Novel Insights into the Links between N6-Methyladenosine and Regulated Cell Death in Musculoskeletal Diseases.

Musculoskeletal diseases (MSDs), including osteoarthritis (OA), osteosarcoma (OS), multiple myeloma (MM), intervertebral disc degeneration (IDD), osteoporosis (OP), and rheumatoid arthritis (RA), present noteworthy obstacles associated with pain, disability, and impaired quality of life on a global scale. In recent years, it has become increasingly apparent that N6-methyladenosine (m6A) is a key regulator in the expression of genes in a multitude of biological processes. m6A is composed of 0.1-0.4% adenylate residues, especially at the beginning of 3'-UTR near the translation stop codon. The m6A regulator can be classified into three types, namely the "writer", "reader", and "eraser". Studies have shown that the epigenetic modulation of m6A influences mRNA processing, nuclear export, translation, and splicing. Regulated cell death (RCD) is the autonomous and orderly death of cells under genetic control to maintain the stability of the internal environment. Moreover, distorted RCDs are widely used to influence the course of various diseases and receiving increasing attention from researchers. In the past few years, increasing evidence has indicated that m6A can regulate gene expression and thus influence different RCD processes, which has a central role in the etiology and evolution of MSDs. The RCDs currently confirmed to be associated with m6A are autophagy-dependent cell death, apoptosis, necroptosis, pyroptosis, ferroptosis, immunogenic cell death, NETotic cell death and oxeiptosis. The m6A-RCD axis can regulate the inflammatory response in chondrocytes and the invasive and migratory of MM cells to bone remodeling capacity, thereby influencing the development of MSDs. This review gives a complete overview of the regulatory functions on the m6A-RCD axis across muscle, bone, and cartilage. In addition, we also discuss recent advances in the control of RCD by m6A-targeted factors and explore the clinical application prospects of therapies targeting the m6A-RCD in MSD prevention and treatment. These may provide new ideas and directions for understanding the pathophysiological mechanism of MSDs and the clinical prevention and treatment of these diseases.

Urinary proteomics for noninvasive monitoring of biomarkers of chronic mountain sickness in a young adult population using data-independent acquisition (DIA)-based mass spectrometry.

Different populations exhibit varying pathophysiological responses to plateau environments. Therefore, it is crucial to identify molecular markers in body fluids with high specificity and sensitivity to aid in determination. Proteomics offers a fresh perspective for investigating protein changes linked to diseases. We utilize urine as a specific biomarker for early chronic mountain sickness (CMS) detection, as it is a simple-to-collect biological fluid. We collected urine samples from three groups: plains health, plateau health and CMS. Using DIA's proteomic approach, we found differentially expressed proteins between these groups, which will be used as a basis for future studies to identify protein markers. Compared with the healthy plain population, 660 altering proteins were identified in plateau health, which performed the resistance to altitude response function by boosting substance metabolism and reducing immune stress function. Compared to the healthy plateau population, the CMS group had 140 different proteins identified, out of which 8 were potential biomarkers for CMS. Our study has suggested that CMS may be closely related to increased thyroid hormone levels, oxidative damage to the mitochondria, impaired cell detoxification function and inhibited hydrolase activity. SIGNIFICANCE: Our team has compiled a comprehensive dataset of urine proteomics for AMS disease. We successfully identified differentially expressed proteins between healthy and AMS groups using the DIA proteomic approach. We discovered that 660 proteins were altered in plateau health compared to the healthy plain population, resulting in a heightened resistance to altitude response function by boosting substance metabolism and reducing immune stress function. Additionally, we pinpointed 140 different proteins in the AMS group compared to the healthy plateau population, with 8 showing potential as biomarkers for AMS. Our findings suggest that the onset of AMS may be closely linked to increased thyroid hormone levels, oxidative damage to the mitochondria, impaired cell detoxification function and inhibited hydrolase activity.

Potential Targets of Natural Products for Improving Cardiac Ischemic Injury: The Role of Nrf2 Signaling Transduction.

