Association between serum magnesium levels and risk of acute kidney injury in patients with traumatic brain injury: A retrospective cohort study from the MIMIC-â £ database.

INTRODUCTION: The occurrence of acute kidney injury (AKI) is associated with a higher risk of mortality in patients with traumatic brain injury (TBI). This study aimed to explore the relationship between serum magnesium levels and the risk of AKI in patients with TBI. METHODS: Patients with TBI were identified from the Medical Information Mart Intensive Care Ⅳ (MIMIC-Ⅳ) 2008-2019. The relationship between serum magnesium levels at admission and magnesium coefficient of variation (CV) during hospitalization and the risk of AKI was analyzed using multivariable logistic regression analysis and expressed as odds ratio (OR) and 95% confidence interval (CI). Subgroup analyses were performed according to Glasgow Coma Scale (GCS) score (<14, ≥14), sepsis (no, yes), and estimated glomerular filtration rate (eGFR; <60, ≥60). RESULTS: Of the 991 patients included, 140 (14.13%) developed AKI during hospitalization. Patients with magnesium levels ≤1.7 mg/dL (tertile 1) (OR=1.68, 95%CI: 1.01-2.81) were associated with a higher risk of AKI compared to those with magnesium levels of 1.7-2.0 mg/dL (tertile 2), but no association was found in those with magnesium levels >2.0 mg/dL (tertile 3) (P=0.479). For magnesium CV, patients with magnesium CV >10% (tertile 3) (OR=2.26, 95%CI: 1.16-4.41) were linked to an increased risk of AKI compared to those with magnesium CV ≤4% (tertile 1), but there may be a slight association between magnesium CV of 4%-10% (tertile 2) and AKI risk (OR=1.86, 95%CI: 0.99-3.48; P=0.053). Subgroup analyses showed that lower magnesium levels (≤1.7 mg/dL) or greater magnesium CV (>10%) were associated with a higher risk of AKI only in patients with a GCS score ≥14, non-sepsis, or eGFR ≥60 mL/min/per1.73m2 (P<0.05). CONCLUSION: Lower serum magnesium levels at admission or greater magnesium CV during hospitalization were associated with a higher risk of AKI in patients with TBI.

PM2.5-induced ferroptosis by Nrf2/Hmox1 signaling pathway led to inflammation in microglia.

Particulate matter (PM) has been a dominant contributor to air contamination, which will enter the central nervous system (CNS), causing neurotoxicity. However, the biological mechanism is poorly identified. In this study, C57BL/6J mice were applied to evaluate the neurotoxicity of collected fine particulate matter (PM2.5), via oropharyngeal aspiration at two ambient equivalent concentrations. The Y-maze results showed that PM2.5 exposure in mice would lead to the damage in hippocampal-dependent working memory. In addition, cell neuroinflammation, microglial activation were detected in hippocampus of PM2.5-exposure mice. To confirm the underlying mechanism, the microarray assay was conducted to screen the differentially expressed genes (DEGs) in microglia after PM2.5 exposure, and the results indicated the enrichment of DEGs in ferroptosis pathways. Furthermore, Heme oxygenase-1 (Hmox1) was found to be one of the most remarkably upregulated genes after PM2.5 exposure for 24 h. And PM2.5 exposure induced ferroptosis with iron accumulation through heme degradation by Nrf2-mediated Hmox1 upregulation, which could be eliminated by Nrf2-inhibition. Meanwhile, Hmox1 antagonist zinc protoporphyrin IX (ZnPP) could protect BV2 cells from ferroptosis. The results taken together indicated that PM2.5 resulted in the ferroptosis by causing iron overload through Nrf2/Hmox1 signaling pathway, which could account for the inflammation in microglia.

[Correlation between intestinal toxicity and composition changes of toxic parts from Euphorbia ebracteolata before and after Terminalia chebula soup processing].

