Multi-sequence generative adversarial network: better generation for enhanced magnetic resonance imaging images.

Introduction: MRI is one of the commonly used diagnostic methods in clinical practice, especially in brain diseases. There are many sequences in MRI, but T1CE images can only be obtained by using contrast agents. Many patients (such as cancer patients) must undergo alignment of multiple MRI sequences for diagnosis, especially the contrast-enhanced magnetic resonance sequence. However, some patients such as pregnant women, children, etc. find it difficult to use contrast agents to obtain enhanced sequences, and contrast agents have many adverse reactions, which can pose a significant risk. With the continuous development of deep learning, the emergence of generative adversarial networks makes it possible to extract features from one type of image to generate another type of image. Methods: We propose a generative adversarial network model with multimodal inputs and end-to-end decoding based on the pix2pix model. For the pix2pix model, we used four evaluation metrics: NMSE, RMSE, SSIM, and PNSR to assess the effectiveness of our generated model. Results: Through statistical analysis, we compared our proposed new model with pix2pix and found significant differences between the two. Our model outperformed pix2pix, with higher SSIM and PNSR, lower NMSE and RMSE. We also found that the input of T1W images and T2W images had better effects than other combinations, providing new ideas for subsequent work on generating magnetic resonance enhancement sequence images. By using our model, it is possible to generate magnetic resonance enhanced sequence images based on magnetic resonance non-enhanced sequence images. Discussion: This has significant implications as it can greatly reduce the use of contrast agents to protect populations such as pregnant women and children who are contraindicated for contrast agents. Additionally, contrast agents are relatively expensive, and this generation method may bring about substantial economic benefits.

Bisphenol a accelerates the glucolipotoxicity-induced dysfunction of rat insulinoma cell lines: An implication for a potential risk of environmental bisphenol a exposure for individuals susceptible to type 2 diabetes.

Epidemiological studies have suggested a correlation between bisphenol A (BPA) and type 2 diabetes (T2DM). The effects of BPA on ß-cell dysfunction may reveal the risks from an in vitro perspective. We used the rat insulinoma (INS-1) cell lines (a type of ß-cells) to set up normal or damaged models (DM), which were exposed to various concentrations of BPA (0.001, 0.01, 0.1, 1, 10 and 100 µM). An increase in reactive oxygen species (ROS) and apoptosis, and a decrease in cell viability were observed in INS-1 cells exposed to high doses of BPA for 48 h. Interestingly, exposure to lower doses of BPA for 24 h resulted in increased ROS levels and apoptosis rates in INS-1 in the DM group, along with decreased cell viability, suggesting that BPA exerts toxicity to INS-1 cells, particularly to the DM group. Insulin levels and Glut2 expression, glucose consumption, intracellular Ca2+ and insulin secretion were increased in INS-1 cells after 48 h exposure to high dose of BPA. Stronger effects were observed in the DM group, even those exposed to low doses of BPA for 24 h. Moreover, BPA inhibited high glucose-stimulated insulin secretion in these cells. Our research suggests that low doses of BPA exacerbate the dysfunction caused by glucolipotoxicity, implying environmental BPA exposure poses a risk for individuals with prediabetes or T2DM.

Primary Robotic Versus Conventional Laparoscopic Roux-en-Y Gastric Bypass in Morbidly Obese Patients: A Systematic Review and Meta-Analysis.

BACKGROUND: Robotic Roux-en-Y gastric bypass (RRYGB) and conventional laparoscopic Roux-en-Y gastric bypass (LRYGB) are commonly performed as primary bariatric procedures. The aim of this article was to assess the role of RRYGB in patients undergoing primary bariatric procedures. METHODS: All of the qualified studies were selected from the PubMed, Embase, and Web of Science databases, etc. We mainly compared the outcomes and safety between RRYGB and LRYGB. The outcomes evaluation included surgical effect and surgical safety. RESULT: In total, 35 studies containing 426,463 patients were selected. The mortalities of patients adopting these 2 bariatric procedures were similar (RRYGB: 59/28,023, 0.21%; LRYGB: 612/397,945, 0.15%). We found no significant difference between RRYGB and LRYGB in the incidence of postoperative complications (30-day: OR=1.06, P=0.18; 1-y: OR=1.06, P=0.92). The incidence of 30-day readmission after the operation was higher in RRYGB patients (OR=1.24, P=0.003). However, we found that the RRYGB group had a lower incidence of anastomotic stricture 1 year after the operation when compared with LRYGB (OR=0.35, P=0.0004). The 1-year %EBMIL of these 2 groups was similar (78.53% vs. 76.02%). There was no significant difference in length of hospital stay (LOS) (WMD=-0.03d, P=0.59), conversion rate (OR=0.84, P=0.75), or anastomotic leak (OR=1.00, P=0.99) between these 2 groups. The mean hospital charges were higher in the RRYGB group ($11234.75 vs. $9468.58). CONCLUSION: This systematic review and meta-analysis showed no significant advantage of RRYGB in surgical effect or reduction of intraoperative complications. RRYGB may reduce the incidence of some postoperative long-term complications. The mean hospital charges of RRYGB were higher.

