Maternal history of Alzheimer's disease predisposes to altered serum cholesterol levels in adult offspring.

Controversial findings regarding the association between serum cholesterol levels and Alzheimer's disease (AD) have been identified through observational studies. The genetic basis shared by both factors and the causality between them remain largely unknown. The objective of this study is to examine the causal impact of maternal history of AD on changes in serum cholesterol levels in adult offspring. By retrieving genetic variants from summary statistics of large-scale genome-wide association study of maternal history of AD (European-based: Ncase = 27 696, Ncontrol = 260 980). The causal association between genetically predicted maternal history of AD and changes in serum cholesterol levels in adult offspring was examined using the two-sample Mendelian randomization (MR) method. Causal impact estimates were calculated using single-nucleotide polymorphisms in both univariable MR (UMR) and multivariable MR (MVMR) analyses. Additionally, other approaches, such as Cochran's Q test and leave-one-out variant analysis, were employed to correct for potential biases. The results of UMR presented that genetically predicted maternal history of AD was positively associated with hypercholesterolemia (OR = 1.014; 95% CI: 1.009-1.018; p < 0.001), total cholesterol (OR = 1.29; 95% CI: 1.134-1.466; p < 0.001) and low-density lipoprotein (OR = 1.525; 95% CI: 1.272-1.828; p < 0.001) among adult offspring. Genetic predisposition for maternal history of AD to be negatively associated with high-density lipoprotein (OR = 0.889; 95% CI: 0.861-0.917; p < 0.001). The MVMR analysis remained robust and significant after adjusting for diabetes and obesity in offspring. Sufficient evidence was provided in this study to support the putative causal impact of maternal history of AD on the change of serum cholesterol profile in adult offspring. In clinical practice, priority should be given to the detection and monitoring of cholesterol levels in individuals with a maternal history of AD, particularly in the early stages.

Polystyrene nanoplastics exposure triggers spermatogenic cell senescence via the Sirt1/ROS axis.

Polystyrene nanoplastics (PS-NPs) have been reported to accumulate in the testes and constitute a new threat to reproductive health. However, the exact effects of PS-NPs exposure on testicular cells and the underlying mechanisms remain largely unknown. The C57BL/6 male mice were orally administered with PS-NPs (80 nm) at different dosages (0, 10, and 40 mg/kg/day) for 60 days, and GC-1 cells were treated with PS-NPs in this study. Enlarged seminiferous tubule lumens and a loose and vacuolated layer of spermatogenic cells were observed in PS-NPs-exposed mice. Spermatogenic cells which may be one of the target cells for this reproductive damage, were decreased in the mice from PS-NPs group. PS-NPs caused spermatogenic cells to undergo senescence, manifested as elevated SA-ß-galactosidase activity and activated senescence-related signaling p53-p21/Rb-p16 pathways, and induced cell cycle arrest. Mechanistically, Gene Ontology (GO) enrichment suggested the key role of reactive oxygen species (ROS) in PS-NPs-induced spermatogenic cell senescence, and this result was confirmed by measuring ROS levels. Moreover, ROS inhibition partially attenuated the senescence phenotype of spermatogenic cells and DNA damage. Using the male health atlas (MHA) database, Sirt1 was filtrated as the critical molecule in the regulation of testicular senescence. PS-NPs induced overexpression of the main ROS generator Nox2, downregulated Sirt1, increased p53 and acetylated p53 in vivo and in vitro, whereas these disturbances were partially restored by pterostilbene. In addition, pterostilbene intervention significantly alleviated the PS-NPs-induced spermatogenic cell senescence and attenuated ROS burst. Collectively, our study reveals that PS-NPs exposure can trigger spermatogenic cell senescence mediated by p53-p21/Rb-p16 signaling by regulating the Sirt1/ROS axis. Importantly, pterostilbene intervention may be a promising strategy to alleviate this damage.

Genetic association between coffee/caffeine consumption and the risk of obstructive sleep apnea in the European population: a two-sample Mendelian randomization study.

