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Adverse intrauterine environments can cause persistent changes in epigenetic profiles of stem cells, increasing susceptibility of the offspring to developing metabolic diseases later in life. Effective approaches to restore the epigenetic landscape and function of stem cells remain to be determined. Here we investigated the effects of pharmaceutical activation of AMPK, an essential regulator of energy metabolism, on mitochondrial programming of Wharton's Jelly mesenchymal stem cells (WJ-MSCs) from women with diabetes during pregnancy. Induction of myogenic differentiation of WJ-MSCs was associated with increased PGC-1α expression and mitochondrial DNA abundance. Inhibition of DNA methylation by 5 Azacytidine significantly increased PGC-1α expression and mitochondrial DNA abundance in WJ-MSCs, which were abolished by AMPK inhibitor Compound C (CC), suggesting an AMPK-dependent role of DNA demethylation in regulating mitochondrial biogenesis in WJ-MSCs. Further, activation of AMPK in diabetic WJ-MSCs by AICAR or metformin decreased the level of PGC-1α promoter methylation and increased PGC-1α expression. Notably, decreased PGC-1α promoter methylation by transient treatment of AMPK activators persisted following myogenic differentiation. This was associated with enhanced myogenic differentiation capacity of human WJ-MSCs and increased mitochondrial function. Taken together, our findings revealed an important role for AMPK activators in epigenetic regulation of mitochondrial biogenesis and myogenesis in WJ-MSCs, which could lead to potential therapeutics for preventing fetal mitochondrial programming and long-term adverse outcome in offspring of women with diabetes during pregnancy.

By utilizing the polar symmetry induced by the directional built-in electric field at the MAPbI3 SC/Si heterostructure interface, large polarization ratios of 3.3 at 785 nm and 2.8 at 940 nm are achieved under the self-driven mode.

Coronavirus disease 2019 (COVID-19), an infectious disease caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), is a global pandemic that has high incidence rates, spreads rapidly, and has caused more than 6.5 million deaths globally to date. Currently, several drugs have been used in the clinical treatment of COVID-19, including antivirals (e.g., molnupiravir, baricitinib, and remdesivir), monoclonal antibodies (e.g., etesevimab and tocilizumab), protease inhibitors (e.g., paxlovid), and glucocorticoids (e.g., dexamethasone). Increasing evidence suggests that circulating microRNAs (miRNAs) are important regulators of viral infection and antiviral immune responses, including the biological processes involved in regulating COVID-19 infection and subsequent complications. During viral infection, both viral genes and host cytokines regulate transcriptional and posttranscriptional steps affecting viral replication. Virus-encoded miRNAs are a component of the immune evasion repertoire and function by directly targeting immune functions. Moreover, several host circulating miRNAs can contribute to viral immune escape and play an antiviral role by not only promoting nonstructural protein (nsp) 10 expression in SARS coronavirus, but among others inhibiting NOD-like receptor pyrin domain-containing (NLRP) 3 and IL-1β transcription. Consequently, understanding the expression and mechanism of action of circulating miRNAs during SARS-CoV-2 infection will provide unexpected insights into circulating miRNA-based studies. In this review, we examined the recent progress of circulating miRNAs in the regulation of severe inflammatory response, immune dysfunction, and thrombosis caused by SARS-CoV-2 infection, discussed the mechanisms of action, and highlighted the therapeutic challenges involving miRNA and future research directions in the treatment of COVID-19.

To develop efficient and durable acidic oxygen–reduction–reaction (ORR) catalysts based on all platinum group metals (PGMs) is crucial for large-scale application of proton-exchange membrane fuel cells (PEMFCs) but challenging. Here, we report a nitrogen coordination-induced strong metal–support interaction that can tune the surface atoms of ORR-inactive PGM clusters into efficient and durable active sites. Taking Rh as an example, the carbonization of Rh-overdoped zeolitic imidazolate framework-8 results in a large number of Rh clusters (with a little atomic Rh) in porous nitrogen-doped carbon. The cluster surface atoms coordinate with the nitrogen of the carbon support, forming much stronger metal–support interactions than that of common N-doped carbon-supported metal nanoparticles. The activity of surface-activated Rh clusters is close to that of Pt/C. The regulation rules for the surface active sites inherit most of the characteristics of the corresponding single-atom catalysts, but without their severe instability problem. This surface activation strategy has also shown applicable to other PGMs, thereby it is a promising way to alleviate the reliance of PEMFCs on platinum.

