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Background: Autoimmune neuropathies are common peripheral nervous system (PNS) disorders. Environmental influences and dietary components are known to affect the course of autoimmune diseases. Intestinal microorganisms can be dynamically regulated through diet, and this study combines intestinal microorganisms with diseases to open up new therapeutic ideas. Methods: In Lewis rats, a model of Experimental Autoimmune Neuritis（EAN）was established with P0 peptide, Lactobacillus were used as treatment, serum T-cell ratio, inflammatory factors, sciatic neuropathological changes, and pathological inflammatory effects on intestinal mucosa were detected, and fecal metabolomics and 16s microbiome analysis were performed to further explore the mechanism. Results: In the EAN rat model, Lactobacillus paracasei L9 (LP) could dynamically regulate the CD4+/CD8+T balance in serum, reduce serum IL-1, IL-6 and TNF-α expression levels, improve sciatic nerve demyelination and inflammatory infiltration, and nervous system scores. Intestinal mucosa was damaged, Lactobacillus paracasei L9 (LP) gavage induced intestinal mucosa recovery; Occludin and ZO-1 upregulation; IL-1, TNF-α and Reg3γ downregulation. Finally, metabolomics and 16s microbiome analysis were performed, and differential metabolites were enriched with an important metabolic pathway, arginine and proline metabolism. Conclusion: LP may improve EAN in rats by influencing intestinal community and the lysine and proline metabolism.

Monkeypox has been spreading worldwide since May 2022, when the World Health Organization (WHO) declared the outbreak of a “Public health emergency of international concern”. The spread of monkeypox has posed a serious threat to the health of people all over the world but few studies have been carried out on it, and the molecular mechanism of monkeypox after infection remains unclear. We therefore implemented a transcriptome analysis to identify signaling pathways and biomarkers in monkeypox-infected cells to help understand monkeypox-host cell interactions. In this study, the dataset GSE36854 and GSE11234 were obtained from GEO. Among them, 84 significantly different genes were identified in the dataset GSE36854, followed by KEGG, GO analysis protein-protein interaction (PPI) construction and Hub gene extraction. We also analyzed the expression regulation patterns of hub genes and screened the drugs targeting the hub genes. The results showed that monkeypox-infected cells significantly activated the cellular immune response, and induced inflammatory response. IER3, IFIT2, IL11, ZC3H12A, EREG, IER2, NFKBIE, FST, IFIT1 and AREG were the top 10 hub genes, in which anti-viral gene IFIT1 and IFIT2 were significantly suppressed. AP-26113 and itraconazole promoting the expression of IFIT1 and IFIT2 may be used as new candidates for the treatment of monkeypox viral infection. Our results provide a new entry point for understanding the mode of interaction between monkeypox virus and its host.

Targeted therapy is an essential treatment for non-small cell lung cancer (NSCLC) that is always associated with the drug resistance. c-ros oncogene 1 (ROS1) gene point mutation is one of the leading factors causing drug resistance. However, the point mutation cell models of crizotinib are challenging to obtain, causing few reports on the drug resistance mechanism and the treatment strategy. We constructed CD74-ROS1 D2033N and CD74-ROS1 S1986F point mutant plasmids by fusion PCR technology and transfected them into A549 cells. Western blot and MTT assay proved that the drug-resistant cell lines were successfully transfected. The transwell assay confirmed that the mutant cells' motor abilities were significantly increased compared with the wild-type group. In addition, focal adhesion kinase (FAK) was significantly increased in mutant cells. Moreover, crizotinib resistance occurred in the mutant cells through the activation of FAK / phosphatidylinositol 3-kinase (PI3K) / protein kinase B (AKT) pathway. Next, crizotinib was combined with defactinib, a FAK inhibitor, to further explore its therapeutic effect. The results showed that the combination could significantly inhibit the proliferation, invasion and migration of mutant cells. In conclusion, we proved that CD74-ROS1 D2033N and CD74-ROS1 S1986F point mutant NSCLC cells were resistant to crizotinib through the activation of FAK/PI3K/AKT signaling pathway, and inhibiting FAK/PI3K/AKT signaling pathway activation by defactinib could overcome drug resistance in mutant cells.

