Insights into the effects of coating and single crystallization on the rate performance and cycle life of LiNi0.9Mn0.1O2 cathode.

Coating and single crystal are two common strategies for cobalt-free nickel-rich layered oxides to solve its poor rate performance and cycle stability. However, the action mechanism of different modification protocols to suppress the attenuation are unclear yet. Herein, the Li2MoO4 layer-coated polycrystalline LiNi0.9Mn0.1O2 (1.0 %-Mo + NM91) and single crystal LiNi0.9Mn0.1O2 (SC-NM91) are prepared to investigate this difference, respectively. By focusing on the interior of particles, the relationship between structure evolution and electrochemical behavior is systematically studied, and the intrinsic mechanism of coating/single-crystallization modifications on suppressing the attenuation is clarified. The results show that microcracks in LiNi0.9Mn0.1O2 (NM91) are the main culprit leading to the rate capability decay, and the coating can effectively prevent the radial diffusion of microcracks from the center to surface, inhibiting the generation of surface side reactions. Therefore, the coating has a more advantage in improving the rate performance at 5.0C, the discharge capacity of 1.0 %-Mo + NM91 (130.6 mAh/g) is 7.9 % higher than that of SC-NM91 (121.0 mAh/g). In contrast, the single-crystallization can effectively prevent the formation of intergranular cracks arising from the anisotropic stress in NM91, which causes the severe cycle degradation. Correspondingly, the grain boundary-free SC-NM91 shows superior cyclability. The capacity retention rate of SC-NM91 (80.8 %) at 0.2C after 100cycles is 6.3 % higher than that of 1.0 %-Mo + NM91 (74.5 %). This work concludes the effect difference of different modification methods on enhancing the electrochemical performance, which provides theoretical and technical guidance for the optimized and targeted modification design in the cobalt-free high nickel cathode materials.

First report of cucumber green mottle mosaic virus infecting Cynanchum rostellatum in China.

Cucumber green mottle mosaic virus (CGMMV) was first discovered on cucumber in the United Kingdom in 1935 (Ainsworth, 1935), and has spread worldwide except to Antarctica (Jones, 2021). Given its extensive damage, it is considered an important pathogen on global cucurbit plants and fruit crops. In China, CGMMV was first reported on pumpkin in Guangxi Province in 2003 (Qin et al., 2005), and occurred on 34 plants species across 23 provinces (Liu et al., 2016). Cynanchum rostellatum is a member of the family Apocynaceae. In July 2021, leaves of C. rostellatum exhibiting virus-like symptoms (yellowing, severe crinkling, deformation) were observed and collected in Liaoning Province, China. Aphids were also observed on the leaves and stems (Fig. S1) of the plants and were collected. Total RNA was extracted from diseased leaves following the CTAB method, followed by the depletion of ribosomal RNAs (rRNA) with TIANSeq rRNA Depletion Kit (Tiangen, China). The RNAs were, then processed into a DNBSEQ LncRNA-Seq library, and sequenced on the MGISEQ-2000 platform at BGI Genomics (Wuhan, China). A total of 106.98 M clean reads were obtained after data filtering using SOAPnuke software (BGI, China). The clean reads were assembled into contigs using CLC Genomics Workbench 11 (Qiagen, USA) and Trinity v2.0.6 (Haas et al., 2013). A contig (4,760 reads, average coverage:73.76) of 6,391 nucleotides was found to share the highest sequence identity (99.83%) with CGMMV isolate GDLZ (MK933286), irrespective of other virus-like contigs related to Polerovirus and Totivirus. Based on the genome of GDLZ isolate, seven specific primers (Table S1) were designed to amplify the full viral genomic sequences using a PrimeScriptTM One-Step RT-PCR Kit. Seven expected amplicons were obtained, cloned, and sequenced. The complete genome was determined to be 6,423 nucleotides (GenBank accession number OR854819) in length and designated as LNMJ isolate. LNMJ shared 96.8%-99.7% nucleotide sequence identities with CGMMV isolates from China. Phylogenetic analysis based on the complete genome sequences showed that LNMJ clustered together with CGMMV isolates hn (GenBank accession number KC851866), GDLZ (GenBank accession number MK933286), and JD8 (GenBank accession number KM873784) from China. The specific primers LM-TJ-3F/3R were designed to determine the virus-symptom association for LNMJ, and all twelve symptomatic C. rostellatum plants collected from fields tested positive for LNMJ. Two out of six randomly selected aphids from the diseased plants also tested positive. To further prove its infectivity, LNMJ was inoculated mechanically onto ten healthy Nicotiana benthamiana plants, and the results indicated a high infection rate of 80% (8/10), at 30 days post-inoculation despite no distinct symptoms observed. To our knowledge, this is the first report of the natural infection of C. rostellatum plants with CGMMV. C. rostellatum is a widespread herb in China (Wei et al., 2019) and more surveys are needed to determine the distribution of CGMMV. The habitats of C. rostellatum span diverse agroecological zones, and thus our study underscores the potential spillover of CGMMV to neighboring crops as a significant risk.

