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ObjectiveTo explore the absorption， distribution， accumulation， and excretion after oral exposure to lanthanum and the effects of lanthanum on the blood element spectrum of rats.Methods48 female SPF-grade rats were randomly divided into 8 groups with a one-time gavage of 700 mg/kg·BW lanthanum nitrate solution using single oral exposure experiment. And the blood， heart， liver， spleen， lung， kidneys， brain， femur， and fecal of rats were collected and measured by ICP-MS after gavage for 1， 2， 4， 8， 16， 32， 64， and 128 h. Another 48 SPF-grade rats were randomly divided into 4 groups （half male and female）， each group with a control and an experimental group was observed in experimental time-point in repeat oral exposure experiment. The experimental group repeatedly gavage lanthanum nitrate solution containing lanthanum 66 mg/kg·BW， and the control group gavage an equal amount of physiological saline. Then， on the 7th， 14th， 21st and 28th days， the rats （including the control group and the experimental group） were taken to determine the contents of 44 elements in blood and the contents of lanthanum in liver， kidney， femur， feces and urine by ICP-MS.ResultsAfter single oral exposure to lanthanum， lanthanum peaked in blood for 2 h， the elimination half-life was 69.315 h， and the overall clearance rate was 1.733 L/h/kg. Lanthanum was widely distributed in the heart， liver， spleen， lung， kidneys， brain， and femur with blood， and the level in the femur was the highest （P0.05）.ConclusionIn this experiment， lanthanum can be rapidly absorbed into the blood after oral exposure and is widely distributed in the heart， liver， spleen， lung， kidneys， brain， and femur. After repeat oral exposure to lanthanum， lanthanum is easily deposited in the liver and femur， feces excretion is the main route of elimination， and no effect of lanthanum on the blood element spectrum of rats has been observed.

ObjectiveTo investigate the contamination status and dietary exposure risk of 3 perfluorinated substances and 2 chlorine substituted perfluoroalkyl ether sulfonate acids in fresh vegetables planted in the vicinity of typical fluorine chemical industry parks located in Guangdong province.MethodsNinety six vegetables were collected from the vicinity of 3 typical fluorine chemical industry parks and local markets in 2019. The concentrations of 3 perfluorinated substances ［perfluorooctane sulfonate acid （PFOS）， perfluorooctanoic acid （PFOA）， perfluorohexanesulfonic acid （PFHxS）］ and 2 chlorine substituted perfluoroalkyl ether sulfonate acids （6：2 Cl-PFESA and 8：2 Cl-PFESA） in fresh vegetables were detected using isotope dilution method by UPLC-QqQ-MS， and the point estimate was employed to estimate the levels of dietary exposure from fresh vegetables.ResultsPFOS and PFOA were detected in all samples， while chlorine substituted perfluoroalkyl ether sulfonates were detected in 2 leafy vegetable samples. The sum of average concentration of PFASs and Cl-PFESAs in vegetable samples was 0.792 ng/g fw （fresh weight， fw）， and it was two-fold higher compared the samples around the fluorine chemical industrial with the samples from local markets. The average concentration of 5 chemicals （1.11 ng/g fw） was the highest in leafy vegetables. The results of dietary exposure assessment indicated that the exposure levels of 3 perfluorinated compounds by consumption of fresh vegetables which planted surrounding fluorine chemical industry parks were 0.185-2.35 ng/kg·BW. The hazard indexes （HI） of PFOS and PFOA were greater than 1. The exposure level of chlorine substituted perfluoroalkyl ether sulfonate acids were lower.ConclusionThe exposures of PFOS and PFOA of local general population exceeded the established thresholds for the adult residents. The risks of 2 chlorine substituted perfluoroalkyl ether sulfonate acids exposure from vegetables were low， which still need to be concerned.

Background Cross-sectional studies have shown that the level of bilirubin in vivo is related to the progression of atherosclerosis, but the data from large-scale studies in China and even in the world are very limited. Objective To investigate the effect of serum total bilirubin (TBIL) and indirect bilirubin (IBIL) on the progression of carotid atherosclerosis in healthy people. Methods Retrospective cohort study was adopted to select 11 394 healthy people who had continuous physical examination and carotid intima-media thickness (cIMT) ≤1 mm displayed by carotid artery ultrasound examination as the research subjects in Hebei General Hospital from January 2010 to December 2019. Demographic characteristics, past medical history, physical examination, laboratory examination results of previous physical examination, carotid artery ultrasound and other information of subjects were collected. The subjects were divided into the progressive carotid atherosclerosis group and the non-progressive group according to whether cIMT increased during follow-up. The Cox proportional regression model was used to explore the effect of bilirubin on the progression of carotid atherosclerosis, and Cox regression analysis was performed by gender, age, body mass index (BMI) , hypertension, diabetes, smoking and alcohol consumption. Results 1 586 cases of carotid atherosclerosis progression were detected in 10 years, with a cumulative incidence rate of 13.9%. The results of Cox regression analysis showed that for every 1 standard deviation increase in TBIL and IBIL levels, the risk of carotid atherosclerosis progression decreased by 6.6% and 17.4%, respectively〔HR (95%CI) =0.934 (0.881, 0.990) ; HR (95%CI) =0.826 (0.777, 0.877) 〕 after adjustment for age, sex, BMI, smoking, alcohol consumption, hypertension, diabetes, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, total cholesterol, triglyceride, alanine aminotransferase and estimated glomerular filtration rate. Subgroup analysis showed that there was no statistical difference in the protective effects of TBIL and IBIL on different subgroups. Conclusion TBIL and IBIL levels are independent protective factors for the progression of carotid atherosclerosis in healthy subjects. Elevated bilirubin levels reduce the risk of carotid atherosclerosis progression, with IBIL being more potent in preventing carotid atherosclerosis progression.