This study aims to explore the correlation between intestinal toxicity and composition changes of Euphorbia ebracteolata before and after Terminalia chebula soup(TCS) processing. Intragastric administration was performed on the whole animal model. By using fecal water content, inflammatory causes, and pathological damage of different parts of the intestinal tract of mice as indexes, the differences in intestinal toxicity of dichloromethane extraction of raw E. ebracteolata(REDE), dichloromethane extraction of TCS, and dichloromethane extraction of E. ebracteolata after simulated TCS processing(STREDE) were compared, so as to investigate the effect of TCS processing on the intestinal toxicity of E. ebracteolata. At the same time, the component databases of E. ebracteolata and T. chebula were constructed, and the composition changes of diterpenoids, tannins, and phenolic acids in the three extracted parts were analyzed by HPLC-TOF-MS. HPLC was used to compare the content of four diterpenoids including ent-11α-hydroxyabicta-8(14), 13(15)-dien-16, 12-olide(HAO), jolkinolide B(JNB), fischeria A(FA), and jolkinolide E(JNE) in the E. ebracteolata before and after processing and the residue of container wall after processing, so as to investigate the effect of TCS processing on the content and structure of the diterpenoids. The results showed that the REDE group could significantly increase the fecal water content and the release levels of TNF-α and IL-1ß from each intestinal segment, and intestinal tissue damage was accompanied by significant infiltration of inflammatory cells. However, compared with the REDE group, the intestinal tissue damage in the STREDE group was alleviated, and the infiltration of inflammatory cells decreased. The intestinal toxicity significantly decreased. Mass spectrometry analysis showed that there was no significant difference in the content of diterpenoids of REDE before and after simulated TCS processing, but a large number of tannins and phenolic acids were added. The results of HPLC showed that the content of four diterpenoids of E. ebracteo-lata decreased to varying degrees after TCS processing, ranging from-0.35% to-19.74%, and the decreased part mainly remained in the container wall, indicating that the structure of toxic diterpenoids of E. ebracteolata was not changed after TCS processing. The antagonistic effect of tannic and phenolic acids in the TCS may be the main reason for the reduced intestinal toxicity of E. ebracteolata after TCS processing. The TCS processing for E. ebracteolata is scientific.

Associations of perfluoroalkyl substances with metabolic-associated fatty liver disease and non-alcoholic fatty liver disease: NHANES 2017-2018.

OBJECTIVES: This study investigated the potential effects of perfluoroalkyl substance (PFAS) in serum on MAFLD, NAFLD, and liver fibrosis. METHODS: Our sample included 696 participants (≥ 18 years) from the 2017-2018 NHANES study with available serum PFASs, covariates, and outcomes. Using the first quartile of PFAS as the reference group, we used weighted binary logistic regression and multiple ordered logistic regression used to analyze the relationship between PFAS and MAFLD, NAFLD, and liver fibrosis and multiple ordinal logistic regression to investigate the relationship between PFAS and MAFLD, NAFLD, and liver fibrosis and calculated the odds ratio (OR) and 95% confidence interval for each chemical. Finally, stratified analysis and sensitivity analysis were performed according to gender, age, BMI, and serum cotinine concentration. RESULTS: A total of 696 study subjects were included, including 212 NAFLD patients (weighted 27.03%) and 253 MAFLD patients (weighted 32.65%). The quartile 2 of serum PFOA was positively correlated with MAFLD and NAFLD (MAFLD, OR 2.29, 95% CI 1.05-4.98; NAFLD, OR 2.37, 95% CI 1.03-5.47). PFAS were not significantly associated with liver fibrosis after adjusting for potential confounders in MAFLD and NAFLD. Stratified analysis showed that PFOA was strongly associated with MAFLD, NAFLD, and liver fibrosis in males and obese subjects. In women over 60 years old, PFHxS was also correlated with MAFLD, NAFLD, and liver fibrosis. CONCLUSION: The serum PFOA was positively associated with MAFLD and NAFLD in US adults. After stratified analysis, the serum PFHxS was correlated with MFALD, NAFLD, and liver fibrosis.

Evaluating public opinions: informing public health policy adaptations in China amid the COVID-19 pandemic.

