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Abstract Chemical weathering modulates carbon transfer between the crust, hydrosphere, and atmosphere. The extent to which microbial processes are involved in mineral dissolution remains elusive. Here, we performed geochemical and molecular analyses of river water and other materials collected from a rapidly exhuming catchment in eastern Taiwan. In addition to solute generation driven primarily by pyrite-induced carbonate weathering, highly skewed microbial community compositions with abundant Sulfuricurvum and Thiobacillus members were detected during high-water periods. The yields of these taxa were also correlated with those of sulfate and sediments, suggesting that pyrite oxidation and carbonate dissolution were facilitated by sulfur-respiring microorganisms inhabiting erodible materials at a pace comparable to the supply of sulfur-bearing minerals through rapid exhumation. The net CO2 export regulated by such potentially supply-limited, microbially-mediated mineral weathering greatly surpasses the global average, highlighting active orogens in high-standing islands as important CO2 contributors rendered by tandem biotic and abiotic processes.

The first outbreak of influenza A virus (IAV), which has been circulating for many decades, has resulted in serious morbidity and mortality. The IAV epidemic has caused serious damage to human life and the economy. Following an IAV infection, lymphatic cells immediately enter the lungs to clear the virus and eliminate damaged cells to maintain normal physiological mechanisms. In this study, we used alpha-lipoic acid (ALA), which has versatile antioxidant functions, as a target to treat and evaluate host antiviral effects and immune mechanisms. We observed that pre-treatment with ALA improved the survival rate and pathological state in a mouse model. A reduction in the inflammatory cytokine tumor necrosis factor-alpha was observed following in vivo experiments. It also increased the release of antiviral cytokines into the lungs by T lymphocytes. ALA pre-treatment effectively prevented acute pneumonia by modulating immune composition and contributing to virus clearance.

With the increasing prominence of environmental and energy issues, electric vehicles (EVs) as representatives of clean energy vehicles have experienced rapid development in recent years, and the charging load has also exhibited statistical characteristics. Accurate prediction of EV charging load is crucial to improve grid load dispatch and intelligent level. However, current research on EV charging load prediction still faces challenges such as data reliability, complexity and variability of charging behavior, uncertainty, and lack of standardization methods. Therefore, this paper proposes an electric vehicle charging load prediction method based on spectral clustering and deep learning network (SC-CNN-LSTM). Firstly, to address the insufficient amount of EV charging load data, this paper proposes to use Monte Carlo simulation to sample and simulate historical load data. Then, in order to identify the internal structure and patterns of charging load, the sampled and simulated dataset is clustered using spectral clustering, dividing the data into different clusters, where each cluster represents samples with similar charging load characteristics. Finally, based on the different sample features of each cluster, corresponding CNN-LSTM models are constructed and trained and predict using the respective data. By modifying the model parameters, the prediction accuracy of the model is improved. Through comparative experiments, the proposed method in this paper has significantly improved prediction accuracy compared to traditional prediction methods without clustering, thus validating the effectiveness and practicality of the method.

AbstractHedychium flavum Roxb. 1820 is a perennial herb mainly distributed in China, India, Myanmar and Thailand with ornamental, edible and medicinal value. It is extensively cultivated as a source of aromatic essential oils, ornamental plant, food flavorings and vegetables, and folk medicine. In this study, we sequence the complete chloroplast genome of H. flavum by de novo assembly. The assembled genome has a typical quadripartite circular structure with 163,909 bp in length, containing a large single-copy region (LSC, 88,589 bp), a small single-copy region (SSC, 15,762 bp), and two inverted repeat regions (IRs, 29,779 bp). The cp genome contains 133 genes, including 87 protein-coding genes, 38 tRNA genes and 8 rRNA genes. Phylogenetic analysis based on the complete cp genome shows a close affinity of H. flavum and H. neocarneum with 100% bootstrap support. This study will provide useful genetic resource for further phylogenetic analysis of the genus Hedychium and Zingiberaceae.