BACKGROUND: The association between coffee/caffeine consumption and obstructive sleep apnea (OSA) risk remains unclear. PURPOSE: To determine the relationship between coffee/caffeine consumption and the risk of OSA, using the Mendelian randomization (MR) method in the European population. METHODS: Two sets of coffee consumption-associated genetic variants were, respectively, extracted from the recent genome-wide meta-analysis (GWMA) and genome-wide association study (GWAS) of coffee consumption. Taking other caffeine sources into account, genetic variants associated with caffeine consumption from tea and plasma caffeine (reflecting total caffeine intake) were also obtained. The inverse variance weighted (IVW) technique was utilized as the primary analysis, supplemented by the MR-Egger, weighted-median, and MR-Pleiotropy RESidual Sum and Outlier (PRESSO) techniques. Leave-one-out (LOO) analysis was performed to assess whether the overall casual estimates were driven by a single SNP. Additional sensitivity analyses were performed using similar methods, while the genetic variants associated with confounders, e.g., body mass index and hypertension, were excluded. RESULTS: The IVW method demonstrated that coffee consumption GWMA (OR: 1.065, 95% CI 0.927-1.224, p = 0.376), coffee consumption GWAS (OR: 1.665, 95% CI 0.932-2.977, p = 0.086), caffeine from tea (OR: 1.198, 95% CI 0.936-1.534, p = 0.151), and blood caffeine levels (OR: 1.054, 95% CI 0.902-1.231, p = 0.508) were unlikely to be associated with the risk of OSA. The other three methods presented similar results, where no significant associations were found. No single genetic variant was driving the overall estimates by the LOO analysis. These findings were also supported by the sensitivity analyses with no confounding genetic variants. CONCLUSION: Our study found no association between coffee/caffeine consumption and the risk of OSA.

Relationship between dietary carotenoid intake and sleep duration in American adults: a population-based study.

OBJECTIVE: To investigate the relationship between dietary carotenoid intake and sleep duration. METHODS: Adults enrolled in the National Health and Nutrition Examination Survey (NHANES) 2007-2018 without missing information on dietary carotenoid intake (α-carotene, ß-carotene, ß-cryptoxanthin, lycopene, and lutein + zeaxanthin), sleep duration, and covariates were included. Participants' carotenoid consumption was divided into three groups by quartiles and sleep duration was grouped as short (< 7 h/night), optimal (7-8 h/night), and long (> 8 h/night). Multinominal logistic regression was constructed to examine the association between dietary carotenoid intake and sleep duration. Restricted cubic spline (RCS) regression was further utilized to explore their dose-response relationship. The weighted quantile sum (WQS) model was adopted to calculate the mixed and individual effect of 5 carotenoid sub-types on sleep duration. RESULTS: Multinominal logistic regression presented that people with higher intakes of α-carotene, ß-carotene, ß-cryptoxanthin, lycopene, and lutein + zeaxanthin were less likely to sleep too short or too long. Consistent with the findings from multinominal logistic regression, the RCS models suggested a reverse U-shaped relationship between sleep duration and carotenoid intakes. The mixed effects were also significant, where ß-cryptoxanthin and lutein + zeaxanthin were the top 2 contributors associated with the decreased risks of short sleep duration, while ß-carotene, α-carotene, and ß-cryptoxanthin were the main factors related to the lower risk of long sleep duration. CONCLUSION: Our study revealed that the American adults with optimal sleep duration were associated with more dietary carotenoid intake, in comparison to short or long sleepers.

Identification and functional analysis of senescence-associated secretory phenotype of premature senescent hepatocytes induced by hexavalent chromium.