Exogenous abscisic acid (ABA) has been implicated in plant response to cadmium (Cd) stress, but the underlying mechanism remains unclear. In the present study, we found that exogenous ABA application decreased Cd fixation in wild type (WT) root cell wall through reducing the hemicelluloses content, in parallel with the decreased expression of IRT1, ZIP1, ZIP4, HMA2 and HMA4, which are related to Cd uptake and translocation, and the increased expression of PDF2.6, PDR8 and AIT1, which are related to Cd chelation, efflux, and accumulation inhibition. These changes might be associated with the reduced Cd accumulation in roots and shoots and the alleviated Cd toxicity. In contrast, the mutation of ABI4, a transcription factor in ABA signaling pathway, significantly increased the expression of IRT1, ZIP1, ZIP4, HMA2 and HMA4, while decreased the expression of AIT1, PDF2.6 and PDR8, enhancing Cd accumulation in roots and shoots of abi4. The enhanced Cd-sensitivity in abi4 mutant could not be rescued by exogenous ABA addition compared with WT. In a word, we conclude that exogenous ABA mitigates Cd toxicity in Arabidopsis thaliana via inhibiting Cd uptake, translocation and accumulation, promoting Cd chelation and efflux, a pathway that might be regulated by ABI4.

Background The third-generation epithelial growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) have shown significant therapeutic effects on patients with non-small cell lung carcinoma (NSCLC) who carry active EGFR mutations, as well as those who have developed acquired resistance to the first-generation of EGFR-TKIs due to the T790M mutation. However, most patients develop drug resistance after 8–10 months of treatment. Currently, the mechanism has not been well clarified, and new therapeutic strategies are urgently needed. Methods Osimertinib resistant cell lines were established by culturing sensitive cells in chronically increasing doses of osimertinib. The anticancer effect of reagents was examined both in vitro and in vivo using the sulforhodamine B assay and a xenograft mouse model. The molecular signals were detected by western blotting. The combination effect was analyzed using CompuSyn software. Results We found that bromodomain and extra-terminal proteins (BETs) were upregulated in osimertinib resistant (H1975-OR) cells compared with those in the paired parental cells (H1975-P), and that knockdown of BETs significantly inhibited the growth of H1975-OR cells. The BET inhibitor JQ1 also exhibited stronger growth-inhibitory effects on H1975-OR cells and a greater expression of BETs and the downstream effector c-Myc than were observed in H1975-P cells. The histone deacetylase (HDAC) inhibitor trichostatin A (TSA) showed stronger growth suppression in H1975-OR cells than in H1975-P cells, but vorinostat, another HDAC inhibitor, showed equal inhibitory efficacy in both cell types. Consistently, downregulation of BET and c-Myc expression was greater with TSA than with vorinostat. TSA restrained the growth of H1975-OR and H1975-P xenograft tumors. The combination of TSA and JQ1 showed synergistic growth-inhibitory effects in parallel with decreased BET and c-Myc expression in both H1975-OR and H1975-P cells and in xenograft nude mouse models. BETs were not upregulated in osimertinib resistant HCC827 cells compared with parental cells, while TSA and vorinostat exhibited equal inhibitory effects on both cell types. Conclusion Upregulation of BETs contributed to the osimertinib resistance of H1975 cells. TSA downregulated BET expression and enhanced the growth inhibitory effect of JQ1 both in vitro and in vivo. Our findings provided new strategies for the treatment of osimertinib resistance.