The change in the operating state of the compressor will cause the variety of working conditions in gas network, affecting the steady-state power flow of electric-gas-heat integrated energy system. In order to calculate the gas network power flow of the comprehensive energy system under different operation states, the sub-networks and energy coupling links of integrated energy system are modeled respectively. Considering five working modes and two driving modes of the compressors, based on Newton-Raphson method, an integrated power flow calculation method which reserves the pipelines of compressors is proposed and an equivalent solution method which separates the pipelines of compressors is developed for gas network with multiple compressors under different operation states. The power flow of integrated energy system is calculated by distributed algorithm. The accuracy and effectiveness of the proposed integrated power flow calculation method are verified through two examples, which remedies the disadvantages of existing power flow calculation models of gas network that cannot deal with complex working conditions in gas network and lack convergence and universality. Then the impacts of the change in compressor operation states on power flow of integrated energy system are revealed.

Triclosan (TCS), employed as an antiseptic and disinfectant, comes into direct contact with humans through a plethora of consumer products and its rising environmental release. We have demonstrated that TCS promotes liver tumorigenesis in mice, yet the biological and molecular mechanisms by which TCS exerts its toxicity, especially in early stages of liver disease, are largely unexplored. When mice were fed a high-fat diet (HFD), we found that fatty liver and dyslipidemia are prominent early signs of liver abnormality induced by TCS. The presumably protective HFD-induced hepatic expression of the metabolic regulator fibroblast growth factor 21 (FGF21) was blunted by TCS. TCS-altered Fgf21 expression aligned with aberrant expression of genes encoding metabolic enzymes manifested as profound systemic metabolic changes that disturb homeostasis of amino acids, fatty acids, and glucose. Using a type 1 diabetic animal model, TCS potentiates and accelerates the development of steatohepatitis and fibrosis, accompanied by increased levels of hepatic lipid droplets and oxidative stress. Analysis of fecal samples revealed that HFD-fed mice exhibited a reduction in fecal species richness, and that TCS further diminished microbial diversity and shifted the bacterial community toward lower Bacteriodetes and higher Firmicutes, resembling changes in microbiota composition in nonalcoholic steatohepatitis (NASH) patients. Using reverse-genetic approaches, we demonstrate that, along with HFD, TCS induces hepatic steatosis and steatohepatitis jointly regulated by the transcription factor ATF4 and the nuclear receptor PPARα, which participate in the transcriptional regulation of the Fgf21 gene. This study provides evidence linking nutritional imbalance and exposure to TCS with the progression of NASH.

The eastern margin of the Tibetan Plateau has given rise to much debate about mechanisms of plateau uplift and evolution and, in particular, the role of the lower crust in crustal thickening. Knowledge of the middle to lower crust conditions is critical for evaluating various models of crustal deformation, but data on crustal evolution through time are lacking. Here, we turn to the Gongga Shan granite, an intrusion along the Xianshuihe fault in easternmost Tibet that directly records local Cenozoic crustal conditions. We present 124 U-Pb samples from the Gongga Shan granite (GSG) that prove that the crust has been stepwise producing partial melt from 56 Ma to 4 Ma. According to the age distribution, the GSG can be separated into four major groups with ages of 4–10 Ma, 12–20 Ma, 25–40 Ma, and 43–56 Ma. Combining the timing information with geophysics and low-temperature thermochronology data, we suggest that events younger than 10 Ma may indicate the onset of recent crustal channel flow in the middle to lower crust. In contrast, the youngest 4 Ma ages indicate the ongoing partial melting of the middle crust. The 12–20 Ma events could be related to an earlier stage of crustal channel flow, consistent with the regional large-scale crustal channel flow in central Tibet.

