Dynamic Hydrogen-Bond Network as a Modulator of Bismuth-Antimony Complex Anodes for Self-Healable and Wider Temperature Adaptive Potassium Ion Batteries.

Antimony (Sb)-based anodes are attractive candidates in potassium-ion batteries (PIBs) due to their superior capacities and rational potassium inserting voltages. However, the sluggish kinetics and poor interface compatibility severely hinder practical application. Herein, Bi0.67 Sb1.33 S3 nanospheres embedded into in situ formed poly(3,4-ethylenedioxythiophene) crosslinked with polythioctic acid (PET@PTA) (Bi0.67 Sb1.33 S3 /PET@PTA) were elaborately conceptualized with hydrogen bonds exchangeable binding (HBEB) sites. Bi0.67 Sb1.33 S3 /PET@PTA exhibits notable self-healing ability and wider temperature adaptability. Bi0.67 Sb1.33 S3 /PET@PTA displays an impressive capacity of 819 mAh g-1 at 0.05 A g-1 , prominent cycle ability with a 73 % capacity conservation after 500 cycles at 2 A g-1 , and high capacity retention of 66 % and 84 % at -40 and 70 °C to that case at room temperature, respectively, for potassium storage. This work provides a new perspective for HBEB sites in maximizing the desirable K+ storage performance.

Circadian clock gene BMAL1 controls testosterone production by regulating steroidogenesis-related gene transcription in goat Leydig cells.

Testosterone is produced by Leydig cells (LCs) and undergoes diurnal changes in serum levels in rats, mice, and humans, but little is known in goats. The present study revealed that goat serum testosterone levels displayed diurnal rhythmic changes (peak time at ZT11.2). Immunohistochemical staining showed that BMAL1, a circadian clock protein, is highly expressed in goat LCs. ELISA revealed that both hCG (0-5 IU/ml) and 22R-OH-cholesterol (0-30 µM) addition stimulated testosterone synthesis in primary goat LCs in a dose-dependent manner. Treating goat LCs with hCG (5 IU/ml) significantly increased intracellular cAMP levels. Additionally, real-time quantitative polymerase chain reaction (PCR) analysis revealed that the circadian clock (BMAL1, PER1, PER2, DBP, and NR1D1) and steroidogenesis-related genes (SF1, NUR77, StAR, HSD3B2, CYP17A1, CYP11A1, and HSD17B3) showed rhythmic expression patterns in goat LCs following dexamethasone synchronization. Several Bmal1-Luc circadian oscillations were clearly observed in dexamethasone-treated goat LCs transfected with the pLV6-Bmal1-Luc plasmid. BMAL1 knockdown significantly downregulated mRNA levels of PER2, NR1D1, DBP, StAR, HSD3B2, SF1, NUR77, and GATA4, and dramatically decreased StAR and HSD3B2 protein levels and testosterone production. In contrast, BMAL1 overexpression significantly increased the mRNA and protein expression levels of StAR and HSD17B3 and enhanced testosterone production. Reporter assays revealed that goat BMAL1, or in combination with mouse CLOCK, activated goat HSD17B3 transcription in vitro. These data indicate that BMAL1 contributes to testosterone production by regulating transcription of steroidogenesis-related genes in goat LCs, providing a basis for further exploring the underlying mechanism by which the circadian clock regulates ruminant reproductive capability.

Bmal1 promotes prostaglandin E2 synthesis by upregulating Ptgs2 transcription in response to increasing estradiol levels in day 4 pregnant mice.

