In Situ Polymerized Quasi-Solid Electrolytes Compounded with Ionic Liquid Empowering Long-Life Cycling of 4.45 V Lithium-Metal Battery.

High-voltage resistant quasi-solid-state polymer electrolytes (QSPEs) are promising for enhancing the energy density of lithium-metal batteries in practice. However, side reactions occurring at the interfaces between the anodes or cathodes and QSPEs considerably reduce the lifespan of high-voltage LMBs. In this study, a copolymer of vinyl ethylene carbonate (VEC) and poly(ethylene glycol) diacrylate (PEGDA) was used as the framework, with a cellulose membrane (CE) as the supporting layer. Based on density functional theory calculations, 1-butyl-1-methylpyrrolidinium bis(trifluoromethanesulfonyl)imide (Pyr14TFSI), an ionic liquid, was screened because of its lowest unoccupied molecular orbital energy level as a modifying agent for the in situ P(VECx-EGy)/Pyrz/LiTFSI@CE QSPEs synthesis. Pyr14+, with a lithiophobic alkyl chain, forms a dense positive ion shielding layer on the protruding tips of deposited lithium, facilitating uniform and smooth lithium deposition. Pyr14TFSI assists in constructing a stable solid electrolyte interphase (SEI) layer on the Li surface enriched with LiF, Li3N, and RCOOLi. The modulation of lithium deposition behavior on the anode by Pyr14TFSI ensures stable Li plating/stripping for >1500 h. A Li-Cu cell exhibits stable cycling for >200 cycles at a current density of 0.05 mA cm-2, with an average Coulombic efficiency of 92.7%. In situ polymerization ensures that P(VECx-EGy)/Pyrz/LiTFSI@CE QSPEs exhibit excellent interface compatibility with the anode and the cathode. The CR2032 button cell Li|P(VEC1-EG0.06)/Pyr0.4/LiTFSI@CE|LiCoO2 demonstrates stable cycling with a negligible capacity decay of 0.083% per cycle for >390 cycles at 25 °C and 0.2 C when using a high-voltage LiCoO2 (4.45 V) cathode. Furthermore, a 7.1 mAh pouch cell achieves stable charge-discharge cycles, confirming the pronounced stability of the as-fabricated QSPE at the interfaces of the high-voltage LiCoO2 cathode and Li anode.

Fine mapping and identifying candidate gene of Y underlying yellow peel in Cucurbita pepo.

As a conspicuous trait, peel color is one of the most important characteristics that affects commodity quality and consumer preferences. The locus Y underlying yellow peel in Cucurbita pepo (zucchini) was first reported in 1922; however, its molecular mechanism is still unknown. In this study, a genetic analysis revealed that yellow peel is controlled by a single dominant genetic factor. Furthermore, Y was mapped in a ~170 kb region on chromosome 10 by bulked segregated analysis (BSA) and fine mapping in F2 and BC1 segregating populations. The candidate region harbors fifteen annotated genes, among which Cp4.1LG10g11560 (CpCHLH) is regarded as a promising candidate gene. CpCHLH encodes a magnesium chelatase H subunit involved in chlorophyll biosynthesis, and its mutation can result in a reduction in chlorophyll content and yellow phenotype. Interestingly, a large fragment (~15 kb) duplication containing incomplete CpCHLH was inserted in the candidate interval, resulting in two reformed CpCHLH proteins in the yellow parental line. It is most likely that the reformed CpCHLH proteins act as a malfunctional competitor of the normal CpCHLH protein to interrupt the formation of chlorophyll. Overall, the isolation of Y will shed light on the molecular mechanism of the peel color regulation of zucchini and lay a foundation for breeding.

Combined analysis of carotenoid metabolites and the transcriptome to reveal the molecular mechanism underlying fruit colouration in zucchini (Cucurbita pepo L.).