Abstract Background Disordered lipid metabolism plays an essential role in both the initiation and progression of alcoholic fatty liver disease (AFLD), and fatty acid β-oxidation is increasingly considered as a crucial factor for controlling lipid metabolism. Hif-2α is a member of the Hif family of nuclear receptors, which take part in regulating hepatic fatty acid β-oxidation. However, its functional role in AFLD and the underlying mechanisms remain unclear. Results Hif-2α was upregulated in EtOH-fed mice and EtOH-treated AML-12 cells. Inhibition or silencing of Hif-2α led to increased fatty acid β-oxidation and BNIP3-dependent mitophagy. Downregulation of Hif-2α activates the PPAR-α/PGC-1α signaling pathway, which is involved in hepatic fatty acid β-oxidation, by mediating BNIP3-dependent mitophagy, ultimately delaying the progression of AFLD. Conclusions Hif-2α induces liver steatosis, which promotes the progression of AFLD. Here, we have described a novel Hif-2α-BNIP3-dependent mitophagy regulatory pathway interconnected with EtOH-induced lipid accumulation, which could be a potential therapeutic target for the prevention and treatment of AFLD.

Fault location is of great significance for fault handling and power restoration of distribution network. In the fault location method for active distribution network,the calculation speed of matrix algorithm is high,but this method has a poor fault tolerance. The fault tolerance of intelligent optimization algorithm is strong,but this method has local convergence problems in large-scale distribution network,and it has a low speed. To solve the problems above,a comprehensive approach for the fault location in distribution network which combines the advantages of both methods is proposed. Firstly,the matrix algorithm is used to locate the fault section rapidly after fault occurs in active distribution network,which uses the alarm information uploaded by the feeder terminal unit (FTU). Then,in order to avoid outputting wrong positioning results caused by poor fault tolerance of matrix algorithm,the positioning results of matrix algorithm is verified by switching function. The location results that fail the verification is included in the suspicious fault set whose dimension is much lower than that of the distribution network. To output the final positioning results,the grey wolf optimization (GWO) algorithm is used to optimize the set above. Finally,the simulation tested by Matlab shows that the proposed method can achieve fault location rapidly with strong fault tolerance in active distribution network.

Abstract The evolution of the Taiwan orogen, an active arc–continent collision zone between the North Luzon Arc (NLA) and the Eurasian continent, is recorded in arc volcanic and sedimentary rocks from the Taiyuan retro‐foredeep basin of the Coastal Range, eastern Taiwan. Arc volcanism in the northern NLA experienced a magmatic culmination at 9–7 Ma and a cessation at 5.3–4.3 Ma, based on new U‐Pb zircon ages. Young zircon U‐Pb ages (1.74, 1.58, and

To address the fault identification challenge in distribution networks, a method leveraging a mixture of the von Mises-Fisher (mov-MF) distribution model for fault probability identification is proposed. Initially, the synchronous phasor measuring unit is employed to gather the post-fault steady-state voltage phase quantities, and then, the voltage phase angle values are combined to form a three-dimensional feature quantity. Subsequently, the mov-MF distribution model is initialized through the spherical K-means algorithm and the minimum message length algorithm. This model is further refined via the expectation-maximization algorithm to iteratively optimize distribution parameters. The test set data are input into the mov-MF distribution model, which has been constructed using typical fault data, to discern fault types. Finally, the efficacy of the proposed method is validated through simulation verification conducted on the IEEE 33-node distribution system. The analysis of the examples demonstrates the accuracy of the mov-MF distribution model-based fault identification method in identifying single-phase ground, two-phase ground, two-phase interphase, and three-phase short-circuit faults. [ABSTRACT FROM AUTHOR]

Photovoltaic (PV) power fluctuates with weather changes, and traditional forecasting methods typically decompose the power itself to study its characteristics, ignoring the impact of multidimensional weather conditions on the power decomposition. Therefore, this paper proposes a short-term PV power generation method based on MVMD (multivariate variational mode decomposition) feature extraction and the Informer model. First, MIC correlation analysis is used to extract weather features most related to PV power. Next, to more comprehensively describe the relationship between PV power and environmental conditions, MVMD is used for time–frequency synchronous analysis of the PV power time series combined with the highest MIC correlation weather data, obtaining frequency-aligned multivariate intrinsic modes. These modes incorporate multidimensional weather factors into the data-decomposition-based forecasting method. Finally, to enhance the model's learning capability, the Informer neural network model is employed in the prediction phase. Based on the input PV IMF time series and associated weather mode components, the Informer prediction model is constructed for training and forecasting. The predicted results of different PV IMF modes are then superimposed to obtain the total PV power generation. Experiments show that this method improves PV power generation accuracy, with an MAPE value of 4.31%, demonstrating good robustness. In terms of computational efficiency, the Informer model's ability to handle long sequences with sparse attention mechanisms reduces training and prediction times by approximately 15%, making it faster than conventional deep learning models. [ABSTRACT FROM AUTHOR]