Background By continually monitoring end-tidal carbon dioxide concentrations, capnography can detect abnormal ventilation or apnoea early. This randomized, controlled study explored the effect of early intervention with capnography on the incidence of hypoxia in mildly obese patients undergoing sedation for esophagogastroduodenoscopy (EGD) and colonoscopy. Methods This is a single-center, randomized, single-blind, parallel-assignment, controlled trial. Mildly obese patients (28 kg/m2 ≤ BMI 2) undergoing sedation for EGD and colonoscopy were randomly assigned to either the standard or capnography group. Standard cardiopulmonary monitoring equipment was used in both groups, and additional capnography was performed in the capnography group. In the event of inadequate alveolar ventilation during sedation, five interventions were administered in sequence (a-e) : a: increasing oxygen flow (5 L/min); b: a chin lift or jaw thrust maneuver; c: placement of the nasopharyngeal airway and chin lift; d: mask positive-pressure ventilation, and e: ventilator-assisted ventilation with tube insertion. The primary outcome was the incidence of hypoxia (SpO2 2 ≤ 85%), subclinical respiratory depression (90% ≤ SpO2 2 during operation, patient satisfaction, endoscopist satisfaction, and other adverse events of anesthesia sedation. Results 228 patients were included (capnography group = 112; standard group = 113; three patients were excluded) in this study. The incidence of hypoxia was significantly lower in the capnography group than in the standard group (13.4% vs. 30.1%, P = 0.002). Subclinical respiratory depression in the capnography group was higher than that of the standard group (30.4% vs. 17.7%, P = 0.026). There was only a 5.4% incidence of severe hypoxia in the capnography group compared with 14.2% in the standard group (P = 0.026). During sedation, 96 and 34 individuals in the capnography and standard groups, respectively, underwent the intervention. There was a statistically significant difference (P 2 during operation, patient satisfaction, or endoscopist satisfaction rating. There was no statistically significant difference in adverse events of anesthesia sedation between the two groups. Conclusion Capnography during sedation for EGD and colonoscopy allows for the detection of apnea and altered breathing patterns in mildly obese patients before SpO2 is reduced. Effective intervention measures are given to patients within this time frame, which reduces the incidence of hypoxia and severe hypoxia in patients. Trial registration Ethical approval was granted by the Medical Ethics Committee (Chairperson Professor Tian Hui) of Qilu Hospital, Shandong University ((Ke) Lun Audit 2021 (186)) on 15/07/2021. The study was registered (https://www.chictr.org.cn) on 23/10/2021(ChiCTR2100052234). Designed and reported using CONSORT statements.

Objective: Attention-Deficit/Hyperactivity Disorder (ADHD) are significantly impaired in social relationships, such as poorer parent-child and peer relationships. However, fewer study to explore sibling relationships in ADHD. Thus, this study is to investigate the quality of sibling relationships among firstborn preschooler with ADHD relative to those without ADHD. Methods: This was a population-based cohort study involving 69634 children enrolled in 234 kindergartens in Longhua District of Shenzhen, China. Sibling relationships were assessed with Sibling Inventory of Behavior (SIB) and ADHD symptoms were assessed with the 18-item Swanson, Nolan, and Pelham Rating Scale (SNAP-IV). Logistic regression and ordinal logistic regression models were performed to examine the associations between ADHD symptoms and sibling relationships among preschoolers. Results: This study included 8419 first-born children with siblings. Of them, 831 children (9.87%) have ADHD symptoms. Children with ADHD showed significantly higher scores of negative sibling relationships in rivalry, aggression and avoidance, and significantly lower scores of positive sibling relationships in involvement, empathy and teaching compared to non-ADHD group. Rivalry, aggression and child gender (boys) were positively correlated with children with ADHD, while involvement (companionship), teaching and household income were negatively correlated with children with ADHD. In ordinal logistic regression models, rivalry, aggregation, involvement and teaching entered the model, while rivalry and aggregation were risk factors of ADHD, and involvement and teaching were protective factors of ADHD. Conclusion It is important to pay more attention to the sibling relationships of children with ADHD.

