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[Display omitted] • Co-exposure of MC-LR and NaNO 2 exacerbates reproductive system oxidative damage. • MC-LR and NaNO 2 have synergistic effect on the reduction of sperm density in mice. • MC-LR and NaNO 2 induce apoptosis and pyroptosis via mtROS. • MC-LR and NaNO 2 induced spermatogenic disorders though cell apoptosis and pyroptosis. Microcystins (MCs) and nitrites are coexisted in the environment and have reproductive toxicity. The combined toxic effect and mechanism of MCs and nitrite on spermatogenesis remain largely unclear. In the present study, co-exposure to microcystin-leucine arginine (MC-LR) and sodium nitrite (NaNO 2) aggravated testicular damage of Balb/c mice and mitochondrial impairment of spermatogonia, Sertoli cells, and sperm. Furthermore, MC-LR and NaNO 2 reduced sperm density with a synergistic effect. In addition, MC-LR and NaNO 2 synergistically induced oxidative stress in the reproductive system by decreasing superoxide dismutase (SOD) activity and glutathione (GSH) levels and increasing levels of mitochondrial reactive oxygen species (mtROS) and reactive oxygen species (ROS). More importantly, mitoquidone mesylate (MitoQ), an inhibitor of mtROS, blocked MC-LR and NaNO 2 -induced spermatogonia and Sertoli cell apoptosis by inhibiting high expression of Bax, Fadd, Caspase-8, and cleaved-Caspase-3. On the other hand, MitoQ suppressed pyroptosis of Sertoli cells by inhibiting the expression of NLRP3, N-GSDMD, and cleaved-Caspase-1. Additionally, MitoQ alleviated co-exposure-induced sperm density reduction and organ index disorders in F1 generation mice. Together, co-exposure of MC-LR and NaNO 2 can enhance spermatogenic disorders by mitochondrial oxidative impairment-mediated germ cell death. This study emphasizes the potential risks of MC-LR and NaNO 2 on reproduction in realistic environments and highlights new insights into the cause and treatment of spermatogenic disorders. [ABSTRACT FROM AUTHOR]

Solar-driven interfacial evaporation technology stands out as a promising solution for sustainable freshwater production. To achieve sustained and efficient water evaporation, it is crucial to carefully modulate the distribution of water content within the solar evaporator. In this study, a novel light-temperature responsive composite hydrogel-based solar evaporator was successful constructed. This involved the incorporation of a hydrophilic backbone (polyacrylamide) and a highly efficient solar absorber (multi-walled carbon nanotubes) into a temperature-sensitive hydrogel polymer backbone (poly (N, N-diethylacrylamide)). Due to its low critical solution temperature, the evaporator can undergo a hydrophilic/hydrophobic phase transition alternating day and night conditions. In natural sunlight, the upper hydrogel evaporation region is rendered hydrophobic, minimizing heat loss and preventing salt crystallization. Simultaneously, the bottom water delivery region is hydrophilic to ensure sufficient water supply. At night, the evaporator absorbs water and dissolves, thereby facilitating the rapid return of highly concentrated brine. Leveraging the spontaneously formed Janus structure, the photo-hydrothermal hydrogel achieves an impressive evaporation rate of 2.74 kg m−2 h−1 and exhibits excellent salt resistance. The notable water evaporation performance and robust salt resistance provide exciting possibilities for achieving ultrafast solar water purification. [Display omitted] • A photothermo-responsive hydrogel solar evaporator was developed, exhibiting high evaporation rates and salt resistance. • In natural sunlight, the hydrogel autonomously generates a Janus structure through inherent light-temperature responsive. • At night, the evaporator absorbs water and dissolves, facilitating the rapid return of highly concentrated brine. [ABSTRACT FROM AUTHOR]

