-magnitude lower intensity than achievable in most optical nonlinear materials. We fabricated a 10,000-pixel array of optoelectronic neurons, and experimentally demonstrated an intelligent imaging system that instantly attenuates intense glares while retaining the weaker-intensity objects captured by a cellphone camera. This intelligent glare-reduction is important for various imaging applications, including autonomous driving, machine vision, and security cameras. The rapid nonlinear processing of incoherent broadband light might also find applications in optical computing, where nonlinear activation functions for ambient light conditions are highly sought.

Ultrasound-Induced Gold Nanoparticle United with Acoustic Reprogramming of Macrophages for Enhanced Cancer Therapy.

Sonodynamic therapy (SDT) has considerable potential in cancer treatment and exhibits high tissue penetration with minimal damage to healthy tissues. The efficiency of SDT is constrained by the complex immunological environment and tumor treatment resistance. Herein, a specific acoustic-actuated tumor-targeted nanomachine is proposed to generate mechanical damage to lysosomes for cancer SDT. The hybrid nanomachine was assembled with gold nanoparticles (GNPs) as the core and encapsulated with macrophage exosomes modified by AS1411 aptamers (GNP@EXO-APs) to optimize the pharmacokinetics and tumor aggregation. GNP@EXO-APs could be specifically transferred to the lysosomes of tumor cells. After induction with ultrasound, GNP@EXO-APs generated strong mechanical stress to produce lysosomal-dependent cell death in cancer cells. Notably, tumor-associated macrophages were reprogrammed in the ultrasound environment to an antitumor phenotype. Enhanced mechanical destruction via GNP@EXO-APs and immunotherapy of cancer cells were verified both in vitro and in vivo under SDT. This study provides a new direction for inside-out killing effects on tumor cells for cancer treatment.

Menin orchestrates hepatic glucose and fatty acid uptake via deploying the cellular translocation of SIRT1 and PPARγ.

BACKGROUND: Menin is a scaffold protein encoded by the Men1 gene, which interacts with various transcriptional proteins to activate or repress cellular processes and is a key mediator in multiple organs. Both liver-specific and hepatocyte-specific Menin deficiency promotes high-fat diet-induced liver steatosis in mice, as well as insulin resistance and type 2 diabetic phenotype. The potential link between Menin and hepatic metabolism homeostasis may provide new insights into the mechanism of fatty liver disease. RESULTS: Disturbance of hepatic Menin expression impacts metabolic pathways associated with non-alcoholic fatty liver disease (NAFLD), including the FoxO signaling pathway, which is similar to that observed in both oleic acid-induced fatty hepatocytes model and biopsied fatty liver tissues, but with elevated hepatic Menin expression and inhibited FABP1. Higher levels of Menin facilitate glucose uptake while restraining fatty acid uptake. Menin targets the expression of FABP3/4/5 and also CD36 or GK, PCK by binding to their promoter regions, while recruiting and deploying the cellular localization of PPARγ and SIRT1 in the nucleus and cytoplasm. Accordingly, Menin binds to PPARγ and/or FoxO1 in hepatocytes, and orchestrates hepatic glucose and fatty acid uptake by recruiting SIRT1. CONCLUSION: Menin plays an orchestration role as a transcriptional activator and/or repressor to target downstream gene expression levels involved in hepatic energy uptake by interacting with the cellular energy sensor SIRT1, PPARγ, and/or FoxO1 and deploying their translocations between the cytoplasm and nucleus, thereby maintaining metabolic homeostasis. These findings provide more evidence suggesting Menin could be targeted for the treatment of hepatic steatosis, NAFLD or metabolic dysfunction-associated fatty liver disease (MAFLD), and even other hepatic diseases.

Investigating a Method for a Horizontal Comprehensive Eco-Compensation Standard of Interregional Ecological Regulating Services.