Low-dose BPA-induced neuronal energy metabolism dysfunction and apoptosis mediated by PINK1/parkin mitophagy pathway in juvenile rats.

Bisphenol A (BPA) is related to neurological disorders involving mitochondrial dysfunction, while the mechanism remains elusive. Therefore, we explored it through in vitro and in vivo experiments. In vitro, hippocampal neurons derived from neonatal rats of different genders were exposed to 1-100 nM and 100 µM BPA, autophagy activator Rapa and inhibitor 3-MA for 7 d. The results suggested that even nanomolar BPA (1-100 nM) disturbed Ca2+ homeostasis and damaged the integrity of mitochondrial cristae in neurons (p < 0.05). Furthermore, BPA increased the number of autophagic lysosomes, LC3II/LC3I ratio, and p62 expression, and decreased parkin expression (p < 0.05), suggesting that the entry of damaged mitochondria into autophagic pathway was prompted, while the autophagic degradation pathway was blocked. This further disrupts neuronal energy metabolism and promotes neuronal apoptosis. However, Rapa attenuated the adverse effects caused by BPA, while 3-MA exacerbated these reactions. In vivo, exposure of juvenile rats to 0.5, 50, 5000 µg/kg‧bw/day BPA during PND 7-21 markedly impaired the structure of hippocampal mitochondria, increased the number of autophagosomes, the rate of neuronal apoptosis, and the expression levels of pro-apoptotic proteins Cyt C, Bax, Bak1, and Caspase3, and decreased the expression of anti-apoptotic protein Bcl2 (p < 0.05). Particularly, male rats are more sensitive to low-dose BPA than females. Overall, environmental-doses BPA can induce the imbalance of energy metabolism in hippocampal neurons via PINK1/parkin mitophagy, thereby inducing their apoptosis. Importantly, this study provides a theoretical basis for attenuating BPA-related neurological diseases.

A high-throughput method for the determination of 14 UV-filters in human plasma by LC-MS/MS: Minimize interferences from proteins and phospholipids in the matrix.

Accurate monitoring of UV-filters exposure levels in human plasma is a challenge because of the significant differences in the physicochemical properties of UV-filters, as well as the matrix effect caused by abundant proteins and phospholipids in plasma. Therefore, an effective and rapid method for simultaneous determination of 14 UV-filters in human plasma using protein precipitation-solid phase extraction (SPE) coupled with liquid chromatography tandem mass spectrometry (LC-MS/MS) was developed. Acetonitrile with 0.1 % formic acid and 10 % isopropanol (v/v) were used as mobile phases. A gradient elution on an ACQUITY UPLC BEH-C18 column at 30 °C and 0.3 mL/min flow rate was applied for separation. The electrospray ionization positive or negative modes were selected to determine the corresponding analyte to increase selectivity and sensitivity. Results showed that acetonitrile-tetrahydrofuran (v/v, 8:2) as the extraction solvent can effectively precipitate protein in plasma and improve the solubility of UV-filters. The HybridSPE cartridge improved the removal efficiency of phospholipids, while 1 mL of methanol elution increased the extraction recoveries of targets. Fourteen UV-filters achieved good linearities, low detection limits (0.050 to 0.10 µg/L) and quantification limits (0.10 to 1.0 µg/L). Method accuracy and precision, extraction recoveries, and storage stabilities of all analytes met the criterion of 80-120 %. Moreover, this method was successfully applied for the determination of UV-filters in plasma randomly collected from adults. Nine of 14 UV-filters were determined and their concentrations were distributed widely, suggesting a big variation of individual UV-filters exposure.