Myocardial ischemia is the leading cause of health loss from cardiovascular disease worldwide. Myocardial ischemia and hypoxia during exercise trigger the risk of sudden exercise death which, in severe cases, will further lead to myocardial infarction. The Nrf2 transcription factor is an important antioxidant regulator that is extensively engaged in biological processes such as oxidative stress, inflammatory response, apoptosis, and mitochondrial malfunction. It has a significant role in the prevention and treatment of several cardiovascular illnesses, since it can control not only the expression of several antioxidant genes, but also the target genes of associated pathological processes. Therefore, targeting Nrf2 will have great potential in the treatment of myocardial ischemic injury. Natural products are widely used to treat myocardial ischemic diseases because of their few side effects. A large number of studies have shown that the Nrf2 transcription factor can be used as an important way for natural products to alleviate myocardial ischemia. However, the specific role and related mechanism of Nrf2 in mediating natural products in the treatment of myocardial ischemia is still unclear. Therefore, this review combs the key role and possible mechanism of Nrf2 in myocardial ischemic injury, and emphatically summarizes the significant role of natural products in treating myocardial ischemic symptoms, thus providing a broad foundation for clinical transformation.

A Feasibility Study on Using Hanging Arm Test to Assess Elbow Stability During Surgical Treatment for Varus Posteromedial Rotatory Instability.

Objectives: The aim of this study to investigate the safety and effectiveness of performing the hanging arm test during surgical treatment for elbow varus posteromedial rotatory instability (VPMRI) to assess elbow stability and determine whether to repair the lateral ulnar collateral ligament (LUCL). Methods: In a retrospective study from August 2014 to March 2019, 27 patients with VPMRI who had a negative result in the hanging arm test after fixation of coronoid fracture were selected. Intraoperative bleeding, operative time, elbow range of motion (ROM), and complications were recorded. Elbow function was evaluated with the Mayo elbow performance score (MEPS) and the disabilities of the arm, shoulder, and hand (DASH) score. Results: The operation time was 85.9 ± 11.06 min (range 65-110). The intraoperative blood loss was 70.7 ± 9.31 ml (range 60-100). At the last follow-up, the elbow joint averaged 73.8° ± 2.931° in pronation, 78.9° ± 2.941° in supination, 7.2° ± 3.207° in extension, and 123.3° ± 6.651° in flexion. The MEPS score was 90.7 ± 4.36 (range 74-95), and the DASH score was 9.8 ± 2.58 (range 6.67-13.3). One patient presented with symptoms of ulnar nerve entrapment 2 months after operation and was treated with ulnar nerve release. The symptom of numbness went away completely 1 week after operation. No complications such as wound infection, arthritis, or chronic instability of the elbow were found in the other patients. Conclusion: Our findings suggest that not all VPMRI patients need the LUCL to be repaired, and the hanging arm test is a safe and reliable method to assess whether to repair the LUCL in the treatment of elbow VPMRI. Level of evidence: Level IV; Retrospective studies.

Noncoding RNAs: the crucial role of programmed cell death in osteoporosis.

Osteoporosis is the most common skeletal disease characterized by an imbalance between bone resorption and bone remodeling. Osteoporosis can lead to bone loss and bone microstructural deterioration. This increases the risk of bone fragility and fracture, severely reducing patients' mobility and quality of life. However, the specific molecular mechanisms involved in the development of osteoporosis remain unclear. Increasing evidence suggests that multiple noncoding RNAs show differential expression in the osteoporosis state. Meanwhile, noncoding RNAs have been associated with an increased risk of osteoporosis and fracture. Noncoding RNAs are an important class of factors at the level of gene regulation and are mainly involved in cell proliferation, cell differentiation, and cell death. Programmed cell death is a genetically-regulated form of cell death involved in regulating the homeostasis of the internal environment. Noncoding RNA plays an important role in the programmed cell death process. The exploration of the noncoding RNA-programmed cell death axis has become an interesting area of research and has been shown to play a role in many diseases such as osteoporosis. In this review, we summarize the latest findings on the mechanism of noncoding RNA-mediated programmed cell death on bone homeostasis imbalance leading to osteoporosis. And we provide a deeper understanding of the role played by the noncoding RNA-programmed cell death axis at the gene regulatory level of osteoporosis. We hope to provide a unique opportunity to develop novel diagnostic and therapeutic approaches for osteoporosis.

Roles and mechanisms of copper homeostasis and cuproptosis in osteoarticular diseases.