The gastrointestinal tract is enriched with xenobiotic processing proteins that play important roles in xenobiotic bioactivation, metabolism, and detoxification. The application of genetically modified mouse models has been instrumental in characterizing the function of xenobiotic processing genes (XPG) and their proteins in drug metabolism. Here, we report the utilization of three-dimensional crypt organoid cultures from these animal models to study intestinal drug metabolism and toxicity. With the successful culturing of crypt organoids, we profiled the abundance of Phase I and Phase II XPG expression, drug transporter gene expression, and xenobiotic nuclear receptor (XNR) gene expression. Functions of XNRs were examined by treating crypt cells with XNR prototypical agonists. Real-time quantitative polymerase chain reaction demonstrated that the representative downstream target genes were induced. These findings were validated from cultures developed from XNR-null mice. In crypt cultures isolated from Pxr-/- mice, pregnenolone 16α-carbonitrile failed to induce Cyp3a11 gene expression; similarly, WY14643 failed to induce Cyp4a10 in the Pparα-/- crypts. Crypt cultures from control (Ugt1F/F ) and intestinal epithelial cell (IEC) specific Ugt1 null mice (Ugt1ΔIEC ) were treated with camptothecin-11, an anticancer prodrug with severe intestinal toxicity that originates from insufficient UGT1A1-dependent glucuronidation of its active metabolite SN-38. In the absence of Ugt1 gene expression, Ugt1ΔIEC crypt cultures exhibit very limited production of SN-38 glucuronide, concordant with increased apoptosis in comparison with Ugt1F/F crypt cultures. This study suggests crypt organoid cultures as an effective in vitro model for studying intestinal drug metabolism and toxicity.

Hyperbilirubinemia, caused by the accumulation of unconjugated bilirubin, is one of the most common clinical diagnoses in both premature and term newborns. Owing to the fact that bilirubin is metabolized solely through glucuronidation by UDP-glucuronosyltransferase (UGT) 1A1, it is now known that immaturity of UGT1A1, in combination with the overproduction of bilirubin during the developmental stage, acts as a bottleneck to bilirubin elimination and predisposes the infant to high total serum bilirubin levels. Although neonatal jaundice is mostly benign, excessively high levels of serum bilirubin in a small percentage of newborns can cause bilirubin-induced neurologic dysfunction, potentially leading to permanent brain damage, a condition known as kernicterus Although a large portion of hyperbilirubinemia cases in newborns are associated with hemolytic diseases, we emphasize here the impaired ability of UGT1A1 to eliminate bilirubin that contributes to hyperbilirubinemia-induced neurotoxicity in the developmental stage. As a series of hereditary UGT1A1 mutations have been identified that are associated with UGT1A1 deficiency, new evidence has verified that delayed expression of UGT1A1 during the early stages of neonatal development is a tightly controlled event involving coordinated intrahepatic and extrahepatic regulation. This review recapitulates the progress that has been made in recent years in understanding the causes and physiopathology of severe hyperbilirubinemia, investigating molecular mechanisms underlying bilirubin-induced encephalopathy, and searching for potential therapies for treating pathologic hyperbilirubinemia. Several animal models have been developed to make it possible to examine bilirubin-induced neurotoxicity from multiple directions. Moreover, environmental factors that may alleviate or worsen the condition of hyperbilirubinemia are discussed.