Environmental dose of 16 priority-controlled PAHs induce endothelial dysfunction: An in vivo and in vitro study.

Polycyclic aromatic hydrocarbons (PAHs) exposure is related to the occurrence of cardiovascular diseases (CVDs). Endothelial dysfunction is considered an initial event of CVDs. To confirm the relationship of PAHs exposure with endothelial dysfunction, 8-week-old male SD rats and primary human umbilical vein endothelial cells (HUVECs) were co-treated with environmental doses of 16 priority-controlled PAHs for 90 d and 48 h, respectively. Results showed that 10× PAHs exposure remarkably raised tumor necrosis factor-α and malonaldehyde levels in rat serum (p < 0.05), but had no effects on interleukin-8 levels and superoxide dismutase activity. The expressions of SIRT1 in HUVECs and rat aorta were attenuated after PAHs treatment. Interestingly, PAHs exposure did not activate the expression of total endothelial nitric oxide synthase (eNOS), but 10× PAHs exposure significantly elevated the expression of phosphorylated eNOS (Ser1177) in HUVECs and repressed it in aortas, accompanied with raised nitrite level both in serum and HUVECs by 48.50-253.70 %. PAHs exposure also led to the augment of endothelin-1 (ET-1) levels by 19.76-38.54 %, angiotensin (Ang II) levels by 20.09-39.69 % in HUVECs, but had no effects on ET-1 and Ang II levels in serum. Additionally, PAHs exposure improved endocan levels both in HUVECs and serum by 305.05-620.48 % and stimulated the THP-1 cells adhered to HUVECs (p < 0.05). After PAHs treatment, the smooth muscle alignment was disordered and the vascular smooth muscle locally proliferated in rat aorta. Notably, the systolic blood pressure of rats exposed to 10× PAHs increased significantly compared with the control ones (131.28 ± 5.20 vs 116.75 ± 5.33 mmHg). In summary, environmental chronic PAHs exposure may result in endothelial dysfunction in SD rats and primary HUVECs. Our research can confirm the cardiovascular damage caused by chronic exposure to PAHs and provide ideas for the prevention or intervention of CVDs affected by environmental factors.

Genome-Wide Identification and Expression Analysis of CCO Gene Family in Liriodendron chinense.

Carotenoid cleavage oxygenase (CCO) is an enzyme that can catalyze carotenoids to volatile aromatic substances and participate in the biosynthesis of two important phytohormones, i.e., abscisic acid (ABA) and strigolactone (SL). However, the genome-wide identification and analysis of the CCO gene family in the rare and endangered woody plant Liriodendron chinense has not been reported. Here, we performed a genome-wide analysis of the CCO gene family in the L. chinense genome and examined its expression pattern during different developmental processes and in response to various abiotic stresses. A total of 10 LcCCO genes were identified and divided into 6 subfamilies according to the phylogenetic analysis. Subcellular localization prediction showed that most of the LcCCO proteins were located in the cytoplasm. Gene replication analysis showed that segmental and tandem duplication contributed to the expansion of this gene family in the L. chinense genome. Cis-element prediction showed that cis-elements related to plant hormones, stress and light response were widely distributed in the promoter regions of LcCCO genes. Gene expression profile analysis showed that LcNCED3b was extensively involved in somatic embryogenesis, especially the somatic embryo maturation, as well as in response to heat and cold stress in leaves. Furthermore, qRT-PCR analysis showed that LcNCED3b obviously responded to drought stress in roots and leaves. This study provides a comprehensive overview of the LcCCO gene family and a potential gene target for the optimization of the somatic embryogenesis system and resistance breeding in the valuable forest tree L. chinense.

Trace metal exposure and risk assessment of local dominant fish species in the Beijiang River Basin of China: A 60 years' follow-up study.

