The adsorption and its mechanism of venlafaxine by original and aged polypropylene microplastic and the changes of joint toxicity.

Conjugation with the increment of consumption of polypropylene (PP) masks and antidepressants during pandemic, PP microplastics (MPs) and Venlafaxine (VEN) widely co-existed in surface waters. However, their environmental fate and the combined toxicity were unclear. Hence, we investigated the adsorption behaviors, and associated mechanisms of PP MPs for VEN. The impact factors including pH, salinity, and MPs aging were estimated. The results indicated PP MPs could adsorb amount of VEN within 24 h. The pseudo second-order kinetic model (R2 = 0.97) and Dubinin-Radushkevich model (R2 = 0.89) fitted well with the adsorption capacity of PP MPs for VEN, implying that chemical adsorption accompanied by electrostatic interaction might be the predominant mode for the interactions between PP MPs and VEN. Meanwhile, the adsorption capacity of PP MPs declined from pH of 2.5-4.5 and then increased from 4.5 to 9.5. The increased salinity (5-35 ppt) significantly suppressed the adsorption capacity. Aging by sunlight and UV triggered the formation of new functional group (carbonyl) on MPs, and then enhanced the adsorption capacity for VEN. Gaussian Model analysis further evidenced the electrostatic adsorption occurring in PP MPs and VEN. The combined exposure to PP MPs and VEN showed significantly antagonistic toxicity on Daphnia magna. The adsorption of VEN by PP MPs mitigated the lethal effects and behavioral function impairment posed by VEN on animals, implying the potential protective effects on zooplankton by PP MPs. This study for the first time provides perspective for assessing the environmental fate of MPs and antidepressants in aquatic system.

Incidence and risk factors of subclinical rejection after pediatric liver transplantation, and impact on allograft fibrosis.

INTRODUCTION: Subclinical rejection (SCR) is a common injury in protocol biopsy after pediatric liver transplantation (pLT), but its effect on the recipient is not clearly understood. We herein investigated the incidence and risk factors involved in SCR and analyzed the relationship between SCR and allograft fibrosis (AF). METHODS: We retrospectively reviewed the biopsy results from 507 children between May 2013 and May 2019, and 352 patients underwent protocol biopsy 2 years after pLT, 203 underwent protocol biopsy 5 years after pLT, and 48 underwent protocol biopsy both 2 and 5 years after pLT. RESULTS: The incidence of SCR in the 5-year group was higher than that in the 2-year group (20.2% vs.13.4%, respectively, p = .033). The number of patients with mild and moderate SCR in the 5-year group was also higher than that in the 2-year group (p = .039). Logistic regression analysis showed that acute rejection before liver biopsy and deceased donor liver transplantation (DDLT) were independent risk factors for SCR in the two groups, and that the incidence and severity of AF in protocol biopsies at both periods in the SCR group were higher than those in the non-SCR group (p < .05). CONCLUSIONS: The incidence and severity of SCR increased with the prolongation of protocol biopsy time. We postulate that acute rejection and DDLT are independent risk factors for SCR after transplantation. As the occurrence of SCR also augmented the incidence and severity of AF.

A novel predictive model of microvascular invasion in hepatocellular carcinoma based on differential protein expression.

BACKGROUND: This study aims to construct and verify a nomogram model for microvascular invasion (MVI) based on hepatocellular carcinoma (HCC) tumor characteristics and differential protein expressions, and explore the clinical application value of the prediction model. METHODS: The clinicopathological data of 200 HCC patients were collected and randomly divided into training set and validation set according to the ratio of 7:3. The correlation between MVI occurrence and primary disease, age, gender, tumor size, tumor stage, and immunohistochemical characteristics of 13 proteins, including GPC3, CK19 and vimentin, were statistically analyzed. Univariate and multivariate analyzes identified risk factors and independent risk factors, respectively. A nomogram model that can be used to predict the presence of MVI was subsequently constructed. Then, receiver operating characteristic (ROC) curve, calibration curve, and decision curve analysis (DCA) were conducted to assess the performance of the model. RESULTS: Multivariate logistic regression analysis indicated that tumor size, GPC3, P53, RRM1, BRCA1, and ARG were independent risk factors for MVI. A nomogram was constructed based on the above six predictors. ROC curve, calibration, and DCA analysis demonstrated the good performance and the clinical application potential of the nomogram model. CONCLUSIONS: The predictive model constructed based on the clinical characteristics of HCC tumors and differential protein expression patterns could be helpful to improve the accuracy of MVI diagnosis in HCC patients.

