"Anions-in-Colloid" Hydrated Deep Eutectic Electrolyte for High Reversible Zinc Metal Anodes.

Zn metal suffers from severe zinc dendrites, anion-related side reactions, hydrogen evolution reaction (HER) and narrow electrochemical stable window (ESW). Herein, an"anions-in-colloid" hydrated deep eutectic electrolyte (ACDE-3) is designed to improve the stability of zinc anode. The ACDE-3 reconfigures the hydrogen-bond (HB) network and regulates the solvation shell. More importantly, the hydroxyl-rich ß-cyclodextrins (ß-CDs) in ACDE-3 self-assemble into micelles, in which the steric effect between the adjacent ß-CDs restricts the movement of anions. This unique "anions-in-colloid" structure enables the eutectic system with a high Zn2+ transference number (tZn2+) of 0.84.  Thus, ACDE-3 inhibits the formation of dendrite, prevents the anion-involved side reactions, suppresses the HER, and enlarges the ESW to 2.32 V. The Zn//Zn symmetric cell delivers a long lifespan of 900 hours at 0.5 mAh cm-2, and the Zn//Cu half cells have a high average columbic efficiency (ACE) of 97.9% at 0.5 mAh cm-2 with a uniform and compact zinc deposition. When matched with a poly(1,5-naphthalenediamine) cathode, the full battery with a low negative/positive capacity ratio of 2 can still cycle steadily for 200 cycles at a current density of 1.0 A g-1. Additionally, this electrolyte can operative over a wide temperature range from -40 °C to 40 °C.

Endodontic microsurgery and prosthodontic treatment of a permanent anterior concrescence: A case report.

Concrescence is a rare dental anomaly in which two adjacent teeth are united only by their cementum. Concrescence most frequently occurs in molars, especially a third mandibular molar and a supernumerary tooth. It is rarely seen in the maxillary anterior teeth. This case report is the first in the literature which details the successful treatment of a concrescence between the maxillary central incisor and a supernumerary tooth through multidisciplinary therapy. The treatment plan included root canal treatment, endodontic microsurgery, and prosthodontic treatment.

Synergistic effect of additional anlotinib and immunotherapy as second-line or later-line treatment in pancreatic cancer: A retrospective cohort study.

Background: Pancreatic ductal adenocarcinoma (PDAC) is in urgent need of a second-line or later-line treatment strategy. We aimed to analyze the efficacy and safety of additional anlotinib, specifically anlotinib in combination with immunotherapy, in patients with PDAC who have failed first-line therapy. Methods: Patients with pathological diagnosis of PDAC were additionally treated with anlotinib, and some patients were treated with anti-PD-1 agents at the same time, which could be retrospectively analyzed. The efficacy and safety of additional anlotinib were evaluated. Results: A total of 23 patients were included. In patients treated with additional anlotinib, the overall median progression-free survival (PFS) was 1.8 months and the median overall survival (OS) was 6.3 months, regardless of anti-PD-1 agents. Among patients receiving additional anlotinib in combination with anti-PD-1 agents, median PFS and OS were 1.8 and 6.5 months, respectively. Adverse events (AEs) were observed in 16 patients (69.6%). In patients treated with additional anlotinib, the majority of AEs were grade 1-3. Univariate analysis revealed that patients with baseline red blood cell distribution width (RDW) <14% treated with additional anlotinib plus anti-PD-1 agents had significantly longer OS than patients with baseline RDW ≥14% (p = 0.025). Patients with additional anlotinib plus anti-PD-1 agents as second-line therapy had a longer OS than those treated as later-line therapy (p = 0.012). Multivariate analysis showed that baseline RDW was the only independent risk factor for OS (p = 0.042). Conclusion: The combination of anlotinib and immunotherapy represents an effective add-on therapy with tolerable AEs as second- or later-line therapy in patients with PDAC, particularly in patients with baseline RDW <14%.

Halofuginone Inhibits Osteoclastogenesis and Enhances Osteoblastogenesis by Regulating Th17/Treg Cell Balance in Multiple Myeloma Mice with Bone Lesions.