Hexavalent chromium [Cr(VI)] is a common heavy metal pollutant that can cause a number of human disease, including inflammation and cancer. Senescent cells can secrete a variety of molecules known as senescence-associated secretory phenotype (SASP). Our previous studies have confirmed that Cr(VI) can induce premature senescence in L02 hepatocytes, but the composition and the function of the related SASP are still unknown. In order to understand the components of SASP secreted by senescent L02 hepatocytes under the action of Cr(VI), we applied LC-MS/MS-based label-free protein quantification. We found that three SASP components including Coactosin-like protein 1 (COTL1), Alpha-enolase (ENO1), and Peroxiredoxin 2 (PRDX2) were up-regulated, which were confirmed by western blotting and qRT-PCR. Evidence suggested that SASP may promote the development of tumor through chronic inflammatory response, therefore we identified and analyzed the potential biological functions and signaling pathways of these three SASP components using GO and KEGG methods. The interaction between SASP components was analyzed by STRING, and verified by Co-IP. We also found that ENO1 and PRDX2, which have direct interaction, can inhibit the growth and proliferation of wildtype hepatocytes and premature senescent hepatocytes, but can promote the proliferation and behavioral changes of liver tumor cells. The present study provides valuable clues for elucidation of the carcinogenic mechanism of Cr(VI), especially for further prevention and targeted treatment of Cr(VI)-related cancer.

The role of PKA/PP2B-mediated Drp1 phosphorylation and the subsequent EGFR inhibition in Cr(VI)-induced premature senescence.

In recent years, frequent hexavalent chromium [Cr(VI)] pollution incidents have severely damaged the ecology and endangered the public health. It is well known that cell senescence could promote the carcinogenesis, thus the related research on the occurrence of premature senescence is of great significance to the elucidation of the carcinogenic mechanism of Cr(VI). We previously confirmed that long-term low-dose Cr(VI) exposure induced premature senescence, but the key molecular events that determine the occurrence of premature senescence are still unclear. In the present study, we found that Cr(VI) induced phosphorylation of dynamin-relatedprotein 1 (Drp1)-S637 site in premature senescent cells, which was accompanied with the decrease of mitochondrial fission. We also demonstrated that the phosphorylation status of Drp1-S637 after Cr(VI) exposure was related to the antagonism of PKA/PP2B, and continuous dephosphorylation of Drp1-S637 attenuated premature senescence caused by Cr(VI). The epidermal growth factor receptor (EGFR) overexpression significantly alleviated the occurrence of premature senescence, and the expressions of EFGR and its downstream molecules were related to the phosphorylation status of Drp1-S637. In brief, we revealed the role of PKA/PP2B-mediated Drp1 phosphorylation and the subsequent EGFR inhibition in Cr(VI)-induced premature senescence. This study is the first time to link the phosphorylation of Drp1 with Cr(VI)-induced premature senescence, in order to find the key molecular events that determine the occurrence of premature senescence and demonstrate the molecular mechanism of abnormal elongated mitochondria formation in the senescence process. The significance of this study is to explore the carcinogenesis of Cr(VI) and provide new ideas and strategies for the targeted treatment of Cr(VI)-related cancers.

Role of Clusterin/NF-κB in the secretion of senescence-associated secretory phenotype in Cr(VI)-induced premature senescent L-02 hepatocytes.

Hexavalent chromium [Cr(VI)] and its compounds have caused serious environmental pollution and health damage. Senescent cells can actively change the surrounding environment by secreting some factors, which are called senescence associated secretory phenotype (SASP). Our previous work has confirmed that premature senescent hepatocytes induced by Cr(VI) expressed high level of Clusterin (CLU) and secrete interleukin-6 (IL-6) and IL-8. CLU is involved in the regulation of tumor development and drug resistance, but whether CLU regulates SASP components and participates in Cr(VI)-induced malignant transformation is unclear. In this study we demonstrated that Cr(VI) induced the secretion of tumor promoting components of SASP such as IL-6, IL-8, and granulocyte-macrophage colony stimulating factor (GM-CSF) in senescent L-02 hepatocytes, while the levels of the anti-tumor components of SASP such as chemokine (c-x-c motif) ligand-1 (CXCL-1) and monocyte chemoattractant protein-1 (MCP-1) were not altered. CLU shRNA interference significantly reduced the levels of IL-6, IL-8, and GM-CSF in the culture medium of senescent cells, suggesting CLU may regulate SASP. The NF-κB inhibitor PDTC significantly alleviated Cr(VI)-induced increase of IL-6, IL-8, and GM-CSF, confirming that NF-κB can regulate the tumor promoting components of SASP. CLU shRNA interference aggravated the inhibitory effect of PDTC on SASP secretion, indicating that CLU regulated the secretion of SASP in Cr(VI)-induced senescent hepatocytes through the NF-κB signaling. We speculated that SASP secreted by Cr(VI)-induced premature senescent hepatocytes was tightly related to the carcinogenic effect of Cr(VI). Therefore, elucidation of upstream regulatory mechanism of SASP is of great significance. In addition to further clarifying the carcinogenic mechanisms associated with Cr(VI), we could also seek out new targets for treatment of Cr(VI)-related cancer.