Severe neonatal hyperbilirubinemia (SNH) and the onset of bilirubin encephalopathy and kernicterus result in part from delayed expression of UDP-glucuronosyltransferase 1A1 (UGT1A1) and the inability to metabolize bilirubin. Although there is a good understanding of the early events after birth that lead to the rapid increase in serum bilirubin, the events that control delayed expression of UGT1A1 during development remain a mystery. Humanized UGT1 (hUGT1) mice develop SNH spontaneously, which is linked to repression of both liver and intestinal UGT1A1. In this study, we report that deletion of intestinal nuclear receptor corepressor 1 (NCoR1) completely diminishes hyperbilirubinemia in hUGT1 neonates because of intestinal UGT1A1 gene derepression. Transcriptomic studies and immunohistochemistry analysis demonstrate that NCoR1 plays a major role in repressing developmental maturation of the intestines. Derepression is marked by accelerated metabolic and oxidative phosphorylation, drug metabolism, fatty acid metabolism, and intestinal maturation, events that are controlled predominantly by H3K27 acetylation. The control of NCoR1 function and derepression is linked to IKKβ function, as validated in hUGT1 mice with targeted deletion of intestinal IKKβ. Physiological events during neonatal development that target activation of an IKKβ/NCoR1 loop in intestinal epithelial cells lead to derepression of genes involved in intestinal maturation and bilirubin detoxification. These findings provide a mechanism of NCoR1 in intestinal homeostasis during development and provide a key link to those events that control developmental repression of UGT1A1 and hyperbilirubinemia.

Humanized UDP-glucuronosyltransferase (UGT)-1 (hUGT1) mice encode the UGT1 locus including the UGT1A1 gene. During neonatal development, delayed expression of the UGT1A1 gene leads to hyperbilirubinemia as determined by elevated levels of total serum bilirubin (TSB). We show in this report that the redox-sensitive NF-κB pathway is crucial for intestinal expression of the UGT1A1 gene and control of TSB levels. Targeted deletion of IKKβ in intestinal epithelial cells (hUGT1/Ikkβ(ΔIEC) mice) leads to greater neonatal accumulation of TSB than observed in control hUGT1/Ikkβ(F/F) mice. The elevation in TSB levels in hUGT1/Ikkβ(ΔIEC) mice correlates with a reduction in intestinal UGT1A1 expression. As TSB levels accumulate in hUGT1/Ikkβ(ΔIEC) mice during the neonatal period, the increase over that observed in hUGT1/Ikkβ(F/F) mice leads to weight loss, seizures and eventually death. Bilirubin accumulates in brain tissue from hUGT1/Ikkβ(ΔIEC) mice inducing an inflammatory state as shown by elevated TNFα, IL-1β and IL-6, all of which can be prevented by neonatal induction of hepatic or intestinal UGT1A1 and lowering of TSB levels. Altering the redox state of the intestines by oral administration of cadmium or arsenic to neonatal hUGT1/Ikkβ(F/F) and hUGT1/Ikkβ(ΔIEC) mice leads to induction of UGT1A1 and a dramatic reduction in TSB levels. Microarray analysis following arsenic treatment confirms upregulation of oxidation-reduction processes and lipid metabolism, indicative of membrane repair or synthesis. Our findings indicate that the redox state in intestinal epithelial cells during development is important in maintaining UGT1A1 gene expression and control of TSB levels.

Triclosan (TCS) is a broad-spectrum antimicrobial agent that has been added to personal care products, including hand soaps and cosmetics, and impregnated in numerous different materials ranging from athletic clothing to food packaging. The constant disposal of TCS into the sewage system is creating a major environmental and public health hazard. Owing to its chemical properties of bioaccumulation and resistance to degradation, TCS is widely detected in various environmental compartments in concentrations ranging from nanograms to micrograms per liter. Epidemiology studies indicate that significant levels of TCS are detected in body fluids in all human age groups. We document here the emerging evidence--from in vitro and in vivo animal studies and environmental toxicology studies--demonstrating that TCS exerts adverse effects on different biological systems through various modes of action. Considering the fact that humans are simultaneously exposed to TCS and many TCS-like chemicals, we speculate that TCS-induced adverse effects may be relevant to human health.