Copper is an essential trace element in the human body that is extensively distributed throughout various tissues. The appropriate level of copper is crucial to maintaining the life activities of the human body, and the excess and deficiency of copper can lead to various diseases. The copper levels in the human body are regulated by copper homeostasis, which maintains appropriate levels of copper in tissues and cells by controlling its absorption, transport, and storage. Cuproptosis is a distinct form of cell death induced by the excessive accumulation of intracellular copper. Copper homeostasis and cuproptosis has recently elicited increased attention in the realm of human health. Cuproptosis has emerged as a promising avenue for cancer therapy. Studies concerning osteoarticular diseases have elucidated the intricate interplay among copper homeostasis, cuproptosis, and the onset of osteoarticular diseases. Copper dysregulation and cuproptosis cause abnormal bone and cartilage metabolism, affecting related cells. This phenomenon assumes a critical role in the pathophysiological processes underpinning various osteoarticular diseases, with implications for inflammatory and immune responses. While early Cu-modulating agents have shown promise in clinical settings, additional research and advancements are warranted to enhance their efficacy. In this review, we summarize the effects and potential mechanisms of copper homeostasis and cuproptosis on bone and cartilage, as well as their regulatory roles in the pathological mechanism of osteoarticular diseases (e.g., osteosarcoma (OS), osteoarthritis (OA), and rheumatoid arthritis (RA)). We also discuss the clinical-application prospects of copper-targeting strategy, which may provide new ideas for the diagnosis and treatment of osteoarticular diseases.

Phytochemicals against Osteoarthritis by Inhibiting Apoptosis.

Osteoarthritis (OA) is a chronic joint disease that causes pathological changes in articular cartilage, synovial membrane, or subchondral bone. Conventional treatments for OA include surgical and non-surgical methods. Surgical treatment is suitable for patients in the terminal stage of OA. It is often the last choice because of the associated risks and high cost. Medication of OA mainly includes non-steroidal anti-inflammatory drugs, analgesics, hyaluronic acid, and cortico-steroid anti-inflammatory drugs. However, these drugs often have severe side effects and cannot meet the needs of patients. Therefore, safe and clinically appropriate long-term treatments for OA are urgently needed. Apoptosis is programmed cell death, which is a kind of physiologic cell suicide determined by heredity and conserved by evolution. Inhibition of apoptosis-related pathways has been found to prevent and treat a variety of diseases. Excessive apoptosis can destroy cartilage homeostasis and aggravate the pathological process of OA. Therefore, inhibition of apoptosis-related factors or signaling pathways has become an effective means to treat OA. Phytochemicals are active ingredients from plants, and it has been found that phytochemicals can play an important role in the prevention and treatment of OA by inhibiting apoptosis. We summarize preclinical and clinical studies of phytochemicals for the treatment of OA by inhibiting apoptosis. The results show that phytochemicals can treat OA by targeting apoptosis-related pathways. On the basis of improving some phytochemicals with low bioavailability, poor water solubility, and high toxicity by nanotechnology-based drug delivery systems, and at the same time undergoing strict clinical and pharmacological tests, phytochemicals can be used as a potential therapeutic drug for OA and may be applied in clinical settings.

Mathematical modeling of combined therapies for treating tumor drug resistance.

Drug resistance is one of the most intractable issues to the targeted therapy for cancer diseases. To explore effective combination therapy schemes, we propose a mathematical model to study the effects of different treatment schemes on the dynamics of cancer cells. Then we characterize the dynamical behavior of the model by finding the equilibrium points and exploring their local stability. Lyapunov functions are constructed to investigate the global asymptotic stability of the model equilibria. Numerical simulations are carried out to verify the stability of equilibria and treatment outcomes using a set of collected model parameters and experimental data on murine colon carcinoma. Simulation results suggest that immunotherapy combined with chemotherapy contributes significantly to the control of tumor growth compared to monotherapy. Sensitivity analysis is performed to identify the importance of model parameters on the variations of model outcomes.

A Hybrid-Salt Strategy for Modulating the Li+ Solvation Sheathes and Constructing Robust SEI in Non-Flammable Electrolyte Lithium Metal Batteries.