[Display omitted] • Thermal crosslinked alkynyl-based polyimide membrane (EBPA-TB-TC) showed high thermal stability and increased microporosity. • EBPA-TB-TC membrane exhibited He permeability (61.14 Barrer) and He/N 2 selectivity (72.78). • EBPA-TB-TC membrane demonstrated excellent anti-aging performance. Membrane separation technology plays a critical role in the utilization of helium (He) resources. Yet, the performance of current polymer membranes is hindered by a trade-off between permeability and selectivity, as well as by physical aging. Solving these problems is vitally crucial for the industrial application of He separation. This study reported controllable thermal crosslinking of alkynyl-based polyimide membrane (EBPA-TB-TC) to improve He permeability and anti-aging performance. The resulting covalently crosslinked structures conferred thermal and chemical stability to the membranes, as well as increased microporosity. It led to a notable 'anti-trade-off' effect and improved anti-aging characteristics. An optimized EBPA-TB-TC membrane exhibited a superior combination with a He permeability of 61.14 Barrer and an He/N 2 selectivity of 72.78. Crucially, mixed-gas He/N 2 (1:1, 50/50) separation results over 50 days revealed minimal reductions in He permeability (1.34 %) and He/N 2 selectivity (2.95 %), indicating fantastic anti-aging performance. These findings demonstrated the significant potential of thermally cross-linked EBPA-TB-TC membrane in long-term stable helium separation. [ABSTRACT FROM AUTHOR]

• Toxic effects and mechanisms of microcystins have been revealed by omics methods. • All 59 existing omics studies on microcystins toxicity were tabulated and discussed. • The application status of omics in toxicology research of microcystins was summarized. • The development direction of Omics in the toxicology study of microcystins was proposed. Microcystins (MCs) are the most widely distributed cyanotoxins, which can be ingested by animals and human body in multiple ways, resulting in a threat to human health and the biodiversity of wildlife. Therefore, the study on toxic effects and mechanisms of MCs is one of the focuses of attention. Recently, the Omics techniques, i.e. genomics, transcriptomics, proteomics and metabolomics, have significantly contributed to the comprehensive understanding and revealing of the molecular mechanisms about the toxicity of MCs. This paper mainly reviews current literature using the Omics approaches to explore the toxicity mechanism of MCs in liver, gonad, spleen, brain, intestine and lung of multiple species. It was found that MCs can exert strong toxic effects on various metabolic activities and cell signal transduction in cell cycle, apoptosis, destruction of cell cytoskeleton and redox disorder, at protein, transcription and metabolism level. Meanwhile, it was also revealed that the alteration of non-coding RNAs (miRNA, circRNA and lncRNA, etc.) and gut microbiota plays an essential regulatory role in the toxic effects of MCs, especially in hepatotoxicity and reproductive toxicity. In addition, we summarized current research gaps and pointed out the future directions for research. The detailed information in this paper shows that the application and development of Omics techniques have significantly promoted the research on MCs toxicity, and it is also a valuable resource for exploring the toxic mechanism of MCs. [ABSTRACT FROM AUTHOR]