Background: Obesity induces adipose tissue chronic inflammation resulting in insulin resistance and metabolic disorders. With light activation, we recently showed that in situ transplantation of photoactivated adipose-derived stem cells (ASCs) improves glucose metabolism by suppressing adipose tissue macrophages in obese mice. Still, the mechanisms have not been thoroughly investigated. Methods: Cultured ASCs were subjected to light treatment, and exosomes (Exos) were subsequently harvested and injected intraperitoneally into HFD mice. High-throughput miRNA sequencing was performed to detect the miRNA profiles of light-activated ASCs-Exos. The roles of miRNA and target gene were predicted and analyzed in vitro or in vivo by dual-luciferase reporter gene assay, specific miRNA mimic, miRNA inhibitor, and siRNA. Results: We showed that light-activated ASCs produce miRNA-containing exosomes (Exos), which significantly prolonged therapeutic effects on the improvement of obesity-associated insulin tolerance when injected intraperitoneally into obese mice. Mechanistically, light-activated ASCs-Exos shift M1 macrophages toward the M2 via miR-3572-5p–mediated targeting of ELVAL1 in vitro and in vivo. Moreover, miR-3572-5p inhibitor delivery significantly modulated insulin sensitivity and macrophage phenotype. Conclusions: These data suggest that light activation is a simple and effective method for generating the functionality of ASCs-Exos, and miR-3572-5p could be a new therapeutic target of adipose tissue inflammation for insulin resistance. This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Fractures are the dominant conditions for rainfall infiltration into slopes, which can aggravate the instability of landslides. However, few studies have been conducted to analyze in detail the instability and deformation characteristics of creeping landslides with fractures. In view of this, this study investigated a landslide in Fu’ao Village, Wencheng County, Zhejiang Province in China to determine how fractures affect landslide deformation and instability during heavy rainfall through an in situ simulation experiment. In the experiment, three consecutive days of rainfall were set up based on Typhoon Megi in 2016, and two conditions were simulated, namely, rainfall + water filling fractures and rainfall + filled fractures (also referred to as the first and second conditions, respectively). The changes in the volumetric water content (VWC), pore water pressure (PWP), and deep displacement of the landslide at a depth of less than 5 m under the two conditions were observed using field monitoring instruments. The simulation results were as follows: (1) The volumetric water content of the shallow soil showed a more sensitive time-varying response to rainfall, while that of the soil at a depth of more than 200 cm showed a lagged response to rainfall, with a lag of about 10 h, which decreased significantly in the case of the unfilled fractures; (2) Under the first condition, the pore water pressure at different depths showed almost the same changing amplitude of 5 kPa or less. Under the second condition, the pore water pressure increased significantly with depth during the rainfall, with the changing amplitude reaching 30 kPa; (3) The displacement of the borehole equipped with the inclinometers near the front of the slope was higher than that at the borehole equipped with the inclinometers near the rear of the slope. The displacement under the first condition was up to 6 mm, which was significantly greater than that under the second condition. Therefore, fractures have significant effects on the instability of landslides induced by typhoon-triggered rainstorms, and one important measure to prevent and control this type of landslides is to fill fractures in the landslides in time.

In vitro flow cytometric analysis of the effects of folic acid on cellular uptake of the synthesized polymers. Flow cytometry demonstrated equivalent forward shifts in A, 4T1 cells stained with P-Alexa647 and B, 4T1 cells stained with P-Alexa647-FA. Equivalent forward shifts are also seen in C, BMMs stained with Alexa647 and D, BMMs stained with P-Alexa647-FA.

Distribution of clonal abnormalities in cell line 4T1

Representative karyotype from A, 4T1 (MSKCC) and B, 4T1 (ATCC).

Copolymer composition

A summary of P-Alexa647-FA synthesis is shown, with the final molecular struture.

Composite karyotype* of cell line 4T1

Leukocyte immunoglobulin-like receptor B4 (LILRB4) is an inhibitory receptor in the LILR family mainly expressed on normal and malignant human cells of myeloid origin. By binding to ligands, LILRB4 is activated and subsequently recruits adaptors to cytoplasmic immunoreceptor tyrosine inhibitory motifs to initiate different signaling cascades, thus playing an important role in physiological and pathological conditions, including autoimmune diseases, microbial infections, and cancers. In normal myeloid cells, LILRB4 regulates intrinsic cell activation and differentiation. In disease-associated or malignant myeloid cells, LILRB4 is significantly correlated with disease severity or patient survival and suppresses T cells, thereby participating in the pathogenesis of various diseases. In summary, LILRB4 functions as an immune checkpoint on myeloid cells and may be a promising therapeutic target for various human immune diseases, especially for cancer immunotherapy.