The decline in high ecological water status in rivers is a significant concern in European countries. It is thus important to investigate the factors that cause sites to lose high status in order to undertake measures to protect and restore high status water quality. Analysis of 20 years of water quality data reveals strong mobility between high status and non-high status (especially good status) rivers. Associations between this mobility and socio-economic and physical environmental variables were estimated by multinomial logistic regression at national scale and regional scale. Based on reported changes in water quality status cross across 1990, 2000 and 2010, four classes of the mobility of high status were defined in this study: those sites that maintain high status (maintain), enter high status (enter), fluctuate between high and non-high status (fluctuate) and exit from high status (exit). The national results indicate that agricultural activity as indicated by variables representing intensity of livestock farming (organic nitrogen) and tillage farming (cereal share) and elevation had significant negative impacts on high status rivers. Meanwhile, significant differences in population density and septic tank density between ‘exit’, ‘maintain’, ‘fluctuate’ and ‘enter’ classes indicate that these factors played important roles in the stability of high status rivers. The regional outcomes reveal differential significant pressures across regions. For example, rainfall and elevation had positive impacts on high status rivers in the north-west region, while organic nitrogen had a negative effect in the south-west. This paper demonstrates the challenge in achieving the Water Framework Directive goal of maintaining high status rivers, given the sensitive and highly differentiated nature of areas that have lost high status or fluctuated in and out of high status. This paper also suggests the necessity for localised policies and mitigation measures.

Nonsmall cell lung cancer (NSCLC) is one of the most common malignancies and needs novel and effective chemotherapy. In this study, our purpose is to explore the anticancer effects of 2-methoxy-5((3,4,5-trimethosyphenyl) seleninyl) phenol (SQ) on human NSCLC (A549 and H460) cells. We found that SQ suppressed the proliferation of NSCLC cells in time- and dose-dependent manners, and blocked the cells at G2/M phase, which was relevant to microtubule depolymerization. Additionally, SQ induced A549 and H460 cell apoptosis by activating the mitochondrial apoptotic pathway. Further, we demonstrated that SQ enhanced the generation of reactive oxygen species (ROS), and pretreatment with N-acetyl- L-cysteine (NAC) attenuated SQ-induced cell apoptosis. Meanwhile, SQ mediated-ROS generation caused DNA damage in A549 and H460 cells. Our data also revealed that SQ-induced apoptosis was correlated with the inhibition of mouse double minute 2 (MDM2) in A549 and H460 cells. In summary, our research indicates that the novel compound SQ has great potential for therapeutic treatment of NSCLC in future.

RNase III DROSHA is upregulated in multiple cancers and contributes to tumor progression by hitherto unclear mechanisms. Here, we demonstrate that DROSHA interacts with β-Catenin to transactivate STC1 in an RNA cleavage-independent manner, contributing to breast cancer stem-like cell (BCSC) properties. DROSHA mRNA stability is enhanced by N(6)-methyladenosine (m(6)A) modification which is activated by AURKA in BCSCs. AURKA stabilizes METTL14 by inhibiting its ubiquitylation and degradation to promote DROSHA mRNA methylation. Moreover, binding of AURKA to DROSHA transcript further strengthens the binding of the m(6)A reader IGF2BP2 to stabilize m(6)A-modified DROSHA. In addition, wild-type DROSHA, but not an m(6)A methylation-deficient mutant, enhances BCSC stemness maintenance, while inhibition of DROSHA m(6)A modification attenuates BCSC traits. Our study unveils the AURKA-induced oncogenic m(6)A modification as a key regulator of DROSHA in breast cancer and identifies a novel DROSHA transcriptional function in promoting the BCSC phenotype.

Existing research has found cross-sectional seasonality of stock returns—the periodic outperformance of certain stocks during the same calendar months or weekdays. We hypothesize that assets’ different sensitivities to investor mood explain these effects and imply other seasonalities. Consistent with our hypotheses, relative performance across individual stocks or portfolios during past high or low mood months and weekdays tends to recur in periods with congruent mood and reverse in periods with noncongruent mood. Furthermore, assets with higher sensitivities to aggregate mood—higher mood betas—subsequently earn higher returns during ascending mood periods and earn lower returns during descending mood periods.