Microcystin-LR (MC-LR) is an emerging water pollutant produced by blooming cyanobacteria. It could be absorbed into human body via contaminated food and drinking water causing severe reproductive toxicity. Previous studies showed that MC-LR could regulate autophagy by inducing endoplasmic reticulum (ER) stress thereby causing female reproductive toxicity. However, the molecular mechanisms of MC-LR-induced autophagy remain to be elucidated. It is known that IRE1 and CaMKKβ pathways are two important pathways involved in autophagy induced by ER stress. Hence, this study investigated the roles of both pathways in MC-LR-induced autophagy in mouse ovarian cells. The results showed that MC-LR significantly up-regulated the expression of autophagy marker proteins LC3Ⅱ and BECLIN1 and down-regulated the expression of P62 in vivo and in vitro. MC-LR-caused increase of autophagosomes could be observed in KK-1 cells by MDC staining. MC-LR induced the formation of autolysosomes as indicated by the overlap of LAMP1 and LC3. Meanwhile, MC-LR significantly activated the proteins in IRE1 pathway (IRE1, XBP1 and JNK) and in CaMKKβ pathway (CaMKKβ, AMPK, mTOR). Furthermore, MC-LR caused weight loss and ovarian histopathological damage in mice. In contrast, after the expression and function of IRE1 and CaMKKβ were inhibited with siRNA in vitro and by inhibitors (4μ8C and STO-609, respectively) in vivo , the up-regulation of LC3Ⅱ and BECLIN1 and the degradation of P62 induced by MC-LR were significantly suppressed. MC-LR-induced autophagosomes in KK-1 cells and autolysosomes in mouse ovarian cells were also decreased. Moreover, the knockdown of IRE1 and CaMKKβ relieved MC-LR-induced histopathological injury to mouse ovaries. These results indicated that MC-LR induced ovarian cell autophagy and ovarian injury via IRE1 and CaMKKβ pathways. This study is the first study revealing the molecular mechanisms of MC-LR-induced autophagy of ovarian cells and providing new insights into the female reproductive toxicity of MC-LR. Image 1 • After absorbed by ovaries, MC-LR can induce autophagy and damage of mouse ovaries. • IRE1 pathway is involved in autophagy and damage of mouse ovaries induced by MC-LR. • CaMKKβ pathway participates in autophagy and damage of mouse ovaries induced by MC-LR. [ABSTRACT FROM AUTHOR]

Microcystin-leucine arginine (MC-LR) is a variant of microcystins (MCs), which poses a serious threat to the reproductive system. Histone acetylation modification can regulate the expressions of apoptosis-related genes. However the mechanisms of histone acetylation involving MC-LR-induced apoptosis were not understood. This study investigated the change of histone acetylation and its role in apoptosis and cell cycle arrest induced by MC-LR. MC-LR enhanced the activity of histone deacetylase (HDAC), decreased the activity of histone acetylase (HAT), up-regulated the expression of HDAC1, and down-regulated the expressions of Ac-H3 and Ac-H4 in vitro and vivo. Meanwhile, MC-LR induced testicular tissue injury and increased the expressions of apoptosis-related genes, such as Bax , Caspase3 and Caspase8 , ultimately causing cells apoptosis in testicular tissues. Furthermore, MC-LR also induced cell cycle arrest in S phase, increased the expression of P21Wif1/Cip1, and inhibited the expressions of cyclinD1, cyclinE1, CDK2 and E2F1. Importantly, HDAC inhibitor Trichostatin A (TSA) could ameliorate MC-LR-induced apoptosis and cell cycle arrest by reverse-regulating the expressions of these proteins. These results indicated that MC-LR could activate the mitochondrial apoptotic pathway and disorder the cell cycle pathway to induce the cell apoptosis by enhancing HDAC activity and reducing histone acetylation of normal testicular cells in SD rats. Hence, histone acetylation has a vital function in MC-LR-induced apoptosis in SD rat testicular cells, which provides a new insight on the reproductive toxicity of male induced by MC-LR. • MC-LR enhanced the activity of HDAC and reduced the acetylation levels of histone H3, H4. • MC-LR induced SD rat testicular cell apoptosis. • MC-LR induced SD rat testicular cell cycle arrest in S phase. • Trichostatin A inhibited MC-LR-induced SD rat testicular cell apoptosis and cell cycle arrest. [ABSTRACT FROM AUTHOR]