Evidences shows that T helper 17 (Th17) and regulatory T (Treg) cells imbalance plays a critical role in bone lesions of MM patients. Therefore, regulating the Th17/Treg imbalance may be beneficial for bone lesions in MM. Ten MM mice complicated with bone lesions were established and divided into the halofuginone (HF) group and the PBS group. After treatment, tibia and fibula from both groups were scanned by micro-CT. Osteoclasts and osteoblasts were validated by histochemical staining and ELISA. Th17 and Treg cells were tested by flow cytometry. The correlations between Th17/Treg cell ratio and osteoclasts, osteoblasts and bone remodeling were analyzed using the Spearman relative analysis. After treatment, mice in the HF group had an increase in trabecular bone volume fraction and thickened cortex, but a decrease in trabecular separation compared to mice in the PBS group.Tartrate-resistant acid phosphase (TRAP) + osteoclasts and its biomarker TRACP5b in serum were reduced, while alkaline phosphatase (ALP) + osteoblasts and its biomarker N-terminal propeptide of type 1precollagen (P1NP) in serum were accreted in the HF group. Th17/Treg cell ratio in halofuginone-treated mice was 0.85 ± 0.05, and was significantly lower than that in PBS-treated mice, which was 1.51 ± 0.03. In addition, it showed that the Th17/Treg cell ratio was significantly and positively associated with osteoclasts, but was significantly and negatively associated with osteoblasts and bone remodeling. Halofuginone plays a critical role in the amelioration bone lesions in MM, as it can inhibit osteoclastogenesis and enhance osteoblastogenesis by regulating the Th17/Treg cell balance. Supplementary Information: The online version contains supplementary material available at 10.1007/s12288-024-01756-4.

Is JAK effective in treating recurrent SAPHO syndrome? TwHF might be a good choice.

BACKGROUND: Recently, JAKi has also been widely proved to be an effective alternative to conventional treatment for Synovitis acne pustulosis-hyperostosis-osteitis (SAPHO) cases, after failure of multiple drugs including those described above. But what to do when all these treatments fail? We report a case of remission from Tripterygium wilfordii Hook (TwHF) treatment. METHODS: The patient was treated with nonsteroidal anti-inflammatory drugs, oral prednisone, minocycline, bisphosphonate injection, etanercept, and tofacitinib, but the symptoms did not change significantly. Treatment with TwHF (1.0 mg/kg/day, patient weight 60 kg) was started for 24 weeks. RESULTS: After 50 months of unsatisfactory treatment, this patient was finally treated with herbal TwHF, and after 6 months of treatment, the patient's magnetic resonance imaging and inflammatory indexes were significantly improved, indicating that the disease had been better controlled. CONCLUSION: In this study, TwHF was successful in treating a patient with refractory SAPHO syndrome who was refractory to multiple Western medications without significant adverse effects or toxicities, but further follow-up is needed to determine long-term efficacy. More case reports as well as clinical trials are still needed to confirm whether TwHF can effectively treat refractory SAPHO syndrome.

Super Hydrous Solvated Structure of Chaotropic Ca2+ Contributes Superior Anti-Freezing Aqueous Electrolytes and Stabilizes the Zn anode.

The further development of aqueous zinc (Zn)-ion batteries (AZIBs) is constrained by the high freezing points and the instability on Zn anodes. Current improvement strategies mainly focus on regulating hydrogen bond (HB) donors (H) of solvent water to disrupt HBs, while neglecting the environment of HB-acceptors (O). Herein, we propose a mechanism of chaotropic cation-regulated HB-acceptor via a "super hydrous solvated" structure. Chaotropic Ca2+ can form a solvated structure via competitively binding O atoms in H2O, effectively breaking the HBs among H2O molecules, thereby reducing the glass transition temperature of hybrid 1 mol L-1 (M) ZnCl2+4 M CaCl2 electrolyte (-113.2 °C). Meanwhile, the high hydratability of Ca2+ contributes to the water-poor solvated structure of Zn2+, suppressing side reactions and uneven Zn deposition. Benefiting from the anti-freezing electrolyte and high reversible Zn anode, the Zn||Pyrene-4,5,9,10-tetraone (PTO) batteries deliver an ultrahigh capacity of 183.9 mAh g-1 at 1.0 A g-1 over 1600-time stable cycling at -60 °C. This work presents a cheap and efficient aqueous electrolyte to simultaneously improve low-temperature performances and Zn stability, broadening the design concepts for antifreeze electrolytes.

