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Abstract Background The initial randomized, double‐blinded, actively controlled, phase III ANEAS study (NCT03849768) demonstrated that aumolertinib showed superior efficacy relative to gefitinib as first‐line therapy in epidermal growth factor receptor (EGFR)‐mutated advanced non‐small cell lung cancer (NSCLC). Metastatic disease in the central nervous system (CNS) remains a challenge in the management of NSCLC. This study aimed to compare the efficacy of aumolertinib versus gefitinib among patients with baseline CNS metastases in the ANEAS study. Methods Eligible patients were enrolled and randomly assigned in a 1:1 ratio to orally receive either aumolertinib or gefitinib in a double‐blinded fashion. Patients with asymptomatic, stable CNS metastases were included. Follow‐up imaging of the same modality as the initial CNS imaging was performed every 6 weeks for 15 months, then every 12 weeks. CNS response was assessed by a neuroradiological blinded, independent central review (neuroradiological‐BICR). The primary endpoint for this subgroup analysis was CNS progression‐free survival (PFS). Results Of the 429 patients enrolled and randomized in the ANEAS study, 106 patients were found to have CNS metastases (CNS Full Analysis Set, cFAS) at baseline by neuroradiological‐BICR, and 60 of them had CNS target lesions (CNS Evaluable for Response, cEFR). Treatment with aumolertinib significantly prolonged median CNS PFS compared with gefitinib in both cFAS (29.0 vs. 8.3 months; hazard ratio [HR] = 0.31; 95% confidence interval [CI], 0.17‐0.56; P < 0.001) and cEFR (29.0 vs. 8.3 months; HR = 0.26; 95% CI, 0.11‐0.57; P < 0.001). The confirmed CNS overall response rate in cEFR was 85.7% and 75.0% in patients treated with aumolertinib and gefitinib, respectively. Competing risk analysis showed that the estimated probability of CNS progression without prior non‐CNS progression or death was consistently lower with aumolertinib than with gefitinib in patients with and without CNS metastases at baseline. No new safety findings were observed. Conclusions These results indicate a potential advantage of aumolertinib over gefitinib in terms of CNS PFS and the risk of CNS progression in patients with EGFR‐mutated advanced NSCLC with baseline CNS metastases. Trial registration ClinicalTrials.gov number, NCT03849768

Abstract Generating co‐speech gestures for interactive digital humans remains challenging because of the indeterministic nature of the problem. The authors observe that gestures generated from speech audio or text by existing neural methods often contain less movement shift than expected, which can be viewed as slow or dull. Thus, a new generative model coupled with memory networks as dynamic dictionaries for speech‐driven gesture generation with improved diversity is proposed. More specifically, the dictionary network dynamically stores connections between text and pose features in a list of key‐value pairs as the memory for the pose generation network to look up; the pose generation network then merges the matching pose features and input audio features for generating the final pose sequences. To make the improvements more accurately measurable, a new objective evaluation metric for gesture diversity that can remove the influence of low‐quality motions is also proposed and tested. Quantitative and qualitative experiments demonstrate that the proposed architecture succeeds in generating gestures with improved diversity.

Abstract The Equilibrium Optimiser (EO) has been demonstrated to be one of the metaheuristic algorithms that can effectively solve global optimisation problems. Balancing the paradox between exploration and exploitation operations while enhancing the ability to jump out of the local optimum are two key points to be addressed in EO research. To alleviate these limitations, an EO variant named adaptive elite‐guided Equilibrium Optimiser (AEEO) is introduced. Specifically, the adaptive elite‐guided search mechanism enhances the balance between exploration and exploitation. The modified mutualism phase reinforces the information interaction among particles and local optima avoidance. The cooperation of these two mechanisms boosts the overall performance of the basic EO. The AEEO is subjected to competitive experiments with state‐of‐the‐art algorithms and modified algorithms on 23 classical benchmark functions and IEE CEC 2017 function test suite. Experimental results demonstrate that AEEO outperforms several well‐performing EO variants, DE variants, PSO variants, SSA variants, and GWO variants in terms of convergence speed and accuracy. In addition, the AEEO algorithm is used for the edge server (ES) placement problem in mobile edge computing (MEC) environments. The experimental results show that the author’s approach outperforms the representative approaches compared in terms of access latency and deployment cost.

Abstract Due to the richness of natural image semantics, natural image colourisation is a challenging problem. Existing methods often suffer from semantic confusion due to insufficient semantic understanding, resulting in unreasonable colour assignments, especially at the edges of objects. This phenomenon is referred to as colour bleeding. The authors have found that using the self‐attention mechanism benefits the model's understanding and recognition of object semantics. However, this leads to another problem in colourisation, namely dull colour. With this in mind, a Position‐Spatial Attention Network(PSANet) is proposed to address the colour bleeding and the dull colour. Firstly, a novel new attention module called position‐spatial attention module (PSAM) is introduced. Through the proposed PSAM module, the model enhances the semantic understanding of images while solving the dull colour problem caused by self‐attention. Then, in order to further prevent colour bleeding on object boundaries, a gradient‐aware loss is proposed. Lastly, the colour bleeding phenomenon is further improved by the combined effect of gradient‐aware loss and edge‐aware loss. Experimental results show that this method can reduce colour bleeding largely while maintaining good perceptual quality.

