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Long noncoding RNAs (lncRNAs) are emerging as critical regulators in the biological development of breast cancer. In this study, we aimed to determine the roles and mechanisms of the lncRNA COX10 divergent transcript (COX10-DT) in breast cancer progression. The relative expression level of COX10-DT was calculated in matched breast cancer tissues and adjacent normal tissues using quantitative real-time PCR. Gain-of-function and loss-of-function approaches further revealed the functions and mechanisms of COX10-DT in breast cancer cells. Clinically, we found that the lncRNA COX10-DT was commonly overexpressed in breast cancer tissues compared to paired peritumoural tissues. Functionally, the lncRNA COX10-DT might promote the proliferation and migration of breast cancer cells. Mechanistically, the lncRNA COX10-DT did not play a role by regulating the expression of its divergent gene COX10 but acted as a competitive endogenous RNA (ceRNA) by directly sponging miR-206, which further regulated the expression of brain-derived neurotrophic factor (BDNF). Taken together, our results proved that the lncRNA COX10-DT could function via the COX10-DT /miR-206/ BDNF axis, thereby promoting the development of breast cancer. These findings indicated that the lncRNA COX10-DT might be a potential biomarker and therapeutic target for breast cancer. • This article firstly studied the role and mechanisms of COX10-DT in breast cancer. • COX10-DT might promote the proliferation and migration of breast cancer cells. • COX10-DT might not play a role by targeting its divergent gene COX10. • COX10-DT promotes the progression of breast cancer via the COX10-DT /miR-206/ BDNF axis. [ABSTRACT FROM AUTHOR]

The toxicity of nanoparticles to freshwater microalgae is of significant importance in maintaining the overall stability of aquatic ecosystems. However, the transport mechanism and toxicity response of microalgae towards nanoplastics (NPs) remain to be further investigated. In this study, we examined the toxicity and internalization mechanisms of polystyrene nanoplastics (PS-NPs) in the microalga Chlorella sorokiniana. The results revealed that the PS-NPs inhibited algal cells' growth and disrupted cell integrity upon contact, leading to cell shrinkage or rupture. Moreover, amino-modified PS-NPs (Nano-PS-NH 2) exhibited greater toxicity to C. sorokiniana than carboxyl-modified PS-NPs (Nano-PS-COOH). Furthermore, significant inhibition of PS-NPs internalization was observed when four different endocytosis-related inhibitors were used, indicating that internalized PS-NPs can enter algal cells through endocytic pathways. More importantly, C. sorokiniana exposed to Nano-PS-NH 2 responded to the reduction in carbon sources and energy resulting from the suppression of photosynthesis by regulating the metabolism of carbohydrates. These findings elucidate the effects of PS-NPs on C. sorokiniana , including their impact on cell morphology and metabolism, while shedding light on the internalization mechanisms of NPs by C. sorokiniana which deepen our understanding of the toxicity of nanoplastics on algae and provide important theoretical support for solving such aquatic ecological environment problems. [Display omitted] • Polystyrene nanoparticles can enter C. sorokiniana cells through endocytosis. • Nano-PS-NH 2 exhibited greater toxicity to C. sorokiniana than Nano-PS-COOH. • Nano-PS-NH 2 disrupted photosynthesis and triggered energy and carbon deficiency in cells. • The cells enhanced the decomposition of carbohydrates in response to the stresses. [ABSTRACT FROM AUTHOR]

