Enhancement of Peroxydisulfate Activation for Complete Degradation of Refractory Tetracycline by 3D Self-Supported MoS2/MXene Nanocomplex.

Antibiotic abuse, particularly the excessive use of tetracycline (TC), a drug with significant environmental risk, has gravely harmed natural water bodies and even posed danger to human health. In this study, a three-dimensional self-supported MoS2/MXene nanohybrid with an expanded layer spacing was synthesized via a facile one-step hydrothermal method and used to activate peroxydisulfate (PDS) for the complete degradation of TC. The results showed that a stronger •OH signal was detected in the aqueous solution containing MoS2/MXene, demonstrating a superior PDS activation effect compared to MoS2 or Ti3C2TX MXene alone. Under the conditions of a catalyst dosage of 0.4 g/L, a PDS concentration of 0.4 mM, and pH = 5.0, the MoS2/MXene/PDS system was able to fully eliminate TC within one hour, which was probably due to the presence of several reactive oxygen species (ROS) (•OH, SO4•-, and O2•-) in the system. The high TC degradation efficiency could be maintained under the influence of various interfering ions and after five cycles, indicating that MoS2/MXene has good anti-interference and reusability performance. Furthermore, the possible degradation pathways were proposed by combining liquid chromatography-mass spectrometry (LC-MS) data and other findings, and the mechanism of the MoS2/MXene/PDS system on the degradation process of TC was elucidated by deducing the possible mechanism of ROS generation in the reaction process. All of these findings suggest that the MoS2/MXene composite catalyst has strong antibiotic removal capabilities with a wide range of application prospects.

Prenatal diesel exhaust exposure alters hippocampal synaptic plasticity in offspring.

Diesel exhaust particles (DEPs) are major air pollutants emitted from automobile engines. Prenatal exposure to DEPs has been linked to neurodevelopmental and neurodegenerative diseases associated with aging. However, the specific mechanism by DEPs impair the hippocampal synaptic plasticity in the offspring remains unclear. Pregnant C57BL/6 mice were administered DEPs solution via the tail vein every other day for a total of 10 injections, then the male offsprings were studied to assess learning and memory by the Morris water maze. Additionally, protein expression in the hippocampus, including CPEB3, NMDAR (NR1, NR2A, NR2B), PKA, SYP, PSD95, and p-CREB was analyzed using Western blotting and immunohistochemistry. The alterations in the histomorphology of the hippocampus were observed in male offspring on postnatal day 7 following prenatal exposure to DEPs. Furthermore, 8-week-old male offspring exposed to DEPs during prenatal development exhibited impairments in the Morris water maze test, indicating deficits in learning and memory. Mechanistically, the findings from our study indicate that exposure to DEPs during pregnancy may alter the expression of CPEB3, SYP, PSD95, NMDAR (NR1, NR2A, and NR2B), PKA, and p-CREB in the hippocampus of both immature and mature male offspring. The results offer evidence for the role of the NMDAR/PKA/CREB and CPEB3 signaling pathway in mediating the learning and memory toxicity of DEPs in male offspring mice. The alterations in signaling pathways may contribute to the observed damage to synaptic structure and transmission function plasticity caused by DEPs. The findings hold potential for informing future safety assessments of DEPs.

Combined effects of polystyrene nanoplastics and lipopolysaccharide on testosterone biosynthesis and inflammation in mouse testis.

