Search

Abstract Mitochondria, responsible for cellular energy synthesis and signal transduction, intricately regulate diverse metabolic processes, mediating fundamental biological phenomena such as cell growth, aging, and apoptosis. Tumor invasion and metastasis, key characteristics of malignancies, significantly impact patient prognosis. Tumor cells frequently exhibit metabolic abnormalities in mitochondria, including alterations in metabolic dynamics and changes in the expression of relevant metabolic genes and associated signal transduction pathways. Recent investigations unveil further insights into mitochondrial metabolic abnormalities, revealing their active involvement in tumor cell proliferation, resistance to chemotherapy, and a crucial role in tumor cell invasion and metastasis. This paper comprehensively outlines the latest research advancements in mitochondrial structure and metabolic function. Emphasis is placed on summarizing the role of mitochondrial metabolic abnormalities in tumor invasion and metastasis, including alterations in the mitochondrial genome (mutations), activation of mitochondrial-to-nuclear signaling, and dynamics within the mitochondria, all intricately linked to the processes of tumor invasion and metastasis. In conclusion, the paper discusses unresolved scientific questions in this field, aiming to provide a theoretical foundation and novel perspectives for developing innovative strategies targeting tumor invasion and metastasis based on mitochondrial biology. Graphical Abstract

Renal cell carcinoma (RCC) is one of the deadliest malignant tumors. Despite significant advances in RCC treatment over the past decade, complete remission is rarely achieved. Consequently, there is an urgent need to explore and develop new therapies to improve the survival rates and quality of life for patients. In recent years, the development of tumor organoid technology has attracted widespread attention as it can more accurately simulate the spatial structure and physiological characteristics of tumors within the human body. In this review, we summarize the main methods currently used to construct kidney cancer organoids, as well as their various biological and clinical applications. Furthermore, combining organoids with other technologies, such as co-culture techniques and microfluidic technologies, can further develop organoids and address their limitations, creating more practical models. This approach summarizes the interactions between different tissues or organs during tumor progression. Finally, we also provide an outlook on the construction and application of kidney cancer organoids. These rapidly evolving kidney cancer organoids may soon become a focal point in the development of in vitro clinical models and therapeutic research for kidney cancer.

Abstract Gene editing of living cells has become a crucial tool in medical research, enabling scientists to address fundamental biological questions and develop novel strategies for disease treatment. This technology has particularly revolutionized adoptive transfer cell therapy products, leading to significant advancements in tumor treatment and offering promising outcomes in managing transplant rejection, autoimmune disorders, and inflammatory diseases. While recent clinical trials have demonstrated the safety of tolerogenic dendritic cell (TolDC) immunotherapy, concerns remain regarding its effectiveness. This review aims to discuss the application of gene editing techniques to enhance the tolerance function of dendritic cells (DCs), with a particular focus on preclinical strategies that are currently being investigated to optimize the tolerogenic phenotype and function of DCs. We explore potential approaches for in vitro generation of TolDCs and provide an overview of emerging strategies for modifying DCs. Additionally, we highlight the primary challenges hindering the clinical adoption of TolDC therapeutics and propose future research directions in this field.

IntroductionPEDV, Brachyspira hyodysenteriae, and Lawsonia intracellularis, are highly contagious diarrheal pathogens that have caused significant harm to the global swine industry. Co-infections with multiple pathogens are common, making it challenging to identify the actual causative agents depending only on clinical information. It is crucial to develop a reliable method to simultaneously detect and differentiate these pathogens.MethodsBased on the conserved regions of the M gene of PEDV, NADH oxidase gene of B. hyodysenteriae, and the 16S rDNA gene of L. intracellularis, specific probes and primers for the multiplex real-time PCR assay were designed. The concentrations of primers and probes were optimized using a matrix method.ResultsThe approach demonstrated high specificity and no cross-reactivity with major pathogens related to diarrheal diseases. It showed high sensitivity with a detection limit of 10 copies/μL for B. hyodysenteriae and L. intracellularis, and 100 copies/μL for PEDV, respectively. It also demonstrated high reproducibility and stability with low coefficients of variation. Results from the multiplex real-time PCR method were in complete agreement with the commercial singleplex real-time PCR kit for detecting PEDV, B. hyodysenteriae and L. intracellularis. Clinical data revealed single infection rates of 31.46% for PEDV, 58.43% for B. hyodysenteriae, and 98.6% for L. intracellularis. The co-infection rates were 16.85% for PEDV + B. hyodysenteriae, 31.46% for PEDV + L. intracellularis, 57.86% for B. hyodysenteriae + L. intracellularis, and 16.85% for PEDV + B. hyodysenteriae + L. intracellularis, respectively.DiscussionThe new multiplex real-time PCR method can simultaneously differentiate PEDV, B. hyodysenteriae and L. intracellularis, making it a valuable diagnostic tool for preventing and controlling infectious diseases, as well as aiding in epidemiological investigations.