Abstract The threat of long‐term low wind output processes (LWOP) on the supply ability of the power system is escalating with the increasing integration of wind power. Accurate prediction of LWOP is crucial for maintaining the stable operation of the power system. However, the occurrence probability of LWOP is low and the available samples are lacking, limiting the high‐accuracy predictive modeling of LWOP. Therefore, a novel prediction method for LWOP under very few samples based on improved Wasserstein deep convolutional generative adversarial networks (W‐DCGAN) is proposed here. Firstly, a multi‐dimensional identification method is proposed to accurately identify historical LWOP. Then, an LWOP sample generation model based on improved W‐DCGAN is established. The model integrates a long short‐term memory layer into the deconvolutional layer of the generator to enhance the temporal characteristics of generated samples. Finally, three prediction algorithms are used to construct LWOP prediction models based on both generated and actual samples, respectively. The wind power operation data from a province in China is taken as an example to verify the effectiveness of the proposed method. The results show that the prediction accuracy of LWOP can be improved by 14.36%–55.85%.

Abstract Multi‐energy microgrids (MEMG) have become an effective means of integrated energy management due to their unique advantages, including area independence, diverse supply, flexibility, and efficiency. However, the uncertain deviation of the renewable energy generators (REGs) output and the uncertain deviation of the multiple energy load response cumulatively lead to the deterioration of the MEMG model performance. To address these issues, this article proposes a cooperative forecasting management model for MEMG that considers multiple uncertainties and load response knowledge characterization. The model combines a multi‐energy load prediction model with a management model based on deep reinforcement learning. It proposes multiple iterations of data, fits the dynamic environment of MEMG by continuously improving the long short‐term memory (LSTM) neural network based on knowledge distillation (KD) architecture, and then optimizes the MEMG state space by considering the knowledge of load response characteristics, Furthermore, it combines multi‐agent deep deterministic policy gradient (MADDPG) with horizontal federated (hF) learning to co‐train multi‐MEMG, addressing the issues of training efficiency during co‐training. Finally, the validity of the proposed model is demonstrated by an arithmetic example.

Abstract Background To explore the utility of 5.0T ultra‐high field magnetic resonance (MR) for the assessment of the superior cerebellar artery (SCA). Methods Imaging data from 55 patients (19 men and 36 women) who underwent three‐dimensional time of flight MR angiography (3D‐TOF‐MRA) with 5.0T MRI in the Shandong University Affiliated Shandong Provincial Third Hospital from May 22, 2023 to June 16, 2023 were retrospectively analyzed. The origin, caliber, and course of the SCA were recorded. An independent sample t‐test was used to compare the differences in quantitative indexes between the two groups. Results A total of 123 superior cerebellar arteries were detected in 55 patients. We found that 86.99% of superior cerebellar arteries were longer than the P3 segment of the posterior cerebral artery. The superior cerebellar arteries were divided into nine types according to the origin of the SCA, with Type A accounting for the highest proportion (approximately 49.09%). The mean diameter of the SCA was 1.11 ± 0.22 mm, while the mean diameters of the right and left sides were 1.13 ± 0.24 mm and 1.07 ± 0.27 mm, respectively. There were no differences in SCA diameters between the two sides (p > 0.05). Conclusions 3D‐TOF‐MRA with ultra‐high field 5.0T MR can effectively evaluate the SCA, and provides a new effective imaging evaluation method for clinical practice.

Abstract Background The integration of 7 Tesla (7T) magnetic resonance imaging (MRI) with advanced multimodal artificial intelligence (AI) models represents a promising frontier in neuroimaging. The superior spatial resolution of 7TMRI provides detailed visualizations of brain structure, which are crucial forunderstanding complex central nervous system diseases and tumors. Concurrently, the application of multimodal AI to medical images enables interactive imaging‐based diagnostic conversation. Methods In this paper, we systematically investigate the capacity and feasibility of applying the existing advanced multimodal AI model ChatGPT‐4V to 7T MRI under the context of brain tumors. First, we test whether ChatGPT‐4V has knowledge about 7T MRI, and whether it can differentiate 7T MRI from 3T MRI. In addition, we explore whether ChatGPT‐4V can recognize different 7T MRI modalities and whether it can correctly offer diagnosis of tumors based on single or multiple modality 7T MRI. Results ChatGPT‐4V exhibited accuracy of 84.4% in 3T‐vs‐7T differentiation and accuracy of 78.9% in 7T modality recognition. Meanwhile, in a human evaluation with three clinical experts, ChatGPT obtained average scores of 9.27/20 in single modality‐based diagnosis and 21.25/25 in multiple modality‐based diagnosis. Our study indicates that single‐modality diagnosis and the interpretability of diagnostic decisions in clinical practice should be enhanced when ChatGPT‐4V is applied to 7T data. Conclusions In general, our analysis suggests that such integration has promise as a tool to improve the workflow of diagnostics in neurology, with a potentially transformative impact in the fields of medical image analysis and patient management.

Abstract Background Concurrent chemoradiotherapy (CCRT) is the standard treatment for locally advanced esophageal squamous cell carcinoma (ESCC). However, the optimal radiotherapy regimen, particularly in terms of total dose and planned range of irradiation field, remains unclear. This phase III clinical trial aimed to compare the survival benefits between different radiation doses and different target fields. Methods This trial compared two aspects of radiation treatment, total dose and field, using a two‐by‐two factorial design. The high‐dose (HD) group received 59.4 Gy radiation, and the standard‐dose (SD) group received 50.4 Gy. The involved field irradiation (IFI) group and elective nodal irradiation (ENI) group adopted different irradiation ranges. The participants were assigned to one of the four groups (HD+ENI, HD+IFI, SD+ENI and SD+IFI). The primary endpoint was overall survival (OS), and the secondary endpoints included progression‐free survival (PFS). The synergy indexwas used to measure the interaction effect between dose and field. Results The interaction analysis did not reveal significant synergistic effects between the dose and irradiation field. In comparison to the target field, patients in IFI or ENI showed similar OS (hazard ratio [HR] = 0.99, 95% CI: 0.80‐1.23, p = 0.930) and PFS (HR = 1.02, 95% CI: 0.82–1.25). The HD treatment did not show significantly prolonged OS compared with SD (HR = 0.90, 95% CI: 0.72–1.11, p = 0.318), but it suggested improved PFS (25.2 months to 18.0 months). Among the four groups, the HD+IFI group presented the best survival, while the SD+IFI group had the worst prognosis. No significant difference in the occurrence of severe adverse events was found in dose or field comparisons. Conclusions IFI demonstrated similar treatment efficacy to ENI in CCRT of ESCC. The HD demonstrated improved PFS, but did not significantly improve OS. The dose escalation based on IFI (HD+IFI) showed better therapeutic efficacy than the current recommendation (SD+ENI) and is worth further validation.