The electrode interface determines the performance of an electrochemical energy storage system. Using traditional electrolyte organic additives and high-concentration electrolyte emerging recently are two generally strategies for improving the electrode interface. Here, a hybrid-salt electrolyte strategy is proposed for constructing the stable electrode interface. Through the solubilization effect of phosphate ester on LiNO3, a hybrid-salts-based non-flammable phosphate ester electrolyte system (HSPE) with LiPF6 and LiNO3 as Li salts has been developed. By the strong interaction between NO3 - and Li+, the Li+ solvation sheath and solvent behaviors have been modulated, thus the undesirable effects of phosphate ester are eliminated and a robust SEI is formed. Experimental results and theoretical calculations illustrate that NO3 - as a kind of strongly coordinating anion can reduce the number of TEP molecules and lower the reduction reactivity of TEP. The reconfigured Li+ solvation structure allows the formation of an inorganic-rich SEI on the electrode surface. As a result, in the designed HSPE, the average coulombic efficiency of lithium plating/stripping is increased to 99.12 %. This work explored a new approach to construct the electrode interface and addressing the poor interface performance issue of phosphate esters.

KLF transcription factors in bone diseases.

Krüppel-like factors (KLFs) are crucial in the development of bone disease. They are a family of zinc finger transcription factors that are unusual in containing three highly conserved zinc finger structural domains interacting with DNA. It has been discovered that it engages in various cell functions, including proliferation, apoptosis, autophagy, stemness, invasion and migration, and is crucial for the development of human tissues. In recent years, the role of KLFs in bone physiology and pathology has received adequate attention. In addition to regulating the normal growth and development of the musculoskeletal system, KLFs participate in the pathological process of the bones and joints and are intimately linked to several skeletal illnesses, such as osteoarthritis (OA), rheumatoid arthritis (RA), osteoporosis (OP) and osteosarcoma (OS). Consequently, targeting KLFs has emerged as a promising therapeutic approach for an array of bone disorders. In this review, we summarize the current literature on the importance of KLFs in the emergence and regulation of bone illnesses, with a particular emphasis on the pertinent mechanisms by which KLFs regulate skeletal diseases. We also discuss the need for KLFs-based medication-targeted treatment. These endeavours offer new perspectives on the use of KLFs in bone disorders and provide prognostic biomarkers, therapeutic targets and possible drug candidates for bone diseases.

Moderate mechanical stress suppresses chondrocyte ferroptosis in osteoarthritis by regulating NF-κB p65/GPX4 signaling pathway.

Ferroptosis is a recently identified form of programmed cell death that plays an important role in the pathophysiological process of osteoarthritis (OA). Herein, we investigated the protective effect of moderate mechanical stress on chondrocyte ferroptosis and further revealed the internal molecular mechanism. Intra-articular injection of sodium iodoacetate (MIA) was conducted to induce the rat model of OA in vivo, meanwhile, interleukin-1 beta (IL-1ß) was treated to chondrocytes to induce the OA cell model in vitro. The OA phenotype was analyzed by histology and microcomputed tomography, the ferroptosis was analyzed by transmission electron microscope and immunofluorescence. The expression of ferroptosis and cartilage metabolism-related factors was analyzed by immunohistochemical and Western blot. Animal experiments revealed that moderate-intensity treadmill exercise could effectively reduce chondrocyte ferroptosis and cartilage matrix degradation in MIA-induced OA rats. Cell experiments showed that 4-h cyclic tensile strain intervention could activate Nrf2 and inhibit the NF-κB signaling pathway, increase the expression of Col2a1, GPX4, and SLC7A11, decrease the expression of MMP13 and P53, thereby restraining IL-1ß-induced chondrocyte ferroptosis and degeneration. Inhibition of NF-κB signaling pathway relieved the chondrocyte ferroptosis and degeneration. Meanwhile, overexpression of NF-κB by recombinant lentivirus reversed the positive effect of CTS on chondrocytes. Moderate mechanical stress could activate the Nrf2 antioxidant system, inhibit the NF-κB p65 signaling pathway, and inhibit chondrocyte ferroptosis and cartilage matrix degradation by regulating P53, SLC7A11, and GPX4.

Comparison of Bone-setting Robots and Conventional Reduction in the Treatment of Intertrochanteric Fracture: A Retrospective Study.