Microplastics (MPs)/nanoplastics (NPs), as a source and vector of pathogenic bacteria, are widely distributed in the natural environments. Here, we investigated the combined effects of polystyrene NPs (PS-NPs) and lipopolysaccharides (LPS) on testicular function in mice for the first time. 24 male mice were randomly assigned into 4 groups, control, PS-NPs, LPS, and PS-NPs + LPS, respectively. Histological alterations of the testes were observed in mice exposed to PS-NPs, LPS or PS-NPs + LPS. Total sperm count, the levels of testosterone in plasma and testes, the expression levels of steroidogenic acute regulatory (StAR) decreased more remarkable in testes of mice treated with PS-NPs and LPS than the treatment with LPS or PS-NPs alone. Compared with PS-NPs treatment, LPS treatment induced more sever inflammatory response in testes of mice. Moreover, PS-NPs combined with LPS treatment increased the expression of these inflammatory factors more significantly than LPS treatment alone. In addition, PS-NPs or LPS treatment induced oxidative stress in testes of mice, but their combined effect is not significantly different from LPS treatment alone. These results suggest that PS-NPs exacerbate LPS-induced testicular dysfunction. Our results provide new evidence for the threats to male reproductive function induced by both NPs and bacterial infection in human health.

TRPML1 contributes to antimony-induced nephrotoxicity by initiating ferroptosis via chaperone-mediated autophagy.

Evidence suggests that ferroptosis participates in kidney injury. However, the role of ferroptosis in antimony (Sb) induced nephrotoxicity and the mechanism are unknown. Here, we demonstrated that Sb induced injury in renal tubular epithelial cells (RTECs) and ferroptosis. Inhibition of ferroptosis reduced RTECs injury. Besides, elimination of reactive oxygen species (ROS) alleviated ferroptosis and RTECs injury. Moreover, exposure to Sb not only increased the co-localization of glutathione peroxidase 4 (GPX4) and LAMP1, but also decreased the levels of MEF2D and LRRK2, while increased the levels of HSC70, HSP90, and LAMP2a. These findings suggest that Sb activates chaperone-mediated autophagy (CMA), enhances lysosomal transport and subsequent degradation of GPX4, ultimately leads to ferroptosis. Additionally, up-regulation of lysosomal cationic channel, TRPML1, mitigated RTECs injury and ferroptosis. Mechanistically, up-regulation of TRPML1 mitigated the changes in CMA-associated proteins induced by Sb, diminished the binding of HSC70, HSP90, and TRPML1 with LAMP2a. Furthermore, NAC restored the decreased TRPML1 level caused by Sb. In summary, deficiency of TRPML1, secondary to increased ROS induced by Sb, facilitates the CMA-dependent degradation of GPX4, thereby leading to ferroptosis and RTECs injury. These findings provide insights into the mechanism underlying Sb-induced nephrotoxicity and propose TRPML1 as a promising therapeutic target.

The role of m6A demethylases in lung cancer: diagnostic and therapeutic implications.

m6A is the most prevalent internal modification of eukaryotic mRNA, and plays a crucial role in tumorigenesis and various other biological processes. Lung cancer is a common primary malignant tumor of the lungs, which involves multiple factors in its occurrence and progression. Currently, only the demethylases FTO and ALKBH5 have been identified as associated with m6A modification. These demethylases play a crucial role in regulating the growth and invasion of lung cancer cells by removing methyl groups, thereby influencing stability and translation efficiency of mRNA. Furthermore, they participate in essential biological signaling pathways, making them potential targets for intervention in lung cancer treatment. Here we provides an overview of the involvement of m6A demethylase in lung cancer, as well as their potential application in the diagnosis, prognosis and treatment of the disease.

A Drosophila model of gestational antimony exposure uncovers growth and developmental disorders caused by disrupting oxidative stress homeostasis.

The toxic heavy metal antimony (Sb) is ubiquitous in our daily lives. Various models have shown that Sb induces neuronal and reproductive toxicity. However, little is known about the developmental toxicity of Sb exposure during gestation and the underlying mechanisms. To study its effects on growth and development, Drosophila stages from eggs to pupae were exposed to different Sb concentrations (0, 0.3, 0.6 and 1.2 mg/mL Sb); RNA sequencing was used to identify the underlying mechanism. The model revealed that prenatal Sb exposure significantly reduced larval body size and weight, the pupation and eclosion rates, and the number of flies at all stages. With 1.2 mg/mL Sb exposure in 3rd instar larvae, 484 genes were upregulated and 694 downregulated compared to controls. Biological analysis showed that the disrupted transcripts were related to the oxidative stress pathway, as verified by reactive oxygen species (ROS) scavenger N-acetylcysteine (NAC) and glutathione (GSH) intervention experiments. Sb exposure induced oxidative stress imbalance could be rectified by chelation and antioxidant effects of NAC/GSH. The Drosophila Schneider 2 (S2) model further demonstrated that NAC and GSH greatly ameliorated cell death induced by Sb exposure. In conclusion, gestational Sb exposure disrupted oxidative stress homeostasis, thereby impairing growth and development.