Public concern regarding safety policies serious consequences is anticipated to persist over an extended duration. A study examining a case of rapid public health policy adaptation in China during the COVID-19 epidemic was conducted by gathering public opinion data from major social media platforms. A systematic approach to comprehend public opinion was developed. Five fundamental elements and four dimensions were delineated. An indicator system was established utilizing the K-means text clustering model. Public prediction, expectation, and their evolution underlying public concern were elucidated employing TF-IDF text mining models. The HMM elucidated the way public opinion influences policy adjustments. The findings underscore that public concern regarding enduring events undergoes temporal shifts, mirroring the evolution of public opinion towards policy. Public opinion aroused by both the original event and derived events collaboratively influence policy adjustments. In China, public opinion serves as a mechanism for policy feedback and oversight; notably, negative public sentiment plays a pivotal role in expediting policy transitions. These findings aid in refining policies to mitigate emergencies through a feedback loop, thereby averting the emergence of safety risks such as social unrest prompted by public opinion.

Response mechanism of a highly efficient partial nitritation-anammox (PN/A) process under antibiotic stress: Extracellular polymers, microbial community, and functional genes.

The Partial nitritation-Anammox (PN/A) process can be restricted when treating high ammonia nitrogen wastewater containing antibiotics. This study aims to explore the response mechanism of the PN/A process under antibiotic stress. Results showed the PN/A process achieved a nitrogen removal rate higher than 1.01 ± 0.03 kg N/m3/d under long-term sulfamethazine stress. The increase of extracellular polymers from 22.52 to 43.96 mg/g VSS was conducive to resisting antibiotic inhibitory. The increase of Denitratisoma and SM1A02 abundance as well as functional genes nirS and nirK indicated denitrifiers should play an important role in the stability of the PN/A system under sulfamethazine stress. In addition, antibiotic-resistant genes (ARGs) sul1 and intI1 significantly increased by 8.78 and 5.12 times of the initial values to maintain the resistance of PN/A process to sulfamethazine stress. This study uncovers the response mechanism of the PN/A process under antibiotic stress, offering a scientific basis and guidance for further application in the future.

Utilizing systematic Mendelian randomization to identify potential therapeutic targets for mania.

Background: Mania has caused incalculable economic losses for patients, their families, and even society, but there is currently no effective treatment plan for this disease without side effects. Methods: Using bioinformatics and Mendelian randomization methods, potential drug target genes and key substances associated with mania were explored at the mRNA level. We used the chip expression profile from the GEO database to screen differential genes and used the eQTL and mania GWAS data from the IEU database for two-sample Mendelian randomization (MR) to determine core genes by colocalization. Next, we utilized bioinformatics analysis to identify key substances involved in the mechanism of action and determined related gene targets as drug targets. Results: After differential expression analysis and MR, a causal relationship between the expression of 46 genes and mania was found. Colocalization analysis yielded six core genes. Five key substances were identified via enrichment analysis, immune-related analysis, and single-gene GSVA analysis of the core genes. MR revealed phenylalanine to be the only key substance that has a unidirectional causal relationship with mania. In the end, SBNO2, PBX2, RAMP3, and QPCT, which are significantly associated with the phenylalanine metabolism pathway, were identified as drug target genes. Conclusion: SBNO2, PBX2, RAMP3, and QPCT could serve as potential target genes for mania treatment and deserve further basic and clinical research. Medicinal target genes regulate the phenylalanine metabolism pathway to achieve the treatment of mania. Phenylalanine is an important intermediate substance in the treatment of mania that is regulated by drug target genes.

Dietary calcium is inversely associated with hepatitis B virus infection: an analysis of US National Health and Nutrition Examination Survey (NHANES) 2007-2020.

BACKGROUND: There have been studies on the relationship between hepatitis B virus (HBV) infection and diet. We hypothesized HBV infection is related to dietary calcium intake, but the evidence is limited. This study aimed to examine whether dietary calcium intake is independently related to HBV infection in the United States population. METHODS: A total of 20,488 participants aged over 20 years from the National Health and Nutrition Examination Survey (NHANES), conducted from 2007 to 2020, were included in this study. Pearson correlation was used to test the association between dietary calcium and serum calcium. The relationships of HBV infection with dietary calcium and serum calcium were assessed by logistic regression models. RESULTS: There was a weak correlation between dietary calcium and serum calcium (r = 0.048). Logistic regression models indicated that HBV infection had a linear negative correlation with dietary calcium (OR 0.37; 95%CI 0.19, 0.76). For each additional 10 mg dietary calcium, the possibility of HBV infection was reduced by 63%. Hepatitis B positive participants had lower serum calcium content than negative participants. Stratified analysis shown the linear relationship between calcium and HBV infection varied among sex, race/ethnicity, and body mass index. CONCLUSION: Our findings demonstrated HBV infection was linearly and inversely correlated with dietary calcium. The current study is expected to offer a fresh perspective on reducing HBV infection.