Atomically Engineered Encapsulation of SnS2 Nanoribbons by Single-Walled Carbon Nanotubes for High-Efficiency Lithium Storage.

Rechargeable lithium-ion batteries are integral to contemporary energy storage, yet current anode material systems struggle to meet the increasing demand for extended range capabilities. This work introduces a novel composite anode material composed of one-dimensional 2H-phase tin disulfide (SnS2) nanoribbons enclosed within cavities of single-walled carbon nanotubes (SnS2@SWCNTs), achieved through precise atomic engineering. Employing aberration-corrected transmission electron microscopy, we precisely elucidated the crystal structure of SnS2 within the confines of the SWCNTs. This deliberate design effectively addresses the inherent limitations of SnS2 as a lithium-ion anode material, including its low electrical conductivity, considerable volume expansion effects, and unstable solid electrolyte interface membrane. Testing confirmed that SnS2 transforms into the Li5Sn2 alloy phase after full lithiation and back to SnS2 after delithiation, showing excellent reversibility. The composite also benefits from edge effects, improving lithium storage through stronger binding and lower migration barriers, which were supported by calculations. This pioneering work advances high-performance anode materials for applications.

Can digital transformation promote green innovation in enterprises? the moderating effect of heterogeneous environmental regulations.

Currently, digital transformation is having various impacts on enterprises around the world, including the green innovation. However, the current literature on the relationship between digitalization and green innovation in enterprises is scarce. What is the relationship between them, and whether heterogeneous environmental regulation has mediating effects, are questions that are worth exploring. Using a sample of listed manufacturing enterprises in China, this paper empirically tests the impact of digital transformation on enterprise green innovation. The results show that: (1) Digital transformation has a significant positive impact on green innovation, including green innovation output and green innovation capability. (2) Diverse environmental regulation may have mediating effects of digital transformation's influence on green innovation. (3) After a number of robustness tests, the conclusions are still valid. This paper can provide a reference for developing green development strategies for manufacturing enterprises.

Mime-seq 2.0: a method to sequence microRNAs from specific mouse cell types.

Many microRNAs (miRNAs) are expressed with high spatiotemporal specificity during organismal development, with some being limited to rare cell types, often embedded in complex tissues. Yet, most miRNA profiling efforts remain at the tissue and organ levels. To overcome challenges in accessing the microRNomes from tissue-embedded cells, we had previously developed mime-seq (miRNome by methylation-dependent sequencing), a technique in which cell-specific miRNA methylation in C. elegans and Drosophila enabled chemo-selective sequencing without the need for cell sorting or biochemical purification. Here, we present mime-seq 2.0 for profiling miRNAs from specific mouse cell types. We engineered a chimeric RNA methyltransferase that is tethered to Argonaute protein and efficiently methylates miRNAs at their 3'-terminal 2'-OH in mouse and human cell lines. We also generated a transgenic mouse for conditional expression of this methyltransferase, which can be used to direct methylation of miRNAs in a cell type of choice. We validated the use of this mouse model by profiling miRNAs from B cells and bone marrow plasma cells.

Regulatory role of the miR-142-3p/CDC25C axis in modulating autophagy in non-small cell lung cancer.