Critical role of VGLL4 in the regulation of chronic normobaric hypoxia-induced pulmonary hypertension in mice.

Pulmonary hypertension (PH), a rare but deadly cardiopulmonary disorder, is characterized by extensive remodeling of pulmonary arteries resulting from enhancement of pulmonary artery smooth muscle cell proliferation and suppressed apoptosis; however, the underlying pathophysiological mechanisms remain largely unknown. Recently, epigenetics has gained increasing prominence in the development of PH. We aimed to investigate the role of vestigial-like family member 4 (VGLL4) in chronic normobaric hypoxia (CNH)-induced PH and to address whether it is associated with epigenetic regulation. The rodent model of PH was established by CNH treatment (10% O2 , 23 hours/day). Western blot, quantitative reverse transcription polymerase chain reaction, immunofluorescence, immunoprecipitation, and adeno-associated virus tests were performed to explore the potential mechanisms involved in CNH-induced PH in mice. VGLL4 expression was upregulated and correlated with CNH in PH mouse lung tissues in a time-dependent manner. VGLL4 colocalized with α-smooth muscle actin in cultured pulmonary arterial smooth muscle cells (PASMCs), and VGLL4 immunoactivity was increased in PASMCs following hypoxia exposure in vitro. VGLL4 knockdown attenuated CNH-induced PH and pulmonary artery remodeling by blunting signal transducer and activator of transcription 3 (STAT3) signaling; conversely, VGLL4 overexpression exacerbated the development of PH. CNH enhanced the acetylation of VGLL4 and increased the interaction of ac-H3K9/VGLL4 and ac-H3K9/STAT3 in the lung tissues, and levels of ac-H3K9, p-STAT3/STAT3, and proliferation-associated protein levels were markedly up-regulated, whereas apoptosis-related protein levels were significantly downregulated, in the lung tissues of mice with CNH-induced PH. Notably, abrogation of VGLL4 acetylation reversed CNH-induced PH and pulmonary artery remodeling and suppressed STAT3 signaling. Finally, STAT3 knockdown alleviated CNH-induced PH. In conclusion, VGLL4 acetylation upregulation could contribute to CNH-induced PH and pulmonary artery remodeling via STAT3 signaling, and abrogation of VGLL4 acetylation reversed CNH-induced PH. Pharmacological or genetic deletion of VGLL4 might be a potential target for therapeutic interventions in CNH-induced PH.

Quantify individual variation of real-time PM2.5 exposure in urban Chinese homes based on a novel method.

Fine particulate matter (PM2.5 ) concentrations show high variations in different microenvironments indoors, which has considerable impact on risk management. However, the real-time variations of PM2.5 exposure associated with per activity/microenvironment and intra-variation among family members remain undefined. In this study, real-time monitors were used to collect real-time PM2.5 data in different microenvironments in 32 households in urban community of China. Peak concentrations of PM2.5 were found in kitchen. The parallel levels of PM2.5 household indoor and outdoor indicated the benefit of clean energies use. To validly assess the health risk of individuals, we proposed a novel method to estimate the real-time exposure of all residents and firstly investigate the intra-variation of PM2.5 exposure among family members. The member who is responsible for cooking in the family had the maximum PM2.5 exposure. The ratios among intraindividual variations demonstrated children usually had lower exposure compared to the adults as they stayed more time in lower polluted microenvironments such as living room and bedroom. The exposure intensity in living room was above 1.0 for most residents, indicating it is warranted to alleviate the air pollution in living room. This study firstly focused on the intra differences of PM2.5 exposure among family members and provided a new insight for indoor air pollution management. The results suggested when adopting measures to reduce exposure, the microenvironments pattern of each member should be taken into consideration. Future work is welcomed to move another big step on this issue to protect the human health.