Gut Microbiota from Short-Chain Chlorinated Paraffin-Exposed Mice Promotes Astrocyte Activation by Disrupting the Intestinal Tight Junction via Zonulin Upregulation.

Short-chain chlorinated paraffins (SCCPs) are novel toxicants in food and are reported to possess neurotoxicity. Here, we investigated the mechanism of SCCP-induced astrocyte activation and neuroinflammation. SCCP gavage induced astrocyte activation and neuronal cell death with the changes of gut microbiome and metabolites. Antibiotic cocktail administration to deplete the gut microbiome ameliorated the astrocyte activation and inflammation induced by SCCPs. In fecal microbiota transplantation (FMT) assays, mice that received transplanted gut microbiome from SCCP-treated mice showed increased astrocyte activation and elevated inflammatory response. In addition, SCCP exposure promotes zonulin expression and tight junction injury, and antibiotic cocktail administration inhibited that in the intestinal tract. Increased zonulin and tight junction injury were also observed in SCCPs_FMT mice. The zonulin inhibition protected the tight junction in the intestinal tract from SCCP exposure and suppressed astrocyte activation. In summary, this study proposes a novel possibility for SCCP-induced astrocyte activation and neurotoxicity by the gut microbiome-mediated zonulin expression and tight junction.

Identification of CLIC5 as a Prognostic Biomarker and Correlated Immunomodulator for Lung Adenocarcinoma.

BACKGROUND: Lung adenocarcinoma (LUAD) is one of the most common pathological types of lung cancer. The gene Chloride Intracellular Channel 5 (CLIC5) has an important role in neurophysiology, cardiovascular biology, and tumour biology. Here, we explored the prognostic value and immune infiltration of CLIC5 expression in LUAD patients. METHODS: We extracted transcriptional LUAD data from The Cancer Genome Atlas (TCGA) and the University of Alabama Cancer Database to explore CLIC5 expression profiles and their relation to CLIC5 and clinicopathological parameters. The relationship between CLIC5 and survival time was explored using Kaplan-Meier Plotter. Then, we integrated the data from TCGA and the Gene Expression Omnibus (GEO) database to perform univariate and multivariate Cox regression. We performed CLIC5 immunohistochemical staining on 167 lung adenocarcinoma samples for further verification. In addition, we analysed the Gene Ontology (GO) database, Kyoto Encyclopaedia of Genes and Genomes pathways and network analysis of protein-protein interactions in lung tissue, to explore the potential mechanism of CLIC5. To analyse the correlation between immune infiltration and CLIC5 expression, we first compared the expression of immune cells in tumour tissues and normal tissues based on the TCGA and GEO databases. We found 51 immunomodulators related to CLIC5 and structured their enrichment pathways as well as those of 50 correlated genes. We used a Cox regression model to identify multiple-gene risk prediction signatures. Finally, we assessed the prognostic accuracy of the risk scores via receiver operating characteristic curves. RESULTS: CLIC5 expression levels were significantly lower in LUAD tissue than in normal tissue. Lower CLIC5 expression was negatively correlated to the overall survival of LUAD patients based on survival analysis. We identified CLIC5 as an independent prognosis predictor. Functional network analysis suggested that CLIC5 is related to multiple pathways. CLIC5 expression is closely related to infiltration levels of many immune cells and immune marker sets in LUAD patients. Furthermore, the risk score based on immunomodulators related to CLIC5 was an independent prognosis predictor in the TCGA lung cohorts. CONCLUSION: Our findings suggest that CLIC5 is a promising molecular marker for the prognosis and immune infiltration of LUAD patients.

