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Tris(2-chloroethyl) phosphate (TCEP) as a new type of flame retardant exists in various water environments, causing great risks to humans and the environment. In this study, shrimp shell was used to prepare an economical and environmental-friendly adsorbent for the efficient removal of TCEP. The systematic studies including characterization, removal performance, and adsorption mechanism of shrimp shell biochar toward TCEP were carried out. Adsorption kinetics and thermodynamics showed that fast equilibrium reached within 30 min, the maximum adsorption capacity q m was 108 μmol g−1 at 298 K, and the adsorption process is spontaneous and exothermic. The environmental factor, such as temperature, pH, inorganic anions and organic matter hardly affected the adsorption performance. Structural characterization indicated that the hierarchical porous structure of shrimp shell biochar is the key to excellent adsorption performance. The adsorption mechanisms were further revealed using density functional theory (DFT) calculations, and the hydrogen bond, van der Waals interactions, Cl–H interactions, and pi-H interactions were identified as potential interaction mechanisms between TCEP and specific biochar structures. The calculated binding energy between TCEP and simplified biochar structure suggested that oxygen-containing groups especially carboxyl, hydroxyl and aldehyde facilitate the adsorption. Our work not only provides a novel strategy for the quick remediation of organophosphate-contaminated water environments but also offers new opportunities for crustacean waste biomass valorization. [Display omitted] • Hierarchical porous shrimp shell biochar exhibted efficient removal of TCEP. • Modified biochar showed good tolerance of pH, anions and HA for TCEP adsorption. • Weak interactions for adsorption were demonstrated by DFT calculations. • Oxygen functional groups influenced the weak interactions. [ABSTRACT FROM AUTHOR]

Accumulating evidence suggests that Liraglutide is a favorable treatment for obese people. Obesity induces cellular senescence and accumulated senescent adipocytes in adipose tissue. However, the role of Liraglutide in adipose tissue (AT) senescence and the underlying mechanisms remain obscure. In this study, we found that HFD induces adipocyte senescence and impaired angiogenesis in AT. The deleterious effects provoked unhealthy adipose tissue remodeling and metabolic disturbance. In contrast, treatment of Liraglutide promoted weight reduction, alleviated adipose tissue senescence, and improved angiogenesis in AT. Notably, we demonstrated that Liraglutide promotes angiogenesis in AT dependent on adipocyte-derived IL-6. These findings revealed distinctive roles of Liraglutide in the regulation of adipocyte senescence and provide a therapeutic potential to obesity-associated metabolic disorders. [Display omitted] • Liraglutide suppressed HFD-induced AT hypertrophy and senescence. • Liraglutide inhibited adipocyte senescence and inflammation. • Adipocyte-mediated endothelial function impairment is dependent on IL-6. [ABSTRACT FROM AUTHOR]

Extensive mineral exploitation activities in history have aggravated potential toxic elements (PTEs) contamination in agricultural soils in China. Comprehensive ecological risk assessment is of great significance to orientate the restoration of contaminated soils, especially for those with high background values and multiple sources. The study area is located in the major rice producing area of China. Historically, there was a silver mine and a lead-zinc mine in the area, which were successively closed during the investigation. The intensive mining activities caused serious PTEs pollution in the agricultural soils around the mining area. In this study, five PTEs (As, Cd, Cr, Hg and Pb) selected to assessed the potential of geoaccumulation index in assessing agricultural soil potential risk assessment by identifying ecological risk sources. 315 of soil samples collected in 2009, 2014, 2018 were comprehensively analyzed by single pollution index evaluation (single factor index, geoaccumulation index), comprehensive evaluation (Nemerow index, potential ecological risk index) and trend analysis. Single factor index analysis showed that geoaccumulation index considered the impact of natural diagenesis of background values and human activities on the environment, ensuring high evaluation accuracy comparing to other methods used in typical complex agricultural soils. The modified potential ecological risk index revealed that the high background area did not represent high risk area, which was consistent with the implementation effect of governance measures. This study can provide important insights for policymakers and environmental engineers to quantitatively recognize the soil pollution and the effectiveness of governance based on applicable and reasonable evaluation methods. [Display omitted] • Modified potential ecological risk index (MRI) by geoaccumulation index. • MRI is more accurate in assessing ecological risks of agricultural soils. • Changes of MRI in 2014 and 2018 were related to mining and remediation activities. • Traditional pollution index results in the high background area were polarized. [ABSTRACT FROM AUTHOR]

