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Blade tip clearance is an important parameter affecting the efficiency, stability, and safety of aero-engines. During the high-speed rotation of the blade, the blade tip clearance changes, which leads to changes in signal amplitude collected by the tip timing sensor. When the rotor is rotating at high speed, it is impractical to measure the tip-timing signal under each tip clearance. Aiming at the previous problems, a prediction method of blade tip-timing sensor waveform based on the combination of the Kriging model and static calibration data are proposed. The relationship between the output voltage of the tip timing sensor and the blade tip clearance and the angle of the blade tip cutting magnetic line is obtained by collecting the data of static calibration. Based on the collected static calibration experimental data and compared with the polynomial fit method and the RBF model, the accuracy of the Kriging model in predicting the waveform of the blade tip timing sensor was verified. The results show that the prediction accuracy of the Kriging model is basically the same as that of the RBF model, but the Kriging model has more advantages in predicting the waveform when the blade tip clearance is unknown. In contrast, the prediction accuracy of the polynomial fit is lower than that of the Kriging and RBF models, and the polynomial fit is prone to significant prediction errors.

Context Diabetes is an age-related disease; however, the mechanism underlying senescent beta cell failure is still unknown. Objective The present study was designed to investigate whether and how the differentiated state was altered in senescent human beta cells by excluding the effects of impaired glucose tolerance. Methods We calculated the percentage of hormone-negative/chromogranin A–positive endocrine cells and evaluated the expressions of forkhead box O1 (FoxO1) and Urocortin 3 (UCN3) in islets from 31 nondiabetic individuals, divided into young (60 years) groups. We also assessed adaptive unfolded protein response markers glucose-regulated protein 94 (GRP94), and spliced X-box binding protein 1 (XBP1s) in senescent beta cells and their possible contributions to maintaining beta cell identity and differentiation state. Results We found an almost 2-fold increase in the proportion of dedifferentiated cells in elderly and middle-aged groups compared with the young group (3.1 ± 1.0% and 3.0 ± 0.9% vs 1.7 ± 0.5%, P < .001). This was accompanied by inactivation of FoxO1 and loss of UCN3 expression in senescent human beta cells. In addition, we demonstrated that the expression levels of adaptive unfolded protein response (UPR) components GRP94 and XBP1s declined with age. In vitro data showed knockdown GRP94 in Min6-triggered cells to dedifferentiate and acquire progenitor features, while restored GRP94 levels in H2O2-induced senescent Min6 cells rescued beta cell identity. Conclusion Our finding highlights that the failure to establish proper adaptive UPR in senescent human beta cells shifts their differentiated states, possibly representing a crucial step in the pathogenesis of age-related beta cell failure.

The prediction of vibration characteristics was studied in the mistuned bladed disk by the mobile interface prestressed component mode synthesis (CMS) superelement method. When the strongly, generally, and weakly coupling in the mistuned bladed disk, according to the results of the direct FEM method, the prediction accuracy of this method was verified and compared with the fixed-interface CMS method by using the relative error of dynamic frequency, vibration mode matching function, and dimensionless root mean square error of vibration amplitudes. It is pointed that for mistuned bladed disk in the strong coupling, the prediction accuracy of dynamic frequency and vibration amplitudes are higher by the mobile interface CMS method and the vibration modes are matched with the direct method. In weak coupling, the results of dynamic frequency and vibration modes predicted by the mobile interface CMS method and the fixed-interface CMS method are consistent with the direct method, but the vibration amplitudes’ prediction error of the mobile interface CMS method is lower than that of the fixed-interface CMS method. In general coupling, the mobile interface CMS method has higher dynamic frequency prediction accuracy at low order, and the two methods have comparable dynamic frequency prediction accuracy at high order. The vibration modes predicted by the two methods are matched with the direct FEM method, and the prediction accuracy of vibration amplitude by the mobile interface CMS method is better than that of the fixed-interface CMS method. The results indicate that the mobile interface CMS method could more accurately predict vibration characteristics of the mistuned bladed disk with different coupling degrees and could be an effective measurement for studying the vibration characteristics of the mistuned bladed disk system.