Long non-coding RNAs HERH-1 and HERH-4 facilitate cyclin A2 expression and accelerate cell cycle progression in advanced hepatocellular carcinoma.

BACKGROUND: The advanced hepatocellular carcinoma (HCC), such as the recurrent tumor after liver transplantation (LT), is an obstacle of HCC treatment. The aim of this study was to discover the underlying mechanism of HCC progression caused by non-coding RNAs (ncRNAs). METHODS: To this end, we investigated the selected patient cohort of matching primary and recurrent HCC after receiving LT. The recurrent tumors after LT were regarded as clinical models of the advanced HCC. Microarrays were used to profile lncRNA and mRNA expression in HCC recurrent and primary tissue samples. The mRNA profile characteristics were analyzed by bioinformatics. Two cell lines, HepG2 and QGY-7703, were used as HCC cell models. The protein-coding potential, length, and subcellular location of the interested lncRNAs were examined by bioinformatics, Northern blot, fluorescent in situ hybridization (FISH), and quantitative RT-PCR (qRT-PCR) assays. HCC cell proliferation was detected by CCK-8, doubling time and proliferation marker gene quantitation assays. DNA replication during the cell cycle was measured by EdU/PI staining and flow cytometry analyses. Promoter activity was measured using a luciferase reporter assay. Interactions between DNA, RNA, and protein were examined by immunoprecipitation and pull-down assays. The miRNA-target regulation was validated by a fluorescent reporter assay. RESULTS: Both lncRNA and mRNA profiles exhibited characteristic alterations in the recurrent tumor cells compared with the primary HCC. The mRNA profile in the HCC recurrent tissues, which served as model of advanced HCC, showed an aberrant cell cycle regulation. Two lncRNAs, the highly expressed lncRNA in recurrent HCC (HERH)-1 and HERH-4, were upregulated in the advanced HCC cells. HERH-1/4 enhanced proliferation and promoted DNA replication and G1-S transition during the cell cycle in HCC cells. HERH-1 interacted with the transcription factor CREB1. CREB1 enhanced cyclin A2 (CCNA2) transcription, depending on HERH-1-CREB1 interaction. HERH-4 acted as an miR-29b/c sponge to facilitate CCNA2 protein translation through a competing endogenous RNA (ceRNA) pathway. CONCLUSIONS: The oncogenic lncRNA HERH-1/4 promoted CCNA2 expression at the transcriptional and post-transcriptional levels and accelerated cell cycle progression in HCC cells. The HERH-1-CREB1-CCNA2 and HERH-4-miR-29b/c-CCNA2 axes served as molecular stimuli for HCC advance.

Impacts of Chinese spring festival on household PM2.5 pollution and blood pressure of rural residents.

BACKGROUND: Household air pollution (HAP) from residential combustion considerably affects human health in rural China. Large-scale population migration and rural lifestyle changes during the Spring Festival are supposed to change the household air pollution and health risks; however, limited field study has determined its impacts on HAP and short-term health outcomes. METHODS: A field study was conducted in rural areas of Southern China before and during the Spring Festival to explore the associations between HAP and blood pressure considering different factors such as cooking fuel, heating fuel, and smoking. Stationary real-time PM2.5 monitors were used to measure PM2.5 concentrations of the kitchen, living room, and yard of 156 randomly selected households. Personal exposure to PM2.5 was calculated based on the results of stationary samplers and corresponding time local residents spent in different microenvironments, and one adult resident was recruited of each family for the blood pressure measurement. RESULTS: Both personal exposure to PM2.5 and blood pressures of local residents increased during Spring Festival compared to the days before the holiday. Based on generalized linear model coupled with dominance analysis approach, it was found that personal PM2.5 exposure was positively associated with the factors of population size and the types of cooking and heating fuels with the relative contributions of approximately 82%, and systolic blood pressure (SBP, 100-120 mmHg as normal range for adults) was positively and significantly associated with personal PM2.5 exposures with the relative contribution of 11%. CONCLUSION: The findings in this study demonstrated that Spring Festival can give rise to increase of HAP and hypertension risks, also related to tremendous solid fuel use, suggesting further policy making on promoting cleaner energy in rural areas and more attention on large population migration during national holidays.