Purpose Excavating valuable outlier information of gray privacy products, the purpose of this study takes the online reviews of women’s underwear as an example, explores the outlier characteristics of online commentary data, and analyzes the online consumer behavior of consumers’ gray privacy products. Design/methodology/approach This research adopts the social network analysis method to analyze online reviews. Based on the online reviews collected from women’s underwear flagship store Victoria’s Secret at Tmall, this study performs word segmentation and word frequency analysis. Using the fuzzy query method, the research builds the corresponding co-word matrix and conducts co-occurrence analysis to summarize the factors affecting consumers’ purchase behavior of female underwear. Findings Establishing a formal framework of gray privacy products, this paper confirms the commonalities among consumers with respect to their perceptions of gray privacy products, shows that consumers have high privacy concerns about the disclosure or secondary use of personal private information when shopping gray privacy products, and demonstrates the big difference between online reviews of gray privacy products and their consumer descriptions. Originality/value The research lays a solid foundation for future research in gray privacy products. The factors identified in this study provide a practical reference for the continuous improvement of gray privacy products and services.

Growing evidence highlights that glycolysis and tumor-derived lactate could skew tumor-associated macrophages (TAMs) toward an immunosuppressive phenotype. However, the updated research has not been systematically summarized yet. TAMs are educated by the tumor microenvironment (TME) and exert immunosuppressive functions and tumorigenic effects via multiple biological processes. It is well known that lactate generated by aerobic glycolysis is significantly accumulated in TME and promotes tumor progression in solid tumors. Moreover, some recent research demonstrated that glycolysis is activated in TAMs to support M2-like polarization, which is absolutely in contrast with the metabolic profile of M2 macrophages in inflammation. Notably, lactate produced by high levels of glycolysis is not only a metabolic by-product but also an oncometabolite. TAMs could access the biological information delivered by lactate and further enhance protumor functions such as immunosuppression and angiogenesis. Here, we outline the connection between glycolysis and TAM phenotype to elucidate the metabolic characteristics of TAMs. Further, insights into the specific molecular mechanisms of lactate-induced TAM polarization and potential therapeutic targets are summarized. We sought to discuss the reciprocal interaction between tumor cells and TAMs mediated by lactate, which will lay a foundation for the research aiming to elucidate the complex functions of TAMs.

The echinoderm microtubule-associated protein-like 4 (EML4)-anaplastic lymphoma kinase (ALK) fusion gene occurs in approximately 5% of non-small-cell lung cancers (NSCLCs). The development of ALK tyrosine kinase inhibitors (ALK-TKIs) is a major advance in treating NSCLC with the ALK fusion gene. Nevertheless, acquired resistance to ALK-TKIs ultimately limits their use. A prevalent mechanism of drug resistance in kinases occurs through the mutation of G1202R in ALK. However, the mechanisms underlying G1202R resistance to ceritinib are not fully understood. Here, we demonstrated that the expression of EML4-ALK G1202R mutation in A549 cells induced an epithelial-mesenchymal transition (EMT) phenotype and significantly increased the migration and invasion abilities. These phenomena may be due to the upregulation of signal transducer and activator of transcription 3 (STAT3), accompanied by the elevated expression of Slug in EML4-ALK G1202R mutant cells. Furthermore, the combination of ALK and STAT3 inhibitors restored the sensitivity of EML4-ALK G1202R mutant cells to ceritinib. In conclusion, these data indicate that the EML4-ALK G1202R mutation mediates the EMT phenotype by activating the STAT3/Slug signaling pathway, resulting in resistance to ceritinib, and that the combination of STAT3 and ALK inhibitors may overcome ALK mutation-driven drug resistance in the clinic.

Severe coronavirus disease 2019 (COVID-19) is characterized by symptoms of lymphopenia and multiorgan damage, but the underlying mechanisms remain unclear. To explore the function of N6-methyladenosine (m6A) modifications in COVID-19, we performed microarray analyses to comprehensively characterize the m6A epitranscriptome. The results revealed distinct global m6A profiles in severe and mild COVID-19 patients. Programmed cell death and inflammatory response were the major biological processes modulated by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Further, RBM15, a major m6A methyltransferase, was significantly elevated and positively correlated with disease severity. Silencing RBM15 drastically reduced lymphocyte death in vitro. Knockdown of RBM15 remarkably suppressed the expression levels of multitarget genes related to programmed cell death and inflammatory response. This study shows that SARS-CoV-2 infection alters the m6A epitranscriptome of lymphocytes, particularly in the case of severe patients. RBM15 regulated host immune response to SARS-CoV-2 by elevating m6A modifications of multitarget genes. These findings indicate that RBM15 can serve as a target for the treatment of COVID-19.