Horizontal eco-compensation lacks effective solutions for implementing comprehensive multifactor compensation and determining the compensation standard. To meet those needs, a method named entropy flat surface was proposed and put into practice. However, some scientific problems were found. More specifically, the measurement method of the ecological value was controversial, and the value diffusion model did not reflect the change in the value gradient caused by spatial distance, while the value diffusion had an unclear scope. Therefore, this work optimized and studied the entropy curved-surface method in the case of E'zhou City. The main goal was to build a value-surface model of ecological regulating services based on maximum entropy production. As far as a tangible normal distribution surface is concerned, the model was more consistent with the ecosystem's energy flow characteristics. The external output of value could be precisely expressed by the dynamic and stable expansion state of the surface model. Therefore, the eco-compensation relations and results were clear. Theoretically, the E'Cheng and Huarong Districts should pay a total of 114 million CNY to the Liangzi Lake District. Our work provided a new perspective, in terms of finding a rule of the ecological regulating service values of the macro morphological structure, simulating the transmission and diffusion of multiple values in interregional areas, solving the calculation problem of the horizontal ecological comprehensive compensation standard, and clarifying the relations of compensation.

WD repeat domain 82 (Wdr82) facilitates mouse iPSCs generation by interfering mitochondrial oxidative phosphorylation and glycolysis.

BACKGROUND: Abundantly expressed factors in the oocyte cytoplasm can remarkably reprogram terminally differentiated germ cells or somatic cells into totipotent state within a short time. However, the mechanism of the different factors underlying the reprogramming process remains uncertain. METHODS: On the basis of Yamanaka factors OSKM induction method, MEF cells were induced and reprogrammed into iPSCs under conditions of the oocyte-derived factor Wdr82 overexpression and/or knockdown, so as to assess the reprogramming efficiency. Meanwhile, the cellular metabolism was monitored and evaluated during the reprogramming process. The plurpotency of the generated iPSCs was confirmed via pluripotent gene expression detection, embryoid body differentiation and chimeric mouse experiment. RESULTS: Here, we show that the oocyte-derived factor Wdr82 promotes the efficiency of MEF reprogramming into iPSCs to a greater degree than the Yamanaka factors OSKM. The Wdr82-expressing iPSC line showed pluripotency to differentiate and transmit genetic material to chimeric offsprings. In contrast, the knocking down of Wdr82 can significantly reduce the efficiency of somatic cell reprogramming. We further demonstrate that the significant suppression of oxidative phosphorylation in mitochondria underlies the molecular mechanism by which Wdr82 promotes the efficiency of somatic cell reprogramming. Our study suggests a link between mitochondrial energy metabolism remodeling and cell fate transition or stem cell function maintenance, which might shed light on the embryonic development and stem cell biology.

Bifunctional Ultrathin RhRu0.5 -Alloy Nanowire Electrocatalysts for Hydrazine-Assisted Water Splitting.

Hydrazine-assisted water electrolysis offers a feasible path for low-voltage green hydrogen production. Herein, the design and synthesis of ultrathin RhRu0.5 -alloy wavy nanowires as bifunctional electrocatalysts for both the anodic hydrazine oxidation reaction (HzOR) and the cathodic hydrogen evolution reaction (HER) is reported. It is shown that the RhRu0.5 -alloy wavy nanowires can achieve complete electrooxidation of hydrazine with a low overpotential and high mass activity, as well as improved performance for the HER. The resulting RhRu0.5 bifunctional electrocatalysts enable, high performance hydrazine-assisted water electrolysis delivering a current density of 100 mA cm-2 at an ultralow cell voltage of 54 mV and a high current density of 853 mA cm-2 at a cell voltage of 0.6 V. The RhRu0.5  electrocatalysts further demonstrate a stable operation at a high current density of 100 mA cm-2 for 80 hours of testing period with little irreversible degradation. The overall performance greatly exceeds that of the previously reported hydrazine-assisted water electrolyzers, offering a pathway for efficiently converting hazardous hydrazine into molecular hydrogen.