[Display omitted] Macrophages have recently been discovered to assume a significant role in the progression of cryptococcosis. However, the potential involvement of macrophage-derived exosomes in the pathogenesis of cryptococcosis remains uncertain. In this study, we investigated the changes of microRNAs in macrophage exosomes (exo -miRNAs) in cryptococcal infections and the role of markedly altered exo -miRNAs in the modulation of Human Umbilical Vein Endothelial Cells (HUVEC) permeability and ROS accumulation and pyroptosis in Human Bronchial Epithelioid Cells (BEAS-2B). Techniques such as microarray analysis and real-time quantitative PCR were used to detect different exo -miRNAs and to screen for the most highly expressed exo -miRNAs. Then its mimics were transfected into HUVEC to study its effect on the monolayer permeability of HUVEC. Finally, the relationship between this exo -miRNAs and the ROS accumulation and pyroptosis was verified by bioinformatics analysis. The results showed that five exo -miRNAs were overexpressed and two exo -miRNAs were reduced, among which, exo -miR-4449 was expressed at the highest level. Exo-miR-4449 could be internalized by HUVEC and enhanced its monolayer permeability. Moreover, exo -miR-4449 was found to promote ROS accumulation and pyroptosis in BEAS-2B through HIC1 pathway. Thus, exo -miR-4449 plays an important role in the pathogenesis of cryptococcosis and holds promise as a significant biomarker for treatment. [ABSTRACT FROM AUTHOR]

• Adenosine differentially regulates the Th1 and Th17 autoimmune responses in EAU. • Adenosine tips the Th1/Th17-balance in favor of Th17 responses. • Reciprocal interactions between γδ- and adenosine-mediated immunoregulation. Th17-type autoreactive T cells contribute to pathogenicity in autoimmune diseases, including autoimmune uveitis. However, the mechanisms of regulation of Th17 cell activities remain unsolved and are likely to be tissue- and disease specific. In this review, we have summarized our studies from the murine model of experimental autoimmune uveitis (EAU). The results demonstrate that γδ T cells have a regulatory effect on Th17 response. The regulatory effects of γδ T cells depend on their action state. Activated γδ T cells express significantly high levels of adenosine receptor A2 (A2AR) but low CD73. Both molecules are crucially involved in adenosine generation, thus modifying T cell responses. While the increased expression of A2AR-allows activated γδ T cells to bind adenosine more effectively than other immune cells, the decreased CD73 restricts their ability to convert AMP to adenosine. Adenosine affects Th1 and Th17 autoimmune responses differently. Its activation of γδ T cells shifts the Th1/Th17 balance towards the Th17 autoreactivity. [ABSTRACT FROM AUTHOR]

Farmed animals produce excrement containing excessive amounts of toxic heavy metals as a result of consuming compound feed as well as receiving medical treatments, and the presence of these heavy metals may aggravate the risk of spreading drug-resistance genes through co-selection during manure treatment and application processes. However, research on the association between heavy metals and antimicrobial resistance is still lacking. In this study, metagenomic sequencing was used to explore the effects of the co-selection of environmentally toxic heavy metals on the resistome in manure. A relevance network analysis showed that metal-resistance genes (MRGs), especially for copper (Cu) and zinc (Zn), were positively correlated with multiple types of antibiotic-resistance genes (ARGs) and formed a complex network. Most bacteria that co-occurred with both MRGs and ARGs simultaneously are members of Proteobacteria and accounted for 54.7% of the total microbial species in the relevance network. The remaining bacteria belonged to Firmicutes, Bacteroidetes and Actinobacteria. Among the four phyla, Cu- and Zn-resistance genes had more complex correlations with ARGs than other MRG types, reflecting the occurrence of ARG co-selection under the selective pressure of high Cu and Zn levels. In addition, approximately 64.8%, 59.1% and 68.4% of MRGs that correlated with the presence of plasmids, viruses and prophages, respectively, are Cu- or Zn-resistant, and they co-occurred with various ARGs, indicating that mobile genetic elements participate in mediating ARG co-selection in response to Cu and Zn pressure. The results indicated that the use of heavy-metal additives in feed induces the increases of drug resistance genes in manure through co-selection, aggravating the risk of antimicrobial resistance diffusion from animal farm to manure land applications. • Heavy metals facilitate ARG proliferation in manure through co-selection. • Heavy metal level determines the complexity of MRG–ARG co-occurrence pattern. • Bacterial preference occurs in ARG co-selection induced by heavy metals. • Proteobacteria are primary resistance gene carriers affected by co-selection. • Cu and Zn trigger wider responses of resistance than other heavy metals. [ABSTRACT FROM AUTHOR]