OBJECTIVE: Intertrochanteric fracture of the femur is a common fracture in older people. Due to the poor systemic condition and prognosis of elderly patients, it is prone to more complications. We introduce the bone-setting concept in the design of the robots, which are used for intertrochanteric fracture of the femur reduction. The purpose of this study is to compare the effect of bone-setting robots and conventional reduction in the treatment of intertrochanteric fracture of the femur (IFF). METHODS: From June 2021 to January 2023, 60 patients with IFF who were treated surgically were assigned to bone-setting robots group and conventional reduction methods group in this retrospective study. The reduction time, operation time, total time, intraoperative blood loss, incision length, fluoroscopy time, and the follow-up time were reviewed. The visual analogue scale (VAS) and Harris scores were used for functional assessment. For continuous variables, independent t-tests were applied; for categorical data, the chi-square test was applied. The significance level as p < 0.05. RESULTS: Among the 60 patients with IFF, 31 were assigned to the bone-setting robots group, and 29 were assigned to the conventional reduction methods group. Both groups with a similar baseline in the number, gender, age, and classification (p > 0.05). The reduction time, operation time, total time, intraoperative blood loss, and fluoroscopy time were less than those in the bone-setting robots reduction group compared to the conventional reduction group. In the bone-setting robots reduction group, the preoperative VAS score was 6.2 ± 1.3, the Harris score was 35.3 ± 3.1, 1 week after surgery VAS score was 3.3 ± 1.2, the Harris score was 57.3 ± 3.7, and at the last follow-up VAS score was 2.4 ± 0.8, and the Harris score was 88.7 ± 3.4. While in the conventional reduction group, the preoperative VAS score was 6.3 ± 1.3, the Harris score was 35.9 ± 2.9, 1 week after surgery VAS score was 4.8 ± 1.4, the Harris score was 46.8 ± 2.8, and at the last follow-up VAS score was 2.6 ± 0.8, and the Harris score was 87.3 ± 3.3. There were no significant differences between the two groups at the preoperative and 6-month postoperative follow-ups in VAS score and Harris score (p > 0.05, p > 0.05, respectively). But the difference was statistically significant at the one-week postoperative follow-up in VAS and Harris scores (p < 0.001). CONCLUSION: The bone-setting robots can better protect the "fracture environment" and have the advantages of being precise, minimally invasive, simple, short time, low radiation, and rapid fracture recovery. The clinical effect of closed repair of IFF is ideal.

Role of the Hippo pathway in autoimmune diseases.

The immune system is an important defense against diseases, and it is essential to maintain the homeostasis of the body's internal environment. Under normal physiological conditions, the steady state of the immune system should be sustained to play normal immune response and immune function. Exploring the molecular mechanism of maintaining immune homeostasis under physiological and pathological conditions will provides understanding of the pathogenesis of autoimmune diseases, infections, metabolic disorders, and tumors, as well as new ideas and molecular targets for the prevention and treatment of these diseases. Hippo signaling pathway can not only regulate immune cells such as macrophages, T cells and dendritic cells, but also interact with immune-related signaling pathways such as NF-kB signaling pathway, TGF-ß signaling pathway and Toll-like receptor signaling pathway, so as to resist the internal environment disorder caused by the invasion of exogenous pathogenic microorganisms and maintain the internal environment stability and physiological balance of the body. Hippo signaling pathway is also involved in the pathological process of immune system-related diseases such as rheumatoid arthritis, inflammatory bowel disease and psoriasis. Hippo pathway is closely related to organ development, stem cell biology, regeneration, and tumor biology. It affects cell differentiation by participating in extracellular and intracellular physiological signal reactions, sensing cell environment, and coordinating cell reactions. This pathway is crucial in maintaining immune homeostasis. This review summarizes the mechanism of Hippo pathway in different immune cells and some autoimmune diseases and the interaction between different immune signaling pathways and Hippo signaling pathway. It aims to explore the role of Hippo in autoimmune diseases and provide theoretical and practical basis for the treatment of autoimmune diseases through Hippo signaling pathway.

Recent advances in polymeric microparticle-based drug delivery systems for knee osteoarthritis treatment.

Due to the poor bioavailability and high joint clearance of drugs, sustained delivery of therapeutic agents has proven difficult in the treatment of osteoarthritis (OA). Intra-articular (IA) drug delivery strategy is an attractive option for enhancing OA patients' prognosis, for which various polymer materials have been used as drug carriers due to their attractive delivery properties, to slow or even reverse the progress of OA by prolonging the duration of therapeutic agent residence in the joint. This article focuses on the recent developments in natural and synthetic polymer-based microsphere drug delivery systems for treating knee osteoarthritis. It evaluates the translational potential of some novel formulations for clinical application.

Protective effects of curcumin against osteoporosis and its molecular mechanisms: a recent review in preclinical trials.