Dynamic models play a critical role in the design of model-based controllers, and therefore have a significant effect on the dynamic characteristics of motion equipment. We mainly focus on the dynamic modeling and parameter identification for a gantry-type automated fiber placement (AFP) machine in this paper. First, a dynamic modeling process combining prismatic axes and revolute axes is conducted by the Newton-Euler method, in which the effects of friction and hydraulic balance system are also considered. Then, as the convenience for parameter identification and the application in linearity control, the methods of dynamic model linearization and determination of minimum inertial parameters based on the multi-body system (MBS) theory are proposed, and a dynamic model in the form of linearized minimum inertial parameters is consequently established. To identify the parameters in the model, key issues regarding excitation trajectory, filtering, and identification algorithm are discussed in detail. Finally, corresponding experiments are performed on the AFP machine, and experimental results show that there is a good agreement between the prediction of the model and the measurement in actuality. Data analysis shows that except for Z-axis, the relative error rates of the others are not greater than 5%, which proves the effectiveness of the established dynamic model and the identified parameters.

Plasmodium falciparum causes the most lethal form of malaria. Peroxide antimalarials based on artemisinin underpin the frontline treatments for malaria, but artemisinin resistance is rapidly spreading. Synthetic peroxide antimalarials, known as ozonides, are in clinical development and offer a potential alternative. Here, we used chemoproteomics to investigate the protein alkylation targets of artemisinin and ozonide probes, including an analogue of the ozonide clinical candidate, artefenomel. We greatly expanded the list of protein targets for peroxide antimalarials and identified significant enrichment of redox-related proteins for both artemisinins and ozonides. Disrupted redox homeostasis was confirmed by dynamic live imaging of the glutathione redox potential using a genetically encoded redox-sensitive fluorescence-based biosensor. Targeted LC-MS-based thiol metabolomics also confirmed changes in cellular thiol levels. This work shows that peroxide antimalarials disproportionately alkylate proteins involved in redox homeostasis and that disrupted redox processes are involved in the mechanism of action of these important antimalarials.ImportanceThe frontline treatments for malaria are combination therapies based on the peroxide antimalarial, artemisinin. Concerningly, artemisinin resistance has emerged in malaria-endemic regions, and now poses a major threat to malaria treatment and eradication efforts. New medicines are urgently required to replace the artemisinins, and some of the most advanced candidates are the fully synthetic peroxide antimalarials, OZ277 (arterolane) and OZ439 (artefenomel). The mechanism of action of peroxide antimalarials involves the reductive activation of the peroxide bond by intra-parasitic haem, but there is no consensus regarding the specific protein targets of the resulting radical species for artemisinins and/or the ozonides. This study provides a comprehensive and unbiased chemoproteomic profile of over 400 target proteins, and confirms the specific impact of peroxide antimalarials on redox metabolism. The key role of redox targets is particularly relevant considering that the mechanism of artemisinin resistance appears to involve modulation of peroxide activation and redox homeostasis.

Centimeter-sized high-quality single crystals made into photodetectors exhibited considerable anisotropic properties and sensitive photodetection capabilities under ultraviolet illumination.

The recent advances in the stability of SACs, including the selection of metals and supports, synthetic strategies, and the catalytic stability in electrocatalysis.

This research explored the influence of Nb5+ doping on the electrical properties and microstructure of [0.852(Bi0.5Na0.5)-0.11(Bi0.5K0.5)-0.038Ba]Ti(1-x)NbxO3 (designated as BNKT-BT). The BNKT-BT samples were fabricated and the XRD results showed that the doping of Nb5+ ions induced a transformation from the coexistence of both rhombohedral and tetragonal phase to a single pseudo cubic phase. Also, the doping of Nb5+ ions caused the temperature of ferroelectric state-ergodic relaxor state transition to decrease below the room temperature (RT). The SEM observations showed that the Nb5+ doping had a minor effect on the grain size of BNKT-BT samples. In addition, the samples achieved a large electrostrain of 0.43% (d*33 = Smax/Emax = 614 pm/V) under 7 kV/mm at RT. Moreover, the aging process employed at 80 °C for two weeks in air could effectively increase the electrostrain from 0.38% to 0.41% under 6 kV/mm (d*33 = 683 pm/V) and reduce the strain hysteresis from 57% to 34%. These results indicated that the B site doping, combined with the aging process, could provide an effective way to enhance the electrostrain performance of lead-free piezoelectric ceramics.