Modulating Electronic Structure of Iridium Single-Atom Anchored on 3D Fe-Doped ß-Ni(OH)2 Catalyst with Nanopyramid Array Structure for Enhanced Oxygen Evolution Reaction.

Developing high-performance electrocatalysts for oxygen evolution reaction (OER) is crucial in the pursuit of clean and sustainable hydrogen energy, yet still challenging. Herein, a spontaneous redox strategy is reported to achieve iridium single-atoms anchored on hierarchical nanosheet-based porous Fe doped ß-Ni(OH)2 pyramid array electrodes (SAs Ir/Fe-ß-Ni(OH)2 ), which exhibits high OER performance with a low overpotential of 175 mV at 10 mA cm-2 and a remarkable OER current density in alkaline electrolyte, surpassing Fe-ß-Ni(OH)2 /NF and IrO2 by 31 and 38 times at 1.43 V versus RHE, respectively. OER catalytic mechanism demonstrates that the conversion of * OH→* O and the active lattice O content can be significantly improved due to the modulation effect of the Ir single atoms on the local electronic structure and the redox behavior of FeNi (oxy) hydroxide true active species. This work provides a promising insight into understanding the OER enhancement mechanism for Ir single-atoms modified FeNi-hydroxide systems.

Chemical profile and difference analysis of four parts of Strobilanthes sarcorrhiza by ultrafast flow liquid chromatography coupled with quadrupole-time-of-flight mass spectrometry and multivariate statistical analysis.

Strobilanthes sarcorrhiza (CTS) is a medicinal plant with various pharmacological effects such as tonifying kidney and anti-inflammatory. However, the chemical composition and difference of its four parts (leaves, stems, rhizomes, and root tubers) have been rarely reported. In this study, ultrafast flow liquid chromatography coupled with quadrupole-time-of-flight MS was applied to analyze the chemical profile of CTS and identify 55 compounds, including terpenoids, phenylethanol glycosides, fatty acid derivatives, chain glycosides, flavonoid glycosides, and others. Among these compounds, 34 compounds were first identified in CTS. They were mainly terpenoids, phenylethanol glycosides, fatty acid derivatives, and so forth. Multivariate statistical analysis, such as principal component analysis and orthogonal partial least squares-discriminant analysis were also used to evaluate the difference in chemical compounds from the four parts of CTS. The results showed that phenylethanol glycosides were the main compounds of the underground parts, while terpenoids were the main compounds of the aboveground parts. This study revealed the chemical diversity and similarity of CTS and suggested that the rhizomes could be used as an alternative medicinal part to improve the resource utilization of CTS.

Identification and validation of cortisol-related hub biomarkers and the related pathogenesis of biomarkers in Ischemic Stroke.

BACKGROUND: Ischemic stroke is a disease in which cerebral blood flow is blocked due to various reasons, leading to ischemia, hypoxia, softening, and even necrosis of brain tissues. The level of cortisol is related to the occurrence and progression of ischemic stroke. However, the mechanism governing their interrelationship is still unclear. The main objective of this study was to identify and understand the molecular mechanism between cortisol and IS. METHODS: The common cortisol-related biological processes were screened by mutual verification of two data sets and the cortisol-related hub biomarkers were identified. Modular analysis of protein interaction networks was performed, and the differential pathway analysis of individual genes was conducted by GSVA and GSEA. Drug and transcription factor regulatory networks of hub genes were excavated, and the diagnostic potential of hub genes was analyzed followed by the construction of a diagnostic model. RESULTS: By screening the two data sets by GSVA, three biological processes with common differences were obtained. After variation analysis, four cortisol-related hub biomarkers (CYP1B1, CDKN2B, MEN1, and USP8) were selected. Through the modular analysis of the protein-protein interaction network and double verification of GSVA and GSEA, a series of potential molecular mechanisms of hub genes were discovered followed by a series of drug regulatory networks and transcription factor regulatory networks. The hub biomarkers were found to have a high diagnostic value by ROC; thus, a diagnostic model with high diagnostic efficiency was constructed. The diagnostic value was mutually confirmed in the two data sets. CONCLUSION: Four cortisol-related hub biomarkers are identified in this study, which provides new ideas for the key changes of cortisol during the occurrence of IS.