Construction and Evaluation of Zeolitic Imidazolate Framework-Encapsulated Hemoglobin Microparticles as Oxygen Carriers.

Artificial oxygen carriers, such as favorably hemoglobin-based oxygen carriers, have received considerable attention due to some drawbacks of human donor blood. Among all oxygen carriers, the metal organic framework (MOF) exhibits excellent oxygen-carrying capacity due to its good encapsulation efficiency and competitive biocompatibility. Recently, zeolitic imidazolate frameworks (ZIFs) with unique structure have attracted much attention due to their outstanding solvothermal stability. Notably, ZIF-8, the prototypical ZIF, has been utilized to load hemoglobin (Hb) as a potential blood substitute. In this work, another ZIF material, which possesses a high oxygen binding/release capability, suitable safety profile, high stability, and efficiency as a potential oxygen carrier, was used to encapsulate Hb in an environment-friendly condition.

Effects of polystyrene nanoplastic gestational exposure on mice.

Airborne plastic particles have received increasing attention due to their ubiquity in the atmosphere and potential human health risks. Previous studies have demonstrated that early-life exposure to environmental toxicants is associated with abnormal metabolic function. However, the impact of exposure to polystyrene nanoplastics (PSNPs) through inhalation on the development of non-alcoholic fatty liver disease (NAFLD) in mothers and offspring remains unknown. In the present study, mice were gestationally exposed to PSNPs at different doses (0, 1, 5, and 25 µg µl-1) through inhalation to investigate health hazards to the dam at weaning and to adult offspring. Gestational exposure to PSNPs at high doses significantly induced hepatic steatosis in the dam and upregulated genes involved in de novo lipogenesis, fatty acids (FAs) uptake, and triacylglycerol (TG) synthesis in the monoacylglycerol acyltransferase pathway. Gestational exposure to high doses of PSNPs led to hepatic steatosis in adult female offspring but not male offspring, and expression levels of genes related to FAs uptake and TG synthesis in the glycerol 3-phosphate pathway were significantly elevated. Collectively, our data demonstrate that gestational exposure to airborne PSNPs induced different development processes of NAFLD in the dam and offspring, providing vital data about plastic particulate toxicology.

Ferroptosis Is Involved in Sex-Specific Small Intestinal Toxicity in the Offspring of Adult Mice Exposed to Polystyrene Nanoplastics during Pregnancy.

Nanoplastics are common contaminants in the living environment. Thus far, no investigations have focused on small intestinal injury in the offspring of adult mice that were exposed to nanoplastics through the respiratory system during pregnancy. Here, we evaluated potential intestinal injury in the offspring of adult mice that were subjected to maternal 80 nm polystyrene nanoparticle (PS-NP) exposure during gestation. PS-NP exposure significantly reduced the birth weight of female mice compared with male mice. However, the adult body weights of the female and male offspring were substantially greater in the PS-NP-exposed groups. Additionally, we found that exposure to PS-NPs during pregnancy caused histological changes in the small intestines of both female and male offspring. Mechanistic analysis revealed upregulation of reactive oxygen species in the small intestines, as indicated by changes in the levels of superoxide dismutase (SOD) and malondialdehyde (MDA). Furthermore, exposure to PS-NPs led to downregulation of GPx4, FTH1, and FTL protein levels, indicating initiation of ferroptosis. Notably, the changes in mRNA expression levels of GPx4, FTH1, and FTL differed between female and male offspring. Although all phenotypes failed to demonstrate classic dose-dependent effects, the data imply that small intestinal toxicity is greater in female offspring than in male offspring. Our results suggest that PS-NP exposure during pregnancy causes sex-specific small intestinal toxicity, which might contribute to reactive oxygen species activation and subsequent ferroptosis. Overall, this study showed toxic effects in offspring after PS-NP exposure during pregnancy.