Background: With its diverse genetic foundation and heterogeneous nature, non-small cell lung cancer (NSCLC) needs a better comprehension of prognostic evaluation and efficient treatment targeting. Methods: Bioinformatics analysis was performed of The Cancer Genome Atlas (TCGA)-NSCLC and GSE68571 dataset. Overlapping differentially expressed genes (DEGs) were used for functional enrichment analysis and constructing the protein-protein interaction (PPI) network. In addition, key prognostic genes were identified through prognostic risk models, and their expression levels were verified. The phenotypic effects of cell division cycle 25C (CDC25C) regulation on NSCLC cell lines were assessed by in vitro experiments using various techniques such as flow cytometry, Transwell, and colony formation. Protein levels related to autophagy and apoptosis were assessed, specifically examining the impact of autophagy inhibition [3-methyladenine (3-MA)] and the miR-142-3p/CDC25C axis on this regulatory system. Results: CDC25C was identified as a key prognostic marker in NSCLC, showing high expression in tumor samples. In vitro experiments showed that CDC25C knockdown markedly reduced the capacity of cells to proliferate, migrate, invade, trigger apoptosis, and initiate cell cycle arrest. CDC25C and miR-142-3p displayed a reciprocal regulatory relationship. CDC25C reversed the inhibitory impacts of miR-142-3p on NSCLC cell cycle proliferation and progression. The synergy of miR-142-3p inhibition, CDC25C silencing, and 3-MA treatment was shown to regulate NSCLC cell processes including proliferation, apoptosis, and autophagy. Conclusions: MiR-142-3p emerged as a key player in governing autophagy and apoptosis by directly targeting CDC25C expression. This emphasizes the pivotal role of the miR-142-3p/CDC25C axis as a critical regulatory pathway in NSCLC.

Causal relationships between Sjögren's syndrome and Parkinson's disease: A Mendelian randomization study.

BACKGROUND: Epidemiological and observational studies have indicated an association between Sjögren's syndrome (SS) and Parkinson's disease (PD). However, consistent conclusions have not been reached due to various limitations. In order to determine whether SS and PD are causally related, we conducted a Mendelian randomization study (MR) with two samples. METHODS: Data for SS derived from the FinnGen consortium's R9 release (2495 cases and 365 533 controls). Moreover, data for PD were acquired from the publicly available GWAS of European ancestry, which involved 33 674 cases and 449 056 controls. The inverse variance weighted, along with four other effective methodologies, were employed to comprehensively infer the causal relationships between SS and PD. To assess the estimation's robustness, a number of sensitivity studies were performed. To determine the probability of reverse causality, we performed a reverse MR analysis. RESULTS: There was no evidence of a significant causal effect of SS on PD risks based on the MR [odds ratio (OR) = 1.03; 95% confidence interval (CI) = 0.95-1.11; p = .45]. Similarly, no evidence supported the causal effects of PD on SS (OR = 0.92; 95% CI = 0.81-1.04; p = .20). These findings held up under rigorous sensitivity analysis. CONCLUSIONS: MR bidirectional analysis did not reveal any cause-and-effect relationship between SS and PD, or vice versa. Further study of the mechanisms that may underlie the probable causal association between SS and PD is needed.

The loss of political connections and the fluctuation of corporate stock prices: Moderating effect based on media attention.

This article examines the impact and mechanism of political connections on stock price fluctuations after the resignation of independent directors with "official" status, based on the exogenous influence of Document No. 18 of the Central Organization Department. Using panel data of A-share listed companies on the Shanghai and Shenzhen stock markets from 2012 to 2020, the experimental group and control group for political affiliation deficiency events were determined through propensity score matching (PSM), and a quasi natural experiment was constructed using differences in differences (DID) for empirical research. By examining the relationship between regional financial development, lack of political connections, and stock price fluctuations, we found that regions with higher levels of financial development are more prone to stock price fluctuations due to the lack of political connections, which is related to higher levels of debt financing in regions with higher levels of financial development. In addition, the increasing level of debt exacerbates conflicts and inconsistencies among stakeholders, which is not conducive to the stability of the company's stock price. Through the above research, relevant suggestions have been provided to enterprises, media, and governments. For example, enterprises should clarify the boundary between government and enterprise, focus on long-term strategic goals, build core competitiveness, and thereby enhance their own value; The media should play a correct role in information transmission and public opinion guidance, and play a positive role in the economic development of the industry; The government should promote market-oriented construction and establish positive government enterprise relationships.

Research trends and frontiers in lupus nephritis: a bibliometric analysis from 2012 to 2022.