Ferulic acid supplementation alleviates hyperuricemia in high-fructose/fat diet-fed rats via promoting uric acid excretion and mediating the gut microbiota.

The prevalence of hyperuricemia (HUA) has been rising, and it is typically accompanied by renal injury and intestinal flora disorder, leading to a non-negligible health crisis. Ferulic acid (FA), as a familiar polyphenol, has been proven to exert anti-hyperuricemic properties via inhibiting uric acid (UA) synthesis; however, the detailed underlying mechanisms remain unclear. The aim of this study was to explore the regulatory effect of FA on UA excretion as a potential strategy for reducing UA levels, and the comorbidities of HUA. FA treatment downregulated the expression of urate absorption transporter genes and repressed the toll-like receptor 4 (TLR4)/nuclear factor kappa-B (NF-κB) pathway in UA-stimulated HK-2 cells. To examine these effects in vivo, FA or allopurinol (positive control) was given to rats with HUA induced by a high-fructose/fat diet (HFFD) for 20 weeks. FA markedly decreased the serum UA, blood urea nitrogen, and creatinine levels. The expression of urate absorption transporters was downregulated, whereas the expression of secretion transporters was upregulated in the kidneys and intestines of FA-treated HUA rats. Additionally, FA mitigated renal oxidative stress, and suppressed the activation of the TLR4/NF-κB pathway and the downstream inflammatory response-related markers in the kidneys. Moreover, FA remodeled the composition of the gut microbiota, characterized by an increase in beneficial bacteria (e.g., Lactobacillus and Ruminococcus) and a decrease in pathogenic bacteria (e.g., Bacteroides). In conclusion, our study validated FA as an effective nutrient to ameliorate HFFD-induced HUA, suggesting its potential to mitigate the HUA-associated renal impairment and intestinal microbiota disturbance.

Identification and virtual screening of novel salty peptides from hydrolysate of tilapia by-product by batch molecular docking.

Introduction: Tilapia produces a large number of by-products during processing, which contain potentially flavorful peptides. Methods: The application of PyRx software enabled batch molecular docking andscreening of 16 potential salty peptides from 189 peptides identified in the enzymaticdigestion of tilapia by-products. Results: According to sensory analysis, all 16 peptides werepredominantly salty with a threshold of 0.256 - 0.379 mmol/L with some sournessand astringency, among which HLDDALR had the highest salty intensity, followedby VIEPLDIGDDKVR, FPGIPDHL, and DFKSPDDPSRH. I addition, moleculardocking results showed these four core peptides with high salt intensity bound to thesalt receptor TRPV1 mainly via van der Waals interactions, hydrogen bonds, andhydrophobic forces; Arg491, Tyr487, VAL441, and Asp708 were the key sites for thebinding of salty peptides to TRPV1. Therefore, the application of batch moleculardocking using PyRx is effective and economical for the virtual screening of saltypeptides.

A Review of the Effects of Puerarin on Glucose and Lipid Metabolism in Metabolic Syndrome: Mechanisms and Opportunities.

Chronic diseases, including metabolic syndrome related to sugar and lipid metabolic disorders, are the leading causes of premature death around the world. Novel treatment strategies without undesirable effects are urgently needed. As a natural functional ingredient, puerarin is a promising alternative for the treatment of sugar and lipid metabolic disorders. However, the applications of puerarin are limited due to its poor solubility and short half-life. Various drug delivery systems have been investigated to improve the bioavailability of puerarin. This review summarizes the mechanisms involved in the beneficial action of puerarin: suppressing the release of glucose and FFA; regulating the transport of glucose and fatty acids; acting on the PI3K-Akt and AMPK signaling pathways to decrease the synthesis of glucose and fatty acids; acting on the PPAR signaling pathway to promote ß-oxidation; and improving insulin secretion and sensitivity. In addition, the preparation technologies used to improve the bioavailability of puerarin are also summarized in this review, in the hope of helping to promote the application of puerarin.