Clusterin inhibits Cr(VI)-induced apoptosis via enhancing mitochondrial biogenesis through AKT-associated STAT3 activation in L02 hepatocytes.

Improper treatment of a large amount of industrial waste makes hexavalent chromium [Cr(VI)] seriously pollute the atmosphere, soil and water, and enter the food chain, seriously affecting the health of workers and local residents. We previously proved that Clusterin (CLU) can inhibit the apoptosis of L02 hepatocytes induced by Cr(VI) through mitochondrial pathway, but the associated molecular mechanism has not been further studied. Mitochondrial biogenesis is an important step in mitochondrial damage repair, but the mechanism of mitochondrial biogenesis in Cr(VI)-induced liver toxicity is still unclear. We demonstrated in the present study that Cr(VI) triggered mitochondrial biogenesis dysfunction-associated apoptosis, and CLU delayed Cr(VI)-induced apoptosis by enhancing mitochondrial biogenesis. Signal transducer and activator of transcription 3 (STAT3) was down-regulated in Cr(VI)-induced apoptosis, and CLU may regulate STAT3 via protein kinase B (PKB/AKT) in Cr(VI)-exposed hepatocytes. We used the STAT3 inhibitor C188-9 and the AKT inhibitor Uprosertib to eliminate the anti-apoptotic effect of CLU, and found that CLU inhibited Cr(VI)-induced apoptosis by up-regulating AKT/STAT3 signal. Based on the fact that both AKT and STAT3 are closely related to mitochondrial biogenesis and mitochondrial pathway-associated apoptosis, this study is the first time to link CLU, STAT3, AKT and mitochondrial biogenesis function after Cr(VI) exposure, to further enrich the experimental basis of Cr(VI)-induced hepatotoxicity, clarify the molecular mechanism of CLU helping cells to escape apoptosis, and also suggest that new ways can be sought to prevent and treat Cr(VI)-induced hepatotoxicity by regulating mitochondrial biosynthesis.

Design, Synthesis, Molecular Docking, and Tumor Resistance Reversal Activity Evaluation of Matrine Derivative with Thiophene Structure.

Nasopharyngeal carcinoma (NPC) frequently occurs in Southern China. The main treatments of NPC are chemotherapy and radiotherapy. However, chemo-resistance arises as a big obstacle in treating NPC. Therefore, there is a great need to develop new compounds that could reverse tumor drug resistance. In this study, eight matrine derivatives containing thiophene group were designed and synthesized. Structures of these 8 compounds were characterized by 1H-NMR, 13C-NMR, and high-resolution mass spectrometer (HRMS). The cytotoxicity and preliminary synergistic effects of these 8 compounds were detected against nasopharyngeal carcinoma (NPC) cells and cisplatin-resistant NPC cells (CNE2/CDDP), respectively. Furthermore, the in vivo and in vitro tumor resistance reversal effects of compound 3f were evaluated. Moreover, docking studies were performed in Bclw (2Y6W). The results displayed that compound 3f showed synergistic inhibitory effects with cisplatin against CNE2/CDDP cells proliferation via apoptosis induction. Docking results revealed that compound 3f may exert its effects via inhibiting anti-apoptosis protein Bcl-w.

Pyrene derivative-functionalized mesoporous silica-Cu2+ hybrid ensemble for fluorescence "turn-on" detection of H2S and logic gate application in aqueous media.