Abstract Background In the era of immunotherapy, neoadjuvant immunochemotherapy (NAIC) for the treatment of locally advanced esophageal squamous cell carcinoma (ESCC) is used clinically but lacks of high‐level clinical evidence. This study aimed to compare the safety and long‐term efficacy of NAIC followed by minimally invasive esophagectomy (MIE) with those of neoadjuvant chemotherapy (NAC) followed by MIE. Methods A prospective, single‐center, open‐label, randomized phase III clinical trial was conducted at Henan Cancer Hospital, Zhengzhou, China. Patients were randomly assigned to receive either neoadjuvant toripalimab (240 mg) plus paclitaxel (175 mg/m2) + cisplatin (75 mg/m2) (toripalimab group) or paclitaxel + cisplatin alone (chemotherapy group) every 3 weeks for 2 cycles. After surgery, the toripalimab group received toripalimab (240 mg every 3 weeks for up to 6 months). The primary endpoint was event‐free survival (EFS). The pathological complete response (pCR) and overall survival (OS) were key secondary endpoints. Adverse events (AEs) and quality of life were also assessed. Results Between May 15, 2020 and August 13, 2021, 252 ESCC patients ranging from T1N1‐3M0 to T2‐3N0‐3M0 were enrolled for interim analysis, with 127 in the toripalimab group and 125 in the chemotherapy group. The 1‐year EFS rate was 77.9% in the toripalimab group compared to 64.3% in the chemotherapy group (hazard ratio [HR] = 0.62; 95% confidence interval [CI] = 0.39 to 1.00; P = 0.05). The 1‐year OS rates were 94.1% and 83.0% in the toripalimab and chemotherapy groups, respectively (HR = 0.48; 95% CI = 0.24 to 0.97; P = 0.037). The patients in the toripalimab group had a higher pCR rate (18.6% vs. 4.6%; P = 0.001). The rates of postoperative Clavien‐Dindo grade IIIb or higher morbidity were 9.8% in the toripalimab group and 6.8% in the chemotherapy group, with no significant difference observed (P = 0.460). The rates of grade 3 or 4 treatment‐related AEs did not differ between the two groups (12.5% versus 12.4%). Conclusions The interim results of this ongoing trial showed that in resectable ESCC, the addition of perioperative toripalimab to NAC is safe, may improve OS and might change the standard treatment in the future.

Abstract Various digital therapeutic products have been validated and approved since 2017. They have demonstrated efficacy and safety as a new therapeutic modality in various disorders or conditions. Hypertension is a common but serious condition that can be prevented or controlled with lifestyle changes and medicines. Although a digital therapeutic in hypertension is validated and approved in Japan, whether digital therapeutics (DTx) can significantly improve sustainable lifestyle changes is still a controversial topic. Most studies did not discuss the long‐term gain challenges. In this review, the authors discuss the definition of DTx, and analyze the motivation, engagement and adherence challenges of DTx in hypertension. Some ongoing artificial intelligence (AI)‐enabled or cognitive behavioral therapy (CBT)‐based digital interventions and behavioral strategies for implementing sustainable lifestyle changes are identified and analyzed. With AI‐enabled interventions and behavioral strategies, DTx might be one of the effective approaches to make sustainable lifestyle changes.

Objective Multitargeted tyrosine kinase inhibitors (TKIs) have been approved as second‐line therapy in refractory sarcoma, prolonging progression‐free survival (PFS) but with short‐lived duration of disease control. Fruquintinib is a TKI that specifically inhibits vascular endothelial growth factor receptor‐1,2,3 with no metabolism by liver enzymes. In this retrospective study, we assessed the efficacy and safety of fruquintinib‐based treatment in patients with refractory sarcoma after developing several lines of TKI resistance. Methods We retrospectively analyzed the clinical data of patients with refractory sarcoma after they had developed several lines of resistance to TKIs and who received fruquintinib‐based treatment from November 2021 to August 2023. The primary endpoint was the progression‐free survival rate at 4 months (4m‐PFSR). Secondary endpoints were the median PFS, overall survival (OS), objective response rate, disease control rate, and adverse effects (AEs). PFS and OS were estimated using the Kaplan–Meier method. A log‐rank test was used to compare survival curves between different clinical and pathological factors. Cox proportional hazards analysis was performed to identify PFS‐related prognostic factors. Results We included 124 patients: 56 (45.2%) with osteosarcoma, 28 (22.6%) with Ewing sarcoma, seven (5.6%) with chondrosarcoma, and 33 (26.6%) with soft tissue sarcomas (STS). Only 18 (14.5%) patients received monotherapy with fruquintinib. With a median follow‐up time of 6.8 (interquartile range [IQR], 4.6–9.4) months, 22 (17.7%) patients had partial response and 78 (62.9%) had stable disease. The 4m‐PFSR was 58.4% (95% confidence interval [CI], 49.6%–67.1%). The median PFS and OS were 4.4 (95% CI, 3.9–5.0) months and 11.4 (95% CI, 10.3–12.5) months. In multivariate analysis, a high hazard ratio for progression was associated with target lesions located outside the lung and bone with 1.79 (95% CI, 1.10–2.93; p = 0.020). Eighty‐eight AEs were recorded in 47 (37.9%) patients; the most common were pneumothorax (18/124, 14.5%), diarrhea (8/124, 6.5%), oral mucositis (7/124, 5.6%), and thrombocytopenia (7/124, 5.6%). Conclusions Fruquintinib may be a potential option for patients with refractory sarcoma after developing several lines of TKI resistance, with a satisfactory efficacy and safety profile in combination therapy. However, the degree of contribution of fruquintinib to results is unclear when combined with other effective substances. Additional prospective trials of fruquintinib should be conducted, especially involving different pathological types and combination regimens.