Functional identification of long non-coding RNAs induced by PM2.5 in microglia through microarray analysis.

As a dominating air pollutant, atmospheric fine particulate matter within 2.5 µm in diameter (PM2.5) has attracted increasing attention from the researchers all over the world, which will lead to various adverse effects on the central nervous system (CNS), yet the potential mechanism is unclear. In this study, the microglia (BV2 cell line) were exposed to different concentrations of PM2.5 (5, 10 and 20 µg/cm2) for 24 h. It was found that PM2.5 could result in adverse effects on microglia such as decreased cell viability, structural damage and even cell death. And it was reported that long non-coding RNAs (lncRNAs) could participate in multitudinous neurological diseases. Therefore, the microarray analysis was conducted in order to disclose the underlying neurotoxicity mechanism of PM2.5 by ascertaining the differentially expressed lncRNAs (DElncRNAs). The consequences indicated that the DElncRNAs were enriched in various biological pathways, including ferroptosis, IL-17 signaling pathway and NOD-like receptor signaling pathway. Moreover, the cis- and trans-regulated mRNAs by DElncRNAs as well as the corresponding transcriptional factors (TFs) were observed, such as CEBPA, MYC, MEIS1 and KLF4. In summary, our study supplies some candidate libraries and potential preventive target against PM2.5-induced toxicity through targeting lncRNAs. Furthermore, the post-transcriptional regulation will contribute to the future research on PM2.5-induced neurotoxicity.

White matter microstructural alterations in patients with anti-N-methyl-D-aspartate receptor encephalitis: A tract-based spatial statistics study.

BACKGROUND: Cognitive impairment is common in patients with anti-N-methyl-D-aspartate receptor (anti-NMDAR) encephalitis; however, neural mechanisms underlying this impairment remain unclear. Diffusion tensor imaging (DTI) is a potential method for studying the condition of white matter fibers in patients with anti-NMDAR encephalitis, allowing for an analysis of the neuroimaging mechanisms of cognitive impairment in conjunction with cognitive scales. This study aimed to explore white matter microstructural alterations and their correlation with cognitive function in patients with anti-NMDAR encephalitis. METHODS: DTI data were collected from 22 patients with anti-NMDAR encephalitis (aged 29.00(19.75, 39.50) years; 12 males, 10 females) and 20 healthy controls (HCs) (aged 24.50(21.25, 32.00); 12 males, 8 females) matched for age, sex, and educational level. Changes in the white matter microstructure were analyzed using tract-based spatial statistics. Pearson correlation analysis was used to explore the correlation between white matter integrity and neuropsychological scores. RESULTS: Compared with HCs, patients with anti-NMDAR encephalitis showed decreased fractional anisotropy and increased mean diffusivity values in extensive white matter regions, which were associated with disease severity, memory, and executive and visuospatial functions. CONCLUSION: Widespread impairment of the structural integrity of the white matter in the brain is significantly associated with cognitive dysfunction in patients with anti-NMDAR encephalitis, providing neuroimaging evidence for studying the underlying mechanisms.

High-contrast NIR fluorescent probes for selective detection of NQO1 in breast cancer.