The complete genome sequence of a putative novel cytorhabdovirus identified in Chelidonium majus in China.

A new cytorhabdovirus, tentatively named "chelidonium yellow mottle associated virus" (CheYMaV), was identified in Chelidonium majus with yellow mottle symptoms by high-throughput sequencing and RT-PCR. Its genome is 12,121 nucleotides in length and contains eight open reading frames (ORFs) in the order 3'-N-P'-P-P3-M-G-P6-L-5'. Amino acid sequence comparisons between the putative proteins of CheYMaV and the corresponding proteins of other cytorhabdoviruses showed that it shares the highest sequence similarity with Trifolium pratense virus A (TpVA, MH982250) and Glehnia littoralis virus 1 (GllV1, BK014304), but with sequence identity values below the species demarcation threshold for cytorhabdoviruses (< 80%). Phylogenetic analysis showed that CheYMaV is most closely related to TpVA and GllV1. CheYMaV should therefore be considered a new member of the genus Cytorhabdovirus. This is the first report of a cytorhabdovirus identified in Chelidonium majus.

Ultrastable Super-Tonks-Girardeau Gases under Weak Dipolar Interactions.

The highly excited super-Tonks-Girardeau (sTG) gas was recently observed to be extremely stable in the presence of a weak dipolar repulsion. Here we reveal the underlying reason for this mysterious phenomenon. By exactly solving the trapped small clusters with both contact and dipolar interactions, we show that the reason lies in the distinct spectral responses between sTG gas and its decaying channel (bound state) when a weak dipolar interaction is present. Specifically, a tiny dipolar force can produce a visible energy shift for the localized bound state, but can hardly affect the extended sTG branch. As a result, the avoided level crossing between two branches is greatly modified in both location and width in the parameter axis of coupling strength, leading to a more (less) stable sTG gas for a repulsive (attractive) dipolar force. These results, consistent with experimental observations, are found to robustly apply to both bosonic and fermionic systems.

Quartet Superfluid in Two-Dimensional Mass-Imbalanced Fermi Mixtures.

Quartet superfluid (QSF) is a distinct type of fermion superfluidity that exhibits high-order correlation beyond the conventional BCS pairing paradigm. In this Letter, we report the emergent QSF in 2D mass-imbalanced Fermi mixtures with two-body contact interactions. This is facilitated by the formation of a quartet bound state in vacuum that consists of a light atom and three heavy fermions. For an optimized heavy-light number ratio 3:1, we identify QSF as the ground state in a considerable parameter regime of mass imbalance and 2D coupling strength. Its unique high-order correlation can be manifested in the momentum-space crystallization of a pairing field and density distribution of heavy fermions. Our results can be readily detected in Fermi-Fermi mixtures nowadays realized in cold atoms laboratories, and meanwhile shed light on exotic superfluidity in a broad context of mass-imbalanced fermion mixtures.

Building a Flexible and Highly Ionic Conductive Solid Electrolyte Interphase on the Surface of Si@C Anodes by Binary Electrolyte Additives.