Objective The exact relationship among atypical periprosthetic femoral fractures (APFFs), typical periprosthetic femoral fractures (PFFs), and atypical femur fractures (AFFs) remains unclear. This study aimed to investigate the prevalence of APFFs among PFFs and to identify the clinical characteristics, management, and prognosis that distinguish APFFs from typical PFFs and AFFs to further determine the relationship among these three fracture types. Methods In this retrospective study, we reviewed the clinical data of 117 consecutive patients who had PFFs after hip arthroplasty between January 2012 and December 2022 and further classified them into an APFF group and a typical PFF group according to the revised ASBMR diagnostic criteria for AFF. Moreover, patients who had subtrochanteric or femoral shaft fractures in the same period and met the diagnostic criteria for AFF were recruited and classified into the AFF group. Demographic information, minor features of AFF, comorbidities, history of medication usage, management, and complications were collected and compared among patients with typical PFFs, APFFs, and AFFs. Results Eleven PFFs were identified as APFFs, and the prevalence of APFFs among PFFs was 9.4%. Significant differences were found in generalized increase in cortical thickness (p = 0.019), prodromal symptoms (p

Abstract Background Cancer cachexia‐induced skeletal muscle fibrosis (SMF) impairs muscle regeneration, alters the muscle structure and function, reduces the efficacy of anticancer drugs, diminishes the patient's quality of life and shortens overall survival. RUNX family transcription factor 2 (Runx2), a transcription factor, and collagen type I alpha 1 chain (COL1A1), the principal constituent of SMF, have been linked previously, with Runx2 shown to directly modulate COL1A1 mRNA levels. l‐Carnitine, a marker of cancer cachexia, can alleviate fibrosis in liver and kidney models; however, its role in cancer cachexia‐associated fibrosis and the involvement of Runx2 in the process remain unexplored. Methods Female C57 mice (48 weeks old) were inoculated subcutaneously with MC38 cells to establish a cancer cachexia model. A 5 mg/kg dose of l‐carnitine or an equivalent volume of water was administered for 14 days via oral gavage, followed by assessments of muscle function (grip strength) and fibrosis. To elucidate the interplay between the deltex E3 ubiquitin ligase 3L(DTX3L)/Runx2/COL1A1 axis and fibrosis in transforming growth factor beta 1‐stimulated NIH/3T3 cells, a suite of molecular techniques, including quantitative real‐time PCR, western blot analysis, co‐immunoprecipitation, molecular docking, immunofluorescence and Duolink assays, were used. The relevance of the DTX3L/Runx2/COL1A1 axis in the gastrocnemius was also explored in the in vivo model. Results l‐Carnitine supplementation reduced cancer cachexia‐induced declines in grip strength (>88.2%, P 57.9%, P

Abstract Background The distribution of fat and muscle mass in different regions of the body can reflect different pathways to mortality in individuals with diabetes. Therefore, we investigated the associations between whole‐body and regional body fat and muscle mass with cardiovascular disease (CVD) and non‐CVD mortality in type 2 diabetes (T2D). Methods Within the National Health and Nutrition Examination Survey 1999–2006, 1417 adults aged ≥50 years with T2D were selected. Dual‐energy X‐ray absorptiometry was used to derive whole‐body, trunk, arm, and leg fat mass and muscle mass indices (FMI and MMI). Mortality data until 31 December 2019 were retrieved from the National Death Index. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated from Cox proportional hazard models. Results A total of 1417 participants were included in this study (weighted mean age [standard error]: 63.7 [0.3] years; 50.5% female). Over a median follow‐up of 13.6 years, 797 deaths were recorded (371 CVD‐related and 426 non‐CVD deaths). Higher FMI in the arm was associated with increased risk of non‐CVD mortality (fourth quartile [Q4] vs. first quartile [Q1]: HR 1.82 [95% CI 1.13–2.94]), whereas higher FMI in the trunk or leg was not significantly associated with CVD or non‐CVD mortality. Conversely, higher arm MMI was associated with a lower risk of both CVD (Q4 vs. Q1: HR 0.51 [95% CI 0.33–0.81]) and non‐CVD (Q4 vs. Q1: HR 0.56 [95% CI 0.33–0.94]) mortality. There was a significant interaction between smoking status and arm FMI on non‐CVD mortality (P for interaction = 0.007). Higher arm FMI was associated with a higher risk of non‐CVD mortality among current or former smokers (Q4 vs. Q1: HR 2.67 [95% CI 1.46–4.88]) but not non‐smokers (Q4 vs. Q1: HR 0.85 [95% CI 0.49–1.47]). Conclusions Fat mass and muscle mass, especially in the arm, are differently associated with CVD and non‐CVD mortality in people with T2D. Our findings underscore the predictive value of body compositions in the arm in forecasting mortality among older adults with T2D.