Background: Glioblastoma (GBM) is a highly aggressive and fast-growing brain tumor, characterized by rapid progression, a very poor prognosis, and a high likelihood of recurrence. Thus, effective new therapeutic targets are urgently needed. Transmembrane proteins (TMEMs) have pro-cancer effects on multiple cancer types, but the mechanisms underlying the effects of TMEM17, particularly its role in GBM, remain unclear. Methods: We conducted bioinformatics analyses and immunohistochemistry to evaluate the role of TMEM17 in a variety of cancer types. Functional assays were conducted included the Cell Counting Kit-8 assay, annexin V-FITC/PI double staining, 5-ethynyl-2′-deoxyuridine (EdU) incorporation assay, wound healing assay, transwell invasion assay, and dual luciferase assay. Results: We found that TMEM17 is associated with a poor prognosis in GBM. Prognostic analyses confirmed that high TMEM17 expression predicted poorer survival, establishing its significance as an independent prognostic factor. Functional assays demonstrated that silencing TMEM17 in GBM cell lines inhibited proliferation and invasion, and induced apoptosis, underscoring its role in tumor aggressiveness. From a mechanistic perspective, we discovered that the Ying Yang 1 (YY1) transcription factor can bind to the promoter of TMEM17, regulating its upregulation. Regarding downstream mechanisms, knocking down TMEM17 inhibited the phosphoinositide 3-kinase/AKT pathway. These findings suggest that TMEM17 plays a significant role in GBM and may be a potential therapeutic target for this cancer. Conclusion: These data prove that TMEM17 plays a key role in the regulation of GBM and has great potential as a clinical therapeutic target for GBM.

Abstract This single‐center, open‐label, non‐randomized, two‐part, phase I study was conducted (1) to evaluate the absolute oral bioavailability of rilzabrutinib 400 mg tablet following an i.v. microtracer dose of ~100 μg [14C]‐rilzabrutinib (~1 μCi) and single oral dose of 400 mg rilzabrutinib tablet (part 1), and (2) to characterize the absorption, metabolism, and excretion (AME) of 14C‐radiolabeled rilzabrutinib following single oral dose (300 mg) of [14C]‐rilzabrutinib (~1000 μCi; administered as a liquid) in healthy male participants (part 2). A total of 18 subjects were enrolled (n = 8 in part 1; n = 10 in part 2). The absolute bioavailability of 400 mg rilzabrutinib oral tablet was low (

AbstractObjective To investigate the predictive value of the prognostic nutritional index (PNI) for the effectiveness of infliximab (IFX) in patients with Crohn's disease (CD).Methods All data were retrospectively collected from Xiangya Hospital, Central South University between January 2016 and September 2021. Clinical remission at 52 weeks is the primary endpoint.Results Altogether, 193 CD patients were enrolled. PNI can identify clinical remission (p = 0.004), and the optimal cut-off value of the PNI was 39.2. 92/116 (79.3%) and 44/77 (57.1%) in the high- and low-PNI groups were in clinical remission at week 52 (p = 0.001). Patients with low PNI have poor general health at baseline. The body mass index, hemoglobin, platelet (PLT), serum creatinine, fibrinogen, erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), Crohn's disease activity index (CDAI), and location of disease significantly differed between the two groups (p

With the progress of molecular diagnosis research on non-small cell lung cancer (NSCLC) cells, four identified categories of microRNAs have been found to be related to disease diagnosis, diagnosis of treatment resistance, prediction of prognosis, and drugs for treatment. To date, nine target mRNA/signal pathways have been confirmed for microRNA drug therapy both in vitro and in vivo. When microRNA drugs enter blood vessels, they target the tumor site and play a similar role to that of targeted drugs. However, whether they will produce serious off-target effects remains unknown, and further clinical research is needed. This review provides the first summary of microRNA therapy for NSCLC.