Based on the thermodynamic descriptions of binary sub-systems as well as the experimental phase equilibria data available in the literature, the Ti-W-B and Ti-W-Si ternary systems have been assessed by the CALPHAD (CALculation of PHAse Diagram) method. The solution phases, i.e. liquid and bcc (βTi, W), are described by the substitutional solution model. The binary phases TiB2, TiB, W2B, αWB, W2B5, W2B9, Ti5Si3 and W5Si3 with the solubilities of the third element are modeled using the sublattice models. Two ternary compounds τ with composition of (Ti1-xWx)B and Ti3W2Si10 are described by two sublattice model (Ti,W)1B1 and (Ti,W)1Si2, respectively. A set of self-consistent thermodynamic parameters is finally obtained for each of the two ternary systems. Some representative isothermal and vertical sections as well as liquidus surface projections are calculated. Comparisons between the calculated and measured phase diagrams show that the most of experimental data are satisfactorily reproduced by the present thermodynamic descriptions.

Cancer-associated fibroblasts (CAFs) play a pivotal role in cancer progression; however, how CAFs are induced remains elusive. Sulfonylurea receptor 1 (SUR1) is a tumor-enhancer in non-small cell lung carcinoma (NSCLC). Here, we probed the influence of SUR1-expressing cancer cells on CAFs. Results showed that high SUR1 expression positively correlated with α-SMA positive staining of CAFs in tumor tissues and poor prognosis of NSCLC patients. SUR1 contributed to normal fibroblast (NF) transformation into CAFs and facilitated the growth and metastasis of NSCLC in vivo. Conditioned medium (CM) and exosomes from SUR1-expressing cancer cells induced CAFs and promoted fibroblast migration. In cancer cells, SUR1 promoted p70S6K-induced KH-type splicing regulatory protein (KHSRP) phosphorylation at S395 to inhibit the binding of KHSRP with let-7a precursor (pre-let-7a) and decreasing mature let-7a-5p expression in cancer cells and exosomes. Let-7a-5p delivered by exosomes blocked NF transformation into CAFs by targeting TGFBR1 to inactivate the TGF-β signaling pathway. Glibenclamide, which targets SUR1, restrained CAFs and suppressed tumor growth in patient-derived xenograft models. Furthermore, we found that let-7a-5p was decreased in the tissues and plasma exosomes of NSCLC patients. In summary, SUR1-expressing cancer cells induce NF transformation into CAFs in the tumor microenvironment and promote NSCLC progression by transferring less exosomal let-7a-5p. Glibenclamide is a promising anti-cancer drug, and plasma exosomal let-7a-5p level is a potential diagnostic biomarker for NSCLC patients. These findings provide new therapeutic strategies by targeting SUR1 in NSCLC.

2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) is one of the most toxic polybrominated diphenyl ethers (PBDEs). The toxic effects of BDE-47 on Chinese cabbage seedlings were analyzed in this study. After a 30-day hydroponic exposure to BDE-47 at different concentrations (25, 50, 75, and 100 µg·L−1), the fresh weight of Chinese cabbage seedlings was significantly decreased, whereas their root:shoot ratio was increased, indicating that BDE-47 inhibited the growth of the plant, especially the overground parts. The water content, chlorophyll content, and protein content of Chinese cabbage leaves also markedly decreased with the increase of the BDE-47 concentration. In addition, BDE-47 weakened the photosynthetic capacity of the leaves, which was supported by the decreased photosynthetic parameters [net photosynthetic rate (Pn) and stomatal conductance (gS)]. Although the activities of superoxide dismutase (SOD), peroxidase (POD), and catalase (CAT) in the leaves were enhanced after exposure to BDE-47, the increased malondialdehyde (MDA) content attested to the existence of membrane lipid peroxidation. The increased plasma membrane permeability and the decreased chlorophyll fluorescence parameters [the maximum quantum yield of PSII photochemistry at t = 0 (Fv/Fm), photosystem II (PSII) reaction centers (RCs) per cross section (CS) (RC/CS), absorption energy flux per CS (ABS/CS), trapped energy flux per CS (TRo/CS), electron transport flux per CS (ETo/CS), performance index on the absorption basis (PIabs), and driving force for photosynthesis (DF)] further proved that the plasma membrane and photosynthetic membrane were damaged by BDE-47. Our study demonstrated the phytotoxicities of BDE-47 to Chinese cabbage, which can provide valuable information for understanding the toxicity of BDE-47 on vegetables.