OBJECTIVES: Lupus nephritis is a prevalent renal manifestation of systemic lupus erythematosus (SLE) and represents a significant cause of morbidity and mortality associated with the disease. This study endeavors to undertake a meticulous bibliometric analysis of LN publications to comprehend the research hotspots and future directions. METHODS: The literature on LN was acquired from the Web of Science Core Collection (WoSCC). Co-occurrence and cooperative relationship analysis of authors, institutions, countries, journals, references and keywords in the publication was performed through CiteSpace, VOSviewer and a bibliometric online analysis platform. The knowledge graphs were created, and clustering and emergence analyses were performed. RESULTS: According to the search strategy, a total of 2077 publications related to lupus nephritis (LN) have been identified, with China being the largest contributor globally. The Ohio State University emerged as the most prolific institution. Lupus is the most cited and published journal. Jan J Weening and Brad Rovin were the most prolific and cocited authors. The current research focus revolved around the "nirp3 inflammasome," "biomarker," and "voclosporin". "international society," "thrombotic microangiopathy (TMA)," and "pathway" were identified to be future research hotpots by keyword burst analysis. CONCLUSIONS: This bibliometric analysis summarizes for the first time the progress of LN research (2012-2022), and qualitatively and quantitatively evaluates the bibliometric information of LN research. There has been a steady increase in the scientific literature on LN over the past 11 years, with an average growth rate of 7.27%. In this field, researchers are primarily based in China and the United States. The pathogenic mechanisms, management strategies and prognostic outcomes of LN are acknowledged as prospective research hotspots. Bibliometrically, the research status and trends of LN publications may greatly assist and be a significant reference for future research in the area.

4EBP2-regulated protein translation has a critical role in high-fat diet-induced insulin resistance in hepatocytes.

A high-fat diet (HFD) plays a critical role in hepatocyte insulin resistance. Numerous models and factors have been proposed to elucidate the mechanism of palmitic acid (PA)-induced insulin resistance. However, proteomic studies of insulin resistance by HFD stimulation are usually performed under insulin conditions, leading to an unclear understanding of how a HFD alone affects hepatocytes. Here, we mapped the phosphorylation rewiring events in PA-stimulated HepG2 cells and found PA decreased the phosphorylation level of the eukaryotic translation initiation factor 4E-binding protein 2 (4EBP2) at S65/T70. Further experiments identified 4EBP2 as a key node of insulin resistance in either HFD mice or PA-treated cells. Reduced 4EBP2 levels increased glucose uptake and insulin sensitivity, whereas the 4EBP2_S65A/T70A mutation exacerbated PA-induced insulin resistance. Additionally, the nascent proteome revealed many glycolysis-related proteins translationally regulated by 4EBP2 such as hexokinase-2, pyruvate kinase PKM, TBC1 domain family member 4, and glucose-6-phosphate 1-dehydrogenase. In summary, we report the critical role of 4EBP2 in regulating HFD-stimulated insulin resistance in hepatocytes.

Reversible Solid-Solid Conversion of Sulfurized Polyacrylonitrile Cathodes in Lithium-Sulfur Batteries by Weakly Solvating Ether Electrolytes.

Despite carbonate electrolytes exhibiting good stability to sulfurized polyacrylonitrile (SPAN), their chemical incompatibility with lithium (Li) metal anode leads to poor electrochemical performance of Li||SPAN full cells. While the SPAN employs conventional ether electrolytes that suffer from the shuttle effect, leading to rapid capacity fading. Here, we tailor a dilute electrolyte based on a low solvating power ether solvent that is both compatible with SPAN and Li metal. Unlike conventional ether electrolytes, the weakly solvating ether electrolyte enables SPAN to undergo reversibly "solid-solid" conversion. It features an anion-rich solvation structure that allows for the formation of a robust cathode electrolyte interphase on the SPAN, effectively blocking the dissolution of polysulfides into the bulk electrolyte and avoiding the shuttle effect. What's more, the unique electrolyte chemistry endowed Li ions with fast electroplating kinetics and induced high reversibility Li deposition/stripping process from 25 °C to -40 °C. Based on tailored electrolyte, Li||SPAN full cells matched with high loading SPAN cathodes (≈3.6 mAh cm-2 ) and 50 µm Li foil can operate stably over a wide range of temperatures. Additionally, Li||SPAN pouch cell under lean electrolyte and 5 % excess Li conditions can continuously operate stably for over a month.