To reveal the molecular mechanism underlying peel colouration, carotenoid metabolites and the transcriptome were jointly analysed in zucchini peels with three different colours: light green (Lg), yellow (Y), and orange (O). Our results showed that the carotenoid levels in O (157.075 µg/g) and Y (22.734 µg/g) were both significantly higher than in Lg (7.435 µg/g), while the chlorophyll content was highest in Lg (32.326 µg/g), followed by O (7.294 µg/g) and Y (4.617 µg/g). A total of 14 carotenoids were detected in zucchini peels, primarily lutein (103.167 µg/g in Lg, 509.667 µg/g in Y, and 1543.333 µg/g in O). In particular, significant accumulation of antheraxanthin, zeaxanthin, neoxanthin, and ß-cryptoxanthin was first reported in orange zucchini in this study. Furthermore, two modules with hub genes related to carotenoid or chlorophyll content were identified through weighted gene coexpression network analysis. Additionally, the transcription level of some hub genes (PIF4, APRR2, bHLH128, ERF4, PSY1, LCYE2, and RCCR3) was highly correlated with pigment content in the peel, which may be responsible for carotenoid accumulation and chlorophyll degradation in the Y and O varieties. Taken together, the results obtained in this study help to provide a novel mechanism underlying peel colouration in zucchini.

Research on the mechanisms of polyacrylamide nanospheres with different size distributions in enhanced oil recovery.

Crosslinked polyacrylamide microspheres are widely used as in-depth flooding agents in petroleum development due to their unique properties of thickening, salt-resistance, high-temperature resistance, low cost, etc. To solve the problem of their injections in heterogeneous reservoirs, polyacrylamide nanospheres were synthesized. However, mechanisms of polymer nanospheres in enhanced oil recovery were not investigated comprehensively. In this study, we synthesized polymer nanospheres with different size distributions and studied their mechanisms in enhancing the oil recovery. First, the effects of polyacrylamide nanospheres in enhanced oil recovery of heterogeneous sand-packed tubes was explored by sand-packed tube oil displacement experiments. Second, the rheological properties of polyacrylamide nanosphere dispersion were explored using a rheometer. Third, through the visual microchannel experiment, the mechanism of polymer nanosphere emulsion on the removal of the residual oil film was explored. Finally, through the crude oil removal experiment, it was found that polymer nanospheres with a particle size of about 54 nm can cooperate with surfactants to accelerate the removal of oil droplets.

Performance evaluation of activated carbon with different pore sizes and functional groups for VOC adsorption by molecular simulation.

Volatile organic compounds (VOCs) are growing pollutants now that cause air pollution and threaten human health. In this paper, the Grand Canonical Monte Carlo was used to simulate the adsorption performance of activated carbon on VOCs (benzene, toluene, acetone and methanol). After simulating different pore sizes (0.902 nm,1.997 nm,3 nm and 4 nm) adsorption performances of activated carbon, activated carbon with a pore size of 1.997 nm was selected to further study the influence of functional groups (carboxyl, amino, hydroxyl and hydrogen), and the capillary condensation was explained by the Kelvin equation. Furthermore, effects of functional groups under saturated vapor pressure (P0) of VOCs that range from 0 to 0.1 P0 were explained by the accessible volume and intermolecular interaction potential, respectively. Under pressure range of 0-0.1 P0, at the beginning of adsorption of acetone and methanol, carboxyl and amino groups could reduce the threshold pressure while hydroxyl and hydrogen have the opposite effect. For benzene and toluene, all functional groups have little effect on the threshold pressure, and they reduce the adsorption capacity instead. It could be concluded that the activated carbon could achieve the best adsorption effect on acetone and methanol, on the contrary, the addition of functional groups on benzene and toluene will weaken their adsorption performance.

Expression and secretion of neuregulin-1 in cardiac microvascular endothelial cells treated with angiogenic factors.