Developing liquid electrolytes with higher kinetics and enhanced interphase stability is one of the key challenges for lithium batteries. However, the poor solubility of lithium salts in solvents sets constraints that compromises the electrolyte properties. Here, it is shown that introducing multiple salts to form a high-entropy solution, alters the solvation structure, which can be used to raise the solubility of specific salts and stabilize electrode–electrolyte interphases. The prepared high-entropy electrolytes significantly enhance the cycling and rate performance of lithium batteries. For lithium-metal anodes the reversibility exceeds 99%, which extends the cycle life of batteries even under aggressive cycling conditions. For commercial batteries, combining a graphite anode with a LiNi0.8Co0.1Mn0.1O2 cathode, more than 1000 charge–discharge cycles are achieved while maintaining a capacity retention of more than 90%. These performance improvements with respect to regular electrolytes are rationalized by the unique features of the solvation structure in high-entropy electrolytes. The weaker solvation interaction induced by the higher disorder results in improved lithium-ion kinetics, and the altered solvation composition leads to stabilized interphases. Finally, the high-entropy, induced by the presence of multiple salts, enables a decrease in melting temperature of the electrolytes and thus enables lower battery operation temperatures without changing the solvents.

The design and fabrication of PEDOT:PSS/n-Si cell have been widely studied in recent years, yet few studies have looked into the effect of Si substrate properties on device’s performance. In this study, the thinning treatment of silicon substrates based on simple and low-cost alkaline etching has been systematically investigated. It is found that the KOH etching could effectively remove the surface damage layer. The series resistance (Rs) of device can be adjusted by silicon wafer thickness, under the optimized etching condition, the power conversion efficiency (PCE) of resulting 338 μm-thick PEDOT:PSS/n-Si could reach up to 5.17%, which is 1.7-times increase by comparing that of 500 μm-thick PEDOT:PSS/n-Si (PCE:2.97%).Furthermore, KOH-isopropanol texturing was incorporated into thinning silicon wafer, the smoothing pyramid structures can further reduce light reflectance and improve the junction contact quality between PEDOT:PSS film and n-Si substrates, and the PCE of 5.49% was finally achieved. This study shows guide value for understanding the influence of substrate thickness and texturing treatment on the performance of PEDOT:PSS/n-Si solar cell.

Context The mechanistic target of rapamycin complex I (mTORC1) is crucial for β-cell identity and function in rodents. However, its possible relevance to the physiopathology of diabetes in humans remains unclear. Objective This work aimed to understand the participation of mTORC1 in human β cells in prediabetes and diabetes. Design We evaluated the PS6 immunofluorescence intensity in islets of pancreatic sections from 12 nondiabetic (ND), 11 impaired fasting glucose (IFG), and 11 glycemic-controlled type 2 diabetic (T2D) individuals. We also assessed the dynamic change of mTORC1 activity in β cells of db/db mice with new-onset diabetes. Results There exists intercellular heterogeneity of mTORC1 activities in human islets. Islet mTORC1 activity was independently and positively correlated with FBG in ND, but not in IFG and T2D. Moreover, we did not detect significant change in mTORC1 activities between T2D and ND. Of note, the islet mTORC1 activities were significantly higher in IFG than in ND. We further stratified IFG individuals according to their islet PS6 levels and found that IFG-PS6high exhibited remarkably higher urocortin3 and glucose transporter 2 expression in their β cells compared to IFG-PS6low. Consistently, we also detected a significant increase in mTORC1 activities in prediabetic db/db mice compared to nondiabetic littermates. Interestingly, mTORC1 activities determined β-cell adaptation or failure in db/db mice: A strong negative correlation was found between islet mTORC1 activities and fasting glucose levels in db/db mice during their diabetes progression. Conclusions Our finding highlights a dynamic islet mTORC1 response in β-cell adaption/failure in human T2D.

Panax notoginseng is a widely used traditional Chinese medicine and has extensive pharmacological effects. In this work, water-soluble polysaccharides from Panax notoginseng were isolated and fractionated. One starch-like polysaccharide (PNPN) and six pectin fractions (PNPA-1A, PNPA-1B, PNPA-2A, PNPA-2B, PNPA-3A and PNPA-3B) were obtained. Monosaccharide composition, enzymatic hydrolysis, nuclear magnetic resonance and methylation analysis were combined to characterize their structures. PNPA-1A and PNPA-2A mainly contained 1,4-β-D-galactans, 1,5-α-L-arabinan and arabinogalactan II (AG-II). PNPA-3A was a typical rhamnogalacturonan I (RG-I) type pectin with 1,4-β-D-galactan and 1,5/1,3,5-α-L-arabinan side chains. PNPA-1B, PNPA-2B and PNPA-3B consisted of homogalacturonan (HG) as major domains, together with different ratios of RG-I and rhamnogalacturonan II (RG-II) domains. These results will provide basis for further investigation of structure-activity relationships of Panax notoginseng polysaccharides and be useful for the application of Panax notoginseng.