Prostaglandin G/H synthase 2 (PTGS2) is a rate-limiting enzyme in prostaglandin synthesis. The present study assessed the role of the uterine circadian clock on Ptgs2 transcription in response to steroid hormones during early pregnancy. We demonstrated that the core clock genes (Bmal1, Per2, Nr1d1, and Dbp), Vegf, and Ptgs2, and their encoded proteins, have rhythmic expression in the mouse uterus from days 3.5 to 4.5 (D3.5-4.5) of pregnancy. Progesterone (P4) treatment of cultured uterus endometrial stromal cells (UESCs) isolated from mPer2Luciferase reporter gene knock-in mice on D4 induced a phase shift in PER2::LUCIFERASE oscillations. This P4-induced phase shift of PER2::LUCIFERASE oscillations was significantly attenuated by the P4 antagonist RU486. Additionally, the amplitude of PER2::LUCIFERASE oscillations was increased by estradiol (E2) treatment in the presence of P4. Consistently, the mRNA levels of clock genes (Bmal1 and Per2), Vegf, and Ptgs2 were markedly increased by E2 treatment of UESCs in the presence of P4. Treatment with E2 also promoted prostaglandin E2 (PGE2) synthesis by UESCs. Depletion of Bmal1 in UESCs by small-interfering RNA (siRNA) decreased the transcript levels of clock genes (Nr1d1 and Dbp), Vegf, and Ptgs2 compared with nonsilencing siRNA treatment. Bmal1 knockdown also inhibited PGE2 synthesis. Moreover, the mRNA expression levels of clock genes (Nr1d1 and Dbp), Vegf, and Ptgs2, and their respective proteins were significantly decreased in the uterus of Bmal1-/- mice. Thus, these data suggest that Bmal1 in mice promotes PGE2 synthesis by upregulating Ptgs2 in response to increases in E2 on D4 of pregnancy.NEW & NOTEWORTHY Rhythmic expression of Bmal1 and Ptgs2 was observed in the uterus isolated from D3.5-4.5 of pregnant mice. E2 increased the expression of Bmal1 and Ptg2 in UESCs isolated from mice on D4. The expression of Ptgs2 was significantly decreased in Bmal1-siRNA treated UESCs. Bmal1 knockdown also inhibited PGE2 synthesis. Thus, these data suggest that Bmal1 in mice promotes PGE2 synthesis by upregulating Ptgs2 in response to increases in E2 on D4 of pregnancy.

Zearalenone perturbs the circadian clock and inhibits testosterone synthesis in mouse Leydig cells.

Zearalenone (ZEA), a mycotoxin, is known to impair reproductive capability by disrupting the synthesis and secretion of testosterone by Leydig cells (LCs), although the mechanism is unknown. Robust rhythmicity of circadian clock and steroidogenic genes were identified in LCs. The aim of this study was to examine whether ZEA significantly attenuated the transcription of core clock genes (Bmal1, Dbp, Per2, and Nr1d1) as well as steroidogenic genes (StAR, Hsd3b2, and Cyp11a1) in mouse testis Leydig cell line (TM3). Western blotting confirmed declines in BMAL1, NR1D1, and StAR protein levels. ZEA also suppressed secreted testosterone levels. In primary LCs, isolated from PER2::LUCIFERASE reporter gene knock in mice, ZEA diminished the amplitude of PER2::LUC expression, and induced a phase shift and period extension. In primary LCs, ZEA also suppressed the expression levels of core clock and steroidogenic genes, reduced protein levels of BMAL1, and decreased testosterone secretion. In vivo expression of core clock and steroidogenic genes were reduced in testes of mice exposed to ZEA for 1 week leading to decreased serum testosterone levels. In summary, data suggest that ZEA may impair testosterone synthesis through attenuation of the circadian clock in LCs culminating in reproductive dysfunction in male mammals .

Coordination between the circadian clock and androgen signaling is required to sustain rhythmic expression of Elovl3 in mouse liver.

ELOVL3 is a very long-chain fatty acid elongase, and its mRNA levels display diurnal rhythmic changes exclusively in adult male mouse livers. This cyclical expression of hepatic Elovl3 is potentially controlled by the circadian clock, related hormones, and transcriptional factors. It remains unknown, however, whether the circadian clock, in conjunction with androgen signaling, functions in maintaining the rhythmic expression of Elovl3 in a sexually dimorphic manner. Under either zeitgeber or circadian time, WT mouse livers exhibited a robust circadian rhythmicity in the expression of circadian clock genes and Elovl3 In contrast, male Bmal1-/- mice displayed severely weakened expression of hepatic circadian clock genes, resulting in relatively high, but nonrhythmic, Elovl3 expression levels. ChIP assays revealed that NR1D1 binds to the Elovl3 promoter upon circadian change in WT mouse livers in vivo, and a diminished binding was observed in male Bmal1-/- mouse livers. Additionally, female mouse livers exhibited constant low levels of Elovl3 expression. Castration markedly reduced Elovl3 expression levels in male mouse livers but did not disrupt circadian variation of Elovl3 Injection of female mice with 5α-dihydrotestosterone induced Elovl3 rhythmicity in the liver. In AML12 cells, 5α-dihydrotestosterone also elevated Elovl3 expression in a time-dependent manner. In contrast, flutamide efficiently attenuated this induction effect. In conclusion, a lack of either the circadian clock or androgen signaling impairs hepatic Elovl3 expression, highlighting the observation that coordination between the circadian clock and androgen signaling is required to sustain the rhythmic expression of Elovl3 in mouse liver.