The Beijiang River, one of the Pearl River tributaries located in Guangdong, China, plays a critical role in providing water and fishery resources for the Pearl River Delta and receiving a large amount of domestic and industrial wastewater. However, due to the lack of historical monitoring data, we are unable to fully understand the relationship between the industrial and agricultural development and the environment. In this study, fish specimens collected from the Beijiang River Basin over a span of nearly 60 years (1963-2021) are used as research objects and the concentrations of ten trace metals (TMs) in two locally dominant fish species were determined by an inductively coupled plasma mass spectrometer. The human health risks caused by consuming fishes were assessed. Results show a correlation between the levels of TMs in fish muscle and the degree of industrialization. The concentrations of Cr, Mn, Ni, and Cu peaked during the period of 1981-1983, when China's industrial development was rapidly expanding while the environmental protection facilities were incomplete. However, with the implementation of Ecological Civilization policy, the levels of Cr, Mn, Ni, Cu, Cd, and Ba showed a downward trend in the period from 2018 to 2021. Cu concentrations in both fish muscle and viscera exhibit analogous change patterns across different periods, indicating that Cu serves as a significant indicator of TM pollution in the Beijiang River Basin. The presence of TMs in fish muscle often exhibits long-term enrichment, while those in the viscera demonstrate short-term accumulation. Based on the estimated daily intake, the target hazard quotient (THQ), and total THQ value, the overall health risk associated with TMs in fish from the Beijiang River Basin is low. However, certain TMs in the fish rebounded during 2018-2021, posing a potential risk for aquatic biology and ecosystems, which is worth our attention.

Low-dose bisphenols exposure sex-specifically induces neurodevelopmental toxicity in juvenile rats and the antagonism of EGCG.

Bisphenols (BPs) can negatively affect neurobehaviors in rats, whereas the mechanism remains unclear. Here, the mechanism of BPs-induced neurodevelopmental toxicity and its effective detoxification measures were investigated in vitro and in vivo. In in vitro experiments, primary hippocampal neurons from neonatal rats of different genders were treated with bisphenol A (BPA), bisphenol S (BPS) and bisphenol B (BPB) at 1 nM-100 µM, epigallocatechin gallate (EGCG) and G15, an antagonist of G protein-coupled estrogen receptor (GPER) for 7 d. Results indicated that BPs affected neuronal morphogenesis, impaired GABA synthesis and Glu/GABA homeostasis. Neuronal morphogenetic damage induced by low-doses BPA may be mediated by GPER. Neurotoxicity of BPS is weaker than BPA and BPB. In in vivo studies, exposure to BPA (0.5 µg/kg·bw/day) on PND 10-40 caused oxidative stress and inflammation in rat hippocampus, disrupted neuronal morphogenesis and neurotransmitter homeostasis, ultimately impaired spatial memory of rats. Males are more sensitive to BPA exposure than females. Both in vivo and in vitro studies indicated that EGCG, a phytoestrogen, can alleviate BPA-induced neurotoxicity. Taken together, low-doses BPA exposure sex-specifically disrupted neurodevelopment and further impaired learning and memory ability in rats, which may be mediated by GPER. Promisingly, EGCG effectively mitigated the BPA-induced neurodevelopmental toxicity.

The effects of large-volume leukapheresis on hemoglobin, platelet and coagulation in patients with hyperleukocytic leukemia.

INTRODUCTION: This study retrospectively analyzed a total of 86 leukapheresis treatments in 55 patients with hyperleukocytic leukemia (HLL). METHODS: In the leukapheresis treatments, the monitoring collection (MNC) program in COBE spectra continuous flow centrifuge (CFC) for blood component separator was used. RESULTS: In this study, the white blood cell (WBC) suspension volume collected in leukapheresis treatment were 870.72±208.40 mL, and significantly larger than that reported in previous study. Compared with before leukapheresis, there were no difference in patient with HLL on the peripheral blood platelet (PLT) count and hemoglobin (HGB) levels. The index plasma fibrinogen (FIB) concentration was slightly reduced by leukapheresis, however, it did not affect a lot the maintenance of normal hemostatic function in patients with HLL. DISCUSSION: Our data provided evidences that large-volume leukapheresis had no obvious effects on HGB level and coagulation functions in patient with HLL. So large-volume leukapheresis by CFC could be widely used in clinic.

Polybrominated diphenyl ethers and bromophenols in paired serum, hair, and urine samples of e-waste dismantlers: Insights into hair as an indicator of endogenous exposure.