The N6-methyladenosine (m6A) RNA modification is essential during embryonic development of various organs. However, its role in embryonic and early postnatal islet development remains unknown. Mice in which RNA methyltransferase-like 3/14 (Mettl3/14) were deleted in Ngn3+ endocrine progenitors (Mettl3/14nKO) developed hyperglycemia and hypoinsulinemia at 2 weeks after birth. We found that Mettl3/14 specifically regulated both functional maturation and mass expansion of neonatal β-cells before weaning. Transcriptome and m6A methylome analyses provided m6A-dependent mechanisms in regulating cell identity, insulin secretion, and proliferation in neonatal β-cells. Importantly, we found that Mettl3/14 were dispensable for β-cell differentiation but directly regulated essential transcription factor MafA expression at least partially via modulating its mRNA stability. Failure to maintain this modification impacted the ability to fulfill β-cell functional maturity. In both diabetic db/db mice and patients with type 2 diabetes (T2D), decreased Mettl3/14 expression in β-cells was observed, suggesting its possible role in T2D. Our study unraveled the essential role of Mettl3/14 in neonatal β-cell development and functional maturation, both of which determined functional β-cell mass and glycemic control in adulthood.

Improving the reversibility of lithium metal batteries is one of the challenges in current battery research. This requires better fundamental understanding of the evolution of the lithium deposition morphology, which is very complex due to the various parameters involved in different systems. Here, we clarify the fundamental origins of lithium deposition coverage in achieving highly reversible and compact lithium deposits, providing a comprehensive picture in the relationship between the lithium microstructure and solid electrolyte interphase (SEI) for lithium metal batteries. Systematic variation of the salt concentration offers a framework that brings forward the different aspects that play a role in cycling reversibility. Higher nucleation densities are formed in lower concentration electrolytes, which have the advantage of higher lithium deposition coverage; however, it goes along with the formation of an organic-rich instable SEI which is unfavorable for the reversibility during (dis)charging. On the other hand, the growth of large deposits benefiting from the formation of an inorganic-rich stable SEI is observed in higher concentration electrolytes, but the initial small nucleation density prevents full coverage of the current collector, thus compromising the plated lithium metal density. Taking advantages of the paradox, a nanostructured substrate is rationally applied, which increases the nucleation density realizing a higher deposition coverage and thus more compact plating at intermediate concentration (∼1.0 M) electrolytes, leading to extended reversible cycling of batteries.

Type 2 diabetes (T2D) is associated with defective insulin secretion and reduced β cell mass. Available treatments provide a temporary reprieve, but secondary failure rates are high, making insulin supplementation necessary. Reversibility of β cell failure is a key translational question. Here, we reverse engineered and interrogated pancreatic islet–specific regulatory networks to discover T2D-specific subpopulations characterized by metabolic inflexibility and endocrine progenitor/stem cell features. Single-cell gain- and loss-of-function and glucose-induced Ca(2+) flux analyses of top candidate master regulatory (MR) proteins in islet cells validated transcription factor BACH2 and associated epigenetic effectors as key drivers of T2D cell states. BACH2 knockout in T2D islets reversed cellular features of the disease, restoring a nondiabetic phenotype. BACH2-immunoreactive islet cells increased approximately 4-fold in diabetic patients, confirming the algorithmic prediction of clinically relevant subpopulations. Treatment with a BACH inhibitor lowered glycemia and increased plasma insulin levels in diabetic mice, and restored insulin secretion in diabetic mice and human islets. The findings suggest that T2D-specific populations of failing β cells can be reversed and indicate pathways for pharmacological intervention, including via BACH2 inhibition.