The commercialization of proton exchange membrane fuel cells (PEMFCs) could provide a cleaner energy society in the near future. However, the sluggish reaction kinetics and harsh conditions of the oxygen reduction reaction affect the durability and cost of PEMFCs. Most previous reports on Pt-based electrocatalyst designs have focused more on improving their activity; however, with the commercialization of PEMFCs, durability has received increasing attention. In-depth insight into the structural evolution of Pt-based electrocatalysts throughout their lifecycle can contribute to further optimization of their activity and durability. The development of in situ electron microscopy and other in situ techniques has promoted the elucidation of the evolution mechanism. This mini review highlights recent advances in the structural evolution of Pt-based electrocatalysts. The mechanisms are adequately discussed, and some methods to inhibit or exploit the structural evolution of the catalysts are also briefly reviewed.

The recent advancement of nanoparticles (NPs) holds significant potential for treating various ailments. NPs are employed as drug carriers for diseases like cancer because of their small size and increased stability. In addition, they have several desirable properties that make them ideal for treating bone cancer, including high stability, specificity, higher sensitivity, and efficacy. Furthermore, they might be taken into account to permit the precise drug release from the matrix. Drug delivery systems for cancer treatment have progressed to include nanocomposites, metallic NPs, dendrimers, and liposomes. Materials’ mechanical strength, hardness, electrical and thermal conductivity, and electrochemical sensors are significantly improved using nanoparticles (NPs). New sensing devices, drug delivery systems, electrochemical sensors, and biosensors can all benefit considerably from the NPs’ exceptional physical and chemical capabilities. Nanotechnology is discussed in this article from a variety of angles, including its recent applications in the medical sciences for the effective treatment of bone cancers and its potential as a promising option for treating other complex health anomalies via the use of anti-tumour therapy, radiotherapy, the delivery of proteins, antibiotics, and vaccines, and other methods. This also brings to light the role that model simulations can play in diagnosing and treating bone cancer, an area where Nanomedicine has recently been formulated. There has been a recent uptick in using nanotechnology to treat conditions affecting the skeleton. Consequently, it will pave the door for more effective utilization of cutting-edge technology, including electrochemical sensors and biosensors, and improved therapeutic outcomes.

Objectives: Placental inflammation possibly underlies preeclampsia pathogenesis. This study aimed to investigate the expression of the high mobility box group 1 (HMGB1)-toll-like receptor 4 (TLR4) signalling pathway in preeclamptic placentas and determine whether HMGB1 regulates the biological behaviour of trophoblasts in vitro. Design: Placental biopsies were taken from 30 preeclamptic patients and 30 normotensive controls. In vitro experiments were carried out in HTR-8/SVneo human trophoblast cells. Participants/Materials, Setting, Methods: HMGB1, TLR4, and nuclear factor kappa B (NF-κB) mRNA and protein were quantified to compare their expression in human placentas from preeclamptic and normotensive pregnancies. HTR-8/SVneo cells were stimulated with HMGB1 (50 – 400 µg/L) for 6 – 48 h, and proliferation and invasion of HTR-8/SVneo cells were measured via Cell Counting Kit-8 and transwell assays. HTR-8/SVneo cells were also transfected with HMGB1 and TLR4 siRNA to investigate the effect of knocking down these proteins. The mRNA and protein expression of TLR4, NF-κB, and matrix metalloproteinase 9 (MMP-9) were determined using qPCR and western blotting, respectively. Data were analysed with either a t-test or one-way analysis of variance. Results The mRNA and protein levels of HMGB1, TLR4, and NF-κB were significantly higher in the placentas from preeclamptic pregnancies than from normal pregnancies (P < 0.05). HMGB1 stimulation (at concentrations up to 200 µg/L) of HTR-8/SVneo cells significantly increased invasion and proliferation over time. However, at an HMGB1 stimulation concentration of 400 µg/L, the invasion and proliferation ability of HTR-8/SVneo cells decreased. Compared to controls, mRNA and protein expression levels of TLR4, NF-κB, and MMP-9 increased (mRNA level fold change: 1.460, 1.921, 1.667; protein level fold change: 1.600, 1.750, 2.047) when stimulated with HMGB1 (P < 0.05) but decreased when HMGB1 was knocked down (P < 0.05). TLR4 siRNA transfection combined with HMGB1 stimulation reduced the mRNA (fold change: 0.451) and protein (fold change: 0.289) expression of TLR4 (P < 0.05), while NF-κB and MMP-9 were unaffected (P > 0.05). Limitations Only one trophoblast cell line was used in this study, and the findings were not confirmed in animal studies. Conclusions This study explored the pathogenesis of preeclampsia from two aspects: inflammation and trophoblast invasion. The overexpression of HMGB1 in placentas from preeclamptic pregnancies suggests this protein may be involved in preeclampsia pathogenesis. In vitro, HMGB1 was found to regulate the proliferation and invasion of HTR-8/SVneo cells by activating the TLR4-NF-κB-MMP-9 pathway. These findings have implications for targetting HMGB1 could be a therapeutic strategy for treating PE. In the future, we will further verify this in vivo and in other trophoblast cell lines, further exploring the molecular interactions of the pathway.