Components analysis of San-Bai decoction, and its pharmacodynamics and mechanism on preventing and treating melasma.

ETHNOPHARMACOLOGICAL RELEVANCE: San-Bai Decoction (SBD) is a classic whitening prescription originally recorded in the 'Introduction to Medicine' of the Ming Dynasty. SBD has been known for invigorating Qi and blood, promoting spleen and stomach, whitening skin, and fading melasma. However, its pharmacodynamic material basis and specific mechanism remain unclear. AIM OF THE STUDY: The aim of this study is to clarify the pharmacodynamic material basis of SBD and its mechanism of removing melasma. MATERIALS AND METHODS: The positive and negative ion mass spectrum data of SBD extract were collected by UHPLC-Q-Exactive Orbitrap MS/MS, imported into Compound Discoverer (CD) 3.1 software, matched through the online database, and manually checked. Finally, the in vitro chemical components of SBD were classified. Similarly, the mass spectrum data of SBD in the serum of normal rats and melasma model rats were also analyzed by CD 3.1 software. The in vitro identified Compound file of SBD was imported into the Expected Compounds and the Generate Expected Compounds project was selected. The SBD compounds were then chosen under the Compound Section. All phase I and II reaction types related to SBD components were selected, and the metabolic platform of CD 3.1 software was utilized to process the results and obtain possible metabolites. The metabolites were scored and products with high scores were subsequently screened. According to literature comparison, the final metabolites of SBD in both normal rats and melasma model rats were determined and comprehensively analyzed. The Melasma model rats were constructed through intramuscular injection of progesterone and ultraviolet radiation B (UVB) irradiation. The preventing and treating effect of SBD on melasma were evaluated by regulating inflammation, epidermal collagen content, and oxidative stress. Additionally, the effect of SBD on the Phosphatidylinositol 3-kinase (PI3K)/Protein kinase B (Akt)/Glycogen synthase kinase 3ß (GSK3ß) pathway was investigated through Western blot (WB) to explore its underlying mechanism on whitening and removing melasma efficacy. RESULTS: Ultimately, 94 components were identified in SBD, including 41 flavonoids, 27 organic acids, and 9 glycosides, 3 terpenoids, 2 amides, 2 aldehydes, 1 phenylpropanoid and 9 other compounds. In the blood of normal rat group, a total of 24 prototype components and 61 metabolites were identified. Similarly, there were19 prototype components and 44 metabolites identified from the blood of melasma model rats. Pharmacodynamic experiment results indicated that SBD effectively reduced the incidence of melasma, prevent the loss of epidermal collagen, and elevate the activity of superoxide dismutase and decrease the malondialdehyde content in both liver and skin. Interestingly, the WB results demonstrated that SBD effectively activated PI3K/Akt/GSK3ß pathway, and down-regulated the expression of melanin-related proteins. CONCLUSIONS: For the first time, the components of SBD extracts, and its prototype components and metabolites in the blood of normal rats and melasma model rats were successfully identified by high-resolution liquid chromatography-mass spectrometry with CD software. Additionally, the differences of in vivo components of SBD between normal rats and melasma model rats were analyzed. The preventive and therapeutic effect of SBD on melasma was verified in the melasma model rats induced by progesterone and UVB irradiation, and its mechanism was related to activating PI3K/Akt/GSK3ß pathway and downregulating the expression of melanin-related proteins. These results provide an experimental foundation for further research on the pharmacodynamic substance basis and pharmacodynamic mechanism of SBD, as well as developing new anti-melasma formula with SBD.

Preparation of paeoniflorin-glycyrrhizic acid complex transethosome gel and its preventive and therapeutic effects on melasma.