Polychlorinated biphenyls (PCBs) are highly hazardous, persistent, and bioaccumulative substances that pose a threat to water quality in a number of locations, including the Beiluo River in Shaanxi Province, China. However, little is known about the contribution of PCBs to the Beiluo River. In this study, in order to look into the impact of sources on the water of the Beiluo River, the discovered PCB congeners in water were examined on a regional scale. The concentration of PCBs in water across Beiluo River was in the range from 0.065 to 1.92 ng L−1, and the average concentration was 0.37 ng L−1. The main PCB sources in the Beiluo River waterbody were found using positive matrix factorization (PMF). Source apportionment results indicated that the PCB pollution of the Beiluo River was mostly caused by industrial emissions, technical PCB mixtures, and coal and wood combustion. According to current ecological risk assessment guidelines, the PCB concentrations found in this study may have a negative impact on biological systems. Overall, the new information about the presence of several PCBs in the water of the Beiluo River justifies the need for urgent management actions, as well as long-term monitoring efforts, to protect ecosystems. Future investigations of these chemicals in China may use the conclusions of this first ecological risk level assessment on the PCB contamination in the waterbody of the Beiluo River as a guide.

Context Beta-cell dedifferentiation was recently proposed as a mechanism of β-cell dysfunction, but whether it can be a trigger of β-cell failure preceding hyperglycemia in humans is uncertain. Pancreatic cancer can cause new-onset diabetes, yet the underlying mechanism is unknown. Objective To investigate whether β-cell dedifferentiation is present in nondiabetic pancreatic ductal adenocarcinoma (PDAC) patients, we examined pancreatic islets from 15 nondiabetic patients with benign tumors (control) and 15 nondiabetic PDAC patients. Design We calculated the number of hormone-negative endocrine cells and evaluated important markers of β-cell dedifferentiation and function in the paraneoplastic islets. We assessed tumor-related inflammatory changes under the pancreatic cancer microenvironment and their influence on β-cell identity. Results We found nearly 10% of nonhormone expressing endocrine cells in nondiabetic PDAC subjects. The PDAC islets were dysfunctional, evidenced by low expression of Glucose transporter 2 (GLUT2) and Urocortin3 (UCN3), and concomitant upregulation of Aldehyde Dehydrogenase 1 Family Member A3 (ALDH1A3) expression and proinsulin accumulation. Pancreatic cancer caused paraneoplastic inflammation with enhanced tissue fibrosis, monocytes/macrophages infiltration, and elevated inflammatory cytokines. Moreover, we detected β-cell dedifferentiation and defects in GSIS in islets exposed to PANC-1 (a cell line established from a pancreatic carcinoma of ductal origin from a 56-year-old Caucasian male)-conditioned medium. In a larger cohort, we showed high prevalence of new-onset diabetes in PDAC subjects, and fasting blood glucose (FBG) was found to be an additional useful parameter for early diagnosis of PDAC. Conclusions Our data provide a rationale for β-cell dedifferentiation in the pathogenesis of pancreatic cancer–associated diabetes. We propose that β-cell dedifferentiation can be a trigger for β-cell failure in humans, before hyperglycemia occurs.

Statins are cholesterol-lowering agents that increase the incidence of diabetes and impair glucose tolerance via their detrimental effects on nonhepatic tissues, such as pancreatic islets, but the underlying mechanism has not been determined. In atorvastatin (ator)-treated high-fat diet–fed mice, we found reduced pancreatic β-cell size and β-cell mass, fewer mature insulin granules, and reduced insulin secretion and glucose tolerance. Transcriptome profiling of primary pancreatic islets showed that ator inhibited the expression of pancreatic transcription factor, mechanistic target of rapamycin (mTOR) signaling, and small G protein (sGP) genes. Supplementation of the mevalonate pathway intermediate geranylgeranyl pyrophosphate (GGPP), which is produced by 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase, significantly restored the attenuated mTOR activity, v-maf musculoaponeurotic fibrosarcoma oncogene homolog A (MafA) expression, and β-cell function after ator, lovastatin, rosuvastatin, and fluvastatin treatment; this effect was potentially mediated by sGP prenylation. Rab5a, the sGP in pancreatic islets most affected by ator treatment, was found to positively regulate mTOR signaling and β-cell function. Rab5a knockdown mimicked the effect of ator treatment on β-cells. Thus, ator impairs β-cell function by regulating sGPs, for example, Rab5a, which subsequently attenuates islet mTOR signaling and reduces functional β-cell mass. GGPP supplementation could constitute a new approach for preventing statin-induced hyperglycemia.