Abstract Background Sarcopenia is an important indicator of ill health and is linked to increased mortality and a reduced quality of life. Age‐associated muscle mass indices provide a critical tool to help understand the development of sarcopenia. This study aimed to develop sex‐ and age‐specific percentiles for muscle mass indices in a Chinese population and to compare those indices with those from other ethnicities using the National Health and Nutrition Examination Survey (NHANES) data. Methods Whole‐body and regional muscle mass was measured by dual‐energy X‐ray absorptiometry (DXA) in participants of the China Body Composition Life‐course (BCL) study (17 203 healthy Chinese aged 3–60 years, male 48.9%) and NHANES (12 663 healthy Americans aged 8–59 years, male 50.4%). Age‐ and sex‐specific percentile curves were generated for whole‐body muscle mass and appendicular skeletal muscle mass using the Generalized Additive Model for Location Scale and Shape statistical method. Results Values of upper and lower muscle mass across ages had three periods: an increase from age 3 to a peak at age 25 in males (with the 5th and 95th values of 41.5 and 66.4 kg, respectively) and age 23 in females (with the 5th and 95th values of 28.4 and 45.1 kg, respectively), a plateau through midlife (30s–50s) and then a decline after their early 50s. The age at which muscle mass began to decline was 52 years in men with the 5th and 95th percentile values of 43.5 and 64.6 kg, and 51 years in women with the 5th and 95th percentile values of 31.6 and 46.9 kg. Appendicular skeletal muscle mass decreased earlier than whole body muscle mass, especially leg skeletal muscle mass, which decreased slightly after age 49 years in both sexes. In comparison with their US counterparts in the NHANES, the Chinese participants had lower muscle mass indices (all P

Abstract Background Sarcopenia, a group of muscle‐related disorders, leads to the gradual decline and weakening of skeletal muscle over time. Recognizing the pivotal role of gastrointestinal conditions in maintaining metabolic homeostasis within skeletal muscle, we hypothesize that the effectiveness of the myogenic programme is influenced by the levels of gastrointestinal hormones in the bloodstream, and this connection is associated with the onset of sarcopenia. Methods We first categorized 145 individuals from the Emergency Room of Taipei Veterans General Hospital into sarcopenia and non‐sarcopenia groups, following the criteria established by the Asian Working Group for Sarcopenia. A thorough examination of specific gastrointestinal hormone levels in plasma was conducted to identify the one most closely associated with sarcopenia. Techniques, including immunofluorescence, western blotting, glucose uptake assays, seahorse real‐time cell metabolic analysis, flow cytometry analysis, kinesin‐1 activity assays and qPCR analysis, were applied to investigate its impacts and mechanisms on myogenic differentiation. Results Individuals in the sarcopenia group exhibited elevated plasma levels of glucagon‐like peptide 1 (GLP‐1) at 1021.5 ± 313.5 pg/mL, in contrast to non‐sarcopenic individuals with levels at 351.1 ± 39.0 pg/mL (P

Abstract Background Hydrogen sulfide (H2S), the third gasotransmitter discovered, regulates a variety of physiological functions. Whether H2S alleviates skeletal muscle ageing by regulating autophagy has not been reported. Methods Mice were administered 150 mg/kg/day of D‐galactose (D‐gal), and C2C12 myotubes were cultured in 20 g/L D‐gal to induce ageing. Sodium hydrosulfide (NaHS) was employed as an exogenous donor in the treatment group. The intracellular concentration of H2S was quantified by the 7‐azido‐4‐methylcoumarin fluorescence probe. The proteins involved in the ubiquitin‐mediated degradation of AMPKα1 were detected by liquid chromatography tandem mass spectrometry (LC–MS/MS) and co‐immunoprecipitation (Co‐IP). S‐sulfhydration of USP5 was tested by a biotin‐switch assay. Associated proteins were analysed by western blot. Results NaHS was found to effectively restore the H2S content in both ageing gastrocnemius (+91.89%, P

Abstract Background Aging negatively impacts tissue repair, particularly in skeletal muscle, where the regenerative capacity of muscle stem cells (MuSCs) diminishes with age. Although aerobic exercise is known to attenuate skeletal muscle atrophy, its specific impact on the regenerative and repair capacity of MuSCs remains unclear. Methods Mice underwent moderate‐intensity continuous training (MICT) from 9 months (aged + Ex‐9M) or 20 months (aged + Ex‐20M) to 25 months, with age‐matched (aged) and adult controls. Histological examinations and MuSC transplantation assays assessed aerobic exercise effects on MuSC function and muscle regeneration. CCN2/connective tissue growth factor modulation (overexpression and knockdown) in MuSCs and AICAR supplementation effects were explored. Results Aged mice displayed significantly reduced running duration (65.33 ± 4.32 vs. 161.9 ± 1.29 min, mean ± SD, P

Abstract Aiming at the problems of traditional ship cold chain monitoring systems being easily affected by environmental factors, difficult to achieve real‐time monitoring in the open sea without network signals, and low efficiency in transmitting Beidou short message data, a multi‐link compressed transmission ship cold chain monitoring system was designed by combining 5G technology, Beidou short message transmission technology, and multi‐protocol transmission technology. The system can adaptively switch the strength of wireless signals to ensure that information transmission is not lost. At the same time, a Beidou short message compressed transmission method was proposed to improve transmission efficiency. Test results show that the system can accurately complete data collection and processing, with small system errors, effectively improving the reliability and efficiency of the monitoring system, and has high application value.

Abstract With a large number of film capacitors being deployed in critical locations in electrical and electronic systems, artificial intelligence (AI) technology is also expected to address the problems encountered in this process. According to our findings, AI applications can cover the entire lifecycle of film capacitors. However, the AI safety hazards in these applications have not received the attention they deserve. To meet this, the authors argue, with specific examples, risks that flawed, erratic, and unethical AI can introduce in the design, operation, and evaluation of film capacitors. Human‐AI common impact and more multi‐dimensional evaluation for AI are proposed to better cope with unknown, ambiguity, and known risks brought from AI in film capacitors now and in the future.