Abstract: Previously, Srinivasula devised a contiguous molecule (C-cp-3 or immunocaspase-3) containing the small and large subunits similar to that in the active form of caspas-3 and found C-cp-3 had similar cleavage activity to the active form of caspase-3. To search for a new clinical application of C-cp-3 to treat hepatocellular carcinoma, recombinant adenoviruses carrying the C-cp-3 and a-fetoprotein (AFP) promoter (Ad-rAFP-C-cp-3) were constructed through a bacterial homologous recombinant system. The efficiency of adenovirus-mediated gene transfer and the inhibitory effect of Ad-rAFP-C-cp-3 on the proliferation of hepatocarcinoma cells were determined by X-gal stain and MTT assay, respectively. The tumorigenicity of hepatocarcinoma cells transfected by Ad-rAFP-C-cp-3 and the antitumor effect of Ad-rAFP-C-cp-3 on transplanted tumor in nude mice were detected in vivo. The results suggested that Ad-rAFP-C-cp-3 can inhibit specifically proliferation of AFP-producing human hepatocarcinoma cells in vitro and in vivo and adenovirus-mediated C-cp-3 transfer could be used as a new method to treat human hepatocarcinoma. [Copyright &y& Elsevier]

Molecular dynamics (MD) computer simulations have been carried out to study the structures, properties, and crystal nucleation of iron nanoparticles with 331 Fe atoms or with diameter around 2 nm. Structure information for the nanoparticles was analyzed from the MD simulations. Three crystalline phases and one amorphous phase were obtained by cooling the nanoparticles from their molten droplets at different cooling rates or with different lengths of cooling time periods. Molten droplets froze into three different solid phases and a solid–solid transition from a disordered body-centered cubic (BCC) phase to an ordered BCC phase were observed during the slow cooling and the quenching processes. Properties of nanoparticle Fe331, such as melting point, freezing temperature, heat capacity, heat of fusion, heat of crystallization, molar volume, thermal expansion coefficient, and diffusion coefficient, have been estimated. Nucleation rates of crystallization to two solid phases for Fe331 at temperatures of 750, 800, and 850 K are presented. Both classical nucleation theory and diffuse interface theory are used to interpret our observed nucleation results. The interfacial free energy and the diffuse interface thickness between the liquid phase and two different solid phases are estimated from these nucleation theories. [Copyright &y& Elsevier]

[Display omitted] Lithium metal is considered as an ideal anode candidate for next generation Li battery systems since its high capacity, low density, and low working potential. However, the uncontrollable growth of Li dendrites and infinite volume expansion impede the commercialized applications of Li-metal anodes. In this work, we rationally designed and constructed a hierarchical porous hollow carbon nanofiber decorated with diverse metal sulfides (MS-ZS@PHC). This composite scaffold has three advantages: First, the synergistic effect of multiple-size lithiophilic phases (nano ZnS and micro MoS 2) can regulate Li ions nuclei and grow up homogenously on the scaffold. Second, the enlarged interplanar spacing of MoS 2 microsphere on the fibers can provide abundant channels for Li ions transportation. Third, the porous scaffold can confine the volume expansion of Li metal anode during cycling. Therefore, in a symmetrical cell, the MS-ZS@PHC host presents a homogenous Li plating/stripping behavior and runs steadily for 1100 h at 5 mA cm−2 with a capacity of 5 mAh cm−2 and even for 700 h at 10 mA cm−2 with a capacity of 1 mAh cm−2. A full cell using MS-ZS@PHC /Li composite as anode and coupled with LiFePO 4 as cathode delivers an excellent cyclic and rate performances. [ABSTRACT FROM AUTHOR]