Preeclampsia (PE) is one of the major causes of maternal and perinatal mortality worldwide. This study aimed to determine the immunological characteristics of PE patients and normal pregnancy at the T cell receptor beta-chain (TRB) level by using high-throughput sequencing. High-throughput sequencing was performed to analyze the expression of TRB-CDR3 in circulating T cells. T cells were isolated from 36 healthy pregnant women, 24 patients with severe PE, and 18 patients with moderate PE. Rearranged mRNA sequences were assigned to their germline V, D, and J counterparts, and translated into proper amino acids by the IMGT database. In general, PE samples had more TRB-CDR3 reads and types than those of normal pregnant woman in the circulation, but the mean number of TRB-CDR3 reads and unique TRB-CDR3 reads in severe group was lower than that in the moderate group. In PE patients, the V7_9 and V20_1 gene loci were more prevalent than in healthy pregnant women. In addition, 4 kinds of TRB-CDR3 peptides were found to be highly relevant to the pathogenesis of PE. Of them, peptides matched to herpes simplex virus antigen-specific T cells were much lower in PE samples.

Immature pancreatic β-cells are highly proliferative, and the expansion of β-cells during the early neonatal period largely determines functional β-cell mass; however, the mechanisms are poorly characterized. We generated Ngn3RapKO mice (ablation of Raptor, an essential component of mechanistic target of rapamycin [mTORC1] in Ngn3+ endocrine progenitor cells) and found that mTORC1 was dispensable for endocrine cell lineage formation but specifically regulated both proliferation and identity maintenance of neonatal β-cells. Ablation of Raptor in neonatal β-cells led to autonomous loss of cell identity, decelerated cell cycle progression, compromised proliferation, and caused neonatal diabetes as a result of inadequate establishment of functional β-cell mass at postnatal day 14. Completely different from mature β-cells, Raptor regulated G1/S and G2/M phase cell cycle transition, thus permitting a high proliferation rate in neonatal β-cells. Moreover, Ezh2 was identified as a critical downstream target of mTORC1 in neonatal β-cells, which was responsible for G2/M phase transition and proliferation. Our discovery of the dual effect of mTORC1 in immature β-cells has revealed a potential target for replenishing functional β-cell pools by promoting both expansion and functional maturation of newly formed immature β-cells.

How to utilize oxygen redox chemistry in oxide electrodes is a promising challenge to realize high-capacity cathodes. Herein, we demonstrate an unexpected strategy, ‘decreasing transition metal (TM)’ to form TM deficiency, to activate non-bonding O 2p orbitals in charge compensation process for the A-deficient (A: alkali metal, e.g., Li, Na) oxide electrodes. Na0.653Mn0.929O2, as a model material, has been successfully prepared and shows an obvious voltage plateau at ~ 4.2 V, corresponding to the oxygen redox (O2-/(O2)n-) with a total capacity of ~ 210 mAh g−1. This proposed strategy reveals that the special structural and chemical features can effectively increase O 2p orbitals near the Fermi level, triggering oxygen oxidation prior to transition metal oxidation towards a high-valence state. Our results provide an insightful guide for the further development of high-capacity materials, particularly for Na-deficient NaxTMO2 (x≤1) electrodes in Na-ion batteries (NIBs).

For the development of national industry green environmental protection, the use of zinc dialkyl dithiophosphate (ZDDP) should be reduced in the process of mechanical lubrication, two novel borate ...

m6A RNA modification is essential during embryonic development of various organs; however, its role in embryonic and early postnatal islet development remains unknown. Mice in which RNA methyltransferase-like 3/14 (Mettl3/14) were deleted in Ngn3+ endocrine progenitors (Mettl3/14nKO) developed hyperglycemia and hypo-insulinemia at 2 weeks after birth. We found that Mettl3/14 specifically regulated both functional maturation and mass expansion of neonatal β cells before weaning. Transcriptome and m6A methylome analyses provided m6A-dependent mechanisms in regulating cell identity, insulin secretion and proliferation in neonatal β cells. Importantly, we found that Mettl3/14 were dispensable for β cell differentiation, but directly regulated essential transcriptional factor MafA expression at least partially via modulating its mRNA stability and failure to maintain this modification impacted the ability to fulfill β cell functional maturity. In both diabetic db/db mice and type 2 diabetes patients, decreased Mettl3/14 expression in β cells were observed, suggesting its possible role in type 2 diabetes. Our stud­­­­­­­­­y unraveled the essential role of Mettl3/14 in neonatal β cell development and functional maturation, both of which determined functional β cell mass and glycemic control in adulthood.