Objective: This study investigated the spinal changes in ligature‐induced periodontitis and the role of periodontitis in cognitive impairment. Methods: Twenty mice were randomized into the control and chronic periodontitis (CP) groups, with the latter receiving ligature‐induced periodontitis. Cognitive performance was assessed by fear conditioning test. Periodontal inflammation and alveolar bone resorption were evaluated by micro‐computed tomography and histopathology. The hippocampal microglial activation was evaluated by immunohistochemistry (IHC). The expressions of hippocampal cytokines (TNF‐α, iNOS, IL‐1β, IL‐4, IL‐10, and TREM2) were measured by reverse transcription–polymerase chain reaction. The morphology and density of the dendritic spines were determined by Golgi–Cox staining. Results: The CP mice reported significant inflammatory cell infiltration and alveolar bone resorption, with marked increases in cytokine levels (TNF‐α, iNOS, IL‐1β, and TREM2) in the brain. Moreover, the CP mice showed significantly reduced freezing to the conditioned stimulus in the cued and contextual tests, indicating impaired memory. Further analyses revealed, in the hippocampus of the CP mice, enhanced microglial activation, decreased dendritic spine density, and increased proportion of thin dendritic spines. Conclusions: Periodontitis‐induced neuroinflammation may impair the cognitive function by activating hippocampal microglia and inducing dendritic spine immaturity. [ABSTRACT FROM AUTHOR]

Pentachlorophenol (PCP) is a ubiquitous emerging persistent organic pollutant detected in the environment and foodstuffs. Despite the dietary intake of PCP being performed using surveillance data, the assessment does not consider the bioaccessibility and bioavailability of PCP. Pork, beef, pork liver, chicken and freshwater fish Ctenopharyngodon Idella-fortified by three levels of PCP were processed by RIVM and the Caco-2 cell model after steaming, boiling and pan-frying, and PCP in foods and digestive juices were detected using isotope dilution–UPLC-MS/MS. The culinary treatment and food matrix were significantly influenced (p < 0.05) in terms of the bioaccessibility and bioavailability of PCP. Pan-frying was a significant factor (p < 0.05) influencing the digestion and absorption of PCP in foods, with the following bioaccessibility: pork (81.37–90.36%), beef (72.09–83.63%), pork liver (69.11–78.07%), chicken (63.43–75.52%) and freshwater fish (60.27–72.14%). The bioavailability was as follows: pork (49.39–63.41%), beef (40.32–53.43%), pork liver (33.63–47.11%), chicken (30.63–40.83%) and freshwater fish (17.14–27.09%). Pork and beef with higher fat content were a key factor in facilitating the notable PCP bioaccessibility and bioavailability (p < 0.05). Further, the exposure of PCP to the population was significantly reduced by 42.70–98.46% after the consideration of bioaccessibility and bioavailability, with no potential health risk. It can improve the accuracy of risk assessment for PCP. [ABSTRACT FROM AUTHOR]

Soluble E‐cadherin (sE‐cad) is an 80 kDa fragment derived from E‐cadherin that is shed from the cell surface through proteolytic cleavage and is a biomarker in various cancers that promotes invasion and migration. Alveolar epithelial destruction, aberrant lung fibroblast migration and inflammation contribute to pulmonary fibrosis. Here, we hypothesized that E‐cadherin plays an important role in lung fibrosis. In this study, we found that E‐cadherin was markedly increased in the bronchoalveolar lavage fluid (BALF) and serum of mice with pulmonary fibrosis and that blocking sE‐cad with HECD‐1, a neutralizing antibody targeting the ectodomain of E‐cadherin, effectively inhibited myofibroblast accumulation and collagen deposition in the lungs after bleomycin (BLM) exposure. Moreover, transforming growth factor‐β (TGF‐β1) induced the shedding of sE‐cad from A549 cells, and treatment with HECD‐1 inhibited epithelial–mesenchymal transition (EMT) stimulated by TGF‐β1. Fc‐E‐cadherin (Fc‐Ecad), which is an exogenous form of sE‐cad, robustly promoted lung fibroblast migration. E‐cadherin participates in bleomycin (BLM)‐induced lung fibrosis by promoting EMT in the alveolar epithelium and fibroblast activation. E‐cadherin may be a novel therapeutic target for lung fibrosis. [ABSTRACT FROM AUTHOR]