Enhancers of the PAIR4 regulatory module promote distal VH gene recombination at the Igh locus.

While extended loop extrusion across the entire Igh locus controls VH -DJH recombination, local regulatory sequences, such as the PAIR elements, may also activate VH gene recombination in pro-B-cells. Here, we show that PAIR-associated VH 8 genes contain a conserved putative regulatory element (V8E) in their downstream sequences. To investigate the function of PAIR4 and its V8.7E, we deleted 890 kb containing all 14 PAIRs in the Igh 5' region, which reduced distal VH gene recombination over a 100-kb distance on either side of the deletion. Reconstitution by insertion of PAIR4-V8.7E strongly activated distal VH gene recombination. PAIR4 alone resulted in lower induction of recombination, indicating that PAIR4 and V8.7E function as one regulatory unit. The pro-B-cell-specific activity of PAIR4 depends on CTCF, as mutation of its CTCF-binding site led to sustained PAIR4 activity in pre-B and immature B-cells and to PAIR4 activation in T-cells. Notably, insertion of V8.8E was sufficient to activate VH gene recombination. Hence, enhancers of the PAIR4-V8.7E module and V8.8E element activate distal VH gene recombination and thus contribute to the diversification of the BCR repertoire in the context of loop extrusion.

PET117 assembly factor stabilizes translation activator TACO1 thereby upregulates mitochondria-encoded cytochrome C oxidase 1 synthesis.

Cytochrome c oxidase, also known as complex IV, facilitates the transfer of electrons from cytochrome c to molecular oxygen, resulting in the production of ATP. The assembly of complex IV is a tightly regulated and intricate process that entails the coordinated synthesis and integration of subunits encoded by the mitochondria and nucleus into a functional complex. Accurate regulation of translation is crucial for maintaining proper mitochondrial function, and defects in this process can lead to a wide range of mitochondrial disorders and diseases. However, the mechanisms governing mRNA translation by mitoribosomes in mammals remain largely unknown. In this study, we elucidate the critical role of PET117, a chaperone protein involved in complex IV assembly, in the regulation of mitochondria-encoded cytochrome c oxidase 1 (COX1) protein synthesis in human cells. Depletion of PET117 reduced mitochondrial oxygen consumption rate and impaired mitochondrial function. PET117 was found to interact with and stabilize translational activator of COX1 (TACO1) and prevent its ubiquitination. TACO1 overexpression rescued the inhibitory effects on mitochondria caused by PET117 deficiency. These findings provide evidence for a novel PET117-TACO1 axis in the regulation of mitochondrial protein expression, and revealed a previously unknown role of PET117 in human cells.

pH-Responsive Selenium Nanoplatform for Highly Efficient Cancer Starvation Therapy by Atorvastatin Delivery.

Recently, starvation-inducing nutrient deprivation has been regarded as a promising strategy for tumor suppression. As a first-line lipid-lowering drug, atorvastatin (ATV) significantly reduces caloric intake, suggesting its potential in starvation therapy for suppressing tumors. Accordingly, we developed a novel starvation therapy agent (HA-Se-ATV) in this study to suppress tumor growth by using hyaluronic acid (HA)-conjugated chitosan polymer-coated nano-selenium (Se) for loading ATV. HA-Se-ATV targets cancer cells, following which it effectively accumulates in the tumor tissue. The HA-Se-ATV nanoplatform was then activated by inducing a weakly acidic tumor microenvironment and subsequently releasing ATV. ATV and Se synergistically downregulate the levels of cellular adenosine triphosphate while inhibiting the expression of thioredoxin reductase 1. Consequently, the starvation-stress reaction of cancer cells is significantly elevated, leading to cancer cell death. Furthermore, the in vivo results indicate that HA-Se-ATV effectively suppresses tumor growth with a low level of toxicity, demonstrating its great potential for clinical translation.