Abstract Bone is a common organ affected by metastasis in various advanced cancers, including lung, breast, prostate, colorectal, and melanoma. Once a patient is diagnosed with bone metastasis, the patient's quality of life and overall survival are significantly reduced owing to a wide range of morbidities and the increasing difficulty of treatment. Many studies have shown that bone metastasis is closely related to bone microenvironment, especially bone immune microenvironment. However, the effects of various immune cells in the bone microenvironment on bone metastasis remain unclear. Here, we described the changes in various immune cells during bone metastasis and discussed their related mechanisms. Osteoblasts, adipocytes, and other non‐immune cells closely related to bone metastasis were also included. This review also summarized the existing treatment methods and potential therapeutic targets, and provided insights for future studies of cancer bone metastasis.

Abstract Dendritic cells (DCs) comprise diverse cell populations that play critical roles in antigen presentation and triggering immune responses in the body. However, several factors impair the immune function of DCs and may promote immune evasion in cancer. Understanding the mechanism of DC dysfunction and the diverse functions of heterogeneous DCs in the tumor microenvironment (TME) is critical for designing effective strategies for cancer immunotherapy. Clinical applications targeting DCs summarized in this report aim to improve immune infiltration and enhance the biological function of DCs to modulate the TME to prevent cancer cells from evading the immune system. Herein, factors in the TME that induce DC dysfunction, such as cytokines, hypoxic environment, tumor exosomes and metabolites, and co‐inhibitory molecules, have been described. Furthermore, several key signaling pathways involved in DC dysfunction and signal‐relevant drugs evaluated in clinical trials were identified. Finally, this review provides an overview of current clinical immunotherapies targeting DCs, especially therapies with proven clinical outcomes, and explores future developments in DC immunotherapies.

Abstract A data‐driven Buck converter model identification method is proposed to deal with missing (incomplete) outputs, which is robust to the data length and percentage of missing data. A nuclear norm based convex optimization problem instead of linear interpolation, to guarantee the recovered missing data satisfying the potential model structured low‐rank character, is constructed to estimate missing outputs. The alternating direction method of multiplier strategy is used to solve the nuclear norm based convex optimization problem. In this way, the high‐quality missing data can be estimated, even for short data length and high percentage of missing data. Based on the recovered data, the subspace identification method provides accurate estimates of the structure and parameter of the Buck converter synchronously. By applying the proposed method to a Buck converter, experimental results demonstrate its effectiveness.

Abstract The ability to effectively classify human emotion states is critically important for human‐computer or human‐robot interactions. However, emotion classification with physiological signals is still a challenging problem due to the diversity of emotion expression and the characteristic differences in different modal signals. A novel learning‐based network architecture is presented that can exploit four‐modal physiological signals, electrocardiogram, electrodermal activity, electromyography, and blood volume pulse, and make a classification of emotion states. It features two kinds of attention modules, feature‐level, and semantic‐level, which drive the network to focus on the information‐rich features by mimicking the human attention mechanism. The feature‐level attention module encodes the rich information of each physiological signal. While the semantic‐level attention module captures the semantic dependencies among modals. The performance of the designed network is evaluated with the open‐source Wearable Stress and Affect Detection dataset. The developed emotion classification system achieves an accuracy of 83.88%. Results demonstrated that the proposed network could effectively process four‐modal physiological signals and achieve high accuracy of emotion classification.

Abstract With the advancements in Industry 4.0 and the global demand for sustainable energy, power electronics devices are emerging as pivotal components for modern industrial, transportation, and energy delivery. Ensuring the security of these devices is of paramount importance for safeguarding the reliable operation of critical systems against any threats. In recent years, the issue of intentional electromagnetic interference (IEMI) attack and their related countermeasures have gained widespread attention in both military and civilian power electronics sectors. Here, a review of IEMI in power electronics is provided. Starting from the electromagnetic compatibility standards, the test setups for evaluating the device immunity are introduced. Due to different attack modes and propagation paths, IEMI illuminations are typically categorized into conduction and radiation, where their susceptibility studies, applications, and defence strategies are discussed, respectively. Finally, the existing challenges, ongoing trends, and future topics in this field are discussed.

Abstract We investigated the clinical characteristics of primary aldosteronism (PA) screened from patients with hypertension in China. The participants were hypertensive patients who were suspected of PA and registered in the China Primary Aldosteronism Prospective Study. Plasma aldosterone‐to‐renin ratio (ARR) was used as the screening test. In patients screened positive for PA, that is, an ARR exceeding the thresholds and plasma aldosterone concentration (PAC) > 100 pg/mL, a confirmatory test was performed for diagnosis. Patients with PA underwent a CT scan and adrenal venous sampling for subtyping. Of the 1497 screened patients, 754 (50.4%) had an ARR exceeding the diagnostic threshold and 637 (84.5% of those eligible) were registered. These registered hypertensive patients with suspected PA had a mean (standard deviation) age of 52.6 ± 12.1 years, and included 442 (58.6%) women. In multiple stepwise logistic regression, the significant odds ratios for the presence of diagnosed (n = 490) versus suspected and non‐diagnosed PA (n = 147) were 4.54 (95% CI: 2.78‐7.39) for a history of hypokalemia, 0.79 (95% CI: 0.64‐0.98) for a 0.9 mmol/l higher serum total cholesterol, and 2.25 (95% CI: 1.63‐3.10) for a doubling of PAC in the supine or standing/sitting position. In multiple stepwise logistic regression, the significant odds ratios for the presence of unilateral (n = 135) versus bilateral PA (n = 53) were 3.04 (95% CI: 1.90‐4.87) for a 0.4 mmol/l lower minimum serum potassium concentration and 1.86 (95% CI: 1.20‐2.86) for a 0.3 mmol/l higher serum high‐density lipoprotein cholesterol. PA might be a biochemical continuum in the adrenal hypersecretion of aldosterone as well as hypokalemia.