Absent in melanoma 2 (AIM2) is a cytoplasmic sensor that recognises the double-strand DNA. AIM2 inflammasome is a protein platform in the cell that initiates innate immune responses by cleaving pro-caspase-1 and converting IL-1β and IL-18 to their mature forms. Additionally, AIM2 inflammasome promotes pyroptosis by converting Gasdermin-D (GSDMD) to GSDMD-N fragments. An increasing number of studies have indicated the important and decisive roles of the AIM2 inflammasome, IL-1β, and pyroptosis in cardiovascular diseases, such as coronary atherosclerosis, myocardial infarction, ischaemia/reperfusion injury, heart failure, aortic aneurysm and ischaemic stroke. Here, we review the molecular mechanism of the activation and effect of the AIM2 inflammasome in cardiovascular disease, revealing new insights into pathogenic factors that may be targeted to treat cardiovascular disease and related dysfunctions. [Display omitted] [ABSTRACT FROM AUTHOR]

Disruption of corticospinal tracts (CST) is a leading factor for motor impairments following intracerebral hemorrhage (ICH) in the striatum. Previous studies have shown that therapeutic hypothermia (HT) improves outcomes of ICH patients. However, whether HT has a direct protection effect on the CST integrity and the underlying mechanisms remain largely unknown. In this study, we employed a chemogenetics approach to selectively activate bilateral warm-sensitive neurons in the preoptic areas to induce a hypothermia-like state. We then assessed effects of HT treatment on the integrity of CST and motor functional recovery after ICH. Our results showed that HT treatment significantly alleviated axonal degeneration around the hematoma and the CST axons at remote midbrain region, ultimately promoted skilled motor function recovery. Anterograde and retrograde tracing revealed that HT treatment protected the integrity of the CST over an extended period. Mechanistically, HT treatment prevented mitochondrial swelling in degenerated axons around the hematoma, alleviated mitochondrial impairment by reducing mitochondrial ROS accumulation and improving mitochondrial membrane potential in primarily cultured cortical neurons with oxyhemoglobin treatment. Serving as a proof of principle, our study provided novel insights into the application of HT to improve functional recovery after ICH. • Chemogenetics-induced hypothermia improved motor function after ICH. • Hypothermia ameliorated axonal and myelin degeneration after ICH. • Hypothermia protected the integrity of the CST after ICH. • Hypothermia alleviated mitochondrial impairment after ICH. [ABSTRACT FROM AUTHOR]

Long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) have been the focus of recent studies of neurodegenerative disorders, including Parkinson's disease (PD). However, the specific mechanism of action of growth arrest-specific 5 (GAS5) in PD has not yet been characterized. First, the GSE8030 and GSE16658 datasets were analyzed to obtain differentially expressed genes (DEGs), followed by the development of a PD mouse model. The effects of shRNA targeting fos-like antigen-1 (shFosl1) and microRNA (miR)-150 agomiR on PD mouse behavior and neuronal injury were evaluated in vitro and in vivo. After the determination of target lncRNAs using bioinformatics tools, cell models were developed in SH-SY5Y and N2a cells using MPP+ to verify the effects of GAS5, miR-150 and Fosl1 on cell viability. Knockdown of Fosl1 and GAS5 or overexpression of miR-150 alleviated neuronal injury in mice after MPTP treatment and significantly increased the activity of SH-SY5Y and N2a cells after MPP treatment. GAS5 bound to miR-150, while miR-150 targeted Fosl1. Fosl1 activated the PTEN/AKT/mTOR pathway, thus promoting apoptosis and inhibiting neuronal activity in the PD model. Overall, our findings illuminated that GAS5 accelerated PD progression by targeting the miR-150/Fosl1 axis. [Display omitted] • Fosl1 is significantly higher in brain tissues of mice treated with MPTP. • Knockdown of Fosl1 reduces apoptosis of SH-SY5Y and N2a cells after MPP treatment. • miR-150 agomiR inhibits PD symptoms and neuronal injury in MPTP-treated mice. • GAS5 promotes Fosl1 expression through competitive binding to miR-150. • GAS5 expedites the PTEN/AKT/mTOR pathway via the miR-150/Fosl1 axis. [ABSTRACT FROM AUTHOR]