For most intellectual property core in System-on-a-chip, larger test set is required to achieve higher fault coverage, which leads to excessive test data volume and high-test power consumption during VLSI testing. Hence, partially compatible test decompression technology oriented RL-HC is proposed to effectively alleviate this thorny problem. The unspecified bit in test data is filled according to the evaluation of Weighted Transition Metric, and then the filled test data are divided into blocks by the smallest entropy value. The determined test vectors are encoded using Run length-based Huffman Code scheme, the more frequent the blocks, the shorter the codewords, which aims at reducing the storage resource occupied by test data in system-on-a-chip. Furthermore, a partially compatible XOR decompression circuit structure is designed to avoid the compatible test vectors repeatedly loaded into scan chain, which leads to less test power consumption during scan testing. Numerous experiments are performed on the representative Benchmark circuits to verify the proposed RL-HC based test decompression scheme well, it outperforms the previous code-based scheme in the overall performance including high test compression ratio, test power consumption reduction.

Coronavirus disease-2019 (COVID-19) is a novel respiratory disease induced by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). It remains poorly understood how the host immune system responds to the infection during disease progression. We applied microarray analysis of the whole genome transcriptome to peripheral blood mononuclear cells (PBMCs) taken from severe and mild COVID-19 patients as well as healthy controls. Functional enrichment analysis of genes associated with COVID-19 severity indicated that disease progression is featured by overactivation of myeloid cells and deficient T cell function. The upregulation of TLR6 and MMP9, which promote the neutrophils-mediated inflammatory response, and the downregulation of SKAP1 and LAG3, which regulate T cells function, were associated with disease severity. Importantly, the regulation of these four genes was absent in patients with influenza A (H1N1). And compared with stimulation with hemagglutinin (HA) of H1N1 virus, the regulation pattern of these genes was unique in PBMCs response to Spike protein of SARS-CoV-2 ex vivo. Our data also suggested that severe SARS-CoV-2 infection largely silenced the response of type I interferons (IFNs) and altered the proportion of immune cells, providing a potential mechanism for the hypercytokinemia. This study indicates that SARS-CoV-2 infection impairs inflammatory and immune signatures in patients, especially those at severe stage. The potential mechanisms underpinning severe COVID-19 progression include overactive myeloid cells, impaired function of T cells, and inadequate induction of type I IFNs signaling.

The bromodomain and extra‑terminal domain (BET) family proteins are essential epigenetic regulators in lung cancer. However, BET inhibitors have not had the anticipated therapeutic efficacy. Combined treatment using BET inhibitors along with other drugs had favorable therapeutic effects but the underlying molecular mechanisms remain elusive. The aim of the present study was to investigate the antineoplastic effects and mechanisms of a combination of a BET inhibitor and paclitaxel or cisplatin in non‑small cell lung cancer (NSCLC). By using the online Kaplan‑Meier plotter, it was revealed that increased mRNA levels of several BET protein‑coding genes were associated with poor prognosis in NSCLC. SRB assay results revealed that pharmaceutical or genetic targeting of BET proteins suppressed the growth of NSCLC cells. Inhibition of BET protein expression, in combination with the use of chemotherapeutic drugs such as paclitaxel and cisplatin, further restrained NSCLC cell growth in a synergistic manner. Mechanistically, this combination of suppression of BET expression and chemotherapeutic treatment blocked NSCLC cell growth by inhibiting autophagy and promoting apoptosis, which were revealed by both western blot and ELISA results. The present findings revealed a new rationale for using a combination of BET inhibitors with chemotherapy in NSCLC treatment.