Background & aimsThe UDP-glucuronosyltransferases (UGTs) are part of the cells machinery that protects the tissues from a toxicant insult by environmental and host cell metabolites. We have investigated the mechanism behind tumor growth and UGT repression.MethodsWe initially silenced the Ugt1 locus in human colon cell lines and investigated markers and responses linked to p53 activation. To examine the role of the Ugt1 locus in p53-directed apoptosis and tumorigenesis, experiments were conducted to induce acute colon inflammation and chemical induced colon cancer in mice where we have selectively deleted the Ugt1 locus in the intestinal epithelial cells (Ugt1ΔIEC mice).ResultsKnockdown of the UGT1A proteins by RNAi in human colon cancer cells and knockout of the Ugt1 locus in intestinal crypt stem cells reduces phosphorylated p53 activation and compromises the ability of p53 to control apoptosis. Targeted deletion of intestinal Ugt1 expression in Ugt1ΔIEC mice represses colon inflammation-induced p53 production and pro-apoptotic protein activation. When we induced colon cancer, the size and number of the tumors were significantly greater in the Ugt1ΔIEC mice when compared to wild type mice. Furthermore, analysis of endoplasmic reticulum (ER) stress-related markers indicated that lack of UGT1A expression causes higher ER stress in intestinal epithelial cells and tissue, which may account for the lower expression of p53.ConclusionsOur results demonstrate that UGT1A expression is required to maintain and sustain p53 activation in stress-induced colon epithelial cells and has a significant impact on p53-mediated apoptosis and tumor suppression, thus protecting the colon tissue from neoplastic transformation.

The quality of fresh products through cross-regional sales has been uncertain to consumers. To improve the quality of fresh products, some fresh product supply chains have implemented blockchain technology to provide traceable information for their products, and some regional governments have subsidized their local firms to incentivize them to implement blockchain-driven traceability systems. However, with regional government subsidy heterogeneity, cross-regional fresh product supply chain firms lack theoretical guidance on their operation decisions. Based on the research gap, we investigate optimal operation policies in a fresh product supply chain consisting of a manufacturer and a retailer located in different regions. The local governments may subsidize the manufacturer or the retailer located in their own regions, which construct four subsidy strategies (SS, SN, NS, and NN) along the supply chain. We find that the optimal operation policies under four subsidy strategies can be affected by the sensitivity to traceability level, cost-sharing rate of the manufacturer, rate of products left after corrosion, and subsidy rate to the manufacturer. Moreover, the government subsidy to the retailer is always beneficial to the retailer and the supply chain but does not affect the manufacturer’s operation policies and profits. The government subsidy to the manufacturer is always beneficial to the manufacturer but not always beneficial to the retailer and the supply chain. Hence the desired subsidy strategy for the manufacturer is SS and SN, and the one for the retailer and the supply chain is either NS or SS with different conditions.

Triclosan [5-chloro-2-(2,4-dichlorophenoxy)phenol; TCS] is a synthetic, broad-spectrum antibacterial chemical used in a wide range of consumer products including soaps, cosmetics, therapeutics, and plastics. The general population is exposed to TCS because of its prevalence in a variety of daily care products as well as through waterborne contamination. TCS is linked to a multitude of health and environmental effects, ranging from endocrine disruption and impaired muscle contraction to effects on aquatic ecosystems. We discovered that TCS was capable of stimulating liver cell proliferation and fibrotic responses, accompanied by signs of oxidative stress. Through a reporter screening assay with an array of nuclear xenobiotic receptors (XenoRs), we found that TCS activates the nuclear receptor constitutive androstane receptor (CAR) and, contrary to previous reports, has no significant effect on mouse peroxisome proliferation activating receptor α (PPARα). Using the procarcinogen diethylnitrosamine (DEN) to initiate tumorigenesis in mice, we discovered that TCS substantially accelerates hepatocellular carcinoma (HCC) development, acting as a liver tumor promoter. TCS-treated mice exhibited a large increase in tumor multiplicity, size, and incidence compared with control mice. TCS-mediated liver regeneration and fibrosis preceded HCC development and may constitute the primary tumor-promoting mechanism through which TCS acts. These findings strongly suggest there are adverse health effects in mice with long-term TCS exposure, especially on enhancing liver fibrogenesis and tumorigenesis, and the relevance of TCS liver toxicity to humans should be evaluated.