Si@C as a high specific capacity anode material for lithium batteries (LIBs) has attracted a lot of attention. However, the severe volume change during lithium de-embedding causes repeated rupture/reconstruction of the solid electrolyte interphase (SEI), resulting in poor cycling stability of the Si-based battery system and thus hindering its application in commercial batteries. Using electrolyte additives to form an excellent SEI is considered to be a cost-effective method to meet this challenge. Here, the classical film-forming additive vinyl carbonate (VC), and the newly emerging lithium salt additive lithium difluorophosphate (LiDFP), are chosen as synergistic additives to improve the electrode-electrolyte interface properties. Final results show that the VC additive generates flexible polycarbonate components at the electrode/electrolyte interface, preventing the fragmentation of Si particles. However, the organic components show high impedance, inhibiting the fast transport of Li+. This defect can be supplemented from the decomposition substances of the LiDFP additive. The derived inorganic products, such as LiF and Li3PO4, can strengthen the reaction kinetics of the electrode, reduce the interfacial impedance, and promote the Li+ transport. Thus, the synergistic effect of VC and LiDFP additives builds an effective SEI with good flexibility and high ionic conductivity and then significantly improves the cycling and rate stability of Si@C anodes. The experimental results show that the utilization of LiDFP and VC additives to modify the Si@C anode interface enhances the capacity retention of the Si@C/Li half-cell after 100 cycles from 68.2% to 85.1%. Besides, the possible mechanism of action between VC and LiDFP is proposed by using the spectral characterization technique and density functional theory (DFT) calculations. This research opens up a new possibility for improvement of SEI, and provides a simple way to achieve high-performance Si-based LIBs.

Inhibition of annexin A7 suppresses senescence-associated heterochromatin foci formation and senescence through the AMPK/mTOR pathway in human dermal fibroblasts.

Senescence-associated heterochromatin foci (SAHF) is often used as a biological marker for senescent cells, but the regulation of its formation process is unclear. To find a new modulator of SAHF, we screened our chemical small molecules and found 7-amino-2,3,4,5-tetrahedrobenzo[b][1,4] oxazepin-3-ol (ABO) that was identified as an inhibitor of annexin A7 GTPase (ANXA7) dramatically suppressed the aggregation of heterochromatin protein (HP1γ), an indicator of SAHF. To understand its action mechanism, we first observed the changes in the karyoplasmic ratio of ANXA7 because HP1γ mainly located in the nucleus. The results showed that ABO elevated the protein level of ANXA7 in the nucleus. Therefore, we raised a hypothesis that ANXA7 interacted with HP1γ and regulated its phosphorylation, which is closely related to the formation of SAHF. The co-immunoprecipitation and Western blot experiment results showed that ANXA7 had no direct interaction with HP1γ, however, the phosphorylation of HP1γ was increased by ABO, which suggested that ANXA7 indirectly regulated HP1γ phosphorylation. Then, based on our previous discovery of ANXA7 interacting with AMP-activated protein kinase (AMPK), we investigated the effect of the AMPK/mammalian target of rapamycin (mTOR) signaling pathway on ABO-increased phosphorylation of HP1γ. We found that ABO decreased AMPK phosphorylation and increased the phosphorylation level and activity of mTOR. In the presence of an AMPK activator or mTOR inhibitor, ABO could not increase HP1γ phosphorylation. As a result, ABO inhibited the senescence of human dermal fibroblasts (HDFs). In this study, we found that ANXA7 was a new regulator of SAHF, it could regulate the formation of SAHF through the AMPK/mTOR pathway. The data suggested that ABO could be used as a powerful tool to inhibit the replicative senescence of HDFs.

Inhibition of transition-metal dissolution with an inert soluble product interface constructed by high-concentration electrolyte.