Polybrominated diphenyl ethers (PBDEs) are important pollutants during dismantling activities of electronic waste (e-waste) in China due to its large production and usage. Bromophenols (BPs), which are a kind of flame retardants and diphenyl ether bond cleavage metabolites of PBDEs, are often neglected in the assessment of human exposure to e-waste. Herein, 22 PBDEs and 19 BPs were determined in paired serum, hair, and urine samples collected from workers and residents of a typical e-waste dismantling site in southern China. Both PBDE and BP congeners were more frequently detected in hair than serum and urine samples. The medians of ΣPBDEs and ΣBPs were 350 and 547 ng/g dw in hair internal (hair-In) of occupational population, respectively, which were significantly higher than non-occupational population. However, a non-significant difference was found in levels of ΣPBDEs and ΣBPs in serum and urine between occupational and non-occupational populations, suggesting that hair analysis could easily differentiate between the exposure intensities of PBDEs and BPs to populations than serum and urine analyses. Moreover, levels of BPs in hair-In were 1-2 orders of magnitude higher than those in hair external (hair-Ex), while a non-significant difference was found in the levels of PBDEs. This result indicated that BPs might have originated from endogenous contribution. Notably, as the predominant congeners, the level of 2,4,6-tribromophenol (2,4,6-TBP) in hair-In was 3-8 times higher than that of BDE-209, while level of 2,4,6-TBP in hair-Ex was 1-3 times lower than that of BDE-209. Furthermore, in vivo experiments performed on Sprague-Dawley rats following a 28-day oral treatment with BDE-209 and 2,4,6-TBP verified that endogenous accumulation of 2,4,6-TBP in hair could be attributed to the metabolism of BDE-209 and exposure to 2,4,6-TBP. In conclusion, compared with PBDEs, biomonitoring phenolic compounds or metabolites with hair could better reflect human endogenous exposure.

In vitro and in silico assessment of GPER-dependent neurocytotoxicity of emerging bisphenols.

To rapidly assess the toxicity of bisphenols (BPs) via the activation of G protein-coupled estrogen receptor (GPER), eight BPs action on GPER were evaluated by molecular docking and molecular dynamics (MD) simulation and then confirmed with IMR-32 cells. The target BPs significantly promoted the production of reactive oxygen species (ROS), reduced cell viability, activated the expression of apoptosis-related proteins and increased the apoptosis rate of IMR-32 cells. Intracellular Ca2+ level increased significantly after the treatments with bisphenol A (BPA), bisphenol E (BPE), bisphenol C (BPC) and bisphenol AP (BPAP), suggesting the activation of GPER. Moreover, the stable binding conformations between GPER and BPA, BPE, BPC and BPAP and their dynamic changes of GPER-BPs via MD simulation also suggest that these BPs may activate GPER. The interaction between bisphenol G/bisphenol P/bisphenol PH and GPER are weak, which is consistent with their low GPER activity in vitro. Notably, after the pretreatment of GPER antagonist, Ca2+ accumulation and ROS production induced by BPA, BPE, BPC and BPAP in IMR-32 cells were attenuated. Overall, MD simulation and in vitro results mutually verified the activation of GPER by BPs, and MD simulation can rapidly evaluate the neurocytotoxicity of BPs.

What adverse health effects will environmental heavy metal co-exposure bring us: based on a biological monitoring study of sanitation workers.

To investigate the relationship between health effect profile and co-exposure to heavy metal, 254 sanitation workers from Guangzhou, China, were recruited. Ten urinary metals were determined by inductively coupled plasma mass spectrometry. Parameters of physical examination, including blood lipid metabolism, renal function, blood pressure, and lung function, were tested for each participant. The hazard quotients (HQs) of eight heavy metals were evaluated. Cobalt, copper (Cu), molybdenum (Mo), nickel (Ni), and tin (Sn) demonstrated the top five associations with human health with the ∑19ß as 2.220, 1.351, 1.234, 0.957, and 0.930, respectively. Most physical examination parameters of workers were under the normal ranges, except the levels of forced mid expiratory flow rate (MMEF75/25), the maximum expiratory flow rate at 25% vital capacity (MEF25) and apolipoprotein B in the first quartile, and the level of uric acid in the third quartile of sanitation works. Moreover, Cu was significantly associated with diastolic pressure, pulse, and high density lipid (p < 0.05). Each unit increase in Mo level was related to a 120% increase odd ratio (OR) of abnormal of systolic pressure, but was significantly and negatively correlated with high density lipoprotein and apolipoprotein A, suggesting that Mo exposure may be a risk factor of cardiovascular disease. Each unit increase in Ni and Sn levels was associated with an increased OR of abnormal rate of MMEF75/25 and MEF25 (p < 0.001), suggesting the increasing risks of respiratory diseases. Sanitation workers exposed to Ni and Pb alone had no carcinogenic risks (HQ < 1). However, 23.8%, 34.6%, and 87.3% of sanitation workers confronted non-carcinogenic risks when exposed to Cu, Mo alone (HQ > 1), or co-exposed to the four heavy metals (HI > 1). Our study preliminarily revealed the potential sensitive health indicators of heavy metal co-exposure, which will provide beneficial health protection suggestions for the occupational populations.