Paeoniflorin (PF) and glycyrrhizic acid (GL) have skin beautifying effects of anti-inflammation, anti-oxidation, inhibition of melanin formation, and reduction of skin pigmentation. To improve the transdermal permeability of PF and GL in transdermal drug delivery system (TDDS) and enhance their anti-melasma efficacy, PF-GL transethosome (PF-GL-TE) was prepared by ethanol injection method, and finally gelled with carbomer-940 to form PF-GL-TE gel. Consequently, the obtained PF-GL-TE is small and uniform, with an average particle size and a PDI value of about 167.9 nm and 0.102. PF-GL-TE gel showed sustained release behavior and high transdermal permeability in vitro release and transdermal tests. Meanwhile, PF-GL-TE gel played significant preventive effects on melasma induced by progesterone injection and ultraviolet radiation B (UVB) irradiation. According to the results of H&E staining and Masson staining of rat skin, PF-GL-TE gel can alleviate the skin inflammation of and reduce the loss of collagen fibers of back skin in the melasma model rats. Compared with the PF-GL mixture gel, PF-GL-TE gel significantly attenuated the oxidative damage of liver and skin by increasing the activity of SOD and reducing the content of MDA. The results of Western blot showed that PF-GL-TE gel might down-regulate melanin-related proteins expressions of MITF/TYR/TRP1 and TRP2 to prevent and treat melasma. These findings indicate that PF-GL-TE gel is an effective TDDS for delivering PF and GL into the skin, providing a promising preparation for effective prevention and treatment of melasma.

Electroacupuncture improves apoptosis of nucleus pulposus cells via the IL-22/JAK2-STAT3 signaling pathway in a rat model of cervical intervertebral disk degeneration.

BACKGROUND: Cervical spondylosis (CS) is a prevalent disorder that can have a major negative impact on quality of life. Traditional conservative treatment has limited efficacy, and electroacupuncture (EA) is a novel treatment option. We investigated the application and molecular mechanism of EA treatment in a rat model of cervical intervertebral disk degeneration (CIDD). METHODS: The CIDD rat model was established, following which rats in the electroacupuncture (EA) group received EA. For overexpression of IL-22 or inhibition of JAK2-STAT3 signaling, the rats were injected intraperitoneally with recombinant IL-22 protein (p-IL-22) or the JAK2-STAT3 (Janus kinase 2-signal transducer and activator of transcription protein 3) inhibitor AG490 after model establishment. Rat nucleus pulposus (NP) cells were isolated and cultured. Cell counting kit-8 and flow cytometry were used to analyze the viability and apoptosis of the NP cells. Expression of IL-22, JAK2 and STAT3 was determined using RT-qPCR. Expression of IL-22/JAK2-STAT3 pathway and apoptosis related proteins was detected by Western blotting (WB). RESULTS: EA protected the NP tissues of CIDD rats by regulating the IL-22/JAK2-STAT3 pathway. Overexpression of IL-22 significantly promoted the expression of tumor necrosis factor (TNF)-α, IL-6, IL-1ß, matrix metalloproteinase (MMP)3 and MMP13 compared with the EA group. WB demonstrated that the expression of IL-22, p-JAK2, p-STAT3, caspase-3 and Bax in NP cells of the EA group was significantly reduced and Bcl-2 elevated compared with the model group. EA regulated cytokines and MMP through activation of IL-22/JAK2-STAT3 signaling in CIDD rat NP cells. CONCLUSION: We demonstrated that EA affected apoptosis by regulating the IL-22/JAK2-STAT3 pathway in NP cells and reducing inflammatory factors in the CIDD rat model. The results extend our knowledge of the mechanisms of action underlying the effects of EA as a potential treatment approach for CS in clinical practice.

Construction of Ultrastable Ultrathin Black Phosphorus Nanodisks Hybridized with Fe3 O4 Nanoclusters and Iron (V)-Oxo Complex for Efficient Potassium Storage.