The ensemble system PyH-SBA-15-Cu2+ was obtained via coordination interaction of pyrene derivative-functionalized mesoporous SBA-15 and Cu2+, and applied for the selective and sensitive detection of H2S over pH 6.0-12.0 in aqueous media. The sensing strategy was designed on the basis of the H2S-induced dissolution of Cu2+ from PyH-SBA-15-Cu2+. Cu2+ has good binding affinity to N atoms in PyH-SBA-15; therefore, the organic-inorganic hybrid ensemble PyH-SBA-15-Cu2+ was formed, which is nonfluorescent in aqueous solution because of the Cu2+-promoted emission quenching of PyH-SBA-15. The addition of H2S induces the dissolution of PyH-SBA-15-Cu2+ by the formation of stable CuS, thereby producing fluorescence revival of PyH-SBA-15. The correlative "turn-on" fluorescence signals of this ensemble system are linearly proportional to [H2S] in the concentration region of 0-1.0 × 10-4 M, showing a low detection limit of 3.7 × 10-7 M. Other common anions do not induce distinct fluorescence changes. When using the fluorescence intensity signal changes of PyH-SBA-15 as outputs and Cu2+ and S2- as inputs, PyH-SBA-15 can act as an XNOR logic gate.

Clusterin alleviates Cr(VI)-induced mitochondrial apoptosis in L02 hepatocytes via inhibition of Ca2+-ROS-Drp1-mitochondrial fission axis.

Hexavalent chromium [Cr(VI)] is ubiquitous in the environment and is commonly used in various industrial processes. Clusterin (CLU) is an extracellular chaperone protein which exerts the anti-apoptotic function. In this study, we aimed to explore the effect of CLU on Cr(VI)-induced mitochondrial fission and apoptosis. We revealed that the apoptosis rate of L02 hepatocytes treated with Cr (VI) was increased. CLU over-expression could protect the hepatocytes from Cr(VI)-induced mitochondrial apoptosis. Furthermore, Cr(VI) triggered the intracellular calcium overload, resulting in the activation of xanthine oxidase (XO). Cr(VI) induced reactive oxygen species (ROS) overproduction, led to dynamin-related protein 1 (Drp1) translocation to mitochondria and the subsequent mitochondrial fission, contributing to the caspase-3-dependent mitochondrial apoptosis as evidenced by higher mitochondrial permeability transition pore (mPTP) opening rate, lower mitochondrial membrane potential (MMP), and more alanine transaminase (ALT)/aspartate transaminase (AST) leakage into the culture medium. However, CLU over-expression could trigger the AMP-activated protein kinase (AMPK) pathway, which was followed by the increase of sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) expression. CLU-induced AMPK/SERCA2a activation attenuated calcium overload, caspase-3 activation, and ultimate mitochondrial apoptosis. All in all, the present study demonstrated that Cr(VI) induced hepatocytes apoptosis via Ca2+-ROS-Drp1-mitochondrial fission axis and CLU alleviated the mitochondrial apoptosis through activation of the AMPK/SERCA2a pathway.

ROS-mediated miR-21-5p regulates the proliferation and apoptosis of Cr(VI)-exposed L02 hepatocytes via targeting PDCD4.

Although much has been determined about the molecular mechanisms of hexavalent chromium [Cr(VI)]-induced hepatotoxicity, more remains to be explored. In particular, explicit epigenetic alterations of microRNAs (miRNAs) which can negatively regulate mRNAs at post transcriptional level remain understudied. In the present study, cell apoptosis was determined using Annexin V/propidium iodide (PI) staining, while proliferative growth was analyzed by colony formation assay and proliferating cell nuclear antigen (PCNA) detection. miRNA microarray was performed to compare the global miRNAs expression patterns. miR-21-5p mimics (mi)/inhibitor (in), and PDCD4-siRNAs were transfected into L02 hepatocytes. Our results revealed that Cr(VI) induced apoptosis and inhibited proliferation in L02 hepatocytes via reactive oxygen species (ROS), the formation of which is closely related to mitochondrial damage, especially the inhibition of mitochondrial respiratory chain complex (MRCC). We also confirmed that ROS-mediated miR-21-5p inhibition participated in cell apoptosis and proliferative inhibition induced by Cr(VI). Furthermore, programmed cell death protein 4 (PDCD4), the up-regulation of which was related to ROS over-production, was predicted and verified as a target of miR-21-5p. Transcription factor PDCD4 silencing suppressed apoptosis and stimulated cell proliferation. In conclusion, from the perspective of epigenetics, the present study revealed that ROS-mediated miR-21-5p regulated the proliferation and apoptosis of Cr(VI)-exposed L02 hepatocytes via targeting PDCD4, which provided the new targets for molecular intervention and treatment of liver damage in Cr(VI)-exposed population.