• A dislocation-based damage-coupled constitutive model for SX superalloys is developed. • The incorporation of structure-induced GND can improve the simulation accuracy. • A heat-resistant speckle pattern that is suitable for long-term applications is developed. • Secondary orientation can significantly influence the creep life of circular hole. • An empirical model for rapid evaluation of creep life is proposed based on high throughput simulations. Circular holes in single crystal (SX) turbine blades are susceptible to creep failure at high temperatures, due to the stress concentrations near the holes. In this study, a dislocation-based damage-coupled constitutive model for SX superalloys is developed, validated, and applied to unveil the effect of secondary orientation on the creep life of circular holes. The structure-induced geometrically necessary dislocations (GND) density resulting from the macroscopic strain gradient is incorporated. The dissipated energy is employed as the indicator to predict crack nucleation. Initially, the specimens without a hole are employed to calibrate the parameters and validate the model in the absence of structure-induced GND. Creep experiments incorporating the digital image correlation technique are conducted on the specimens with a hole under different secondary orientations, which aims to validate the simulated strain distribution, crack nucleation location, and creep life under the influence of structure-induced GND. The results indicate that the incorporation of structure-induced GND contributes to mitigating the conservatism in the creep life prediction of circular holes. Because, the GND can enhance dislocation hardening near the hole, extending the predicted life and improving the accuracy of life prediction. Meanwhile, both experiments and simulations indicate that the secondary orientation influences the crack nucleation locations at the hole edge. The variation in the creep life at different secondary orientations is attributed to the changes in both the maximum value and uniformity of resolved shear stresses distributed across slip systems. Finally, the model is applied to simulate the creep behavior of a circular hole under various secondary orientations, stresses, and temperatures. An empirical model is developed to rapidly evaluate the creep life of a circular hole in the SX superalloy, which facilitates the engineering application of the proposed model. [Display omitted] [ABSTRACT FROM AUTHOR]

Abstract The liver is an important iron storage site and a primary MC-LR target. C57BL/6 and Hfe −/− mice were used to investigate effects and mechanisms of MC-LR on systematic iron homeostasis. Body weight, tissue iron content, hematological and serological indexes, and histopathological were evaluated. Ultrastructure and iron metabolism-related genes and proteins were analyzed. MC-LR induced dose-dependent increases in red blood cells, hemoglobin, and hematocrit. In contrast MC-LR-induced dose-dependent decreases in mean corpuscular volume, hemoglobin, and hemoglobin concentration were observed both C57BL/6 and Hfe −/− mice. In both mouse species, serological indexes increased. Aggravated liver and spleen iron were observed in C57BL/6 mice, consistent with Perls' Prussian blue staining. However, an opposite trend was observed in Hfe −/− mice. C57BL/6 mice had lower Hamp1 (Hepcidn), Bmp6 , Il-6 , and Tmprss6. Significant increased Hjv , Hif-1α and Hif-2α were observed in both C57BL/6 and Hfe −/− mice. MC-LR-induced pathological lesions were dose-dependent increase in C57BL/6 mice. More severe pathological injuries in MC-LR groups (25 μg/kg) were observed in Hfe −/− mice than in C57BL/6 mice. In Hfe −/− mice, upon exposure to 25 μg/kg MC-LR, mitochondrial membranes were damaged and mitochondrial counts increased with significant swelling. These results indicated that MC-LR can induce the accumulation of iron in C57BL/6 mice with the occurrence of anemia, similar to thalassemia. Moreover, dysregulation of iron homeostasis may be due to MC-LR-induced Hamp1 downregulation, possibly mediated by hypoxia or the IL6–STAT3 and BMP–SMAD signaling pathways. Highlights • MC-LR induced the accumulation of iron in C57BL/6 mice with the occurrence of anemia that similar to thalassemia. • MC-LR reduced the expression of hepcidin that is the central hormone in regulating iron homeostasis in the body. • The downregulation of hepcidin induced by MC-LR may be related to hypoxia, IL-6-STAT3, and BMP-SMAD signaling pathway and HIFs play important roles. [ABSTRACT FROM AUTHOR]

The top-coal caving mining method, developed steadily in the past two decades, has become the main method for thick seam coal mining in China. In recent years, the core research areas in the top-coal caving mining are the mechanisms of top-coal caving and the improvement of top-coal recovery ratio. In this paper, the mechanisms of the top-coal caving are illustrated by a large number of physical simulation experiments and numerical modelings of actual cases. The marker method, which has sufficient accuracy to calculate the top-coal recovery ratio, is also described in detail. [ABSTRACT FROM AUTHOR]