The practical application of metalloid black phosphorus (BP) based anodes for potassium ion batteries is mainly impeded by its instability in air and irreversible/sluggish potassium storage behaviors. Herein, a 2D composite is purposefully conceptualized, where ultrathin BP nanodisks with Fe3 O4 nanoclusters are hybridized with Lewis acid iron (V)-oxo complex (FC) nanosheets (denoted as BP@Fe3 O4 -NCs@FC). The introduced electron coordinate bridge between FC and BP, and hydrophobic surface of FC synergistically assure that BP@Fe3 O4 -NCs@FC is ultrastable in humid air. With the purposeful structural and componential design, the resultant BP@Fe3 O4 -NCs@FC anode is endowed with appealing electrochemical performance in terms of reversible capacity, rate behavior, and long-duration cycling stability in both half and full cells. Furthermore, the underlying formation and potassium-storage mechanisms of BP@Fe3 O4 -NCs@FC are tentatively proposed. The in-depth insights here will provide a crucial understanding in rational exploration of advanced anodes for next-generation PIBs.

Phytochemical profile and protective effects on myocardial ischaemia-reperfusion injury of sweated and non-sweated Salvia miltiorrhiza. Bge alcoholic extracts.

OBJECTIVES: This study aims to compare the fingerprint and the content of the three components of sweated and non-sweated Salvia miltiorrhiza alcoholic extracts (SSAE and NSAE). It also aims to investigate the difference in protective effects of SSAE and NSAE on myocardial ischaemia-reperfusion injury (MIRI). METHODS: The fingerprints of SSAE and NSAE were established by HPLC with a UV detector to identify the common peaks and detect the content of the three major components (cryptotanshinone, tanshinone I and tanshinone IIA). The protective effects of SSAE and NSAE were compared with MIRI rat model after orally administered SSAE and NSAE (2 g/kg of raw drug) for 7 days. The ST segment, PR and QT interval changes and the infarct size were assessed in the rat hearts. Moreover, the activity of aspartate transaminase (AST), lactate dehydrogenase (LDH), superoxide dismutase (SOD) and the level of cardiac troponin I (cTn I) in serum as well as the cardiac H&E staining were evaluated. KEY FINDINGS: The results showed that the fingerprints of SSAE and NSAE were similar, and cluster analysis showed that the sweating methods had effects on the alcoholic extracts. The content determination showed that sweating could increase the total content of cryptotanshinone, tanshinone I and tanshinone IIA of S. miltiorrhiza. The results of electrocardiograms (ECG) showed that SSAE could make the ST segment drop more obviously, PR and QT intervals become shorter, and the size of the infarct much smaller. Compared with NSAE, SSAE had more significant effects on the enzymatic activity of AST, LDH and the level of cTn I in serum. The H&E staining showed that both SSAE and NSAE could reduce the degree of heart damage. CONCLUSIONS: The present investigation results demonstrated that sweating increased the content of tanshinone components in S. miltiorrhiza alcoholic extracts, and SSAE had a better protective effect on MIRI.

Spectrum-effect relationship between HPLC fingerprint and antioxidant of "San-Bai Decoction" extracts.

"San-Bai Decoction" (SBD) has been a traditional Chinese medicine compound preparation for replenishing Qi and promoting blood circulation, whitening skin, and removing blemishes since ancient times. However, its chemical composition and antioxidant activity are not clear thus far, which limits the in-depth study on its pharmacodynamic material basis and efficacy. The objective of this study was to establish the fingerprint profile of SBD, assess its antioxidant activity by measuring 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging ability, and find the spectrum-effect relationship of SBD by Grey Relation Analysis (GRA) and Partial Least Squares Regression (PLS). In this study, the fingerprint of SBD was established by high performance liquid chromatography (HPLC), and 20 common peaks were found, among which 6 peaks were designated. The similarities between the fingerprints of 12 batches of SBD and the reference fingerprint (R) were all greater than 0.900. Meanwhile, the antioxidant activities of all batches were concentration-dependent in their linear regression equation. The result of GRA showed that the correlation order of 20 common peaks for DPPH radical scavenging was X13 > X7 > X3 > X6 > X10 > X11 > X4 > X12 > X2 > X18 > X9 > X5 > X19 > X1 > X20 > X16 > X17 > X15 > X8 > X14. At the same time, PLS study demonstrated that the contribution of six identified characteristic peaks to DPPH radical scavenging ability was X1 = X7 > X6 > X19 > X20 > X16. In this study, the spectrum-effect relationship of SBD between its HPLC fingerprint and the antioxidant activity can be used to screen the pharmacodynamic substance basis of its antioxidant action and lay the foundation for establishing quality standards and product development.