Protective Effects of Several Common Amino Acids, Vitamins, Organic Acids, Flavonoids and Phenolic Acids against Hepatocyte Damage Caused by Alcohol.

With the increase in alcohol consumption, more and more people are suffering from alcoholic liver disease (ALD). Therefore, it is necessary to elaborate the pathogenesis of ALD from the aspects of alcohol metabolism and harm. In this study, we established an alcoholic liver injury model in vitro by inducing L02 cells with different concentration of ethanol and acetaldehyde. Results showed that the metabolism of ethanol can promote the content of ROS, MDA, TNF-α, IL-6, and caspase 3, causing oxidative and inflammatory stress and membrane permeability changes. However, unmetabolized ethanol and acetaldehyde had little effect on cell membrane permeability and inflammation, indicating that ethanol metabolites were the main reason for cell membrane damage. We also evaluated the effects of amino acids (taurine and methionine), vitamins (E and vitamin D), organic acids (malic acid and citric acid), flavonoids (rutin and quercetin), and phenolic acids (ferulic acid and chlorogenic acid) on alcohol-induced cell membrane damage of L02 cells. Chlorogenic acid, taurine, vitamin E, and citric acid had remarkable effects on improving cell membrane damage. Malic acid, rutin, quercetin, and ferulic acid had obvious therapeutic effects, while vitamin D and methionine had poor therapeutic effects. The relationship between the structure and effect of active ingredients can be further studied to reveal the mechanism of action, and monomers can be combined to explore whether there is a synergistic effect between functional components, in order to provide a certain theoretical basis for the actual study of liver protection.

Breaking down the cell wall: Still an attractive antibacterial strategy.

Since the advent of penicillin, humans have known about and explored the phenomenon of bacterial inhibition via antibiotics. However, with changes in the global environment and the abuse of antibiotics, resistance mechanisms have been selected in bacteria, presenting huge threats and challenges to the global medical and health system. Thus, the study and development of new antimicrobials is of unprecedented urgency and difficulty. Bacteria surround themselves with a cell wall to maintain cell rigidity and protect against environmental insults. Humans have taken advantage of antibiotics to target the bacterial cell wall, yielding some of the most widely used antibiotics to date. The cell wall is essential for bacterial growth and virulence but is absent from humans, remaining a high-priority target for antibiotic screening throughout the antibiotic era. Here, we review the extensively studied targets, i.e., MurA, MurB, MurC, MurD, MurE, MurF, Alr, Ddl, MurI, MurG, lipid A, and BamA in the cell wall, starting from the very beginning to the latest developments to elucidate antimicrobial screening. Furthermore, recent advances, including MraY and MsbA in peptidoglycan and lipopolysaccharide, and tagO, LtaS, LspA, Lgt, Lnt, Tol-Pal, MntC, and OspA in teichoic acid and lipoprotein, have also been profoundly discussed. The review further highlights that the application of new methods such as macromolecular labeling, compound libraries construction, and structure-based drug design will inspire researchers to screen ideal antibiotics.

Puerarin ameliorates nonalcoholic fatty liver in rats by regulating hepatic lipid accumulation, oxidative stress, and inflammation.