Relationship of polycyclic aromatic hydrocarbons exposure with vascular damages among sanitation workers.

Chronic exposure to polycyclic aromatic hydrocarbons (PAHs) leads to a high incidence of cardiovascular diseases. To assess the effects of PAHs exposure on vascular damages in occupationally exposed populations, 196 sanitation workers were recruited. According to the differences of occupation or operation, they were divided into exposure group (n = 115) and control group (n = 81). Sixteen serum PAHs were determined by gas chromatography-tandem mass spectrometery. Tumor necrosis factor ɑ (TNF-ɑ) and angiotensin II (ANG-II) in serum, blood lipids and blood pressure were also measured. Results showed that, except for indeno(1,2,3-cd)pyrene, dibenzo(a,h)anthracene and benzo(g,h,i)perylene, the detection frequencies of other PAHs were above 85%, showing that subjects are generally exposed to PAHs. The top three compounds in serum concentrations of PAHs were phenanthrene, acenaphthylene and anthracene. Moreover, the concentrations of total serum PAHs in the exposure group were significantly higher than those in the control (p < 0.05), suggesting a higher PAHs exposure in the former. Though there was no significant difference in blood lipids and blood pressure between groups (p > 0.05), TNF-ɑ and ANG-II levels in the exposure group were significantly higher than those in the control group (p < 0.05), suggesting that PAHs exposure may be related to pro-inflammatory effects and vascular endothelial damages.

Four-year population exposure study: Implications for the effectiveness of e-waste control and biomarkers of e-waste pollution.

E-waste pollution has emerged as a significant environmental concern. To assess the impact of e-waste control on human pollutant exposure risk and identify appropriate biomarkers to classify e-waste pollution levels, we performed longitudinal population exposure monitoring research in an e-waste recycling area in China after e-waste control. The urinary levels of oxidative stress markers and typical pollutants emitted during e-waste recycling, including heavy metals, polycyclic aromatic hydrocarbons (PAHs), and volatile organic compounds (VOCs), were continuously monitored in the surrounding population (including 275 children and 485 adults) from 2016 to 2019 using high-performance liquid chromatography-tandem mass spectrometry and inductively coupled plasma-mass spectrometry. The results showed that exposure to PAHs, VOCs and heavy metals was significantly associated with oxidative stress levels in urine. After e-waste control, the exposure levels of most PAHs and VOCs and a few heavy metals in the population significantly decreased. Interestingly, the level of 8-hydroxy-2'-deoxyguanosine (a biomarker of oxidative DNA damage) in children significantly decreased by 17.6 %, from 9.45 µg/g CRE in 2017 to 7.79 µg/g CRE in 2019 (p < 0.01). Thus, implementing e-waste control measures effectively reduced the human exposure risk to e-waste pollutants. Urinary tin (Sn), s-phenylmercapturic acid (PMA), 2-&3-hydroxyfluorene (2-&3-OHF), 3-hydroxyphenanthrene (3-OHPhe), and 1-hydroxypyrene (1-OHP) levels decreased significantly and monotonically over time (p < 0.01). The levels of urinary Sn and PMA in combination with 1-OHP, 2-&3-OHF, or 3-OHPhe as biomarkers demonstrated an excellent ability to classify e-waste pollution. These biomarkers will facilitate evaluations of the effectiveness of the governmental pollution regulations and policy measures. Additionally, children were generally exposed to higher levels of heavy metals and VOCs and suffered higher levels of oxidative stress damage than adults, suggesting that children are more vulnerable to e-waste pollution. This work will provide a reference for e-waste management and control.