Identification of diagnostic cytosine-phosphate-guanine biomarkers in patients with gestational diabetes mellitus via epigenome-wide association study and machine learning.

OBJECTIVE: To explore gestational diabetes mellitus (GDM) diagnostic markers and establish the predictive model of GDM. METHODS: We downloaded the DNA methylation data of GSE70453 and GSE102177 from the Gene Expression Omnibus database. Epigenome-wide association study (EWAS) was performed to analyze the relationship between cytosine-phosphate-guanine (CpG) methylation and GDM. And then the logistic regression models were constructed, with the ß-values of CpG sites as predictor variable and the GDM occurrence as binary outcome variable. Data from GSE70453 served as training sets and data from GSE102177 served as verification sets. RESULTS: The EWAS and overlap analysis identified nine-shared significant CpGs in the two DNA methylation data sets. Remarkably, these nine CpGs were differently methylated in GDM samples compared to their matched normal specimens, among which five fully methylated CpGs were finally selected. Importantly, we established a binary logistic regression model based on the above five CpGs, in which cg11169102, cg21179618 and cg21620107 were critical. Hence, we further built a logistic regression model by using the three CpGs and found that the area under the curve was 0.8209. The validation of the model by using the verification sets indicated the area under the curve was 0.8519. CONCLUSIONS: We identified potential CpG biomarkers for the diagnosis of gestational diabetes mellitus patients through using EWAS and Logistic regression models in combination.

Assessment on the lung injury of mice posed by airborne PM2.5 collected from developing area in China and associated molecular mechanisms by integrated analysis of mRNA-seq and miRNA-seq.

Some epidemiological evidences showed exposure of airborne fine particulate matter (PM2.5) was associated with lung dysfunction. However, the adverse effects of PM2.5 from mid-scale city of China on the respiratory system were unknown. Correspondingly, the mechanisms, especially the epigenetic mechanism regulated by miRNAs, involved in PM2.5-induced lung injury has not been fully understood. In this study, male Balb/C mice were exposed to PM2.5 collected from mid-scale city (Baoji), China for 8 weeks (mean concentration 298.52 ± 25.86 µg/m3 at exposure chamber) using a whole-body exposure system. The carbon component was the main ingredient (45.80%) of PM2.5 followed by ions (43.19%). Meanwhile, the sum concentrations of polycyclic aromatic hydrocarbons (PAHs) and n-alkanes (C18-C33) were 570.48 and 2029.13 ng/m3 in the exposure chamber, respectively. Obvious lung injury including pulmonary inflammation and fibrosis (p < 0.05 compared with the control) were found from PM2.5 exposure group determined by micro-CT and histopathological assays, respectively, suggesting the health risk posed by PM2.5 from mid-scale city of China should be concerned. The integrated analysis between mRNA-seq and miRNA-seq revealed the differentially expression genes in lung tissues were enriched in immune pathways including B cell receptor signaling (p = 0.078) and cell adhesion molecules (CAMs) (p = 0.0068). The expression profiles of the genes and corresponding mRNAs involved into the immune pathways determined by RT-qPCR analysis were consistent with them conducted by transcriptome. Moreover, the expression levels of the proteins (i.e., CD19, CD81, PIK3CD, and CD22) involved into B cell receptor signaling pathway from exposure group were 1.71- to 6.948- folds compared with the control, validating the results of the genes expression profiles. Further, canonical correlation analysis (CCA) and multiple correlation analysis between the target genes and components of PM2.5 documented the organic compounds (i.e., Benzo(a)pyrene (p = 0.012) and octadecane (p = 0.05)) and inorganic elements (i.e., Cl-, Ti, Al, and Zn) was the key environmental factors. Cd19, Pik3cd, and Cd8b1 might be the key genes for lung dysfunction induced by PM2.5 illuminated using interactive analysis (p < 0.05). This work for the first time showed the adverse effects of PM2.5 in mid-scale city in China on respiratory system should be concerned, and the associated epigenetic mechanism regulated by miRNA were revealed. These results may provide new insight into the development of future assessment on the air pollution associated respiratory disease.

