Search

A new binder, poly(2-propenoic acid, 2-methyl-, 3-[(2-aminoethyl) amino]-2-hydroxypropyl ester) (P-HAEAPMA), is synthesized and applied to silicon/graphite (Si/graphite) anodes in lithium-ion batteries. The Si/graphite anode with the binder exhibits good electrochemical stability. Furthermore, the materials on the discarded Si/graphite/P-HAEAPMA electrode can be recycled for use based on water because the P-HAEAPMA binder is easily soluble in water. The discharge capacity and capacity retention rate of the electrode with reused materials are slightly lower than those of the original Si/graphite/P-HAEAPMA electrode. The binder is rich in polar amino and hydroxyl groups, which not only helps to form strong adhesion between the electrode active material and copper foil but also promotes the transport of Li ions. The electrochemical performance of the electrode with the P-HAEAPMA binder is significantly enhanced compared with that of the electrode with the traditional PVDF binder or water-based LA133 binder. After 305 cycles, a specific capacity of 485.0 mA h g−1 and a capacity retention rate of 74.8% are achieved for the Si/graphite/P-HAEAPMA electrode. A binder, poly(2-propenoic acid, 2-methyl-, 3-[(2-aminoethyl) amino]-2-hydroxypropyl ester) (P-HAEAPMA), is synthesized and applied to silicon/graphite anodes in lithium-ion batteries, which exhibits good electrochemical stability. After 305 cycles, a specific capacity of 485.0 mA h g−1 and a capacity retention rate of 74.8% are achieved. Moreover, the discarded electrode with P-HAEAPMA binder can be reused just based on water because the P-HAEAPMA binder is easily soluble in water, and the electrochemical properties of the electrode with reused materials are slightly lower than those of the original electrode.

Additional file 1. SPIRIT Checklist for Trials.

Additional file 1: Fig. S1. The generation principle and identification of TRPC6 knockout mice. (A) The generation principle of TRPC6 knockout mice. (B) The scheme for identifying the genotype of TRPC6 knockout mice (C) The results of real-time PCR showed that the expression of TRPC6 was knocked out in mBMSCs from TRPC6 knockout mice. Fig. S2. PCA, cluster and heatmap analyses under stress conditions. (A) PCA under tension. (B) PCA under compression. (C) Cluster analysis under tension. (D) Cluster analysis under compression. (E) Heatmap analysis under tension. (F) Heatmap analysis under compression. Fig. S3. Mechanical force upregulated TRPC4 expression in periodontal ligament stem cells. (A) The expression of TRPC4 as determined by western blotting and quantitative analysis of TRPC6 expression in hPDLSCs are shown. (B) The expression of TRPC4 increased after orthodontic force application in rats; a representative image of TRPC4 immunohistochemical staining on the tension and compression sides of molars subjected to orthodontic force is shown. The black arrow indicates the direction of orthodontic force. Black scale bar, 1 mm; White scale bar, 500 μm; Blue scale bar, 200 μm; Semiquantitative analysis of TRPC4-positive cells. The results are expressed as the mean ± standard deviation of three independent experiments. *P < 0.05; ***P < 0.001.

Qingqing Chen,1,2 Xinxin Han,2 Meihua Chen,2,3 Bingjiao Zhao,1,2 Bingjing Sun,1,2 Liangyan Sun,1,2 Weihua Zhang,1,2 Liming Yu,1,2 Yuehua Liu1,2 1Department of Orthodontics, Shanghai Stomatological Hospital, Fudan University, Shanghai, People’s Republic of China; 2Shanghai Key Laboratory of Craniomaxillofacial Development and Diseases, Fudan University, Shanghai, People’s Republic of China; 3Department of Periodontology, Shanghai Stomatological Hospital, Fudan University, Shanghai, People’s Republic of ChinaCorrespondence: Yuehua Liu; Liming YuShanghai Stomatological Hospital, Fudan University, No. 356 East Beijing Road, Shanghai, 200001, People’s Republic of ChinaTel +86 2163298475Fax +86 2163614515Email liuyuehua@fudan.edu.cn; ylmphoebe@126.comPurpose: Obesity is a worldwide metabolic disease and a critical risk factor for several chronic conditions. Obstructive sleep apnea (OSA) is an important complication of obesity. With the soaring morbidity of obesity, the prevalence of OSA has markedly increased. However, the underlying mechanism of the high relevance between obesity and OSA has not been elucidated. This study investigated the effects of obesity on the structure and function of the genioglossus to explore the possible mechanisms involved in OSA combined with obesity.Methods: Six-week-old male C57BL/6J mice were fed high-fat diet (HFD, 60% energy) or normal diet (Control, 10% energy) for 16 weeks. The muscle fibre structure and electromyography (EMG) activity of genioglossus were measured. The ultrastructure and function of mitochondrial, oxidative damage and apoptosis in genioglossus were detected by transmission electron microscopy (TEM), qPCR, Western blotting, immunohistochemistry and TUNEL staining. We further studied the influence of palmitic acid (PA) on the proliferation and myogenic differentiation of C2C12 myoblasts, as well as mitochondrial function, oxidative stress, and apoptosis in C2C12 myotubes.Results: Compared with the control, the number of muscle fibres was decreased, the fibre type was remarkably changed, and the EMG activity had declined in genioglossus. In addition, a HFD also reduced mitochondria quantity and function, induced excessive oxidative stress and increased apoptosis in genioglossus. In vitro, PA treatment significantly inhibited the proliferation and myogenic differentiation of C2C12 myoblasts. Moreover, PA decreased the mitochondrial membrane potential, upregulated mitochondrial reactive oxygen species (ROS) levels, and activated the mitochondrial-related apoptotic pathway in myotubes.Conclusion: Our findings suggest that a HFD caused genioglossus injury in obese mice. The mitochondrial dysfunction and the accompanying oxidative stress were involved in the genioglossus injury, which may provide potential therapeutic targets for OSA with obesity.Keywords: obesity, obstructive sleep apnea, genioglossus, muscle, mitochondria