Neuregulin-1 (NRG-1) is a positive regulator of angiogenesis, which suggests there may be an association between NRG-1 and angiogenic factors. The aim of the present study was to investigate the effect of treating human cardiac microvascular endothelial cells (HCMECs) with angiogenic factors on NRG-1 expression and secretion. HCMECs were cultured and stimulated with vascular endothelial growth factor (VEGF; 100 ng/ml), angiopoietin (Ang)-1 (100 ng/ml) or Ang-2 (100 ng/ml) under normal or hypoxia/serum deprivation (Hypo/SD) conditions for 24 h. The expression of ErbB receptors and NRG-1 in HCMECs was measured by western blot analysis and the secretion of NRG-1 in HCMECs was determined by ELISA. The results demonstrated that ErbB2, ErbB3 and ErbB4 were expressed in HCMECs and that ErbB2 expression levels were notably higher than those of ErbB3 and ErbB4. Under normal culture conditions the expression and secretion of NRG-1 was significantly increased in HCMECs treated with VEGF or Ang-1 (P<0.05), however levels significantly decreased in HCMECs treated with Ang-2 (P<0.05). Under Hypo/SD conditions the expression and secretion of NRG-1 significantly increased (P<0.05) and VEGF or Ang-1 treatment significantly increased these effects further (P<0.05). Conversely Ang-2 treatment significantly decreased these effects (P<0.05). The expression and release of NRG-1 were significantly increased in HCMECs with VEGF or Ang-1 treatment (P<0.05), which suggests that VEGF and Ang-1 may regulate myocardial angiogenesis and survival via the NRG-1/ErbB signaling pathway.

Coronary Microembolization Induces Cardiomyocyte Apoptosis in Swine by Activating the LOX-1-Dependent Mitochondrial Pathway and Caspase-8-Dependent Pathway.

BACKGROUND: Cardiomyocyte apoptosis by coronary microembolization (CME) contributes to myocardial dysfunction, in which mitochondrial pathway and death receptor pathway are activated. Lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1) is a membrane protein involved in apoptosis. The study aimed to explore the role of LOX-1 in the activation of these 2 major apoptotic pathways. METHODS: Twenty Bama miniature swine were randomized into 4 groups (n = 5 per group). The groups were Sham, CME, LOX-1 small-interfering RNA (siRNA), and control siRNA. Microspheres were injected into the left anterior descending artery of swine to establish CME model. Twelve hours after operation, cardiac function, serum c-troponin I level, microinfarct, and apoptotic index were examined. The levels of LOX-1, Bcl-2, Bax, cytochrome c as well as cleaved caspase 9, -8, and -3 were detected. RESULTS: Myocardial dysfunction, enhanced serum c-troponin I, microinfarct, and apoptosis were induced following CME. Moreover, CME induced increased expression of LOX-1, Bax, cytochrome c, cleaved caspase 9, -8, and -3 as well as decreased Bcl-2 expression levels. The LOX-1 siRNA reversed these effects by CME except cleaved caspase 8 expression, while the control siRNA had no effect. CONCLUSION: Coronary microembolization induces cardiomyocyte apoptosis via the LOX-1-dependent mitochondrial pathway and caspase 8-dependent pathway.

Coronary Microembolization Induces Cardiomyocyte Apoptosis Through the LOX-1-Dependent Endoplasmic Reticulum Stress Pathway Involving JNK/P38 MAPK.

BACKGROUND: Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is a membrane protein associated with apoptosis. Endoplasmic reticulum (ER) stress-induced apoptosis has been determined in several cardiovascular diseases. Mitogen-activated protein kinase (MAPK) signalling is involved in apoptosis. The aim of this study was to investigate whether LOX-1, ER stress, and MAPKs play a role in cardiomyocyte apoptosis after coronary microembolization (CME) and the exact mechanisms involved. METHODS: Thirty swine were randomized into the following groups (n = 5 per group): sham, CME, CME + LOX-1 small-interfering RNA (siRNA), CME + control siRNA, CME + JNK inhibitor, and CME + p38 inhibitor. The CME model was established by injecting microspheres into the left anterior descending (LAD) artery, whereas swine in the sham group received normal saline instead. Twelve hours after the sham operation or CME, cardiac function, serum c-troponin I level, microinfarcts, and apoptotic index were determined. Relative expression levels of LOX-1, ER stress markers (glucose-regulated protein 78 [GRP 78], C/EBP homologous protein [CHOP], and cleaved caspase-12), cleaved caspase-3, c-Jun NH2-terminal protein kinases (JNK), p38, and extracellular signal-related protein kinases (ERK1/2) were measured. RESULTS: CME induced cardiac dysfunction, microinfarction, increased serum c-troponin I levels, and cardiomyocyte apoptosis. Additionally, the expression of LOX-1, ER stress markers, and cleaved caspase-3, and the phosphorylation of JNK, p38, and ERK1/2 were all enhanced. LOX-1 siRNA inhibited these effects except the phosphorylation of ERK1/2. Pretreatment with a JNK inhibitor or a p38 inhibitor attenuated the expression of ER stress markers and apoptosis. CONCLUSIONS: Our results indicated that CME induced cardiomyocyte apoptosis through the LOX-1-dependent ER stress pathway, in which the phosphorylation of JNK and p38 were involved. This might provide a new approach for the prevention and treatment of CME.