Human exposure to BTEX emitted from a typical e-waste recycling industrial park: External and internal exposure levels, sources, and probabilistic risk implications.

Benzene, toluene, ethylbenzene, and xylene (BTEX) can be released during extensive activities associated with the disposal of electronic waste (e-waste), which might pose deleterious health effects on workers. In this study, pollution profiles of BTEX in air and their urinary excretive profiles in occupational workers were investigated in a typical e-waste recycling industrial park. The results showed that the workers in the park were generally exposed to high levels of BTEX. The median levels of urinary metabolites were approximately 6-orders of magnitude higher than those of unmetabolized BTEX, indicating that pollutants efficiently metabolize at those occupational levels. The analytes presented differential profiles in external and internal exposure. Among the metabolites, significant correlation (p < 0.05) was observed between N-acetyl-S-benzyl-L-cysteine (S-BMA) concentration and atmospheric individual BTEX derived from the e-waste recycling area, suggesting that S-BMA is a potential marker for BTEX exposure to e-waste occupational workers. Notably, 95.2 % of all the workers showed a cumulative carcinogenic risk induced by BTEX exposure via inhalation, with 99.9 % of the carcinogenic risk distribution based on concentration of benzene metabolite (N-acetyl-S-(phenyl)-L-cysteine) exceeding 1.0E-6. This study holds potential in providing valuable inferences for the development of remediation strategies focusing on BTEX exposure reduction to protect workers' health at e-waste recycling industries.

Identification, Phylogenetic and Expression Analyses of the AAAP Gene Family in Liriodendron chinense Reveal Their Putative Functions in Response to Organ and Multiple Abiotic Stresses.

In this study, 52 AAAP genes were identified in the L. chinense genome and divided into eight subgroups based on phylogenetic relationships, gene structure, and conserved motif. A total of 48 LcAAAP genes were located on the 14 chromosomes, and the remaining four genes were mapped in the contigs. Multispecies phylogenetic tree and codon usage bias analysis show that the LcAAAP gene family is closer to the AAAP of Amborella trichopoda, indicating that the LcAAAP gene family is relatively primitive in angiosperms. Gene duplication events revealed six pairs of segmental duplications and one pair of tandem duplications, in which many paralogous genes diverged in function before monocotyledonous and dicotyledonous plants differentiation and were strongly purification selected. Gene expression pattern analysis showed that the LcAAAP gene plays a certain role in the development of Liriodendron nectary and somatic embryogenesis. Low temperature, drought, and heat stresses may activate some WRKY/MYB transcription factors to positively regulate the expression of LcAAAP genes to achieve long-distance transport of amino acids in plants to resist the unfavorable external environment. In addition, the GAT and PorT subgroups could involve gamma-aminobutyric acid (GABA) transport under aluminum poisoning. These findings could lay a solid foundation for further study of the biological role of LcAAAP and improvement of the stress resistance of Liriodendron.

[Reform of the bio-separation engineering curriculum under the context of "Emerging Engineering Education"].

"Bio-separation engineering" is a compulsory course for undergraduate students majored in bioengineering, and an important part of the "emerging engineering education" system for bioengineering. Our teaching team follows the principle of "student development as the center, innovation thinking as the core". Guided by the concept of "learning achievement", we reconstructed the teaching contents of this course, and carried out the teaching reform aiming at solving several long-standing problems. These include, for instance, the theoretical teaching is separated from the experimental practice, and students cannot internalize the theoretical knowledge into practical ability in time. Moreover, the contents of course is out-of-date and out of line with industry demand, the teaching form and assessment methods are relatively single, and the students' professional ability and quality are not effectively cultivated. In the new curriculum system, in which the "online" and "offline" teaching are both applied, we broke the boundary between theoretical and experimental courses, and made the contents keep up with the forefront of industry development through research-based teaching. In terms of teaching methods and teaching evaluation, we made full use of modern information technology to enrich classroom teaching activities, and carried out complete, dynamic and diversified assessment for students. These teaching reform measures greatly improved the students' interest in learning this course, as well as their professionalism and research ability.