Background: A proper stem cell source is key to muscle injury repair. Dental pulp stem cells (DPSCs) are an available source for the treatment of muscle injury due to their high reproductive and differential activities. However, the application of DPSCs in muscle regeneration is incompletely understood. Noggin, a secreted BMP antagonist promoted by Wnt-1, is required for embryonic myogenesis. Our research is to study whether Noggin can promote myogenic differentiation of DPSCs, and then to investigate the repair effect of Noggin combined with DPSCs in muscle injury.Methods: DPSCs were treated with Noggin to induce myogenic differentiation in vitro. The levels of myogenic markers (MyoD, Desmin, MRF4 and MyHC), and satellite cell markers (Pax3, Pax7, Six1 and Eya2) were detected during this process. Next, we blocked the effect of Noggin by adding BMP, and Samd phosphorylation level was tested. Then, we implanted Noggin-pretreated DPSC combined Matrigel into the mouse tibialis anterior muscle with volumetric muscle loss (VML). After 30-day recovery, morphometric analysis of the tibialis anterior muscle was performed.Results: Noggin effectively increased myotube formation in DPSCs. We also found Noggin accelerated the skeletal myogenic differentiation of DPSCs and promote Pax7+ satellite-like cell generation. These satellite-like cells had the capacity to generate myofibers and could self-renew. Pax7 and Pax3 levels were repressed when blocked the effect of Noggin by adding BMP, and Noggin eliminated the level of BMP/Smad phosphorylation. This suggested that Noggin facilitated the skeletal myogenic differentiation of DPSCs via Smad/Pax7 pathway. Morphometric analysis of muscle cross-sections revealed that DPSCs therapy could increase repair size and decrease scar tissue in tibialis anterior muscle of VML. Moreover, Noggin-treated DPSCs can benefit to Pax7+ satellite cell pool and promote muscle regeneration. Conclusions: This work reveals that Noggin can promote the generation of satellite-like cells for the myogenic process in DPSCs through Smad/Pax7 signaling pathway, and these satellite-like cells bioconstructs might possess a relatively fast capacity to regenerate for muscle injury.

Background: As the last link in the chain of cardiovascular events, chronic heart failure (CHF) has high morbidity, high mortality, and poor prognosis. It is one of the main causes of death and disability worldwide. As a new drug for the treatment of chronic cardiovascular disease, dapagliflozin, the efficacy, and safety issues are still the focus of attention. Therefore, we conducted a meta-analysis to evaluate the efficacy and safety of dapagliflozin in the treatment of CHF. Methods: According to the search strategy, regardless of publication date or language, randomized controlled trials (RCTs) of dapagliflozin for CHF will be retrieved from 8 databases. First of all, the literature was screened according to the eligibility criteria, and use the Cochrane Collaboration's tool to assess the quality of the included literature. Then, using Rev Man 5.3 and STATA 14.2 software for traditional meta-analysis. Finally, the evaluation of the quality of the evidence and the strength of the recommendations will adopt the Grading of Recommendations, Assessment, Development and Evaluation method. Results: This study will evaluate the efficacy and safety of dapagliflozin for CHF, thereby providing more evidence support for clinical decision-making in CHF. Conclusion: Our research will provide more references for the clinical medication of patients with CHF. Protocol registration number: INPLASY202150046