Polystyrene nanoplastics inhibit StAR expression by activating HIF-1α via ERK1/2 MAPK and AKT pathways in TM3 Leydig cells and testicular tissues of mice.

Microplastics (MPs) and nanoplastics (NPs) are widely found in water, food and air, and have been found in human blood, lung and feces. Several studies in vivo have shown that MPs and NPs decrease testosterone level. However, the molecular mechanism of MPs and NPs leading to testosterone reduction remains unclear. In the present study, mice were treated with 50 µg/kg·day polystyrene (PS)-NPs by tail vein injection once daily for two consecutive days, the mRNA and protein levels of steroidogenic acute regulatory protein (StAR) decreased significantly in testis. TM3 Leydig cells were treated with non-toxic doses of PS-NPs, hypoxia-inducible factor-1α (HIF-1α) mRNA translation was induced by PS-NPs through mTOR/4E-BP1 pathway, which was activated by the ERK1/2 MAPK and AKT pathways. Simultaneously, increased HIF-1α protein inhibited StAR transcription. Additionally, reactive oxygen species production induced by PS-NPs played a central role in the activation of ERK1/2 MAPK/mTOR and AKT/mTOR signaling pathways. These results suggest that PS-NPs down-regulate StAR expression by increasing HIF-1α, which is induced by activation of mTOR/4E-BP1 through the ERK1/2 MAPK and AKT signaling pathways. Our findings provide new insight into the potential molecular mechanism by which PS-NPs impair testosterone synthesis and male reproductive function.

Arsenic trioxide promotes ERK1/2-mediated phosphorylation and degradation of BIMEL to attenuate apoptosis in BEAS-2B cells.

Inorganic arsenic is highly toxic, widely distributed in the human environment and may result in multisystem diseases and several types of cancers. The BCL-2-interacting mediator of cell death protein (BIM) is a key modulator of the intrinsic apoptosis pathway. Interestingly, in the present study, we found that arsenic trioxide (As2O3) decreased BIMEL levels in human bronchial epithelial cell line BEAS-2B and increased BIMEL levels in human lung carcinoma cell line A549 and mouse Sertoli cell line TM4. Mechanismly, the 26S proteasome inhibitors MG132 and bortezomib could effectively inhibit BIMEL degradation induced by As2O3 in BEAS-2B cells. As2O3 activated extracellular signal-regulated kinase (ERK) 1/2, c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) signaling pathways, but only the ERK1/2 MAPK inhibitor PD98059 blocked BIMEL degradation induced by As2O3. Furthermore, As2O3 induced-phosphorylation of BIMEL at multiple sites was inhibited by ERK1/2 MAPK inhibitor PD98059. Inhibition of As2O3-induced ERK1/2 MAPK phosphorylation increased the levels of BIMEL and cleaved-caspase-3 proteins and decreased BEAS-2B cell viability. As2O3 also markedly mitigated tunicamycin-induced apoptosis of BEAS-2B cells by increasing ERK1/2 phosphorylation and BIMEL degradation. Our results suggest that As2O3-induced activation of the ERK1/2 MAPK pathway increases phosphorylation of BIMEL and promotes BIMEL degradation, thereby alleviating the role of apoptosis in As2O3-induced cell death. This study provides new insights into how to maintain the survival of BEAS-2B cells before malignant transformation induced by high doses of As2O3.

Polystyrene nanoplastics promote CHIP-mediated degradation of tight junction proteins by activating IRE1α/XBP1s pathway in mouse Sertoli cells.