Non-alcohol fatty liver disease (NAFLD) is the most prevalent hepatopathy in China, with few effective cures currently. This work aimed to confirm the effect of DHM in vivo /vitro and explore the potential mechanism based on a network pharmacology-based approach. The rats were fed using a high-fat diet (HFD) to accumulate lipid. DHM at different concentrations was used to treat the HFD rats. The serum total cholesterol (TC), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were detected using ELISA kits. The target genes of DHM against NAFLD were screened by online databases. Then, the cytotoxicity of DHM in primary hepatocytes and HepG2 cells was determined by MTT reagent. qRT-PCR was used to quantify the expression level of PPAGR and CASP3 mRNA. Cell apoptosis and intracellular triglyceride (TG) were detected. HFD diet increased rat liver weight/body weight ratio, serum TC, ALT, and AST. But DHM treatment can reduce these elevated indicators. DHM targeted 14 potential genes in NAFLD. PPARG and CASP3 were two hub genes for DHM against NAFLD, with score factor coefficients of −7.1 and −6.8 kcal/mol. DHM reduced the increased PPARG mRNA level and intracellular TG induced by palmitic acid. DHM can reduce the increased CASP3 mRNA level and cell apoptosis induced by palmitic acid. This work demonstrates a mechanism of DHM that alleviates lipid metabolism disorder and cell apoptosis for the treatment of NAFLD, evidencing the potential application of DHM in NAFLD. • DHM can alleviate dyslipidemia induced by high-fat diet in rats. • DHM may inhibit PA-induced lipid accumulation via PPARG in HepG2 cells. • DHM may inhibit primary hepatocytes and HepG2 cell apoptosis via CASP3. [ABSTRACT FROM AUTHOR]

• Knockdown of ACSL4 reduced proinflammatory cytokine production. • Knockdown of ACSL4 inhibited the activation of NF-κB signaling. • ACSL4 promoted neuroinflammation by reducing VGLL4 expression. • Knockdown of ACSL4 alters lipid metabolism. • ACSL4 knockdown attenuated LPS and MPTP-induced neuroinflammation in vivo. Acyl-CoA synthetase long-chain family member 4 (ACSL4) is an important isozyme in polyunsaturated fatty acid (PUFA) metabolism. The role of ACSL4 in the lipopolysaccharide (LPS)-induced inflammation of microglia, and the effects of ACSL4-mediated inflammation on the progression of Parkinson's disease (PD) are unknown. In this study, we found that ACSL4 expression was increased after LPS stimulation. Knocking down ACSL4 in microglia decreased proinflammatory cytokine production. Mechanistically, ACSL4 reduced vestigial-like family member 4(VGLL4) expression to promote NF-κB signal transduction; and ACSL4 regulated lipid composition after LPS stimulation. In addition, knocking down ACSL4 alleviated neuroinflammation in a systemic LPS model and acute l-methyl-4-phenyl-l,2,3,6-tetrahydropyridine (MPTP) model. These data revealed ACSL4 to be a novel regulator that promotes microglia-mediated neuroinflammation by regulating VGLL4 expression and lipid metabolism. [ABSTRACT FROM AUTHOR]

The ATM protein kinase, is a serine/threonine protein kinase that is recruited and activated by DNA double-strand breaks, mediates responses to ionizing radiation in mammalian cells. Here we show that ATM is held inactive in unirradiated cells as a dimer and phosphorylates the opposite strand of the dimer in response to DNA damage. Cellular irradiation induces rapid intermolecular autophosphorylation of serine 1981 that causes dimer dissociation and initiates cellular ATM kinase activity. ATM cannot phosphorylate the substrates when it could not undergo dimer monomer transition. After DNA repair, the active monomer will undergo dephosphorylation to form dimer again and dephosphorylation is critical for dimer re-formation. Our work reveals novel function of ATM dimer monomer transition and explains why ATM dimer monomer transition plays such important role for ATM cellular activity during DNA repair. [ABSTRACT FROM AUTHOR]