Involvement of NLRP3/Caspase-1/GSDMD-Dependent pyroptosis in BPA-Induced apoptosis of human neuroblastoma cells.

Bisphenol A (BPA) induces neurotoxicity via enhancing cell apoptosis and inflammation potently (effective at nanomolar concentrations), but its mechanisms remain unidentified. In this study, human neuroblastoma cell lines, IMR-32 and SK-N-SH cells, isolated from a male and a female subject, respectively, were exposed to BPA at various concentrations, with epigallocatechin gallate (EGCG, an antioxidant from green tea), Z-YVAD-FMK (a caspase-1 inhibitor), and ICI182.780 [an estrogen receptor (ER) inhibitor] as modulators. The results showed that BPA increased the mRNA levels of IL-18, ASC, GSDMD and protein levels of NLRP3, caspase-1 and GSDMD in both cell lines in a nonlinear manner. Noticeably, the direction of changes in the mRNA levels of caspase-1 and IL-1ß were opposite, so did each of them in different cell lines: caspase-1 was enhanced in IMR-32 cells but suppressed in SK-N-SH cells, while IL-1ß was suppressed in IMR-32 cells but enhanced in SK-N-SH cells. The level of GSDMD in situ increased along with the leakage of IL-1ß, IL-18, caspase-1 and lactate dehydrogenase (LDH). Moreover, all the above effects of BPA were reversed by Z-YVAD-FMK, ICI182.780, and EGCG. Besides, BPA significantly increased reactive oxygen species production, LDH leakage and apoptosis, with reduced cell viability and mitochondrial membrane potential, in both cell lines, whereas Z-YVAD-FMK and ICI182.780 significantly alleviated the induction of Bak1, Bax, Bcl-2 and caspase-3 proteins by BPA. In summary, BPA may induce pyroptosis in neuroblastoma cells through NLRP3/caspase-1/GSDMD pathway, as mediated by ER; caspase-1-dependent pyroptosis may also contribute to BPA-induced apoptosis, an effect alleviated by EGCG.

Impaired nitrergic relaxation in pyloric sphincter of the 6-OHDA Parkinson's disease rat.

Patients with Parkinson's disease (PD) often suffer from delayed gastric emptying, but the underlying mechanism remains unclear. We have shown previously that a PD rat model comprising bilateral substantia nigra destruction by 6-hydroxydopamine (6-OHDA rats) exhibits gastroparesis with alteration of neural nitric oxide synthase (nNOS) and acetylcholine in gastric corpus. However, changes in pyloric motility in the 6-OHDA rats have not been characterized. Solid gastric emptying test, immunofluorescence, Western blot, and in vitro pyloric motility recordings were used to assess pyloric motor function in the 6-OHDA rats. The 6-OHDA-treated rats displayed delayed solid gastric emptying and a lower basal pyloric motility index. In the 6-OHDA rats, high K+-induced transient contractions were weaker in pyloric sphincters. Electric field stimulation (EFS)-induced pyloric sphincter relaxation was lower in the 6-OHDA rats. NG-nitro-l-arginine methyl ester (l-NAME), a nonselective inhibitor of NOS, markedly inhibited the EFS-induced relaxation in both control and 6-OHDA rats. Pretreatment of tetrodotoxin abolished the effect of EFS on the pyloric motility. In addition, nNOS-positive neurons were extensively distributed in the pyloric myenteric plexus, whereas the number of nNOS-immunoreactive neurons and the protein expression of nNOS were significantly decreased in the pyloric muscularis of 6-OHDA rats. However, sodium nitroprusside-induced pyloric relaxations were similar between the control and 6-OHDA rats. These results indicate that the pyloric sphincters of 6-OHDA rats exhibit both weakened contraction and relaxation. The latter may be due to reduced nNOS in the pyloric myenteric plexus. The dysfunction of the pyloric sphincter might be involved in the delayed gastric emptying.NEW & NOTEWORTHY Reduced nitrergic neurons in pyloric myenteric plexus potently contributed to the attenuated relaxation in 6-hydroxydopamine (6-OHDA) rats, subsequently affecting gastric emptying. SNP could well improve the relaxation of pylori in 6-OHDA rats. The present study provides new insight into the diagnosis and treatment of delayed gastric emptying in patients with PD.