Abstract Background The aim of the present study was to investigate the function of novel circular RNA hsa_circ_0036683 (circ‐36683) in non‐small cell lung cancer (NSCLC). Methods RNA sequencing was used to screen out differentially expressed miRNAs. Expression levels of miR‐4664‐3p and circ‐36683 were evaluated in lung carcinoma cells and tissues by quantitative reverse transcription‐polymerase chain reaction (qRT‐PCR). The effects of miR‐4664‐3p and circ‐36683 on proliferation and migration were assessed using cell counting kit‐8 (CCK‐8), wound healing and transwell migration assays and xenograft experiments. The targeting relationship of circ‐36683/miR‐4664‐3p/CDK2AP2 was assessed by luciferase reporter assays, western blot, qRT‐PCR and argonaute2‐RNA immunoprecipitation (AGO2 RIP). Co‐immunoprecipitation (Co‐IP), 5‐ethynyl‐2′‐deoxyuridine (EdU) staining and CCK‐8 were used to validate the indispensable role of CDK2AP2 in suppressing cell proliferation as a result of CDK2AP1 overexpression. Results By RNA sequencing, miR‐4664‐3p was screened out as an abnormally elevated miRNA in NSCLC tissues. Transfection of miR‐4664‐3p could promote cell proliferation, migration and xenograft tumor growth. As a target of miR‐4664‐3p, CDK2AP2 expression was downregulated by miR‐4664‐3p transfection and CDK2AP2 overexpression could abolish the proliferation promotion resulting from miR‐4664‐3p elevation. Circ‐36683, derived from back splicing of ABHD2 pre‐mRNA, was attenuated in NSCLC tissue and identified as a sponge of miR‐4664‐3p. The functional study revealed that circ‐36683 overexpression suppressed cell proliferation, migration and resulted in G0/G1 phase arrest. More importantly, the antioncogenic function of circ‐36683 was largely dependent on the miR‐4664‐3p/CDK2AP2 axis, through which circ‐36683 could upregulate the expression of p53/p21/p27 and downregulate the expression of CDK2/cyclin E1. Conclusion The present study revealed the antioncogenic role of circ‐36683 in suppressing cell proliferation and migration and highlighted that targeting the circ‐36683/miR‐4664‐3p/CDK2AP2 axis is a promising strategy for the intervention of NSCLC.

Abstract Background Methyltransferase 3 (METTL3) accelerates N6‐methyladenosine (m6A) modifications and affects cancer progression, including non‐small‐cell lung cancer (NSCLC). In this study, we aimed to explore the regulatory mechanisms of METTL3 underling NSCLC. Methods Immunohistochemical assay, quantitative real‐time polymerase chain reaction (qRT‐PCR) assay, and western blot assay were conducted for gene expression. MTT assay and colony formation assay were performed to explore cell proliferation capacity. Cell apoptosis and THP‐1 cell polarization were estimated by flow cytometry analysis. Cell migration and invasion capacities were evaluated by transwell assay. Methylated RNA immunoprecipitation assay, dual‐luciferase reporter assay, actinomycin D treatment and RIP assay were performed to analyze the relationships of METTL3, insulin‐like growth factor 2 mRNA binding protein 1 (IGF2BP1), and transient receptor potential cation channel subfamily V member 1 (TRPV1). The functions of METTL3 and TRPV1 in vivo were investigated through establishing the murine xenograft model. Results TRPV1 expression was upregulated in NSCLC and related poor prognosis. TRPV1 silencing inhibited NSCLC cell growth and metastasis, induced NSCLC cell apoptosis, and repressed M2 macrophage polarization. The results showed that METTL3 and IGF2BP1 could regulate TRPV1 expression through m6A methylation modification. Moreover, METTL3 deficiency inhibited NSCLC cell growth, metastasis, and M2 macrophage polarization and facilitated NSCLC cell apoptosis, while TRPV1 overexpression restored the impacts. In addition, METTL3 knockdown restrained tumor growth in vivo via regulating TRPV1 expression. Conclusion METTL3 bound to IGF2BP1 and enhanced IGF2BP1's m6A recognition of TRPV1 mRNA, thereby promoting NSCLC cell growth and metastasis, and inhibiting M2 macrophage polarization.

Abstract Background Lung cancer is one of the major threats to human life worldwide. MiR‐190 has been found to perform essential roles in multiple cancer progression; however, there have been no studies focused on its function and underlying regulatory mechanism in lung cancer. Method The miR‐190 expression was detected by real‐time quantitative polymerase chain reaction (RT‐qPCR). The cell functional experiments, including cell counting kit‐8 (CCK‐8), colony formation and transwell assay were conducted in vitro, as well as animal experiments performed in vivo. The regulation and potential binding sites of CBX4 on miR‐190 were predicted by TCGA data set and JASPAR website and verified by ChIP assay and dual‐luciferase reporter assay. The prospects binding site of miR‐190‐3p on CBX4 3′UTR region was predicted by StarBase and verified by dual‐luciferase reporter assay. Results MiR‐190 was decreased in lung cancer cells. The overexpression of miR‐190 had no effects on cell proliferation, but significantly inhibited cancer metastasis both in vitro and in vivo. Moreover, miR‐190 expression could be transcriptionally inhibited by CBX4, and CBX4 was the direct target of miR‐190‐3p. Conclusion MiR‐190 served as a cancer metastasis inhibitor in lung cancer and formed a regulatory loop with CBX4. These findings provided emerging insights into therapeutic targets and strategies for metastatic lung cancer.