The formation of a compact and stable cathode electrolyte interphase (CEI) film is a promising way to improve the high voltage resistance of lithium-ion batteries (LIBs). However, challenges arise due to the corrosion of hydrogen fluoride (HF) and the dissolution of transition metal ions (TMs) in harsh conditions. To address this issue, researchers have constructed an anion-derived CEI film enriched with LiF and LiPO2F2 soluble product on the surface of LiNi0.5Mn1.5O4 (LNMO) cathode in highly concentrated electrolytes (HCEs). The strong binding of LiF and LiPO2F2 generated an inert LiPO2F2 soluble product interface, which inhibited HF corrosion and maintained the spinel structure of LNMO, contributing to a capacity retention of 92% after 200 cycles at 55°C in the resulting cell with a soluble LiPO2F2-containing CEI film. This new approach sheds light on improving the electrode/electrolyte interface for high-energy LIBs.

Esterase D interacts with metallothionein 2A and inhibits the migration of A549 lung cancer cells in vitro.

Esterase D (ESD) is a nonspecific esterase widely distributed in various organisms. ESD plays an important role in regulating cholesterol efflux, inhibiting viral replication and lung cancer growth. MT2A (metallothionein 2A) is the most important isoform of metallothionein (MTs) in human and high expression of MT2A in tumors represents poor prognosis and metastatic behavior. However, there are no reports about the molecular mechanism of ESD in the regulation of tumor metastasis. In this study, we found for the first time that activation ESD promoted its interaction with MT2A and decreased the protein level of MT2A, which resulting in the concentration of free zinc ions up-regulated, and inhibited the migration of A549 lung cancer cells in vitro.

Activation of GRP78 ATPase suppresses A549 lung cancer cell migration by promoting ITGB4 degradation.

Hypochlorous acid (HOCl) is an essential signal molecule in cancer cells. Activated GRP78 ATPase by a HOCl probe named ZBM-H inhibits lung cancer cell growth. However, the role and underlying mechanism of GRP78 ATPase in lung cancer cell migration have not been established. Here, we reported that activation of GRP78 ATPase by ZBM-H suppressed A549 cell migration and inhibited EMT process. Notably, ZBM-H time-dependently decreased the protein level of integrin ß4 (ITGB4) in A549 cells. Combinatorial treatment of 3BDO (an autophagy inhibitor) and ZBM-H partially rescued the protein level of ITGB4. Consistently, 3BDO partially reversed ZBM-H-inhibited cell migration. Furthermore, ZBM-H promoted the interaction between ANXA7 and Hsc70, which participated in the regulation of selective autophagy and degradation of ITGB4.

Identification of a new way to induce differentiation of dermal fibroblasts into vascular endothelial cells.

BACKGROUND: Human dermal fibroblasts (HDFs) have the potential to differentiate into vascular endothelial cells (VECs), but their differentiation rate is low and the mechanism involved is not clear. The small molecule pathway controls the phenotype of fibroblasts by activating cellular signaling pathways, which is a more convenient method in the differentiation strategy of HDFs into VECs. METHODS: In this study, HDFs were treated with the different doses of CPP ((E)-4-(4-(4-(7-(diethylamino)-2-oxo-2H-chromene-3-carbonyl) piperazin-1-yl) styryl)-1-methylpyridin-1-ium iodide), and the mRNA and protein levels of HDFs were detected by qPCR, Western blot, flow cytometry and immunofluorescent staining. The matrigel assays, acetylated-LDL uptake and angiogenesis assays of chick embryo chorioallantoic membrane (CAM) and hindlimb ischemia model of nude mice were performed to evaluate the functions of VECs derived from HDFs. RESULTS: Here, we report that the small chemical molecule, CPP, can effectively induce HDFs to differentiate into VECs. First, we observed the morphological changes of HDFS treated with CPP. Flow cytometry, Western blot and qRT-PCR analyses showed that CPP effectively decreased the level of the HDFs-marker Vimentin and increased levels of the VEC-markers CD31, CD133, TEK, ERG, vWF, KDR and CDH5. Detection of the percentage of CD31-positive cells by immunofluorescent staining confirmed that CPP can effectively induce HDFs to differentiate into VECs. The results of Matrigel assays, DiI-ac-LDL uptake, angiogenesis assays on CAM and hindlimb ischemia model of nude mice showed that CPP-induced HDFs have the functions of VECs in vitro and in vivo. Western blot and qRT-PCR analysis showed that CPP induces HDFs to differentiate into VECs by promoting the expression of pro-angiogenic factors (VEGF, FGF-2 and PDGF-BB). CONCLUSIONS: Our data suggest that the small chemical molecule CPP efficiently induces the differentiation of HDFs into VECs. Simultaneously, this new inducer provides a potential to develop new approaches to restore vascular function for the treatment of ischemic vascular diseases.