Atherosclerosis is an early pathological basis of numerous cardiovascular events that result in death or disability. Recent studies have described PCSK9 as a novel target for the treatment of atherosclerosis; PCSK9 is capable of degrading LDLR on the surface of hepatocytes through the regulation of lipid metabolism, and it can function as a novel inflammatory modulator in atherosclerosis. Inflammasomes are important intracellular multiprotein complexes that promote the inflammatory response in atherosclerosis. Among inflammasomes, the NLRP3 inflammasome is particularly notable because of its important role in the development of atherosclerotic disease. After activation, NLRP3 forms a complex with ASC and pro-caspase-1, converting pro-caspase-1 into activated caspase-1, which may trigger the release of IL-1β and IL-18 and contribute to the inflammatory response. Several recent studies have indicated that there may be interactions between PCSK9 and the NLRP3 inflammasome, which may contribute to the inflammatory response that drives atherosclerosis development and progression. On the one hand, the NLRP3 inflammasome plays an important role via IL-1β in regulating PCSK9 secretion. On the other hand, PCSK9 regulates caspase-1-dependent pyroptosis by initiating mtDNA damage and activating NLRP3 inflammasome signaling. This paper reviews the mechanisms underlying PCSK9 and NLRP3 inflammasome activation in the context of atherosclerosis. Furthermore, we describe the current understanding of the specific molecular mechanism underlying the interactions between PCSK9 and NLRP3 inflammasome signaling as well as the drug repositioning events that influence vascular cells and exert beneficial antiatherosclerotic effects. This review may provide a new therapeutic direction for the effective prevention and treatment of atherosclerosis in the clinic.

Background Severe hindlimb ischemia is a chronic disease with poor prognosis that can lead to amputation or even death. This study aimed to assess the therapeutic effect of liraglutide on hind‐limb ischemia in type 2 diabetic mice and to elucidate the underlying mechanism. Methods and Results Blood flow reperfusion and capillary densities after treatment with liraglutide or vehicle were evaluated in a mouse model of lower‐limb ischemia in a normal background or a background of streptozotocin‐induced diabetes. The proliferation, migration, and tube formation of human umbilical vein endothelial cells were analyzed in vitro upon treatment with liraglutide under normal‐glucose and high‐glucose conditions. Levels of phospho‐Akt, phospho‐endothelial nitric oxide synthase, and phospho‐extracellular signal‐related kinases 1 and 2 under different conditions in human umbilical vein endothelial cells and in ischemic muscle were determined by western blotting. Liraglutide significantly improved perfusion recovery and capillary density in both nondiabetic and diabetic mice. Liraglutide also promoted, in a concentration‐dependent manner, the proliferation, migration, and tube formation of normal glucose– and high glucose–treated human umbilical vein endothelial cells, as well as the phosphorylation of Akt, endothelial nitric oxide synthase, and extracellular signal‐related kinases 1 and 2 both in vitro and in vivo. The liraglutide antagonist exendin (9–39) reversed the promoting effects of liraglutide on human umbilical vein endothelial cell functions. Furthermore, exendin (9–39), LY294002, and PD98059 blocked the liraglutide‐induced activation of Akt/endothelial nitric oxide synthase and extracellular signal‐related kinases 1 and 2 signaling pathways. Conclusions These studies identified a novel role of liraglutide in modulating ischemia‐induced angiogenesis, possibly through effects on endothelial cell function and activation of Akt/endothelial nitric oxide synthase and extracellular signal‐related kinases 1 and 2 signaling, and suggested the glucagon‐like peptide‐1 receptor may be an important therapeutic target in diabetic hind‐limb ischemia.