Inhalation exposure to size-segregated fine particles and particulate PAHs for the population burning biomass fuels in the Eastern Tibetan Plateau area.

Indoor biomass burning produces large amounts of small particles and hazardous contaminants leading to severe air pollution and potentially high health risks associated with inhalation exposure. Personal samplers provide more accurate estimates of inhalation exposure. In this study, inhalation exposure to size-segregated particles and particulate polycyclic aromatic hydrocarbons (PAHs) for the biomass user was studied by deploying personal samplers. The study found that daily PM2.5 inhalation exposure level was as high as 121 ± 96 µg/m3, and over 84% was finer PM1.0. For PAHs, the exposure level was 113 ± 188 ng/m3, with over 77% in PM1.0. High molecular weight PAHs with larger toxic potentials enriched in smaller particles resulting in much high risks associated with PAHs inhalation exposure. Indoor exposure contributed to ~80% of the total inhalation exposure as a result of high indoor air pollution and longer residence spent indoor. The highest exposure risk was found for the male smoker who conducted cooking activities at home.

Temporal responses of hydrochemical variables and dissolved Fe(II) to flooding at a lake riparian wetland under different vegetation revealing by high resolution DGT.

The interplay between hydrological and biogeochemical processes in riparian wetland was recognized to lead directly to the temporal variations of surface water quality. However, the effects of flooding and vegetation on the release and entrapment of heavy metals and nutrients in riparian wetland remain poorly understood. The study aimed at investigating the influences of flooding and vegetation on the hydrochemical and Fe-redox change in the soil porewater and shallow groundwater, in Poyang lake riparian wetland through hydrochemical monitoring and diffusive gradient technology (DGT). The hydrochemical profiles and results of PCA analysis on the temporal datasets both demonstrated that vegetation had significant influences on the hydrochemistry of rhizosphere depth zone (RDZ) and shallow groundwater depth zone (SGZ). The Ca, K, Na, Mg, Mn and DOC at RDZ of both plants showed significant increasing trends from pre-to post-flooding while were observed minor change at the SGZ. The extracted PC1-PC3 from PCA analysis suggested that mineral dissolution and fermentation were dominating processes that explained 64.1% of the hydrochemical variability under the wetting-drying cycle. The synchronous changes of Fe(II), SO42-, DOC and ORP were found to occur at the SGZ of Carex, implying the likely occurrence of Fe- and S- redox reactions. The Fe(II) DGT profiles evidenced the temporal iron reduction and oxidation occurring at the rhizosphere following the wetting-drying cycle, as also reflected by the high opposite Fe2+ and DO association through PCA analysis. The high resolution temporal-spatial Fe(II) distribution suggested also the interface between lake water and groundwater was relatively stable under flooding. These results highlight that the release of dissolved Fe(II) from the wetland rhizosphere driven by flood may result in the release of Fe-associated heavy metals from riparian wetland to surface water, and hence pose potential threats to the surface water quality. Thereby, the flow and flood should be properly controlled and vegetation effects need to be carefully considered in the water resources management of lake-floodplain system.

New sights on the associations between the XRCC1 gene polymorphisms and hepatocellular carcinoma susceptibility.