Design, synthesis and biological evaluation of 1,4-dihydroxyanthraquinone derivatives as anticancer agents.

The novel hydroxyanthraquinone derivatives containing nitrogen-mustard and thiophene group were designed to covalently bind to topoisomerase II, and their structures were confirmed by nuclear magnetic resonance and high resolution mass spectrometer technologies in this article. The in vitro cytotoxicity against different cancer cell lines and one normal liver cell line (L02) was evaluated by MTT assay. Compound A1 was the most potent anti-proliferative agent against the human liver cancer HepG-2 cells (IC50 = 12.5 µM), and there is no obvious growth inhibitory effect on normal liver tissue L02 cells. The good cytotoxicity and selectivity of compound A1 suggest that it could be a promising lead for further optimization. The mechanisms of action about compound A1 and A4 were further investigated through analysis of cell apoptosis. Confocal microscopy tracks the location of compound A1 in the cell, which could enter the cytoplasm and nucleus, and induce severe deformation of the nucleus. The docking study demonstrated that A1 could interact with the catalytic active site in topoisomerase II.

Blockage of ROS-ERK-DLP1 signaling and mitochondrial fission alleviates Cr(VI)-induced mitochondrial dysfunction in L02 hepatocytes.

Hexavalent chromium [Cr(VI)] is a common heavy metal pollutant widely used in various industrial fields. It is well known that mitochondria are the most vulnerable targets of heavy metals, but the key molecule/event that directly mediated mitochondrial dysfunction after Cr(VI) exposure is still unclear. The present study was aimed to explore whether Cr(VI) exposure could affect the mitochondrial fission/fusion process, and whether the related abnormal mitochondrial dynamics have been implicated in Cr(VI)-induced mitochondrial dysfunction. We found that the mitochondrial dysfunction caused by Cr(VI) exposure was characterized by decreased mitochondrial respiratory chain complex (MRCC) I/II activities and levels, collapsed mitochondrial membrane potential (MMP), depleted ATP, and increased reactive oxygen species (ROS) level. Cr(VI) induced abnormal mitochondrial fission/fusion events, the antioxidant Nacetyl-L-cysteine (NAC) restored the abnormal mitochondrial function as well as the fission/fusion dynamics. ROS was the up-stream regulator of extracellular regulated protein kinases (ERK) signaling, and the application of a specific ERK1/2 inhibitor PD98059 confirmed that activation of ERK1/2 signaling was associated with the abnormal mitochondrial fission/fusion and mitochondrial dysfunction. We also demonstrated that treatment with dynamic-like protein 1 (DLP1)-siRNA rescued mitochondrial dysfunction in Cr(VI)-exposed L02 hepatocytes. We reached the conclusion that blockage of ROS-ERK-DLP1 signaling and mitochondrial fission alleviates Cr(VI)-induced mitochondrial dysfunction in L02 hepatocytes, which may provide the new avenue for developing effective strategies to protect against Cr(VI)-induced hepatotoxicity.

Ultrasonic-assisted in situ synthesis of MOF-199 on the surface of carboxylated cellulose fibers for efficient adsorption of methylene blue.