HOCI Probe CPP Induces the Differentiation of Human Dermal Fibroblasts into Vascular Endothelial Cells through PHD2/HIF-1α/HEY1 Signaling Pathway.

Human dermal fibroblasts (HDFs) have the potential to differentiate into endothelial cells (VECs). In our previous research, we reported that a hypochlorous acid (HOCl) probe CPP efficiently induced the differentiation of HDFs into VECs, however, the mechanism of differentiation was not clear. As an HOCI probe, CPP binds HOCI to modulate its effects. In this study, through Western blotting, qPCR, and PHD2 enzyme activity assay, we found that CPP inhibited the enzyme activity of prolyl-4-hydroxylase 2 (PHD2), thereby stabilizing HIF-1α. To further clarify the mechanism by which CPP inhibits PHD2 enzyme activity, we constructed plasmids, and found that CPP inhibited PHD2 activity to increase the HIF-1α level through the modulation of PHD2 at Cys302 by HOCl in HDFs. Furthermore, RNA-seq experiments showed that CPP could induce the expression of HEY1, which is not only a target gene regulated by HIF1α, but also a key transcription factor for VECs. We used siRNA transfection and in vivo experiments to confirm that CPP could induce HDFs to differentiate into VECs by HEY1. In summary, we identified a new inhibitor of PHD2, demonstrated the new role of HOCl in cell differentiation, and elucidated the mechanism by which HOCl probe CPP induced the differentiation of HDFs into VECs.

Grp94 Inhibitor HCP1 Inhibits Human Dermal Fibroblast Senescence.

Researchers are paying more and more attention to aging, especially skin aging. Therefore, it is urgent to find an effective way to inhibit aging. Here, we report a small chemical molecule, HCP1, that inhibited the senescence of human dermal fibroblasts (HDFs). First, we performed morphological experiment and found that HCP1-treated HDFs were no longer elongated and flat compared to DMSO-treated groups. Next, we found that the number of ß-gal positive cells decreased compared to DMSO-treated groups. Through flow cytometry, western blot, and immunofluorescence, we found that HCP1 could inhibit the senescence of HDFs. In the study of the mechanism, we found that HCP1 could regulate the AMPK/mTOR signal pathway through glucose-regulated protein 94 (Grp94). In addition, we found that HCP1 could promote the interaction between Grp94 and lysosomes, which led to an increase in the activity of lysosomes and inhibited the senescence of HDFs. At the same time, we found that HCP1 decreased the concentration of Ca2+ in mitochondria, inhibiting the senescence of HCP1. Therefore, we propose that HCP1 is a potential aging-inhibiting compound, and provide a new idea for the development of senescence-inhibiting drugs.

Universal Tetramer and Pentamer Bound States in Two-Dimensional Fermionic Mixtures.

We study the emergence of universal tetramer and pentamer bound states in the two-dimensional (N+1) system, which consists of N identical heavy fermions interacting with a light atom. We show that the critical heavy-light mass ratio to support a (3+1) tetramer below the trimer threshold is 3.38, and to support a (4+1) pentamer below the tetramer threshold is 5.14. While the ground state tetramer and pentamer are both with zero total angular momentum, they exhibit very different density distributions and correlations in momentum space, due to their distinct angular momentum decompositions in the dimer-fermion frame. These universal bound states can be accessible by a number of Fermi-Fermi mixtures now realized in cold atoms laboratories, which also suggest novel few-body correlations dominant in their corresponding many-body systems.