NAD(P)H:quinone oxidoreductase 1 (NQO1) is a potential biomarker for breast cancer (BC) diagnosis and prognosis. However, existing fluorescent probes for NQO1 detection have limitations such as short emission wavelength, weak fluorescence response, or large background interference. Here, we developed two novel near-infrared (NIR) fluorescent probes, DCl-Q and DCl2-Q, that selectively detect NQO1 activity in BC cells and tissues. They consist of a trimethyl-locked quinone as the recognition group and a donor-π-acceptor structure with halogen atoms as the reporter group. They exhibit strong fluorescence emission at around 660 nm upon binding to NQO1. We demonstrated that they can distinguish BC cells with different NQO1 expression levels and image endogenous NQO1 in tumor-bearing mice. Our probes provide a convenient and highly sensitive tool for BC diagnosis and prognosis based on NQO1 detection.

Indirubin mediates adverse intestinal reactions in guinea pigs by downregulating the expression of AchE through AhR.

Indirubin is the main component of the traditional Chinese medicine Indigo naturalis (IN), a potent agonist of aryl hydrocarbon receptors (AhRs). In China, IN is used to treat psoriasis and ulcerative colitis, and indirubin is used for the treatment of chronic myelogenous leukaemia. However, IN and indirubin have adverse reactions, such as abdominal pain, diarrhoea, and intussusception, and their specific mechanism is unclear.The purpose of our research was to determine the specific mechanism underlying the adverse effects of IN and indirubin. By tracking the modifications in guinea pigs after the intragastric administration of indirubin for 28 days.The results demonstrate that indirubin could accelerate bowel movements and decrease intestinal acetylcholinesterase (AchE) expression. Experiments with NCM460 cells revealed that indirubin significantly reduced the expression of AchE, and the AchE levels were increased after the silencing of AhR and re-exposure to indirubin.This study showed that the inhibition of AchE expression by indirubin plays a key role in the occurrence of adverse reactions to indirubin and that the underlying mechanism is related to AhR-mediated AchE downregulation.

Effects of functional training on muscle strength, jumping, and functional movement screen in wushu athletes: A systematic review.

This study aims to analyse the effects of functional training on muscle strength, jumping, and functional movement screen in wushu athletes. METHODS: This study followed the guidelines of the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). A systematic search of electronic databases was also conducted, including EBSCOhost, Scopus, PubMed, Web of Science, CNKI, Google Scholar, and Wanfang. The Physiotherapy Evidence Database (PEDro) scale was an effective indicator to evaluate the quality of studies included in the systematic review. RESULTS: This systematic review included 474 participants aged 8-24 years old. The intervention period for most studies was 12 weeks. Among the included studies, 6 focused on muscle strength, 4 on jumping performance, and 11 on functional movement screen. CONCLUSION: These articles have been analysed, and the positive impact of functional training interventions on muscle strength, jumping, and functional movement screen of wushu athletes has been verified.

Ursodeoxycholic acid and 18ß-glycyrrhetinic acid alleviate ethinylestradiol-induced cholestasis via downregulating RORγt and CXCR3 signaling pathway in iNKT cells.

Estrogen-induced intrahepatic cholestasis (IHC) is a mild but potentially serious risk and urges for new therapeutic targets and effective treatment. Our previous study demonstrated that RORγt and CXCR3 signaling pathway of invariant natural killer T (iNKT) 17 cells play pathogenic roles in 17α-ethinylestradiol (EE)-induced IHC. Ursodeoxycholic acid (UDCA) and 18ß-glycyrrhetinic acid (GA) present a protective effect on IHC partially due to their immunomodulatory properties. Hence in present study, we aim to investigate the effectiveness of UDCA and 18ß-GA in vitro and verify the accessibility of the above targets. Biochemical index measurement indicated that UDCA and 18ß-GA presented efficacy to alleviate EE-induced cholestatic cytotoxicity. Both UDCA and 18ß-GA exhibited suppression on the CXCL9/10-CXCR3 axis, and significantly restrained the expression of RORγt in vitro. In conclusion, our observations provide new therapeutic targets of UDCA and 18ß-GA, and 18ß-GA as an alternative treatment for EE-induced cholestasis.

Detrimental Role of CXCR3 in α-Naphthylisothiocyanate- and Triptolide-Induced Cholestatic Liver Injury.