Microplastics (MPs) and nanoplastics (NPs) widely exist in human living environment and enter the body through water, food chain and breathing. Several studies have shown that MPs or NPs disrupt the blood-testis barrier in rodents. However, the molecular mechanism by which MPs and NPs damage the blood-testis barrier remains unclear. In the present study, our aim was to investigate the molecular mechanism of the destruction of blood-testis barrier induced by polystyrene (PS)-NPs. Mice were treated with 50 µg/kg·day PS-NPs by tail vein injection once daily for two consecutive days. The results showed that PS-NPs exposure significantly decreased the levels of tight junction (TJ) proteins ZO-2, occludin and claudin-11 in testis of mice. In vitro, we used TM4 Sertoli cells to explore the underlying mechanism of the decrease in TJ proteins induced by PS-NPs. We found that PS-NPs activated IRE1α and induced its downstream XBP1 splicing, which in turn elevated the expression of the E3 ubiquitin ligase CHIP, then CHIP triggers proteasomal degradation of ZO-2, occludin, and claudin-11 proteins. Our findings suggest that IRE1α/XBP1s/CHIP pathway is a pivotal mechanism of TJ proteins degradation induced by PS-NPs in mouse Sertoli cells. In conclusion, our results reveal that the degradation of TJ proteins is one of the mechanisms of blood-testis barrier destruction caused by acute exposure to PS-NPs.

Exposure to short-chain chlorinated paraffins induces astrocyte activation via JAK2/STAT3 signaling pathway.

In the last few decades, short-chain chlorinated paraffins (SCCPs) have become the most heavily produced monomeric organohalogen compounds, and have been reported to induce multiple organ toxicity. However, the effects of SCCPs on the central nervous system are unknown. In the present study, we show that SCCP exposure induced astrocyte proliferation and increased the expression of two critical markers of astrocyte activation, glial fibrillary acidic protein and inducible nitric oxide synthase, in vivo and in vitro. SCCP exposure also increased inflammatory factory gene expression. Moreover, SCCP treatment triggered Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signalling, as shown by increased phosphorylation and STAT3 translocation to the nucleus. Both JAK2 and STAT3 inhibition effectively attenuated SCCP-induced astrocyte activation. Finally, JAK2 inhibition significantly rescued STAT3 phosphorylation and nuclear translocation. Taken together, JAK2/STAT3 pathway activation contributed to SCCP-induced astrocyte activation. These data will help elucidate the molecular mechanism underlying SCCP-induced neurotoxicity.

The TGF-ß/SMAD Signaling Pathway Prevents Follicular Atresia by Upregulating MORC2.

In mammals, female fertility is determined by the outcome of follicular development (ovulation or atresia). The TGF-ß/SMAD signaling pathway is an important regulator of this outcome. However, the molecular mechanism by which the TGF-ß/SMAD signaling pathway regulates porcine follicular atresia has not been fully elucidated. Microrchidia family CW-type zinc finger 2 (MORC2) is anovel epigenetic regulatory protein widely expressed in plants, nematodes, and mammals. Our previous studies showed that MORC2 is a potential downstream target gene of the TGF-ß/SMAD signaling pathway. However, the role of MORC2 in porcine follicular atresia is unknown. To investigate this, qRT-PCR, western blotting, and TdT-mediated dUTP nick-end labeling were performed. Additionally, the luciferase activity assay was conductedto confirm that the TGF-ß/SMAD signaling pathway regulates MORC2. Our results demonstrate that MORC2 is animportant anti-apoptotic molecule that prevents porcine follicular atresia via a pathway involving mitochondrial apoptosis, not DNA repair. Notably, this studyrevealsthat the TGF-ß/SMAD signaling pathway inhibits porcine granulosa cell apoptosis by up-regulating MORC2. The transcription factor SMAD4 regulated the expression of MORC2 by binding to its promoter. Our results will help to reveal the mechanism underlying porcine follicular atresia and improve the reproductive efficiency of sows.

Relationships between urinary metals concentrations and cognitive performance among U.S. older people in NHANES 2011-2014.