Activation of Esterase D by FPD5 Inhibits Growth of A549 Lung Cancer Cells via JAB1/p53 Pathway.

Esterase D (ESD) is widely distributed in mammals, and it plays an important role in drug metabolism, detoxification, and biomarkers and is closely related to the development of tumors. In our previous work, we found that a chemical small-molecule fluorescent pyrazoline derivative, FPD5, an ESD activator, could inhibit tumor growth by activating ESD, but its molecular mechanism is still unclear. Here, by using RNA interference (RNAi), andco-immunoprecipitation techniques, we found that ESD suppressed the nucleus exportation of p53 through reducing the interaction between p53 and JAB1. The protein level of p53 in the nucleus was upregulated and the downstream targets of p53 were found by Human Gene Expression Array. p53 inhibited the expression of CDCA8 and CDC20. Lastly, the cell cycle of A549 cells was arrested at the G0/G1 phase. Together, our data suggest that ESD inhibited the cancer cell growth by arresting the cell cycle of A549 cells via the JAB1/p53 signaling pathway. Our findings provide a new insight into how to inhibit the growth of lung cancer with the activation of ESD by FPD5.

ZBM-H-induced activation of GRP78 ATPase promotes apoptosis via annexin A7 in A549 lung cancer cells.

Hypochlorous acid (HOCl) is an essential signal for the regulation of cancer cell fate, including autophagy and apoptosis. HOCl regulated autophagy by affecting the oxidation modification of glucose-regulated protein 78 (GRP78) and the activity of GRP78 ATPase. The mechanism of GRP78 ATPase in cell apoptosis has however not yet been clarified. Here we reported that ZBM-H, as a probe of HOCl, was able to directly bind to GRP78 in the presence or absence of ATP. Following ZBM-H treatment, the interaction between GRP78 and annexin A7 (ANXA7) was promoted, and this was accompanied by increased phosphorylation of integrin ß4 (ITGB4). In addition, ZBM-H enhanced the phosphorylation of ANXA7. ABO, an inhibitor of ANXA7, inhibited ZBM-H-induced ITGB4 phosphorylation and apoptosis, while ANXA7 activator SEC had opposite effect. Collectively, these data provide new evidence for the mechanism by which ZBM-H-induced activation of GRP78 ATPase regulates apoptosis of A549 lung cancer cells.

Two simple but effective turn-on benzothiazole-based fluorescent probes for detecting hydrogen sulfide in real water samples and HeLa cells.

Two simple turn-on fluorescent probes, containing a benzothiazole and the 2,4-dinitrobenzenesulfonyl group, were designed for detecting H2S. Two probes exhibited good selectivity and high sensitivity, which were applied to detect the H2S in real water samples. Probe P2 with a positive charge had better solubility than probe P1 in water; therefore, probe P2 was successfully applied to detect both the endogenous and exogenous H2S in lysosomes of living HeLa cells.

Efficient catalyst prepared from water treatment residuals and industrial glucose using hydrothermal treatment: Preparation, characterization and its catalytic performance for activating peroxymonosulfate to degrade imidacloprid.

Water treatment residuals (WTRs), as by-products of drinking water treatment plant, were used as catalyst for persulfate activation to degrade organic pollutants. In this study, G-HWTRs were successfully prepared by hydrothermal treatment, which combined WTRs and a hydrothermal reducing agent (industrial glucose) in different ratios. These materials manifested upgraded performance compared with raw WTRs and HWTRs (prepared only with WTRs under hydrothermal condition) in imidacloprid (IMD) degradation. The elemental composition, structure, morphological and magnetic properties of the G-HWTRs were investigated. And the influences of peroxymonosulfate (PMS) concentration, G-HWTRs dosage, initial pH, water matrix on IMD degradation were determined. The results demonstrated that G-HWTRs-3 had the best catalytic performance, 10 µM IMD was almost completely degraded in the system of G-HWTRs (0.2 g L-1) and PMS (0.1 mM) within 2 h without pH adjustment. Based on the results of the electron spin-resonance spectroscopy (ESR) tests and radicals scavenging experiments, all of SO4-, OH, 1O2 and O2- were the reactive oxygen species driving the IMD degradation, and OH was regarded as the main role of IMD degradation. The possible degradation pathways of IMD were further proposed based on the degradation intermediates that identified by LC-MS. Besides, further experiments indicated G-HWTRs has degradation potential for various pollutants, the degradation rate of atrazine (ATZ), acetochlor (ACE) and simazine (SMX) within 2 h achieved 92.54%, 83.88% and 90.25%, respectively. These results confirmed G-HWTRs has good catalytic performance and activation potential on PMS, providing an effective method for remediating organic polluted wastewater.