Cognitive impairment is a serious nonmotor symptom in patients with Parkinson's disease (PD). Currently, there are few studies investigating the relationship of serum markers and retinal structural changes with cognitive function in PD. To investigate the relationship between retinal structural changes, serum high mobility group box-1 (HMGB1) levels and cognitive function and motor symptoms in PD patients. Eighty-nine participants, including 47 PD patients and 42 healthy subjects, were enrolled. PD patients were divided into Parkinson's disease with normal cognitive (PD-NC), Parkinson's disease with mild cognitive impairment (PD-MCI), and Parkinson's disease with dementia (PDD) groups. The motor and nonmotor symptoms of PD patients were evaluated with clinical scale. Serum HMGB1 levels were detected by enzyme-linked immunosorbent assay (ELISA), and ganglion cell-inner plexiform layer complex (GCIPL) thickness changes in the macula were quantitatively analyzed by swept source optical coherence tomography (SS-OCT) in all patients. Compared with the control group, the macular GCIPL (t = −2.308, P = 0.023) was thinner and serum HMGB1 (z = −2.285, P = 0.022) was increased in PD patients. Macular GCIPL thickness in patients with PD-MCI and PDD were significantly lower than that in PD-NC patients, but there were no significant difference between the PD-MCI and PDD groups. Serum HMGB1 levels in patients with PD-MCI and PDD were significantly higher than those in PD-NC patients, and serum HMGB1 levels in PDD patients were higher than those in PD-MCI patients. Correlation analysis showed that serum HMGB1 levels in PD patients were positively correlated with disease duration, H Y stage, UPDRS-I score, UPDRS-III score, and UPDRS total score and negatively correlated with MOCA score. Macular GCIPL thickness was negatively correlated with H Y stage and positively correlated with MOCA score, and macular GCIPL thickness was negatively correlated with serum HMGB1 level. Logistic regression analysis showed that elevated serum HMGB1 level, thinner macular GCIPL thickness, and higher H Y stage were independent risk factors for Parkinson's disease with cognitive impairment (PD-CI). The areas under the receiver operating characteristic curve (AUC) for the serum HMGB1 level and macular GCIPL thickness-based diagnosis of PD-MCI, PDD and PD-CI based on in patients with PD were 0.786 and 0.825, 0.915 and 0.856, 0.852 and 0.841, respectively. The AUC for the diagnosis of PD-MCI, PDD and PD-CI with serum HMGB1 level and GCIPL thickness combined were 0.869, 0.967 and 0.916, respectively. The macular GCIPL thickness and serum HMGB1 level are potential markers of cognitive impairment in PD patients, and their combination can significantly improve the accuracy of the diagnosis of cognitive impairment in PD. • The serum HMGB1 level of PD patients were higher than that of the controls, and the GCIPL in the macular area was thinner than that of the control group. • Serum HMGB1 levels were negatively correlated with the GCIPL thickness in the macula. • Elevated serum HMGB1 levels and thinning of the macular GCIPL correlated with the severity of cognitive dysfunction in PD patients. • Serum HMGB1 level and GCIPL thickness can accurately predict different degrees of cognitive function status in PD patients, and their combination can improve the accuracy of predicting PD-related cognitive impairments. [ABSTRACT FROM AUTHOR]