Diabetes mellitus is a chronic metabolic disease, characterized by high blood sugar levels; it affects more than 500 million individuals worldwide. Type 1 diabetes mellitus (T1DM) is results from insufficient insulin secretion by islets; its treatment requires lifelong use of insulin injections, which leads to a large economic burden on patients. Islet transplantation may be a promising effective treatment for T1DM. Clinically, this process currently involves directly infusing islet cells into the hepatic portal vein; however, transplantation at this site often elicits immediate blood-mediated inflammatory and acute immune responses. Subcutaneous islet transplantation is an attractive alternative to islet transplantation because it is simpler, demonstrates lower surgical complication risks, and enables graft monitoring and removal. In this article, we review the current methods of subcutaneous device-free islet transplantation. Recent subcutaneous islet transplantation techniques with high success rate have involved the use of bioengineering technology and biomaterial cotransplantation—including cell and cell growth factor co-transplantation and hydrogel– or simulated extracellular matrix–wrapped subcutaneous co-transplantation. In general, current subcutaneous device-free islet transplantation modalities can simplify the surgical process and improve the posttransplantation graft survival rate, thus aiding effective T1DM management.

Methionine sulfoxide reductase (Msr) is a kind of antioxidant enzyme that can scavenge free radicals and repair oxidized proteins by reducing methionine sulfoxide to active methionine. Studies have shown that Msr play an important role in regulating ripening, senescence, and stress resistance of fruit and vegetable. In this paper, the classification of Msr is summarized. In addition, the research progresses on the substrates of Msr, gene families encoding Msr, and its role in regulating fruit and vegetable metabolism and stress response are reviewed. This paper would provide theoretical references for further studying the types and functions of Msr in fruit and vegetable crops, as well as improving the quality and stress resistance of fruit and vegetables by genetic engineering.

Context Sevoflurane (Sev) is a commonly used surgical anaesthetic; it has neurotoxic effects on the brain. Echinatin (Ech) is reported to have anti-inflammatory and antioxidant activity.Objective This research confirms the effect of Ech on Sev-induced neurotoxicity and cognitive deficits.Materials and methods Primary rat hippocampal neurons were treated with 4.1% Sev for 6 h in the presence of Ech (5, 10, and 20 μM) or vehicle, followed by a further 42 h of culture. Male Sprague-Dawley aged rats were divided into 6 groups (n = 6): control, Sev, Sev + Ech (20 mg/kg;), Sev + Ech (40 mg/kg), and Sev + Ech (80 mg/kg). Rats were intraperitoneally injected with Ech or vehicle 1 h before Sev exposure (2% Sev for 5 h).Results We found that Ech (5, 10, and 20 μM) elevated cell viability (1.29-, 1.51-, 1.68-fold) but mitigated apoptosis (23.87% vs. 16.48%, 12.72%, 9.02%), oxidative stress, and ferroptosis in hippocampal neurons with Sev treatment. Ech activated the Nrf2 expression in Sev-induced in vitro and in vivo models of anaesthetic neurotoxicity. Ech also weakened neurotoxicity in hippocampal neurons with Sev treatment by increasing Nrf2 expression level. Moreover, Ech alleviated hippocampus neurons apoptosis (19.38% vs. 16.05%, 11.71%, 8.88%), oxidative stress, and ferroptosis in rats with Sev treatment. Ech improved Sev-induced cognitive deficits in rats.Conclusions Ech alleviates Sev-induced neurotoxicity and cognitive deficits by mitigation of ferroptosis and oxidative stress. Ech may be developed as a new promising therapeutic drug for treatment of cerebral nerve injury caused by surgical anaesthesia.

BackgroundParkinsonism and akinetic mutism (AM) following ventriculo-peritoneal shunt (VPS) without underdrainage used to be considered rare, but may be underdiagnosed in daily clinical practice. Although the pathophysiology is still unclear, in several case reports, the parkinsonism and AM after VPS shows responsiveness to dopaminergic treatment.Case presentationWe report a 19-year-old male that presented with severe parkinsonism and AM after VPS. Meanwhile, 18F-FDG-PET showed a cortical and subcortical hypometabolism. Fortunately, levodopa dramatically improved patient's symptoms and brain hypometabolism. This report provides support for the possibility that dopamine deficiency inhibits brain metabolism, and further elucidates the pathogenesis of parkinsonism and AM.ConclusionThis report highlights the presentation of a treatable parkinsonism and points out that Levodopa and/or dopamine agonist should be the first choice if the patients develop parkinson-like symptoms after VPS.