Nonalcoholic fatty liver disease (NAFLD) has become one of the public health problems globally. The occurrence of NAFLD is usually accompanied by a series of chronic metabolic diseases, with a prevalence rate is 25.24% among adults worldwide. Therefore, NAFLD seriously affects the quality of life in patients and causes a large economic burden. It has been reported that puerarin has the function of lowering the serum lipids, but due to the complexity of NAFLD, the specific mechanism of action has not been clarified. The aim of this study was to evaluate the preventive or ameliorating effects of two doses of puerarin (0.11% and 0.22% in diet) on high-fat and high-fructose diet (HFFD)-induced NAFLD in rats. The rats were fed with HFFD-mixed puerarin for 20 weeks. The results showed that puerarin ameliorated the levels of lipids in the serum and liver. Further exploration of the mechanism found that puerarin ameliorated hepatic lipid accumulation in NAFLD rats by reducing the expression of Srebf1, Chrebp, Acaca, Scd1, Fasn, Acacb, Cd36, Fatp5, Degs1, Plin2, and Apob100 and upregulating the expression of Mttp, Cpt1a, and Pnpla2. At the same time, after administration of puerarin, the levels of antioxidant markers (superoxide dismutase, glutathione peroxidase, and catalase) were significantly increased in the serum and liver, and the contents of serum and hepatic inflammatory factors (interleukin-18, interleukins-1ß, and tumor necrosis factor α) were clearly decreased. In addition, puerarin could ameliorate the liver function. Overall, puerarin ameliorated HFFD-induced NAFLD by modulating liver lipid accumulation, liver function, oxidative stress, and inflammation.

Hongqu Rice Wines Ameliorate High-Fat/High-Fructose Diet-Induced Metabolic Syndrome in Rats.

AIM: This study evaluated the possible protective impact of different vintages of Hongqu rice wines on metabolic syndrome (MetS) in rats induced by high-fat/high-fructose diet (HFFD). METHODS: Rats were randomly divided into six groups and treated with (a) basal diet (13.9 kJ/g); (b) HFFD (20.0% w/w lard and 18.0% fructose, 18.9 kJ/g) and (c-f) HFFD with 3-, 5-, 8- and 15-year-aged Hongqu rice wines (9.96 ml/kg body weight), respectively, at an oral route for 20 weeks. RESULTS: Hongqu rice wines could alleviate HFFD-induced augment of body weight gain and fat accumulation, and the release of pro-inflammatory cytokines. Glycolipid metabolic abnormalities caused by HFFD were ameliorated after Hongqu rice wines consumption by lowering levels of fasting insulin, GSP, HOMA-IR, AUC of OGTT and ITT, and lipid deposition (reduced contents of TG, TC, FFA and LDL-C, and elevated HDL-C level) in the serum and liver, probably via regulating expressions of genes involving in IRS1/PI3K/AKT pathway, LDL-C uptake, fatty acid ß-oxidation, and lipolysis, export and synthesis of TG. In addition, concentrations of MDA and blood pressure markers (ANG-II and ET-1) declined, and activities of antioxidant enzymes (SOD and CAT) were improved in conditions of Hongqu rice wines compared to those in the HFFD group. Eight-year-aged Hongqu rice wine produced a more effective effect on alleviating HFFD-caused MetS among different vintages of Hongqu rice wines. CONCLUSION: To sum up, Hongqu rice wines exhibited ameliorative effects on HFFD-induced MetS in rats based on antiobesity, antihyperlipidemic, antihyperglycemic, antioxidant, anti-inflammatory and potential antihypertensive properties.

Use of the systemic inflammation response index (SIRI) as a novel prognostic marker for patients on peritoneal dialysis.

BACKGROUND: The systemic inflammatory response index (SIRI), a novel inflammation maker, has proven to be associated with prognostic outcomes in various diseases. However, few studies have been conducted assessing how SIRI may influence outcomes of patients on peritoneal dialysis (PD). Herein, we assessed the predictive value of SIRI on mortality all-cause mortality, including cardiovascular disease (CVD) in PD patients. METHODS: A total of 646 PD patients were enrolled in this study. PD patients received regular PD treatments at the Zhujiang Hospital from 1 January 2011 to 31 December 2018. SIRI values could be computed as follows: neutrophil count × monocyte count/lymphocyte count. Patients were divided into two groups according to the median level of SIRI. Cox regression analysis and Kaplan-Meier methods were applied to analyze the relationship between SIRI and mortality outcomes in PD patients. RESULTS: During the median 31-month follow-up period, 97 (15.0%) PD patients died from all-causes, and 47 (49.0%) died of CVD. Kaplan-Meier analyses revealed that a high SIRI corresponded to the high mortality of all-cause deaths, including CVD (both p < 0.001) in patients on PD. After adjusting for potential confounders, the higher SIRI level was significantly associated with an increased all-cause mortality (HR: 2.007, 95% CI: 1.304-3.088, p = 0.002) and cardiovascular mortality (HR: 2.847, 95% CI: 1.445-5.608, p = 0.002). CONCLUSIONS: SIRI was a promising predictor of mortality in PD patients, with a higher SIRI corresponding to increased risk of mortality.