Urbanization-related human activities, such as population aggregation, rapid industrial expansion, and intensified traffic, are key factors that impact local polycyclic aromatic hydrocarbon emissions and their associated health risks. Consequently, regions with varying degrees of urbanization within a megacity may exhibit diverse spatiotemporal patterns in the presence and distribution of soil polycyclic aromatic hydrocarbons, resulting in different levels of ecological risks for local inhabitants following the same period of development. In this study, we measured the concentrations of 16 polycyclic aromatic hydrocarbons in soil samples collected from industrial district and rural district in Tianjin (China) in 2018, and compared with polycyclic aromatic hydrocarbon data in 2001 from a previous study to characterize these regional variations in occurrence, source, and human risk of polycyclic aromatic hydrocarbons induced by urbanization with time and space. The results indicate the 20-year rapid urbanization and industrialization has differentially affected the composition, distribution and sources of polycyclic aromatic hydrocarbons in soils from different economic functional zones in Tianjin. Additionally, its impact on health risks in rural district appeared to be more significant than that in industrial district. • Urbanization had different effects on industrial and rural soil PAHs. • Regional socioeconomic patterns and residential behaviors influenced local PAH source profiles. • Risk regions and affected population were estimated quantitatively. • Urbanization-related impact on cancer risks in rural district seemed more notable. [ABSTRACT FROM AUTHOR]

N6-methyladenosine (m6A) is a major type of RNA modification implicated in various pathophysiological processes. Transforming growth factor β2 (TGF-β2) induces epithelial-mesenchymal transition (EMT) in retinal pigmental epithelial (RPE) cells and promotes the progression of proliferative vitreoretinopathy (PVR). However, the role of m6A methylation in the EMT of human telomerase reverse transcriptase (hTERT) retinal pigmental epithelium (RPE)-1 cells has not been clarified. Here, we extracted RNA from RPE cells subjected to 0 or 20 ng/mL TGF-β2 for 72 h and identified differentially methylated genes (DMGs) by m6A-Seq and differentially expressed genes (DEGs) by RNA-Seq. We selected the genes related to EMT by conjoint m6A-Seq/RNA-Seq analysis and verified them by qRT-PCR. We then confirmed the function of m6A methylation in the EMT of RPE cells by knocking down the methyltransferase METTL3 and the m6A reading protein YTHDF1. Sequencing yielded 5814 DMGs and 1607 DEGs. Conjoint analysis selected 467 genes altered at the m6A and RNA levels that are closely associated with the EMT-related TGF-β, AGE-RAGE, PI3K-Akt, P53, and Wnt signaling pathways. We also identified ten core EMT genes ACTG2 , BMP6 , CDH2 , LOXL2 , SNAIL1 , SPARC , BMP4 , EMP3 , FOXM1 , and MYC. Their RNA levels were evaluated by qRT-PCR and were consistent with the sequencing results. We observed that METTL3 knockdown enhanced RPE cell migration and significantly upregulated the EMT markers N-cadherin (encoded by CDH2), fibronectin (FN), Snail family transcription repressor (SLUG), and vimentin. However, YTHDF1 knockdown had the opposite effects and decreased both cell migration and the N-cadherin, FN, and SLUG expression levels. The present study clarified TGF-β2-induced m6A- and RNA-level differences in RPE cells, indicated that m6A methylation might regulate EMT marker expression, and showed that m6A could regulate TGF-β2-induced EMT. • m6A methylation regulates hTERT RPE-1 cell EMT. • TGF-β2 induces m6A- and RNA-level differences. • METTL3 and YTHDF1 affect TGF-β2-induced EMT. [ABSTRACT FROM AUTHOR]

Abstract: In this paper, we shall firstly illustrate why we should consider integral of a stochastic process with respect to a set-valued square integrable martingale. Secondly, we shall prove the representation theorem of set-valued square integrable martingale. Thirdly, we shall give the definition of stochastic integral of a stochastic process with respect to a set-valued square integrable martingale and the representation theorem of this kind of integrals. Finally, we shall prove that the stochastic integral is a set-valued sub-martingale. [Copyright &y& Elsevier]