A sodium (Na) metal anode plays a pivotal role in realizing long-term cycling stability in promising Na-based batteries. However, the uncontrollable plating-stripping process and unstable solid electrolyte interphase (SEI) layer can induce electrode degradation, which hinders its potential applications. In this work, the synergy effects of a composite Na metal anode and fluorine-rich electrolyte were introduced to investigate the Na+ plating-stripping process and its potential use in Na-metal batteries (SMBs). The composite anode was fabricated via alloying and capillary action between the sodiophilic carbon matrix and molten Na metal, thus forming an integrated structure, which effectively improved the interconnection between Na and carbon scaffold to obtain uniform deposition. Combined with the fluorine-rich electrolyte, stable SEI layers consisting of ion-permeable NaF and mechanically durable organic components were obtained. When coupled with an Na3V2(PO4)3 cathode with a high mass loading of ∼9 mg cm−2, an ultra-stable cycling behaviour (capacity retention of >90% over 1000 cycles) and outstanding rate performance (capacity retention of >80% at 15C) were observed due to the improved Na deposition process and interface stability. This work demonstrates that the synergy effects of the composite metal anode and electrolyte modification can be an effective strategy to fabricate highly stable SMBs.

Layered Na-based oxides with the general composition of NaxTMO2 (TM: transition metal) have attracted significant attention for their high compositional diversity that provides tunable electrochemical performance for electrodes in sodium-ion batteries. The various compositions bring forward complex structural chemistry that is decisive for the layered stacking structure, Na-ion conductivity, and the redox activity, potentially promising new avenues in functional material properties. In this work, we have explored the maximum Na content in P2-type layered oxides and discovered that the high-content Na in the host enhances the structural stability; moreover, it promotes the oxidation of low-valent cations to their high oxidation states (in this case Ni2+). This can be rationalized by the increased hybridization of the O(2p)-TM(3d-eg*) states, affecting both the local TM environment as well as the interactions between the NaO2 and TMO2 layers. These properties are highly beneficial for the Na storage capabilities as required for cathode materials in sodium-ion batteries. It leads to excellent Na-ion mobility, a large storage capacity (>100 mAh g-1 between 2.0-4.0 V), yet preventing the detrimental sliding of the TMO2 layers (P2-O2 structural transition), as reflected by the ultralong cycle life (3000 (dis)charge cycles demonstrated). These findings expand the horizons of high Na-content P2-type materials, providing new insights of the electronic and structural chemistry for advanced cathode materials.

Sodium-ion batteries (NIBs) show great prospect on the energy storage applications benefiting from their low cost and the abundant Na resources despite the expected lower energy density compared with lithium-ion batteries (LIBs). To further enhance the competitive advantage, especially in energy density, developing the high-capacity carbon anode materials can be one of the effective approaches to realize this goal. Herein, we report a novel carbon anode made from charcoal with a high capacity of ∼400 mAh g−1, wherein about 85% (>330 mAh g−1) of its total capacity is derived from the long plateau region below ∼0.1 V, which differs from those of typical hard carbon materials (∼300 mAh g−1) in NIBs but is similar to the graphite anode in LIBs. When coupled with air-stable Na0.9Cu0.22Fe0.30Mn0.48O2 oxide cathode, a high-energy density of ∼240 Wh kg−1 is achieved with good rate capability and cycling stability. The discovery of this promising carbon anode is expected to further improve the energy density of NIBs towards large-scale electrical energy storage.

Here we report a high-capacity cathode, Na2Mn3+0.3Mn4+2.7O6.85, based on simultaneous cationic (Mn4+/Mn3+) and anionic (O2-/(O2)n-) redox process in Na-Mn-O system for Na-ion batteries (NIBs). An obvious voltage plateau at ~ 4.2 V vs. Na+/Na is reversibly presented during Na+ deinsertion/insertion demonstrated by XPS analysis of the participation of oxygen redox. This cathode delivers ~ 213 mA h g-1 in the voltage range of 1.5–4.5 V composed of two voltage plateaus from both cationic and anionic redox reaction. The two voltage plateaus exhibit the reversible phase transition upon Na+ insertion/deinsertion corresponding to a solid-solution region (high plateau) and a two-phase region (low plateau), respectively. The results indicate that anionic redox activity is available to develop high-capacity cathodes for NIBs.