Dynamic response and failure characteristics of combined rocks under confining pressure.

Gas explosions or coal and gas outbursts can cause transient destruction of combined coal-rock, and the dynamic mechanical response of combined coal-rock masses plays a key role in accident failure, but we now know little about the dynamic mechanical responses of combined coal-rock. In this article, we selected three rocks (limestone, shale, sandstone) and two coals (bituminous coal and anthracite coal) to form combined coal-rock, and analyze their dynamic mechanical properties by using the SHPB system. We find that the dynamic compressive strength and elastic modulus of combined rock-coal are lower than the average value of single rock and coal, while the ultimate strain and strain rate of combined coal-rock are higher than the average values of single rock and coal. Compressive strength and elastic modulus of the combined body increase gradually with increasing confining pressure, and the strain decreases accordingly. The dynamic stress-strain curve demonstrates an obvious double-peak at high strain rate (85.55 s-1 and above in the present work), while there is no obvious double-peak of the curve at low strain rate. Dynamic compressive strength of combined coal-rock body increases significantly with increasing confining pressure at low strain rate, but it increases more smoothly at higher strain rate. The elastic modulus also increases with increasing confining pressure, and it seems to be stable as confining pressure increases at low strain rate. The ultimate strain decreases gradually with increasing confining pressure but more gently compared with that at low strain rate. Besides, longitudinal fractures of combined coal-rock bodies include penetrating fractures, partially penetrating fractures, and interrupted fractures stopped at the coal-rock interface. The dynamic mechanical response of combined coal-rock is of guiding significance for maintaining the stability of the roadway and formulating the support measures for the roadway.

Dietary Ferulic Acid Ameliorates Metabolism Syndrome-Associated Hyperuricemia in Rats via Regulating Uric Acid Synthesis, Glycolipid Metabolism, and Hepatic Injury.

Ferulic acid is a well-known phenolic acid compound and possesses multiple health-promoting and pharmacological effects. Metabolic syndrome (MetS) and hyperuricemia (HUA) have become health problems worldwide and are closely connected. The aim of this study was to explore the influence of ferulic acid on MetS-related HUA and its underlying mechanisms. Rats were administered high-fructose and high-fat diet (HFFD) with or without ferulic acid (0.05 and 0.1%) for 20 weeks. Intake of HFFD resulted in obesity, hyperglycemia, insulin resistance, and dyslipidemia, which were alleviated by ferulic acid consumption. Treatment of rats with ferulic acid diminished the levels of lipids and inflammatory cytokines and enhanced the activities of antioxidant enzymes in the liver caused by HFFD. Additionally, administration of ferulic acid blocked a HFFD-induced elevation in activities and mRNA expression of enzymes involving in uric acid (UA) synthesis. Molecular docking analysis denoted that ferulic acid bound to the active center of these enzymes, indicative of the potential interaction with each other. These two aspects might partially be responsible for the decrement in serum UA content after ferulic acid ingestion. In conclusion, ferulic acid supplementation ameliorated lipid and glucose metabolic abnormalities, hepatic damage, and UA formation in MetS rats. There was a dose correlation between lipid deposition and UA synthesis-related indicators. These findings implied that ferulic acid could be applied as a promising dietary remedy for the management of MetS-associated HUA.