A high-efficiency porous adsorbent, MOF-199/carboxylated cellulose fibers (MOF-199/CCF), was synthesized in situ at room temperature through carboxylation modification, simple sonication, and vacuum drying. The sonication method produced small MOF-199 particles (tens of nanometers), which allowed for uniform distribution of MOF-199 on CCF and improved its efficiency. The presence of CCF carriers reduces the agglomeration of MOF-199 and enhances its performance. The BET-specific surface area of MOF-199/CCF is 264.83 m2 g-1, which is much larger than that of CCF (2.31 m2 g-1), proving the successful modification of CCF by MOF-199. MOF-199/CCF exhibits better adsorption capacity than CCF, with an adsorption capacity of 659.6 mg g-1 of methylene blue within 30 minutes, and good recycling performance. This work presents a straightforward method for preparing efficient cellulose-based adsorbent materials and offers a novel approach for synthesizing MOF composites.

Experimental Study on Coal and Gas Outburst Risk under Different Water Content Rates in Strong Outburst Coal Seams.

To investigate the alleviation potency of coal seam water infusion on coal and gas outburst, this paper focuses on the Qidong coal mine outburst coal seam, where outburst accidents have occurred many times, and obtains the impact of water content on outburst prediction parameters by studying the features of outburst parameters and gas desorption law under different water content rates. How water content affects outburst was also researched through the use of a self-made outburst simulation test system, and the relationship between water content and outburst intensity and critical gas pressure was studied. It can be concluded that with the rise of water content, the initial velocity of gas diffusion, the gas desorption index of drilling cuttings, and the adsorption constant a decrease, but the firmness coefficient (f) increase, and these indicators are exponentially related to the water content. Meanwhile, as the water content raises, the outburst pressure threshold increases, the outburst intensity gradually decreases, and the less likely outburst occurs. Under 0.5 MPa pressure, as the water content arose from 2.02 to 5.14%, the outburst intensity was significantly weakened, while no outburst occurred as the water content reached to 10.25%. Fitting analysis of the influence curve of outburst parameters and comparing the vital values of outburst prediction indexes finally determined that the water content rate of 5.14% could be used as a key index for water injection measures for coal and gas outburst prevention coal seam in Qidong coal mine no. 9. This research offers a guiding significance for the outburst prevention measures of water infusion in outburst coal seams and gives a feasible scheme for the safe mining of outburst coal mines.

Anisotropic Damage Mechanism of Coal Seam Water Injection with Multiphase Coupling.

After coal seam water injection, coal mechanical properties will change with brittleness weakening and plasticity enhancement. Aiming at the problem of coal damage caused by the coal seam water injection process, based on nonlinear pore elasticity theory and continuum damage theory, a nonlinear pore elastic damage model considering anisotropic characteristics is proposed to calculate and analyze the gas-liquid-solid multiphase coupling effect with the fully coupled finite element method during the coal seam water injection process. The research results indicate that the wetting radius of calculated results by the model agrees well with the in situ test results, and the relative errors are less than 10%. Water saturation and induced damage of the coal body in the parallel bedding direction are greater than that in the vertical bedding direction during the coal seam water injection process, which exhibits significant anisotropic characteristics. With the increasing water injection time, the induced damage of the coal body also increases near the water injection hole. Considering the inherent permeability arising with damage, it has a significant impact on both water saturation and induced damage, which also indicates that there is a strong interaction between water saturation and induced damage. The theoretical model reveals the coal damage mechanism of gas-liquid-solid multiphase coupling after coal seam water injection and provides a theoretical prediction of coal containing water characteristics in engineering practice.

Desorption Characteristics of CH4-C2H6 Mixed Gas in Heavy Hydrocarbon-Rich Coal Seams.