Studies investigating the relationships between the polymorphisms in the X-ray repair cross complementing 1 (XRCC1) gene and the susceptibility of hepatocellular carcinoma (HCC) remained controversial, therefore, we assessed this associations by metaanalysis and trial sequential analysis (TSA). PubMed, Embase, Google Scholar, Chinese National Knowledge Infrastructure and Baidu Scholar were comprehensively screened to retrieve relevant studies up to May 20, 2019. A total of 32 studies was included. Significant associations were discovered in the overall and subgroup analysis in these three polymorphisms. Interestingly, the decreased risk of HCC was detected in the Indians for the rs24587 polymorphism. TSA indicated the required information size for the rs25487 polymorphism were reached, but for the rs25489 and rs1799782 polymorphisms, more well-designed trials were required. Sensitivity analysis implied our results were stable; no publication bias was observed in the rs25487 and rs1799782 polymorphisms. The bioinformatic analysis indicate that the rs1799782 polymorphism is probably damaging and has an influence on the XRCC1 protein function. Our study indicated that the XRCC1 rs25487 was a risk factor for the susceptibility of HCC, which was verified by the TSA. In addition, the rs25489 and rs1799782 polymorphisms were associated with increased risk of HCC. In the subgroup analysis, increased risks were detected in some subgroups (in accordance with Hardy-Weinberg equilibrium, Chinese groups, Mongoloid subgroup, polymerase chain reaction-restriction fragment length polymorphisms and more than 300 subgroups), moreover, decreased HCC risk of the rs25487 polymorphism was firstly observed, which required further studies to verify.

Prognostic evaluation of NANOG and OCT4 expression for posttransplantation hepatocellular carcinoma recurrence.

Postoperative hepatocellular carcinoma (HCC) recurrence and metastasis throw great threaten to its overall survival (OS). This paper focus on exploring the prognostic significance of NANOG and OCT4 expression in HCC recurrence and OS after liver transplantation. Eighty-six patients who meet University of California San Francisco (UCSF) criteria and underwent liver transplantation in Tianjin First Central Hospital between August 2010 and August 2013 were included. Expression of NANOG and OCT4 was determined by immunohistochemistry. The relationships between NANOG and OCT4 expression with tumor recurrence, tumor count, histology stage, lymph node metastasis (LNM) and microvascular invasion (MVI) were explored through the χ2 test and Cox regression analysis. We found that 19/26 and 20/24 patients with positive expression of NANOG and OCT4 relapsed. Combination of NANOG and OCT4 expression was indicated as valuable prognostic signature for HCC recurrence prediction (P < 0.0011). Besides, we identified other key factors with significant correlations with recurrence, such as LNM (P = 0.011) and MVI (P = 0.024). Strikingly, recurrence sites could significantly affect recurrence time (P = 0.0062) and patients with recurrence in transplanted liver have longer recurrence time. In conclusions, we analyzed the relationships between NANOG/OCT4 expression, clinicopathology features, HCC recurrence, and OS after liver transplantation for the first time. Combination of NANOG, OCT4, LNM, histopathological stage, and MVI may be predictor for HCC recurrence posttransplantation. Comprehensive of histopathological stage grade and LNM were considered as prognosis factor for OS after liver transplantation. This should be helpful for treatment method selection for HCC patients after liver transplantation.

Alterations of Serum IP-10 and TARC in Patients with Early Acute Rejection after Liver Transplantation.

BACKGROUND/AIMS: To analyze alterations of interferon-γ-induced protein 10 (IP-10) and thymus and activation-regulated chemokine (TARC) levels in early acute liver transplantation rejection. METHODS: Thirty-six patients with early acute liver transplantation rejection were classified as non-, mild, moderate, and severe rejection groups. The levels of serum IP-10 and TARC were determined on days 3, 2, 1, and 0 before biopsy. RESULTS: The IP-10 activities in all rejection groups were significantly higher (p < 0.05) than those in the non-rejection group at all time points and correlated with the extent of rejection (p < 0.05). The differences in TARC among the three rejection groups were significant (p < 0.05), and its highest level was found in the mild rejection group at all observed time points, whereas its lowest level was detected in the severe rejection group. The analysis of the TARC/IP-10 ratio revealed that the volume was correlated with the rejection degree. This ratio in the moderate and severe rejection groups on days 2, 1, and 0 before biopsy were 20% lower than that before transplantation. CONCLUSION: Serum IP-10 showed an increasing trend during early acute liver transplantation rejection. IP-10 increase or TARC/IP-10 ratio decrease combining with abnormal hepatic enzymatic alteration could be a valuable and specific sign for early rejection of the transplanted liver.

[The risk factors of splenic arterial steal syndrome after orthotopic liver transplantation].