Rapamycin insensitive companion of mechanistic target of Rapamycin (Rictor), the key component of mTOR complex 2 (mTORC2), controls both β-cell proliferation and function. We sought to study whether long chain acyl-CoA synthetase 4 (Acsl4) worked downstream of Rictor/mTORC2 to maintain β-cell functional mass. We found Acsl4 was positively regulated by Rictor at transcriptional and posttranslational levels in mouse β-cell. Infecting adenovirus expressing Acsl4 in β-cell-specific-Rictor-knockout (βRicKO) islets and Min6 cells knocking down Rictor with lentivirus-expressing siRNA-oligos targeting Rictor(siRic), recovered the β-cell dysplasia but not dysfunction. Cell bioenergetic experiment performed with Seahorse XF showed that Acsl4 could not rescue the dampened glucose oxidation in Rictor-lacking β-cell, but further promoted lipid oxidation. Transposase-Accessible Chromatin (ATAC) and H3K27Ac chromatin immunoprecipitation (ChIP) sequencing studies reflected the epigenetic elevated molecular signature for β-cell dedifferentiation and mitigated oxidative defense/response. These results were confirmed by the observations of elevated acetylation and ubiquitination of FoxO1, increased protein levels of Gpx1 and Hif1an, excessive reactive oxygen species (ROS) production and diminished MafA in Acsl4 overexpressed Rictor-lacking β-cells. In these cells, antioxidant treatment significantly recovered MafA level and insulin content. Inducing lipid oxidation alone could not mimic the effect of Acsl4 in Rictor lacking β-cell. Our study suggested that Acsl4 function in β-cell was context dependent and might facilitate β-cell dedifferentiation with attenuated Rictor/mTORC2 activity or insulin signaling via posttranslational inhibiting FoxO1 and epigenetically enhancing ROS induced MafA degradation.

Genetic variation in specific transcription factors during heart formation may lead to congenital heart disease (CHD) or even miscarriage. The aim of the present study was to identify CHD‑associated genes using next generation sequencing (NGS). The whole exome DNA sequence was obtained from a stillborn fetus diagnosed with tricuspid atresia and complete transposition of the great arteries using high‑throughput sequencing methods. Subsequently, genetic variants of CHD‑associated genes were selected and verified in 215 non‑syndromic CHD patients and 249 healthy control subjects using polymerase chain reaction combined with Sanger sequencing. Genetic variants of previously reported CHD‑inducing genes, such as cysteine rich with EGF like domains 1 and cbp/p300‑interacting transactivator with Glu/Asp rich carboxy‑terminal domain 2, were discovered through the NGS analysis. In addition, a novel non‑synonymous mutation of the iroquois homeobox 1 (IRX1) gene (p.Gln240Glu) was identified. A total of three non‑synonymous mutations (p.Gln240Glu, p.Ser298Asn and p.Ala381Glu) of the IRX1 gene were verified in 215 non‑syndromic CHD patients, but not in 249 healthy volunteers. The results demonstrated that NGS is a powerful tool to study the etiology of CHD. In addition, the results suggest that genetic variants of the IRX1 gene may contribute to the pathogenesis of CHD.

Metallic lithium is a promising anode to increase the energy density of rechargeable lithium batteries. Despite extensive efforts, detrimental reactivity of lithium metal with electrolytes and uncontrolled dendrite growth remain challenging interconnected issues hindering highly reversible Li-metal batteries. Herein, we report a rationally designed amide-based electrolyte based on the desired interface products. This amide electrolyte achieves a high average Coulombic efficiency during cycling, resulting in an outstanding capacity retention with a 3.5 mAh cm−2 high-mass-loaded LiNi0.8Co0.1Mn0.1O2 cathode. The interface reactions with the amide electrolyte lead to the predicted solid electrolyte interface species, having favorable properties such as high ionic conductivity and high stability. Operando monitoring the lithium spatial distribution reveals that the highly reversible behavior is related to denser deposition as well as top-down stripping, which decreases the formation of porous deposits and inactive lithium, providing new insights for the development of interface chemistries for metal batteries., Interface chemistry is essential for highly reversible lithium-metal batteries. Here the authors investigate amide-based electrolyte that lead to desirable interface species, resulting in dense Li-metal plating and top-down Li-metal stripping, responsible for the highly reversible cycling.

The