Antioxidation Mechanism of Highly Concentrated Electrolytes at High Voltage.

It has been researched that highly concentrated electrolytes (HCEs) can solve the problem of the excessive decomposition of dilute electrolytes at a high voltage, but the mechanism is not clear. In this work, the antioxidation mechanism of HCE at a high voltage was investigated by in situ electrochemical tests and theoretical calculations from the perspective of the solvation structure and physicochemical property. The results indicate that compared with the dilute electrolyte, the change of solvation structures in HCE makes more PF6- anions easier to be oxidized prior to the dimethyl carbonate solvents, resulting in a more stable cathode-electrolyte interphase (CEI) film. First, the lower oxidation potential of the solvation structure with more PF6- anions inhibits the side effects of the electrolyte effectively. Second, the CEI film, consisted of LiF and LixPOyFz generated from the oxidation of PF6- and Li3PO4 generated from the hydrolysis of LiPF6 via the soluble PO2F2- intermediate, can reduce the interface impedance and improve the conductivity. Intriguingly, the high viscosity of HCEs and the hydrolysis of LiPF6 are proven to play a positive role in enhancing the interfacial stability of the electrolyte/electrode at a high voltage. This study builds a deep understanding of the bulk and interface properties of HCEs and provides theoretical support for their large-scale application in high-voltage battery materials.

Esterase D stabilizes FKBP25 to suppress mTORC1.

BACKGROUND: Esterase D (ESD) is a nonspecific esterase that detoxifies formaldehyde. Many reports have stated that ESD activity is associated with a variety of physiological and pathological processes. However, the detailed signaling pathway of ESD remains poorly understood. METHODS: Considering the advantages of the small chemical molecule, our recent work demonstrated that 4-chloro-2-(5-phenyl-1-(pyridin-2-yl)-4,5-dihydro-1H-pyrazol-3-yl) phenol (FPD5) activates ESD, and will be a good tool for studying ESD further. Firstly, we determined the interaction between ESD and FK506 binding protein 25 (FKBP25) by yeast two-hybrid assay and co-immunoprecipitation (CO-IP) and analyzed the phosphorylation levels of mTORC1, P70S6K and 4EBP1 by western blot. Furthermore, we used the sulforhodamine B (SRB) and chick chorioallantoic membrane (CAM) assay to analyze cell viability in vitro and in vivo after treatment with ESD activator FPD5. RESULTS: We screened FKBP25 as a candidate protein to interact with ESD by yeast two-hybrid assay. Then we verified the interaction between ESD and endogenous FKBP25 or ectopically expressed GFP-FKBP25 by CO-IP. Moreover, the N-terminus (1-90 aa) domain of FKBP25 served as the crucial element for their interaction. More importantly, ESD reduced the K48-linked poly-ubiquitin chains of FKBP25 and thus stabilized cytoplasmic FKBP25. ESD also promoted FKBP25 to bind more mTORC1, suppressing the activity of mTORC1. In addition, ESD suppressed tumor cell growth in vitro and in vivo through autophagy. CONCLUSIONS: These findings provide novel evidence for elucidating the molecular mechanism of ESD and ubiquitination of FKBP25 to regulate autophagy and cancer cell growth. The ESD/FKBP25/mTORC1 signaling pathway is involved in inhibiting tumor cell growth via regulating autophagy.