Trimetazidine pretreatment inhibits myocardial apoptosis and improves cardiac function in a Swine model of coronary microembolization.

OBJECTIVE: Trimetazidine (TMZ) is a well-known anti-ischemic agent; however, its efficacy and mechanism of cardioprotection on coronary microembolization (CME) are largely unknown. The present study was undertaken to determine whether TMZ pretreatment could attenuate myocardial apoptosis and improve cardiac function in a swine model of CME. METHODS: Fifteen swine were randomly and equally divided into a sham-operated (control) group, CME group and CME plus TMZ (TMZ) group. CME was induced by injecting inert plastic microspheres (42 µm in diameter) into the left anterior descending artery. For the control group, the same dose of normal saline was substituted for the microspheres, and the TMZ group was pretreated with TMZ 30 min before microsphere injection. Cardiac function was assessed by echocardiography, myocardial apoptosis was detected by TUNEL staining, and the expression levels of cleaved caspase-9/3 were measured by Western blot 12 h after operation. RESULTS: Compared to the control group, cardiac function in the CME group was significantly decreased (p < 0.05); however, TMZ pretreatment showed significantly improved cardiac function as compared to the CME group (p < 0.05). The myocardial apoptotic rate and the expression levels of cleaved caspase-9/3 increased remarkably in CME group as compared with the control group (p < 0.001). Again, TMZ pretreatment significantly reduced the apoptotic rate and also the expression levels of cleaved caspase-9/3 (p < 0.001). CONCLUSION: The present study demonstrated that TMZ pretreatment could significantly inhibit CME-induced myocardial apoptosis and improve cardiac function, and that the cardioprotective effect appeared to be mediated by the blockade of the mitochondrial apoptotic pathway. These results emphasize the importance of TMZ pretreatment in the therapy of CME-induced myocardial injury.

The involvement of phosphatase and tensin homolog deleted on chromosome ten (PTEN) in the regulation of inflammation following coronary microembolization.

BACKGROUND/AIMS: Growing evidence shows that phosphatase and tensin homolog deleted on chromosome ten (PTEN) is involved in regulating inflammation in different pathological conditions. Therefore, we hypothesized that the upregulation of PTEN correlates with the impairment of cardiac function in swine following coronary microembolization (CME). METHODS: To possibly disclose an anti-inflammatory effect of PTEN, we induced swine CME by injecting inertia plastic microspheres (42 µm in diameter) into the left anterior descending coronary artery and analyzed the myocardial tissue by immunochemistry, qRT-PCR and western blot analyses. In addition, we downregulated PTEN using siRNA. RESULTS: Following CME, PTEN mRNA and protein levels were elevated as early as 3 h, peaked at 12 h, and then continuously decreased at 24 h and 48 h but remained elevated. Through linear correlation analysis, the PTEN protein level positively correlated with cTnI and TNF-α but was negatively correlated with LVEF. Furthermore, PTEN siRNA reduced the microinfarct volume, improved cardiac function (LVEF), reduced the release of cTnI, and suppressed PTEN and TNF-α protein expression. CONCLUSION: This study demonstrated, for the first time, that PTEN is involved in CME-induced inflammatory injury. The data generated from this study provide a rationale for the development of PTEN-based anti-inflammatory strategies.