Induction of monocytic differentiation by bryostatin1 (bryo1) conferred on THP-1 leukemia cells the ability to resist Z-LLL-CHO-induced apoptosis. The mechanism of resistance developed during this process was investigated. Apoptosis resistance was associated with an enhanced expression of X-linked inhibitor of apoptosis protein (XIAP), an endogenous caspase inhibitor, in differentiated THP-1 cells. Bryo1 also increased the level of c-IAP-1, yet decreased the level of c-IAP-2 in THP-1 cells, indicating that distinct regulatory mechanisms are operative. In addition, treatment of THP-1 cells with bryo1 induced a rapid and sustained activation of MEK, prior to the upregulation of XIAP and monocytic differentiation. Pretreatment of THP-1 cells with MEK inhibitors (U0126 and PD98059) prior to bryo1 induction blocked the expression of both XIAP and the c-fms product (M-CSF receptor), a hallmark of monocytic differentiation, but not Bcl-2. In addition, the expression of XIAP in bryo1-treated cells was inhibited by CAPE, a NF-κB-specific inhibitor, indicating that its expression is under the transcriptional regulation of NF-κB downstream of the MEK/MAPK pathway. The importance of XIAP in mediating apoptosis resistance was illustrated in cells transiently transfected with XIAP, which conferred on THP-1 cells the ability to resist Z-LLL-CHO-induced apoptosis. These findings suggest that the expression of XIAP is linked to monocytic differentiation in bryo1-treated THP-1 cells and represents one of the potential antiapoptotic mechanisms acquired during this process. [Copyright &y& Elsevier]

Anemone flaccida Fr. Shmidt (Ranunculaceae), known as ‘Di Wu’ in China, is a perennial herb which has long been used to treat arthritis. The rhizome of A. flaccida contains pharmacologically active components i.e. oleanane-type triterpenoid saponins. Oleanolic acid is natural triterpenoid in plants with diverse biological activities. The biosynthesis of oleanolic acid involves cyclization of 2,3-oxidosqualene to the oleanane-type triterpenoid skeleton, followed by a series of oxidation reactions catalyzed by cytochrome P450 monooxygenase (CYP450). Previously, we identified four possible cytochrome P450 genes belonging to CYP716A subfamily from the transcriptome of A. flaccida . In this study, we identified one of those genes “CYP716A254” encoding a cytochrome P450 monooxygenase from A. flaccida that catalyzes the conversion of the β-amyrin into oleanolic acid. The heterologous expression of CYP716A254 in yeast resulted in oxidation of β-amyrin at the C-18 position to oleanolic acid production. These results provide an important basis for further studies of oleanane-type triterpenoid saponins synthesis in A. flaccida. [ABSTRACT FROM AUTHOR]

Induced (natural) mixing proposed by our teams can solve a big problem of low-energy water situation improvement of stratified reservoirs by minimizing operating periods of water-lifting aerators (WLAs) to advance a complete natural mixing. Here, the mechanisms influencing water situation via induced mixing were systematically explored using a combination of multi-water-environment assessment methods including trophic level index (TLI), water quality index (WQI), and minimum WQI (WQI min) based on long-term field data (i.e., non-operational and operational years of WLAs). The results showed that induced mixing after WLA deactivation improved the levels of eutrophication and water quality (into "light-eutrophic" and "good" status) with a decrease in TLI values (56.0–56.2) and increase in WQI (79.0–79.9) and WQI min (81.5–89.3) values, compared to mixing of the non-operational year (TLI: 69.6, WQI: 73.4, WQI min : 76.1). Induced mixing was launched by deactivating the WLAs in cooling seasons (i.e., in late September within a subtropical monsoon climate zone), which advanced and prolonged the periods of naturally complete mixing by 2–3 months. Water temperature (WT), Dissolved oxygen (DO), relative water column stability (RWCS) and inflow were primary drivers for the water situation succession in the study years. Induced mixing extended the well-oxygenated and mixed conditions (temperature difference <1.0 °C, DO > 8.5 mg/L, RWCS< 20) following artificial mixing to improve the water status from single index level (improvement of 18.8%–73.7% than mixing before the operational years) to integrated evaluation results by changing WT, DO, and RWCS. This study presents a successful case for energy-saving pollution control using mixing systems. [Display omitted] • Induced natural mixing was proposed to achieve low-energy water status improvement. • A naturally complete mixing was extended by 2.2 times using a mixing system (WLAs). • Temperature, oxygen, water stability (RWCS), and inflow affected water situation. • Induced natural mixing improved water status by changing temperature, oxygen, RWCS. • WLA deactivation in proper conditions can advance/extend a naturally complete mixing. [ABSTRACT FROM AUTHOR]