OBJECTIVE: To discuss the risk factors of splenic arterial steal syndrome (SASS) after orthotopic liver transplantation. METHODS: Twenty-four cases who confirmed SASS after liver transplantation in Tianjin First Central Hospital between June 2005 and June 2013 were analyzed retrospectively. Another 96 cases were selected randomly from those patients of the same time with no complication of SASS patients postoperatively as control group. Clinical data of two groups including diameter of splenic artery and hepatic artery preoperatively, weight of graft, weight of recipients, cold/warm ischemia time, an hepatic period and operation time and so on were collected. Others including hepatic artery peak systolic velocity (PSV), end diastolic velocity (EDV), blood flow resistance index and portal vein average velocity (PVF) on the first day after liver transplantation, the day before diagnosis, the day when diagnosed, the 1, 3, 7 days after treatment in SASS group and on 1, 3, 7, 9, 11, 14 days after liver transplantation in control group. Statistical analysis were made between two groups. RESULTS: The splenic artery/hepatic artery ratio preoperatively and weight of donor liver,and the GRWR in SASS group and control group were 1.26 and 1.00, 1 032 g and 1 075 g, (1.40±0.30)% and (1.82±0.21)% respectively, with significantly statistical differences (Z=-6.40, Z=-2.22, t=-6.50; all P<0.05). The warm ischemia time, the cold ischemia time, the anhepatic period and operation time in SASS group and control group were 3.5 minutes and 4.0 minutes, 10.25 hours and 10.10 hours, 43 minutes and 45 minutes, 8.7 hours and 8.7 hours, with no significantly statistical differences (all P>0.05). RI of hepatic went up gradually in the early time after transplantation while dropped obviously when spleen artery spring coils embolization was received (P<0.01) and trended to stable two weeks later. CONCLUSIONS: Splenic artery/hepatic artery ratio and GRWR are the positive and negative risk factors respectively for SASS. The gradual rising of hepatic RI in the early time after transplantation may be the warning signal SASS and spleen artery spring coils embolization is the effective strategy for SASS after liver transplantation.

Caenorhabditis elegans as an In Vivo Model Organism to Elucidate Teratogenic Effects.

Exogenous teratogens contribute to approximately 10% of the human abnormality with exposure occurrence during the prenatal and fetal period. However, the assessment methods and underlying mechanism remain unclear. The nematode Caenorhabditis elegans has been recognized as one of the ideal model animals for toxicologic research as convenient culture, low cost, and complete phenotypes and genomic profiling. This chapter describes the protocols about the estimations on the teratogenic effects using nematodes as model organisms, including the growth, development, behavior, reproduction, energy balance, and transgenes.

Wastewater surveillance for antibiotics and resistance genes in a river catchment: Spatiotemporal variations and the main drivers.

Wastewater-based epidemiology (WBE) is used for mining information about public health such as antibiotics resistance. This study investigated the distribution profiles of six types of antibiotic resistance genes (ARGs) in wastewater and rivers in Wuhu City, China. The levels of ARGs found in the Qingyijiang River were significantly higher than other rivers, and were comparable to effluent levels. Among the ARGs, sulfonamides ARGs and intI1 were the predominant in both wastewaters and rivers. Additionally, the concentrations of ARGs were higher on weekends as opposed to weekdays. Their distribution patterns remained consistent inter-week and inter-season using linear regression analysis (p < 0.001). Interestingly, the occurrence levels of ARGs in wastewaters during spring were significantly higher than in autumn, although insignificant in rivers. The apparent removal rate of ARGs in domestic wastewater sources ranged from 61.52-99.29%, except for qepA (-1.91% to 81.09%), whereas the removal rates in mixed domestic and industrial wastewaters showed a marked decrease (-92.94% to 76.67%). A correlation network analysis revealed that azithromycin and erythromycin were key antibiotics, while blaNDM-1, tetM, tetB, and ermB were identified as key ARGs. Sulfonamide and fluoroquinolone antibiotics, and tetracycline and macrolide ARGs were the primary contributors. Linear mixed models demonstrated that socio-economic variables positively impacted the occurrence levels of ARGs, whereas wastewater flow and river runoff were the negative drivers for their concentrations in wastewaters and surface waters, respectively. Overall, this WBE study contributes to the understanding of spatiotemporal profiles and main drivers of the occurrence of ARGs in wastewater and receiving water.