Background: Epidemiological evidence on Urine metals and cognitive impairment in older individuals is sparse and limited. The goal of this study was to analyze if there was a link between urinary metal levels and cognitive performance in U.S. people aged 60 and up. Methods: The National Health and Nutrition Examination Survey (NHANES) data from 2011 to 2014 were utilized in this cross-sectional analysis. Memory function was quantified using the following methods: Established Consortium for Word Learning in Alzheimer's Disease (CERAD-WL) (immediate learning and recall and delayed recall), Animal Fluency Test (AFT), and Digit Symbol Substitution Test (DSST). An inductively coupled plasma mass spectrometry (ICP-MS) was used to estimate urine metal concentrations. The connection of Urine metals level with cognitive function was investigated employing binary logistic regression and restricted cubic spline models. Results: A total of 840 participants aged 60 years and over were enrolled in this study. After controlling for confounders, the association between cadmium, barium, cobalt, cesium, manganese, and thallium and poor cognitive performance showed significance in multiple logistic regression compared to the lowest quartile of metals. In the DSST test, the weighted multivariate adjusted ORs (95% CI) for cadmium in the highest quartile, barium and cesium in the third quartile were 2.444 (1.310-4.560), 0.412 (0.180-0.942) and 0.440 (0.198-0.979), respectively. There were L-shaped associations between urine cesium, barium, or manganese and low cognitive performance in DSST. Urine lead, molybdenum and uranium did not show any significant relationships with cognitive impairment, respectively, compared to the respective lowest quartile concentrations. Conclusion: The levels of barium (Ba), cobalt (Co), cesium (Cs), manganese (Mn), and thallium (Tl) in urine were found to be negatively related to the prevalence of impaired cognitive performance in our cross-sectional investigation. Higher cadmium (Cd) levels were associated with cognitive impairment.

Level-specific associations of urinary antimony with cognitive function in US older adults from the National Health and Nutrition Examination Survey 2011-2014.

BACKGROUND: We have looked at antimony (Sb) as a new neurotoxin which causes neuronal apoptosis in animal studies. At the population level, however, there is no direct evidence for a relationship between Sb exposure and cognitive performance. METHOD: The study comprehensively assessed the correlation between urinary antimony levels and cognitive test scores in 631 creatinine-corrected older persons using data from the National Health and Nutrition Examination Survey (NHANES) from 2011 to 2014. RESULTS: Using logistic regression, the study looked at the prevalence of cognitive impairment at different levels of urine antimony concentrations and found that, after controlling for covariates, higher doses of urinary antimony were positively associated with cognitive function compared to controls, odds ratio (ORs) with 95% confidence interval (CI) were 0.409 (0.185-0.906) and 0.402 (0.186-0.871) respectively. Restricted cubic spline curves showed a non-linear and dose-specific correlation between urinary antimony and cognitive performance, with lower doses associated with better cognitive performance, while higher doses may be associated with cognitive impairment. CONCLUSIONS: Our data provide evidence for a correlation between Sb and cognitive function at the population level, although the specific mechanisms need to be investigated further.

Betaine Promotes Fat Accumulation and Reduces Injury in Landes Goose Hepatocytes by Regulating Multiple Lipid Metabolism Pathways.

Betaine is a well-established supplement used in livestock feeding. In our previous study, betaine was shown to result in the redistribution of body fat, a healthier steatosis phenotype, and an increased liver weight and triglyceride storage of the Landes goose liver, which is used for foie-gras production. However, these effects are not found in other species and strains, and the underlying mechanism is unclear. Here, we studied the underpinning molecular mechanisms by developing an in vitro fatty liver cell model using primary Landes goose hepatocytes and a high-glucose culture medium. Oil red-O staining, a mitochondrial membrane potential assay, and a qRT-PCR were used to quantify lipid droplet characteristics, mitochondrial ß-oxidation, and fatty acid metabolism-related gene expression, respectively. Our in vitro model successfully simulated steatosis caused by overfeeding. Betaine supplementation resulted in small, well-distributed lipid droplets, consistent with previous experiments in vivo. In addition, mitochondrial membrane potential was restored, and gene expression of fatty acid synthesis genes (e.g., sterol regulatory-element binding protein, diacylglycerol acyltransferase 1 and 2) was lower after betaine supplementation. By contrast, the expression of lipid hydrolysis transfer genes (mitochondrial transfer protein and lipoprotein lipase) was higher. Overall, the results provide a scientific basis and theoretical support for the use of betaine in animal production.