To investigate the roles of Harvista (a sprayable 1-methylcyclopropene, 1-MCP, available component is 150 g · hm-2) and Ethephon (1 mL · L-1) applied at preharvest in apple (Malus domestica Borkh. 'Golden Delicious') fruit cuticular wax biosynthesis, the expression of genes related to fruit cuticular wax biosynthesis and ethylene biosynthesis and signaling, ethylene production rate, respiration rate, wax constituents and structure, and fruit quality were determined at harvest and during cold storage. The results showed that 1-MCP inhibited the expression levels of ethylene biosynthesis and signaling-related genes, decreased fruit ethylene production, and inhibited the expression of MdLACS1, MdCER6, MdCER4 and MdWSD1, which resulted in decreases in alcohols, acids, and esters content in fruit cuticular wax. 1-MCP also reduced fruit dropping rate from 17.17% to 12%; maintained fruit firmness, soluble solids, titratable acidity during cold storage; showed about as one fifth in the total length and one third in the widest width of wax crack as that in control at harvest. In contrast, Ethephon produced the opposite effects. In conclusion, 1-MCP inhibited fruit ethylene biosynthesis and signaling, and influenced fruit cuticular wax biosynthesis. Thus, the fruit cuticular wax constituents and structure was altered, and the fruit quality were maintained at harvest and during cold storage. The results provide a new technology for improving apple fruit harvest and postharvest quality by preharvest application of sprayable 1-MCP.

PurposeOur previous study observed that long non-coding RNA PKD2-2-3 (lnc-PKD2-2-3) is related to advanced tumor features and worse prognosis in cholangiocarcinoma (CCA). Then, this study aimed to further explore the linkage between lnc-PKD2-2-3, miR-328, and GPAM, as well as their effects on regulating CCA viability, mobility, and chemosensitivity.MethodsLnc-PKD2-2-3, miR-328, and GPAM expression in 30 pairs of CCA tumor and adjacent tissues, as well as in CCA cell lines, were determined. Two CCA cell lines (HuCCT1 and TFK1) were transfected by lnc-PKD2-2-3 overexpression plasmid, lnc-PKD2-2-3 siRNA, miR-328 inhibitor, and GPAM siRNA alone or in combination, followed by cell proliferation, apoptosis, invasion, and 5-FU chemosensitivity detection. Besides, xenograft mice were established for validation.ResultsLnc-PKD2-2-3 and GPAM were higher, whereas miR-328 was lower in CCA tissues versus adjacent tissues and also in CCA cell lines versus control cells; meanwhile, they were correlated with each other (all P

High-capacity and structural stable cathode materials are challenges for sodium-ion batteries. Here, the authors report a layered P2-Na0.612K0.056MnO2 with large-sized K+ riveted in the Na-layers to enable 0.9 Na+ (de)insertion with a reversible phase transition of P2-P’2.

Abstract Background The main objectives of this study were as follows: (1) evaluate the prevalence of burnout syndrome among doctors, (2) establish associations with demographic factors in China, and (3) examine the mediating role of psychological attachment in the relationship between job burnout and career calling. Methods This cross-sectional survey was conducted by administering an online questionnaire in May 2016. The survey was performed across Thirty provinces. In total, A total of 3016 Chinese doctors were selected as participants, of which 2617 completed valid questionnaires (effective response rate: 86.77%). Results The overall prevalence of burnout symptoms among Chinese doctors was 85.79%. Little variance was reported for burnout symptoms according to age (Waldχ 2 = 6.843, P 1), and daily working hours (Waldχ 2 = 7.226, P 1). However, the burnout of Chinese doctors was found to be associated with psychological attachment (B = − 0.6433, P

Abstract Background Tamoxifen resistance presents a huge clinical challenge for breast cancer patients. An understanding of the mechanisms of tamoxifen resistance can guide development of efficient therapies to prevent drug resistance. Methods We first tested whether peptidylarginine deiminase 2 (PAD2) may be involved in tamoxifen-resistance in breast cancer cells. The effect of depleting or inhibiting PAD2 in tamoxifen-resistant MCF-7 (MCF7/TamR) cells was evaluated both in vitro and in vivo. We then investigated the potential of Cl-amidine, a PAD inhibitor, to be used in combination with tamoxifen or docetaxel, and further explored the mechanism of the synergistic and effective drug regimen of PADs inhibitor and docetaxel on tamoxifen-resistant breast cancer cells. Results We report that PAD2 is dramatically upregulated in tamoxifen-resistant breast cancer. Depletion of PAD2 in MCF7/TamR cells facilitated the sensitivity of MCF7/TamR cells to tamoxifen. Moreover, miRNA-125b-5p negatively regulated PAD2 expression in MCF7/TamR cells, therefore overexpression of miR-125b-5p also increased the cell sensitivity to tamoxifen. Furthermore, inhibiting PAD2 with Cl-amidine not only partially restored the sensitivity of MCF7/TamR cells to tamoxifen, but also more efficiently enhanced the efficacy of docetaxel on MCF7/TamR cells with lower doses of Cl-amidine and docetaxel both in vivo and in vivo. We then showed that combination treatment with Cl-amidine and docetaxel enhanced p53 nuclear accumulation, which synergistically induced cell cycle arrest and apoptosis. Meanwhile, p53 activation in the combination treatment also accelerated autophagy processes by synergistically decreasing the activation of Akt/mTOR signaling, thus enhancing the inhibition of proliferation. Conclusion Our results suggest that PAD2 functions as an important new biomarker for tamoxifen-resistant breast cancers and that inhibiting PAD2 combined with docetaxel may offer a new approach to treatment of tamoxifen-resistant breast cancers.