Osteoporosis (OP) is one of the most common metabolic skeletal disorders and is commonly seen in the elderly population and postmenopausal women. It is mainly associated with progressive loss of bone mineral density, persistent deterioration of bone microarchitecture, and increased fracture risk. To date, drug therapy is the primary method used to prevent and treat osteoporosis. However, long-term drug therapy inevitably leads to drug resistance and specific side effects. Therefore, researchers are constantly searching for new monomer compounds from natural plants. As a candidate for the treatment of osteoporosis, curcumin (CUR) is a natural phenolic compound with various pharmacological and biological activities, including antioxidant, anti-apoptotic, and anti-inflammatory. This compound has gained research attention for maintaining bone health in various osteoporosis models. We reviewed preclinical and clinical studies of curcumin in preventing and alleviating osteoporosis. These results suggest that if subjected to rigorous pharmacological and clinical trials, naturally-derived curcumin could be used as a complementary and alternative medicine for the treatment of osteoporosis by targeting osteoporosis-related mechanistic pathways. This review summarizes the mechanisms of action and potential therapeutic applications of curcumin in the prevention and mitigation of osteoporosis and provides reference for further research and development of curcumin.

Conservative versus surgical management of isolated O'Driscoll II coronoid fracture: A systematic review.

PURPOSE: The purpose of this systematic review is to summarize the current literature on conservative and surgical management of isolated O'Driscoll II coronoid fracture. STUDY DESIGN: Systematic review. METHODS: We systematically searched Medline, Embase, Google Scholar, and Web of Science databases for published studies by complying with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines and using the keywords "isolated coronoid fracture," "O'Driscoll type 2 coronoid fracture," "anteromedial coronoid fracture," "anteromedial facet coronoid fracture," "posteromedial rotatory instability," and "varus posteromedial rotatory instability." Patients were divided into conservative treatment and surgical treatment groups. Oxford Centre for Evidence-Based Medicine and Methodological Index for Non-Randomized Studies were assessed to determine each article's quality. The primary outcomes of the present reviews were the Mayo elbow performance score (MEPS) and the disabilities of the arm, shoulder, and hand (DASH) score, and the secondary outcomes were associated with complications and reoperations. Eligible trials were independently chosen by two review authors, and a third reviewer resolved all disagreements. RESULTS: The search yielded 458 records, among which 446 articles were of relevance, and 12 were included. In the final review, 138 patients were evaluated-98 (71%) who received surgical treatment and 40 (29%) who received conservative treatment. The mean MEPS score and the DASH score of surgical treatment were 91 and 8, respectively; 69.8% of patients had excellent scores, and 27.0% had good scores. The mean MEPS score and the DASH score of conservative treatment were 92 and 12, respectively; 70.6% of patients had excellent scores, and 23.5% had good scores. CONCLUSIONS: In select cases, conservative treatment can achieve good results in the treatment of isolated O'Driscoll II coronoid fracture when a stricter indication is followed. However, there is insufficient evidence to recommend the appropriate treatment for a particular fracture subtype, and there is a need for more high-quality randomized controlled trials to determine which treatment is superior.

An intrinsic polymer electrolyte via in situ cross-linked for solid lithium-based batteries with high performance.

Since the introduction of poly(ethylene oxide) (PEO)-based polymer electrolytes more than 50 years, few other real polymer electrolytes with commercial application have emerged. Due to the low ion conductivity at room temperature, the PEO-based electrolytes cannot meet the application requirements. Most of the polymer electrolytes reported in recent years are in fact colloidal/composite electrolytes with plasticizers and fillers, not genuine electrolytes. Herein, we designed and synthesized a cross-linked polymer with a three-dimensional (3D) mesh structure which can dissolve the Li bis(trifluoromethylsulfonyl)imide (LiTFSI) salt better than PEO due to its unique 3D structure and rich oxygen-containing chain segments, thus forming an intrinsic polymer electrolyte (IPE) with ionic conductivity of 0.49 mS cm-1 at room temperature. And it can hinder the migration of large anions (e.g. TFSI-) in the electrolyte and increase the energy barrier to their migration, achieving Li+ migration numbers (tLi+) of up to 0.85. At the same time, IPE has good compatibility with lithium metal cathode and LiFePO4 (LFP) cathode, with stable cycles of more than 2,000 and 700 h in Li//Li symmetric batteries at 0.2 and 0.5 mAh cm-2 current densities, respectively. In addition, the Li/IPE/LFP batteries show the capacity retention >90% after 300 cycles at 0.5 C current density. This polymer electrolyte will be a pragmatic way to achieve commercializing all-solid-state, lithium-based batteries.