The chemokine receptor CXCR3 is functionally pleiotropic, not only recruiting immune cells to the inflamed liver but also mediating the pathological process of cholestatic liver injury (CLI). However, the mechanism of its involvement in the CLI remains unclear. Both alpha-naphthylisothiocyanate (ANIT) and triptolide are hepatotoxicants that induce CLI by bile acid (BA) dysregulation, inflammation, and endoplasmic reticulum (ER)/oxidative stress. Through molecular docking, CXCR3 is a potential target of ANIT and triptolide. Therefore, this study aimed to investigate the role of CXCR3 in ANIT- and triptolide-induced CLI and to explore the underlying mechanisms. Wild-type mice and CXCR3-deficient mice were administered with ANIT or triptolide to compare CLI, BA profile, hepatic recruitment of IFN-γ/IL-4/IL-17+CD4+T cells, IFN-γ/IL-4/IL-17+iNKT cells and IFN-γ/IL-4+NK cells, and the expression of ER/oxidative stress pathway. The results showed that CXCR3 deficiency ameliorated ANIT- and triptolide-induced CLI. CXCR3 deficiency alleviated ANIT-induced dysregulated BA metabolism, which decreased the recruitment of IFN-γ+NK cells and IL-4+NK cells to the liver and inhibited ER stress. After triptolide administration, CXCR3 deficiency ameliorated dysregulation of BA metabolism, which reduced the migration of IL-4+iNKT cells and IL-17+iNKT cells and reduced oxidative stress through inhibition of Egr1 expression and AKT phosphorylation. Our findings suggest a detrimental role of CXCR3 in ANIT- and triptolide-induced CLI, providing a promising therapeutic target and introducing novel mechanisms for understanding cholestatic liver diseases.

Sex-specific grey matter abnormalities in individuals with chronic insomnia.

Previous studies have reported sex differences in altered brain function in patients with chronic insomnia (CI). However, sex-related alterations in brain morphology have rarely been investigated. This study aimed to investigate sex-specific grey matter (GM) alterations in patients with CI and to examine the relationship between GM alterations and neuropsychological assessments. Ninety-three (65 females and 28 males) patients and 78 healthy (50 females and 28 males) controls were recruited. Structural magnetic resonance imaging data were analysed using voxel-based morphometry to test for interactions between sex and diagnosis. Spearman's correlation was used to assess the associations among structure, disease duration, and sleep-, mood-, and cognition-related assessments. Males with CI showed reduced GM volume in the left inferior parietal lobe, left middle cingulate cortex, and right supramarginal gyrus. Females with CI showed increased GM volume in the right Rolandic operculum. Moreover, mood-related assessments were negatively correlated with GM volumes in the right supramarginal gyrus and left inferior parietal lobe in the male patients, and cognitive-related assessments were positively correlated with GM volumes in the Rolandic operculum in the female patients. Our findings indicate sex-specific alterations in brain morphology in CI, thereby broadening our understanding of sex differences in CI and potentially providing complementary evidence for the development of more effective therapies and individual treatments.

Effects of high-intensity functional training on physical fitness and sport-specific performance among the athletes: A systematic review with meta-analysis.

OBJECTIVE: This study aims to meta-analyze the impact of high-intensity functional training on athletes' physical fitness and sport-specific performance. METHODS: A systematic search was conducted in five well-known academic databases (PubMed, Scopus, Web of Science, EBSCOhost, and the Cochrane Library) up to July 1, 2023. The literature screening criteria included: (1) studies involving healthy athletes, (2) a HIFT program, (3) an assessment of outcomes related to athletes' physical fitness or sport-specific performance, and (4) the inclusion of randomized controlled trials. The Physical Therapy Evidence Database (PEDro) scale was used to evaluate the quality of studies included in the meta-analysis. RESULTS: 13 medium- and high-quality studies met the inclusion criteria for the systematic review, involving 478 athletes aged between 10 and 24.5 years. The training showed a small to large effect size (ES = 0.414-3.351; all p < 0.05) in improving upper and lower body muscle strength, power, flexibility, and sport-specific performance. CONCLUSION: High-intensity functional training effectively improves athletes' muscle strength, power, flexibility, and sport-specific performance but has no significant impact on endurance and agility. Future research is needed to explore the impact of high-intensity functional training on athletes' speed, balance, and technical and tactical performance parameters.