Abstract Background Primary cutaneous malignant melanoma is a cancer of the pigment cells of the skin, some of which are accompanied by BRAF mutation. Melanoma incidence and mortality rates have been rising around the world. As the current knowledge about pathogenesis, clinical and genetic features of cutaneous melanoma is not very clear, we aim to use bioinformatics to identify the potential key genes involved in the expression and mutation status of BRAF. Methods Firstly, we used UCSC public hub datasets of melanoma (Lin et al., Cancer Res 68(3):664, 2008) to perform weighted genes co-expression network analysis (WGCNA) and differentially expressed genes analysis (DEGs), respectively. Secondly, overlapping genes between significant gene modules and DEGs were screened and validated at transcriptional levels and overall survival in TCGA and GTEx datasets. Lastly, the functional enrichment analysis was accomplished to find biological functions on the web-server database. Results We performed weighted correlation network and differential expression analyses, using gene expression data in melanoma samples. We identified 20 genes whose expression was correlated with the mutation status of BRAF. For further validation, three of these genes (CYR61, DUSP1, and RNASE4) were found to have similar expression patterns in skin tumors from TCGA compared with normal skin samples from GTEx. We also found that weak expression of these three genes was associated with worse overall survival in the TCGA data. These three genes were involved in the nucleic acid metabolic process. Conclusion In this study, CYR61, DUSP1, and RNASE4 were identified as potential genes of interest for future molecular studies in melanoma, which would improve our understanding of its causes and underlying molecular events. These candidate genes may provide a promising avenue of future research for therapeutic targets in melanoma.

Berberine, which is a traditional Chinese medicine can inhibit tumorigenesis by inducing tumor cell apoptosis. However, the immunoregulatory of effects berberine on T cells remains poorly understood. Here, we first examined whether berberine can prolong allograft survival by regulating the recruitment and function of T cells. Using a major histocompatibility complex complete mismatch mouse heterotopic cardiac transplantation model, we found that the administration of moderate doses (5 mg/kg) of berberine significantly prolonged heart allograft survival to 19 days and elicited no obvious berberine-related toxicity. Compared to that with normal saline treatment, berberine treatment decreased alloreactive T cells in recipient splenocytes and lymph node cells. It also inhibited the activation, proliferation, and function of alloreactive T cells. Most importantly, berberine treatment protected myocardial cells by decreasing CD4+ and CD8+ T cell infiltration and by inhibiting T cell function in allografts. In vivo and in vitro assays revealed that berberine treatment eliminated alloreactive T lymphocytes via the mitochondrial apoptosis pathway, which was validated by transcriptome sequencing. Taken together, we demonstrated that berberine prolongs allograft survival by inducing apoptosis of alloreactive T cells. Thus, our study provides more evidence supporting the potential use of berberine in translational medicine.

Aprotic Na-O2 batteries attract increasing attention for the low charging/discharging overpotentials, high energy density, and low cost. Significant progress has been achieved in the battery system, but challenges remain in constructing reliable Na anodes. This review presents an overview of the fundamental understanding of Na anodes in aprotic Na-O2 batteries, including chemical reactivity of Na metal and dendrite formation mechanism. The constructing strategies are summarized as mechanical reinforcement of separators, electrolyte modifications, and electrode structure and material design. Perspectives are envisioned for the further development of durable Na anodes for aprotic Na-O2 batteries.