Age-related endoplasmic reticulum stress represses testosterone synthesis via attenuation of the circadian clock in Leydig cells.

Senile animals exhibit a high risk of elevated endoplasmic reticulum (ER) stress, attenuated circadian clock, and impaired steroidogenesis in testes. However, how these three processes are intertwined in mouse Leydig cells remains unclear. In this study, a mouse model of aging and hydrogen peroxide (H2O2)-induced senescent TM3 Leydig cells were used to dissect the connections among ER stress, circadian oscillators, and steroidogenesis in Leydig cells. Additionally, thapsigargin (Tg, 60 nM)/tunicamycin (Tm, 60 ng/mL)-induced ER stress were established to investigate the underlying mechanisms by which ER stress regulated testosterone synthesis via circadian clock-related signaling pathways in TM3 cells and primary Leydig cells. Elevated ER stress, attenuated circadian clock, and diminished steroidogenesis were detected in the testes of aged mice (24-month-old) and H2O2-induced (200 µM) senescent TM3 cells in comparison with their control groups. Tg/Tm-induced ER stress reduced the transcription of the circadian clock and steroidogenic genes in TM3 cells and LH-treated (100 ng/mL) primary Leydig cells. Furthermore, 4-phenylbutyric acid (4-PBA, 1 µM), an inhibitor of ER stress, alleviated the inhibitory effect of Tg-mediated ER stress on Per2:Luc oscillations in primary Leydig cells isolated from mPer2Luc knock-in mice, and attenuated the repressive effect of H2O2-induced or Tg-mediated ER stress on the transcription of circadian clock and steroidogenic genes expression and testosterone synthesis in TM3 cells. Collectively, these data indicate that age-related ER stress represses testosterone synthesis via attenuation of the circadian clock in Leydig cells.

Bisphenol A attenuates testosterone production in Leydig cells via the inhibition of NR1D1 signaling.

Bisphenol A (BPA) is an endocrine-disrupting compound that impairs testosterone synthesis in male mammals. A circadian clock gene deficiency leads to diminished fertility and even infertility in male mice. However, whether circadian clock signaling pathways mediate the suppressive effect of BPA on testosterone synthesis in Leydig cells (LCs) remains unknown. The present study aims to detect the effect of BPA on cellular circadian clock and testosterone synthesis in mouse LCs, and examine the mechanisms underlying NR1D1 signaling. BPA treatment significantly attenuated the transcription levels of Nr1d1 and steroidogenic genes (Hsd3b2 and Hsd17b3) in TM3 cells, but increased other circadian clock gene levels (Per2 and Dbp). BPA treatment also significantly downregulated NR1D1 and StAR protein expression, but upregulated BMAL1 protein expression in TM3 cells. Furthermore, there was a marked decline in testosterone production in BPA-treated TM3 cells. Intraperitoneal injection of BPA profoundly reduced NR1D1 and StAR protein levels and steroidogenic gene transcription levels (Cyp11a1, Hsd3b2, and Hsd17b3), while enhancing BMAL1 protein and other circadian clock gene (Per2 and Dbp) levels in mouse testes. Notably, serum testosterone levels were also drastically reduced in BPA-treated mice. Moreover, SR9009, an NR1D1 agonist, augmented testosterone production in TM3 cells via elevated expression of steroidogenic genes (StAR, Cyp11a1 and Hsd17b3). Conversely, Nr1d1 knockdown inhibited testosterone accumulation and attenuated steroidogenic gene expression. Moreover, treatment with SR9009 partially reversed the BPA effect on the circadian clock and testosterone production. Taken together, our study demonstrates that BPA perturbs testosterone production, at least partially, via inhibiting NR1D1 signaling in LCs.

Unveiling a bimetallic FeCo-coupled MoS2 composite for enhanced energy storage.