The gas desorption characteristics of coal are closely related to the gas content of the coal seam. The gas in heavy hydrocarbon-rich coal seams contains CH4 and C2H6 heavy hydrocarbons. However, most current research on the gas desorption characteristics of coal seams focuses on CH4 analysis, ignoring the influence of the C2H6 heavy hydrocarbon gas. To accurately determine the gas content of a heavy hydrocarbon-rich coal seam, methods based on CH4 analysis are inadequate and the desorption characteristics of CH4-C2H6 mixed gas must be clarified. This work experimentally and theoretically studies the desorption characteristics of single-component gas and CH4-C2H6 mixed gas from coal samples. The results show that increasing the adsorption-equilibrium pressure was found to increase the desorption quantity and desorption speed of single-component gas and increase the desorption quantity, desorption ratio, and diffusion coefficient of mixed gas. Under the same adsorption-equilibrium pressure, the desorption quantity and rate of single-component CH4 gas exceeded those of C2H6. The quantity and speed of mixed gas desorption increased with rising CH4 concentration and decreased with rising C2H6 concentration. The change in the mixed gas concentration during desorption reflects the distribution characteristics of light hydrocarbon components on the outer surface and heavy hydrocarbon components on the inner surface of coal. From the desorption characteristics of mixed gas, desorption models of mixed gas were obtained at different concentrations, laying a theoretical foundation for accurate determinations of gas contents in heavy hydrocarbon-rich coal seams.

Anti-adhesion multifunctional poly(lactic-co-glycolic acid)/polydimethylsiloxane wound dressing for bacterial infection monitoring and photodynamic antimicrobial therapy.

Wound infection and adhesion are important factors affecting wound healing. Early detection of pathogen infection and reduction of wound-to-dressing adhesion are critical for improving wound healing. Herein, Ester-J, which can rapidly respond to lipase secreted by bacteria, was designed and synthesized. Then, Ester-J was co-spun with poly(lactic-co-glycolic acid) (PLGA) and polydimethylsiloxane (PDMS) to prepare a PP-EsJ hydrophobic anti-adhesion dressing with a contact angle of 140.7°. When the PP-EsJ membrane came into contact with the bacteria, the loaded Ester-J was hydrolyzed to Tph-TSF-OH, releasing bright cyan-blue fluorescence, thus providing a fluorescence switch for an early warning of infection. The detection limits of PP-EsJ for Pseudomonas aeruginosa and Staphylococcus aureus were 1.0 × 105 and 1.0 × 106 CFU/mL, respectively. Subsequently, Tph-TSF-OH released 1O2 through light irradiation, which rapidly killed P. aeruginosa and S. aureus, and accelerated wound healing. Compared with the control group, enhanced wound closure (up to 99.80 ± 1.10 %) was observed in mice treated with the PP-EsJ membrane. The PP-EsJ membrane not only effectively reduced the risk of external infection but also reduced adhesions to the skin during dressing changes. These characteristics make PP-EsJ membranes potentially useful for clinical treatment.

Dietary choline intake and non-alcoholic fatty liver disease (NAFLD) in U.S. adults: National Health and Nutrition Examination Survey (NHANES) 2017-2018.

BACKGROUND: Whether there is an association between dietary choline intake and non-alcoholic fatty liver disease (NAFLD) in American adults remains unclear. METHODS: Data came from the National Health and Nutrition Examination Survey 2017-2018. Choline intake was defined by the mean amounts of two 24 h dietary recalls, and choline intake was categorized into three groups according to the quartiles: inadequate (P75). Hepatic steatosis was assessed with FibroScan®, in which VCTE was employed with controlled attenuation to derive the controlled attenuation parameter (CAP), and NAFLD was defined as a CAP score ≥285 dB/m. Multivariable linear regression was performed to assess the linear relationship between choline intake and CAP. Multivariable logistics regression models were conducted to assess the association between choline intake status and NAFLD in the final sample and subgroup analysis was then performed in men and women. RESULTS: The amount of dietary choline was inversely associated with CAP score (ß = -0.262, 95% CI: -0.280, -0.245). Compared to inadequate choline intake, optimal choline intake was related to a lower risk of NAFLD (OR: 0.705, 95% CI: 0.704-0.706) in the final sample. Subgroup analysis by gender revealed that the highest choline intake status was associated with a lower risk of NAFLD both in females (OR: 0.764, 95% CI: 0.762-0.766), and males (OR: 0.955, 95% CI: 0.953-0.958) when compared to the lowest choline intake. CONCLUSIONS: With the latest NHANES data, we found that higher dietary choline was associated with a lower risk of NAFLD in American adults, and such a relationship exists in both females and males.