Low impact development (LID) practices, such as bioretention and green roof, aim to increase infiltration and retention to manage urban flood. Flood simulation model is an effective tool for scheme comparison at the design stage. In addition, it is also a good method to evaluate the effects of LID after construction. The Flood Risk Analysis Software (FRAS), developed independently by China Institute of Water Resources and Hydropower Research (IWHR), is integrated software that can simulate the whole flood process, mainly including 1D-2D coupling hydraulic model, hydrological model and drainage model. And FRAS also has accurate and reasonable structure routines for urban flood simulation because of the coupling calculation of different models. In order to reflect the influences of LID measures on runoff generation and confluence more accurately, the following improvements were made based on the original software: (1) The SCS method is added to the original rainfall-runoff model due to its simple but sensitive parameter, which can comprehensively reflect initial soil moisture, soil type and land use type of different LID measures. Additionally, it is coupled with the 2D surface hydraulic model in real-time to precisely describe the infiltration process. (2) According to the main functions and characteristics of different LID practices, three typical measures, i.e., green roof, bioretention and porous pavement, are set as special land use types, respectively. The parameters and calculation methods are adjusted accordingly in the model. After these improvements, the model can have more precise simulation about the increased infiltration and flood retention of LID measures.

The fabrication of graphitized diamond covered with polypyrrole (D@G@PPy) core-shell nanocomposites has been achieved by using a superficial electrochemical polymerization and self-assembly strategy. The conductivity of the core-shell nanocomposites was influenced by polymerization time, current as well as the concentration of ions. The obtained excellent conductivity appeared with the current of 0.6 mA and the duration time of 1 h. In addition, the corresponding enhanced electrochemical performance of polypyrrole grown on graphitized diamond substrate is demonstrated compared with pristine polypyrrole. The morphologies of the obtained composites were illuminated through scanning electron microscopy (SEM) and the conductivity was demonstrated by electrochemical impedance spectroscopy (EIS). The characteristic peaks of polypyrrole and qualitative analysis of surface elements have been investigated by Raman spectra and X-ray photoelectron spectroscopy (XPS). The present research could demonstrate a new aspiration for the design and preparation of novel polypyrrole core-shell composites materials.

To investigate the toxic effect and mechanism of 2,2′,4,4′-tetrabromodiphenyl ether (BDE-47) in aquatic plants, in vivo and in vitro exposure to BDE-47 were conducted. After 14-d exposure to 5–20 μg/L BDE-47, the growth of Lemna minor plants was significantly suppressed, and the chlorophyll and soluble protein contents in fronds markedly decreased. Accordingly, the photosynthetic efficiency (Fv/Fm, PI) decreased. When the thylakoid membranes isolated from healthy fronds was exposed to 5–20 mg/L BDE-47 directly in vitro for 1 h, the photosynthetic efficiency also decreased significantly. In both the in vitro (5–20 μg/L) and in vivo (5–20 mg/L) experiments, BDE-47 led to an increased plasma membrane permeability. Hence, we concluded that BDE-47 had a direct toxicity to photosynthetic membranes and plasma membranes. However, direct effects on the activities of peroxidase (POD), malate dehydrogenase (MDH) and nitroreductase (NR) were not observed by adding 5–20 mg/L BDE-47 into crude enzyme extracts. The malondialdehyde (MDA) and superoxide anion radical (O2− ) contents in the BDE-47 treated fronds were higher than those in the control fronds, suggesting that L. minor can not effectively relieve reactive oxygen species (ROS). The data above indicates that BDE-47 is toxic to L. minor through acting directly on biomembranes, which induces the production of ROS and thus causes remarkable oxidative damage to cells.