A multi-omics investigation of the lung injury induced by PM2.5 at environmental levels via the lung-gut axis.

Long-term exposure to fine particulate matter (PM2.5) posed injury for gastrointestinal and respiratory systems, ascribing with the lung-gut axis. However, the cross-talk mechanisms remain unclear. Here, we attempted to establish the response networks of lung-gut axis in mice exposed to PM2.5 at environmental levels. Male Balb/c mice were exposed to PM2.5 (dose of 0.1, 0.5, and 1.0 mg/kg) collected from Chengdu, China for 10 weeks, through intratracheally instillation, and examined the effect of PM2.5 on lung functions of mice. The changes of lung and gut microbiota and metabolic profiles of mice in different groups were determined. Furthermore, the results of multi-omics were conjointly analyzed to elucidate the primary microbes and the associated metabolites in lung and gut responsible for PM2.5 exposure. Accordingly, the cross-talk network and key pathways between lung-gut axis were established. The results indicated that exposed to PM2.5 0.1 mg/kg induced obvious inflammations in mice lung, while emphysema was observed at 1.0 mg/kg. The levels of metabolites guanosine, hypoxanthine, and hepoxilin B3 increased in the lung might contribute to lung inflammations in exposure groups. For microbiotas in lung, PM2.5 exposure significantly declined the proportions of Halomonas and Lactobacillus. Meanwhile, the metabolites in gut including L-tryptophan, serotonin, and spermidine were up-regulated in exposure groups, which were linked to the decreasing of Oscillospira and Helicobacter in gut. Via lung-gut axis, the activations of pathways including Tryptophan metabolism, ABC transporters, Serotonergic synapse, and Linoleic acid metabolism contributed to the cross-talk between lung and gut tissues of mice mediated by PM2.5. In summary, the microbes including Lactobacillus, Oscillospira, and Parabacteroides, and metabolites including hepoxilin B3, guanosine, hypoxanthine, L-tryptophan, and spermidine were the main drivers. In this lung-gut axis study, we elucidated some pro- and pre-biotics in lung and gut microenvironments contributed to the adverse effects on lung functions induced by PM2.5 exposure.

The Exploration of Joint Toxicity and Associated Mechanisms of Primary Microplastics and Methamphetamine in Zebrafish Larvae.

The co-existence of microplastics (MPs) and methamphetamine (METH) in aquatic ecosystems has been widely reported; however, the joint toxicity and associated mechanisms remain unclear. Here, zebrafish larvae were exposed individually or jointly to polystyrene (PS) and polyvinyl chloride (PVC) MPs (20 mg/L) and METH (1 and 5 mg/L) for 10 days. The mortality, behavioral functions, and histopathology of fish from different groups were determined. PS MPs posed a stronger lethal risk to fish than PVC MPs, while the addition of METH at 5 mg/L significantly increased mortality. Obvious deposition of MPs was observed in the larvae's intestinal tract in the exposure groups. Meanwhile, treatment with MPs induced intestinal deposits and intestinal hydrops in the fish, and this effect was enhanced with the addition of METH. Furthermore, MPs significantly suppressed the locomotor activation of zebrafish larvae, showing extended immobility duration and lower velocity. METH stimulated the outcome of PS but had no effect on the fish exposed to PVC. However, combined exposure to MPs and METH significantly increased the turn angle, which declined in individual MP exposure groups. RNA sequencing and gene quantitative analysis demonstrated that exposure to PS MPs and METH activated the MAPK signaling pathway and the C-type lectin signaling pathway of fish, while joint exposure to PVC MPs and METH stimulated steroid hormone synthesis pathways and the C-type lectin signaling pathway in zebrafish, contributing to cellular apoptosis and immune responses. This study contributes to the understanding of the joint toxicity of microplastics and pharmaceuticals to zebrafish, highlighting the significance of mitigating microplastic pollution to preserve the health of aquatic organisms and human beings.