Abstract: The mouse corneal thickness is very important for research into the fields of eye disease. However, the in vivo corneal thickness for the entire cornea from the pupil to the limbus was not determined. We measured in vivo corneal layer thicknesses in different corneal areas, from the central cornea to the limbus, in the widely used inbred C57BL/6 and BALB/c mouse strains using two-photon (2 PH) imaging. Eight corneas of the C57BL/6 or BALB/c were scanned using a 2 PH laser scanning fluorescence microscopy system. A total of 14 thicknesses of the different corneal layers, from different corneal regions, were measured using image processing software. In both C57BL/6 and BALB/c mice, the thickness of the corneal layers was inhomogeneous in different areas of the cornea, and all of the layers had their minimum thickness at the limbus. In C57BL/6 mice, the thickness of the corneal layers gradually increased from the central to the paracentral cornea, peaked at the fifth measurement point in the paracentral area, and decreased from this point to the limbus. In BALB/c mice, the thickness of the entire cornea and corneal epithelium had its maximum at the central cornea and gradually decreased from the central cornea to the peripheral cornea and to the limbus. The thickness of the corneal stroma and endothelium had its maximum at the fourth measurement point in the paracentral cornea and gradually decreased from the paracentral cornea to the limbus. The ratio of epithelial thickness to the total corneal thickness gradually decreased from the central cornea to the limbus in both C57BL/6 and BALB/c mice. The minimum ratio was observed at the fourteenth measurement point in both C57BL/6 and BALB/c mice. The ratio of stromal and endothelial to the total corneal thickness gradually increased from the central cornea to the limbus in both C57BL/6 and BALB/c mice. The maximum ratio was observed at the fourteenth measurement point in C57BL/6 mice. The ratio at the first eight measurement points was significantly lower in BALB/c than in C57BL/6 mice (P < 0.05). Our study demonstrated that the thickness of the entire cornea, the corneal epithelium, the corneal stroma and the endothelium was inhomogeneous in different areas of the cornea. Moreover, all of the layers exhibited a minimum thickness at the limbus in both C57BL/6 and BALB/c mice. Furthermore, the corneal thickness in different areas varied between C57BL/6 and BALB/c mice, and the variation in thickness with respect to corneal location for these strains was dissimilar. When using the mouse as an animal model to examine the cornea, it is important to note the differences between humans and mice. [Copyright &y& Elsevier]