Platinum-based catalysts are widely used for efficient catalysis of the acidic oxygen reduction reaction (ORR). However, the agglomeration and leaching of metallic Pt nanoparticles limit the catalytic activity and durability of the catalysts and restrict their large-scale commercialization. Therefore, this study aimed to achieve a uniform distribution and strong anchoring of Pt nanoparticles on a carbon support and improve the ORR activity and durability of proton-exchange membrane fuel cells. Herein, we report on the facile one-pot synthesis of a novel ORR catalyst using metal–nitrogen–carbon (M–N–C) bonding, which is formed in situ during the ion exchange and pyrolysis processes. An ion-exchange resin was used as the carbon source containing R-N+(CH3)3 groups, which coordinate with PtCl62− to form nanosized Pt clusters confined within the macroporous framework. After pyrolysis, strong M-N-C bonds were formed, thereby preventing the leaching and aggregation of Pt nanoparticles. The as-synthesized Pt supported on the N-doped hierarchically porous carbon catalyst (Pt/NHPC-800) showed high specific activity (0.3 mA cm−2) and mass activity (0.165 A mgPt−1), which are approximately 2.7 and 1.5 times higher than those of commercial Pt/C, respectively. The electrochemical surface area of Pt/NHPC-800 remained unchanged (~1% loss) after an accelerated durability test of 10,000 cycles. The mass activity loss after ADT of Pt/NHPC-800 was 18%, which is considerably lower than that of commercial Pt/C (43%). Thus, a novel ORR catalyst with highly accessible and homogeneously dispersed Pt-N-C sites, high activity, and durability was successfully prepared via one-pot synthesis. This facile and scalable synthesis strategy for high-efficiency catalysts guides the further synthesis of commercially available ORR catalysts.

ObjectiveTo observe and analyze the surgical efficacy of arthroscopic debridement of calcified deposits and arthroscopic debridement combined with subacromial decompression in patients with supraspinatus tendon calcific myositis. To observe the effect of Subacromial decompression on the efficacy of arthroscopic treatment of shoulder calcific tendinitis.Patients and methodsFrom 2016 to 2021, 48 cases of shoulder arthroscopic debridement due to supraspinatus calcific tendinitis met the inclusion criteria and were included, with 24 cases assigned to the arthroscopic debridement group and 24 cases to the arthroscopic debridement combined with subacromial decompression group. Changes between preoperative and postoperative shoulder pain and shoulder function were statistically analyzed.ResultsThe 24 patients in the arthroscopic debridement group were better than the arthroscopic debridement combined with subacromial decompression group in terms of short-term postoperative shoulder pain and shoulder joint function recovery (P P > 0.05).ConclusionsCompared with arthroscopic debridement combined with subacromial decompression, arthroscopic debridement alone is a better surgical option for the treatment of calcific tendinitis.

Methylammonium lead iodide (MAPbI

The development of polymer-based composites with self-healing and recyclable capability has attracted the attention of several researchers for resource recycling and environment protection. In this work, Halloysite nanotubes (HNTs) reinforced polyurethane materials (PU) with self-healing and recyclable ability were constructed by in situ polymerization method. The mechanical, thermal amd morphological properties of PU and related composites were studied. The morphology of samples fracture surface ensured the homogeneous dispersion of HNTs in the polymer matrix. Moreover, thermal stability was improved with the incorporation of the HNTs. The tensile test showed strength increased with HNTs content increased. The tensile strength of composites increases from 23.38 to 34.92 MPa at 2 wt% HNTs. Therefore, the designed strategy provides a simple approach for preparing high mechanical properties, reprocessing and self-healing ability polyurethane composites.