A “Laiyang” pear is a climacteric fruit with a special taste and nutritional value but is prone to a post-harvest aroma compound loss and a loss in fruit quality. In this study, pears were pretreated with 0.5 μl L–1 1-methylcyclopropene (1-MCP) at 20°C for 12 h and then stored at 0 ± 1°C for 150 days to evaluate the influence of 1-MCP on fruit quality and the changes in components of volatile aromas. In addition, pears were further treated with 2 mmol L–1 ethephon. The effects of ethephon on the recovery of aroma production were investigated during the 150 day storage at 0 ± 1°C and the subsequent 7 day shelf life at 20 ± 1°C. Treatment with 1-MCP inhibited firmness loss, increased electrical conductivity, reduced respiration and ethylene production rates as well as the contents of soluble solids, and maintained the storage quality of the fruits. However, 1-MCP treatment inhibited the emission of volatile aromas in pear fruits by decreasing the activities of various enzymes, such as lipoxygenase (LOX), hydroperoxide lyase (HPL), alcohol dehydrogenase (ADH), pyruvate carboxylase (PDC), and alcohol acetyltransferase (AAT). During the shelf-life, activities of the above mentioned enzymes were significantly enhanced, and a higher content of volatile aromas were found in fruits treated with 1-MCP + ethephon, while other qualities were not compromised. These results showed that 1-MCP treatment could effectively maintain the quality of the “Laiyang” pear during cold storage, and the additional application of ethephon on fruits during shelf-life may be a promising way to restore volatile aromas in pear fruits after long-term storage.

The development of rechargeable aqueous zinc batteries are challenging but promising for energy storage applications. With a mild-acidic triflate electrolyte, here the authors show a high-performance Zn-MnO2 battery in which the MnO2 cathode undergoes Zn2+ (de)intercalation.

Na-O2 and K-O2 batteries have attracted extensive attention in recent years. However, the parasitic reactions involving the discharge product of NaO2 or K anode with electrolytes and the severe Na or K dendrites plague their rechargeability and cycle stability. Herein, we report a hybrid Na//K+-containing electrolyte//O2 battery consisting of a Na anode, 1.0 M of potassium triflate in diglyme, and a porous carbon cathode. Upon discharging, KO2 is preferentially produced via oxygen reduction in the cathode with Na+ stripped from the Na anode, and reversely, the KO2 is electrochemically decomposed with Na+ plated back onto the anode. The new reaction pathway can circumvent the parasitic reactions involving instable NaO2 and active K anode, and alternatively, the good stability and conductivity of KO2 and stable Na stripping/plating in the presence of K+ enable the hybrid battery to exhibit an average discharge/charge voltage gap of 0.15 V, high Coulombic efficiency of >96%, and superior cycling stability of 120 cycles. This will pave a new pathway to promote metal-air batteries.

The aim of this paper is to determine the modulatory effects of Lactobacillus acidophilus on the IL-23/Th17 immune axis in experimental colitis. DSS-induced mouse models of UC were to be saline, hormones, and different concentrations of Lactobacillus acidophilus intervention. The expression of interleukin- (IL-) 17, tumor necrosis factor α (TNFα), IL-23, transforming growth factor β1 (TGFβ1), signal transducer and activator of transcription 3 (STAT3), and phosphorylated (p)-STAT3 was examined by RT-PCR, Western blotting, and immunohistochemical analysis. And the results showed that administration of L. acidophilus suppressed Th17 cell-mediated secretion of proinflammatory cytokine IL-17 through downregulation of IL-23 and TGFβ1 expression and downstream phosphorylation of p-STAT3.

High-performance sodium storage at low temperature is urgent with the increasingly stringent demand for energy storage systems. However, the aggravated capacity loss is induced by the sluggish interfacial kinetics, which originates from the interfacial Na+ desolvation. Herein, all-fluorinated anions with ultrahigh electron donicity, trifluoroacetate (TFA-), are introduced into the diglyme (G2)-based electrolyte for the anion-reinforced solvates in a wide temperature range. The unique solvation structure with TFA- anions and decreased G2 molecules occupying the inner sheath accelerates desolvation of Na+ to exhibit decreased desolvation energy from 4.16 to 3.49 kJ mol-1 and 24.74 to 16.55 kJ mol-1 beyond and below -20 °C, respectively, compared with that in 1.0 M NaPF6-G2. These enable the cell of Na||Na3V2(PO4)3 to deliver 60.2% of its room-temperature capacity and high capacity retention of 99.2% after 100 cycles at -40 °C. This work highlights regulation of solvation chemistry for highly stable sodium-ion batteries at low temperature. [ABSTRACT FROM AUTHOR]