• A novel framework is built for quantifying post-earthquake capacity of buildings. • Fatigue damage evolution law is developed to predict local damage accumulations. • Updating damage variable identifies asymmetric crack propagation in beam joints. This paper presents a framework combining theoretical, numerical, and experimental approaches for evaluating the remaining-life of high-rise steel buildings based on earthquake-induced fatigue damage propagation in local beam-to-column connections. A mesh-independent finite element model is developed and implemented using the concept of lumped damage mechanics to estimate the fatigue-induced life loss associated with the extent of crack propagation until complete rupture failure occurred in beam-to-column connection substructure of high-rises. In this framework, a damage state variable is introduced at each end of beam elements and can be linked to the extension of the fatigue fracture in real frame building joints. Then, the damage evolution law is developed by extending the conventional Manson–Coffin law and a new crack-driving parameter to quantify the extent of damage states and predict the remaining life of the associated components in high-rises buildings. The proposed model is validated by a damage index measured from the local wireless sensors in substructure tests of ductile steel beam-to-column connections subjected to ultra-low cycle fatigue loadings. The residual resistance can be quantified by updating the damage curve with the identified damaged conditions. [ABSTRACT FROM AUTHOR]

An effective antioxidant is crucial to prevent deterioration of lipid. This study aimed to investigate the antioxidant properties of vine tea extracts and evaluate their inhibition effect on lipid oxidation. In this study, total flavonoids, phenolics, and anthocyanins content of four leaf extracts were determined from leaves of different ages and colors. In addition, the antioxidant ability of these extracts was evaluated by determining the ferric reducing antioxidant power, DPPH· and OH scavenging activity, and lipid peroxidation inhibitory activity. The results revealed that the extracts, especially from young leaf samples, could effectively scavenge radicals and inhibit lipid oxidation, indicating their antioxidant ability. Compared to BHT, vine tea extracts significantly inhibited the increase of POV and TBARS in sunflower and rapeseed oils. This result may be vital for searching natural antioxidants that prolong the shelf life of food products. • The young leaves of A. grossedentata contained higher flavonoids content. • The anti-oxidation of GYL, GOL, RYL & ROL are evaluated in different oils. • The level of oxidation products and fatty acids were determined with 1H-NMR. • The leaf extracts showed a better effect on retarding oil oxidation than BHT. [ABSTRACT FROM AUTHOR]

Cyanobacterial blooms are a worldwide environmental problem, which is partly attributed to their access to excessive nitrogen (N) and phosphorus (P). Preventing the blooms by reducing N and P from internal inputs is viewed as a challenge. To evaluate the effects of dredging on cyanobacterial abundances and bacterioplankton communities, water and sediment samples were collected from eutrophic Lake Nanhu (Wuhan, China) before dredging (2017) and after dredging (2018). After dredging, significant decreases were observed for sediment nutrients (e.g., C, N, and P sources); C-, N-, P-, and S-cycling-related enzyme activity; N- and P-cycling-related gene abundance; microbial abundance; and dramatic changes were observed in the composition of the sediment microbial community. The release rates of nutrient including nitrogen, phosphorus, and organic matter decreased after dredging, and sediment biogeochemistry was closely correlated to nutrient release rates. Additionally, our observations and analyses indicated that the abundance and diversity of the bacterioplankton community decreased significantly, the composition and interaction of the bacterioplankton community dramatically changed, and the bacterioplankton community function (e.g., N, P-cycling-related enzymes and proteins) down regulated after dredging. Water and sediment physicochemical factors explained 72.28% variation in bacterioplankton community composition, and these physicochemical factors were significantly correlated with diversity, composition, and function of bacterioplankton community. Our findings emphasized that cyanobacterial blooms in freshwater ecosystems were closely correlated with noncyanobacterial bacterioplankton that were largely conserved at the phylum level, with Proteobacteria , Actinobacteria , and Bacteroidetes as the main taxa. To our knowledge, this is the first report clarifying the mechanism of cyanobacterial blooms mitigation by dredging, via changing the association between the bacterioplankton community and sediment biogeochemistry. Our findings are of significance and indicate that dredging is effective for mitigating cyanobacterial blooms. • Dredging caused the deficiency of both water and sediment nutrient. • Sediment biogeochemical processes affected hydrochemistry. • Dredging decreased diversity and function of bacterioplankton community. • Dredging caused relatively less competition between bacterioplankton. • Dredging-driven nutrient deficiency could mitigate cyanobacterial blooms. [ABSTRACT FROM AUTHOR]