Sodium and potassium-ion batteries are promising for energy storage owing to their source abundance and low cost; however, most active materials still suffer from sluggish kinetics, huge volume variations, and poor conductivity and cycle stability. It remains a great challenge to explore appropriate electrode materials for scaled practical applications. Herein, mesoporous FeCo-incorporated MoS2 nanosheets encapsulated into a porous carbon framework (FeCo@C@MoS2) are smartly designed, artistically fabricated and evaluated for sodium and potassium storage. The FeCo@C@MoS2 electrode displays high reversible capacities of 380 mA h g-1 and 147 mA h g-1 at 500 mA g-1 for sodium and potassium storage, respectively. FeCo derived from a Prussian blue analogue promotes fast reaction kinetics of Na+/K+ transport, introduces the formation of a stable solid electrolyte interphase layer (SEI) in both the interior and exterior of the cube-like porous nanostructure and controls the Na+/K+ fluxes, suppressing the growth of metal dendrites. The porous carbon framework with large interstitial voids can effectively buffer volume variations and mitigate mechanical stress, contributing significantly to alleviate strain intensification on the surface layer between MoS2 and FeCo during repeated plating/stripping processes. Density functional theoretical calculations (DFT) further confirm that the synthesized nanostructure shows an intensified electron state, elevated anti-stress ability, high-quality SEI film and preferable Na+/K+ adsorption energies. This in-depth investigation of the electrochemical performance and the extended energy storage mechanism based on metal alloy/sulfide nanostructures for sodium and potassium storage provides guidance for the smart design of heterojunctions for remarkable energy storage.

Fabricating ferromagnetic MoS2-based composite exposed to simulated sunlight for sodium storage.

A light- and magnetic stimuli-responsive MoS2 composite electrode material is designed and evaluated as an anode material of sodium ion batteries. Through the assistance of simulated sunlight, suppressed dendritic sodium growth, buffered volume deformation, promoted electrochemical reaction kinetics, and improved structural stability are simultaneously achieved. Meanwhile, ferroelectric polarization enhances the separation efficiency of photogenerated carriers. The collisions among electrons are dramatically decreased; in turn, the thermal stability of the battery is improved via the tailored orientation of active materials. A stable protective solid-state electrolyte interface film is formed via the photogenerated electrons and the magnetohydrodynamics effect, depressing the growth of sodium dendrites. The porous three-dimensional heterostructure is conducive for promoting transmission of charges and the diffusion of ions, effectively reducing the local current density of metals, further inhibiting the growth of sodium dendrites during deposition and peeling processes. Density functional theoretical calculations also verify that the fabricated MoS2 composite possesses intensified electron density, and exhibits fast reaction kinetics in repeated cycles and lowered sodium adsorption energy. The optical field and the rational magnetic fabrication technology can fundamentally solve the bottleneck problems restricting the development of batteries, mitigating the energy crisis.

ER stress activation impairs the expression of circadian clock and clock-controlled genes in NIH3T3 cells via an ATF4-dependent mechanism.

Endoplasmic reticulum (ER) stress and circadian clockwork signaling pathways mutually regulate various cellular functions, but the details regarding the cross-talk between these pathways in mammalian cells are unclear. In this study, whether perturbation of ER stress signaling affects the cellular circadian clockwork and transcription of clock-controlled genes was investigated in NIH3T3 mouse fibroblasts. An NIH3T3 cell model stably expressing luciferase (Luc) under the control of the Bmal1 clock gene promoter was established using a lentiviral system. Then, Luc activity was monitored in real-time to detect Bmal1-Luc oscillations. The ER stress activators thapsigargin (Tg) and tunicamycin (Tm) markedly reduced Bmal1-Luc oscillation amplitudes and induced phase delay shifts in NIH3T3 cells. Treatment with Tg/Tm activated ER stress signaling by upregulating GRP78, CHOP, ATF6, and ATF4 and simultaneously significantly decreased BMAL1 protein levels and inhibited the transcription of circadian clock (Bmal1, Per2, Nr1d1, and Dbp) and clock-controlled (Scad1, Fgf7, and Arnt) genes. 4-Phenylbutyric acid, an ER stress inhibitor, alleviated the transcriptional repression of the circadian clock genes and partially restored Bmal1-Luc oscillation amplitudes in Tg- or Tm-treated NIH3T3 cells. More importantly, knock-down of ATF4, but not ATF6, in Tg-treated NIH3T3 cells partially rescued Bmal1-Luc oscillation amplitudes and mRNA expression of the four circadian clock genes. Taken together, our study demonstrates that ER stress activation inhibits the transcription of circadian clock and clock-controlled genes via an ATF4-dependent mechanism.