Two-dimensional memristive hyperchaotic maps with different coupling frames and its hardware implementation.

Continuous-time memristors have been used in numerous chaotic circuit systems. Similarly, the discrete memristor model applied to a discrete map is also worthy of further study. To this end, this paper first proposes a discrete memristor model and analyzes the voltage-current characteristics of the memristor. Also, the discrete memristor is coupled with a one-dimensional (1D) sine chaotic map through different coupling frameworks, and two different two-dimensional (2D) chaotic map models are generated. Due to the presence of linear fixed points, the stability of the 2D memristor-coupled chaotic map depends on the choice of control parameters and initial states. The dynamic behavior of the chaotic map under different coupled map frameworks is investigated by using various analytical methods, and the results show that different coupling frameworks can produce different complex dynamical behaviors for memristor chaotic maps. The dynamic behavior based on parameter control is also investigated. The numerical experimental results show that the change of parameters can not only enrich the dynamic behavior of a chaotic map, but also increase the complexity of the memristor-coupled sine map. In addition, a simple encryption algorithm is designed based on the memristor chaotic map under the new coupling framework, and the performance analysis shows that the algorithm has a strong ability of image encryption. Finally, the numerical results are verified by hardware experiments.

Comparison of buttress plate and cannulated screw in the treatment of anteromedial coronoid fracture with elbow posteromedial rotatory instability.

PURPOSE: The purpose of this study is to compare the effect of buttress plate and cannulated screw in the treatment of anteromedial coronoid fracture with posteromedial rotatory instability (PMRI). METHODS: We retrospectively evaluated patients who were diagnosed with O'Driscoll type 2 fractures combined with elbow posteromedial rotatory instability and underwent surgery for anteromedial coronoid fracture between August 2014 and March 2019. They were divided into buttress plate (n=16) and cannulated screw (n=11) groups. The elbow range of motion, visual analog scale (VAS), Mayo elbow performance score (MEPS), and disabilities of the arm, shoulder, and hand score (DASH) were used for clinical outcome assessment. RESULT: There were no significant differences in clinical outcomes. However, the surgical time was significantly shorter in cannulated screw group (85.45±4.156) compared to the buttress plate group (93.81±8.863, P=0.008), and the surgical time was associated with internal fixation (P=0.008). CONCLUSION: Although there was selection of cases in that small fragments were treated with buttress plate and large fragments with cannulated screw, the buttress plate and cannulated screw have comparable functional outcomes on fixation of the anteromedial coronoid fracture with elbow PMRI. The fixation of the anteromedial coronoid fracture with large fragments using the cannulated screw has a shorter operation time.

Comprehensive analysis of immune implication and prognostic value of DHX33 in sarcoma.

DEAH-box helicase 33 (DHX33) is an RNA helicase that has been identified to promote the progression of a variety of cancers. However, the relationship between DHX33 and sarcoma remains unknown. RNA expression data with clinical information for the sarcoma project was collected from TCGA database. The association between the differential expression of DHX33 and the prognosis for sarcoma was assessed using survival analysis. CIBERSORT was used to evaluate the immune cell infiltration in sarcoma sample tissues. We then further investigated the association between DHX33 and tumor-infiltrating immune cells in sarcoma using the TIMER database. Finally, the immune/cancer-related signaling pathways involved in DHX33 were analyzed using gene set enrichment analysis. High DHX33 expression was discovered to be a poor prognostic indicator in TCGA-SARC. Immune subpopulations in the TCGA-SARC microenvironment are dramatically altered compared to normal tissues. The tumor immune estimation resource analysis revealed a strong correlation between the expression of DHX33 and the abundance of CD8+ T cells and dendritic cells. Changes in copy number also affected neutrophils, macrophages, and CD4+ T cells. According to gene set enrichment analysis, DHX33 may be involved in a number of cancer- and immune-related pathways, such as the JAK/STAT signaling pathway, P53 signaling pathway, chemokine signaling pathway, T cell receptor signaling pathway, complement and coagulation cascades, and cytokine-cytokine receptor interaction. Our study emphasized that DHX33 may be involved in the immune microenvironment of sarcoma and play an important role. As a result, it is possible that DHX33 might serve as an immunotherapeutic target for sarcoma.