Abstract Background Patient navigators, whose value has become increasingly apparent, still face significant challenges, including a lack of support, funding, and recognition. These challenges have been exacerbated in the wake of COVID‐19 pandemic. Methods This study explored the potential use of artificial intelligence (AI) in patient navigation. Data were collected through structured surveys and individual interviews with patient navigators from a variety of institutions and professional backgrounds. The data were analyzed to understand the current state of patient navigation, identify existing gaps, and suggest best practices for the future. Results The findings showed that patient navigators (a) have diverse backgrounds and responsibilities, (b) lack technology support for their work, (c) are at risk for burnout, with the extent varying based on the level of technical support received, and (d) report significant overlap between current barriers and those that could potentially be addressed with AI‐driven technologies. Conclusion A novel intervention, that is enabled by AI and other technologies and tailored to individual needs, has the potential to reduce burnout, increase capacity, and help ensure the sustainability of patient navigation and other areas of healthcare. By addressing the specific needs of individual patients, this type of intervention could help improve the overall effectiveness of patient navigation and support the long‐term sustainability of the role.

Abstract Background Ferroptosis is a type of regulated necrosis and glutathione peroxidase 4 (GPX4) has been recognized as a key enzyme that protects against ferroptosis. However, the significance of GPX4 in polymorphonuclear neutrophils (PMNs) of systemic lupus erythematosus (SLE) has not been explored. So we examined GPX4 mRNA in PMNs and analyzed its association with serological and clinical features. Methods A single center research from the Department of Rheumatology and Immunology of the Third Affiliated Hospital, Southern Medical University was conducted between December 2020 and September 2022. Real‐time transcription‐polymerase chain reaction analysis was used to determine the expression of GPX4 mRNA in PMNs from patients suffering from different rheumatoid immune diseases and healthy controls. The associations of GPX4 RNA levels in SLE patients with serological and clinical indicators were assessed by Spearman's correlation analysis. Receiver operating characteristic curve analysis was performed to evaluate the diagnostic value of GXP4 mRNA for SLE. Results GPX4 mRNA levels were lower in SLE patients than those in healthy individuals, patients with rheumatoid arthritis and axial spondyloarthritis. GPX4 mRNA levels were negatively correlated with the number of positive autoantibodies (r = −0.3072, p = 0.0300), anti‐dsDNA antibody (r = −0.3654, p = 0.0336), antinucleosome antibody (r = −0.4052, p = 0.0263), erythrocyte sedimentation rate (r = −0.3773, p = 0.0069), C‐reactive protein (r = −0.4037, p = 0.0036), and SLE disease activity index (r = −0.3072, p = 0.0300). GPX4 mRNA levels were downregulated in patients with alopecia compared with patients without alopecia (p

Abstract The human gut microbiota significantly impacts health, including liver conditions like liver cirrhosis (LC) and spontaneous bacterial peritonitis (SBP). Immunoglobulin A (IgA) plays a central role in maintaining gut microbial balance. Understanding IgA's interplay with gut microbiota and liver health is crucial. This study explores the relationship between fecal IgA levels, gut microbiota, and liver injury severity. A total of 69 LC patients and 30 healthy controls were studied. Fecal IgA levels were measured using ELISA, and IgA‐coated bacteria were quantified via flow cytometry. Microbiota diversity and composition were assessed through 16S rRNA sequencing. Liver injury severity was graded using the Child–Pugh score. Statistical analyses determined correlations. LC patients had higher fecal IgA levels than controls, correlating positively with liver injury severity. Microbiota diversity decreased with severity, accompanied by shifts in composition favoring pro‐inflammatory species. Ralstonia abundance positively correlated with liver injury, whereas Faecalibacterium showed a negative correlation. Specific microbial markers for SBP were identified. Functional profiling revealed altered microbial functionalities in LC and SBP. Elevated fecal IgA levels, coupled with microbiota alterations, correlate with liver injury severity in LC patients. Modulating gut microbiota could be a promising strategy for managing liver‐related conditions. Further research is needed to understand underlying mechanisms and translate findings into clinical practice, potentially improving patient outcomes.

Abstract Long noncoding RNAs are key players in the development of lung adenocarcinoma (LUAD). The present study elucidated the role of LINC01087 in LUAD development. Cell vitality and apoptosis were assessed by the CCK‐8 assay and flow cytometry, respectively. The transwell assay was adopted to evaluate cell migration and invasion. Levels of m6A modification of LINC01087 were determined using the methylated RNA binding protein immunoprecipitation assay. The interactions among LINC01087, miR‐514a‐3p, and centrosome protein 55 (CEP55) were evaluated using dual‐luciferase reporter, RNA immunoprecipitation, and RNA–RNA pull‐down assays. LINC01087 was highly expressed in LUAD, and its downregulation restrained cancer cell proliferation, migration, invasion, and epithelial–mesenchymal transition in vitro as well as tumor growth in a xenograft tumor model. Overexpression of miR‐514a‐3p inhibited malignant phenotypes in LUAD cells by inactivating RhoA/ROCK1 signaling via the suppression of CEP55 expression. Mechanistically, RBM15 increased the expression and mRNA stability of LINC01087 by mediating its m6A modification and LINC01087 induced CEP55 expression by sponging miR‐514a‐3p. RBM15‐induced LINC01087 upregulation accelerated LUAD progression by regulating the miR‐514a‐3p/CEP55/RhoA/ROCK1 axis, illustrating the potential of LINC01087 as a novel target for LUAD therapy.

Abstract Background Despite the adverse effects of ambient fine particulate matter (PM2.5) on type 2 diabetes and the beneficial role of physical activity (PA), the influence of PM2.5 on the relationship between PA and type 2 diabetes remains unclear. Methods In this prospective study with 71,689 participants, PA was assessed by a questionnaire and was categorized into quartiles for volume and three groups for intensity. Long‐term PM2.5 exposure was calculated using 1‐km resolution satellite‐based PM2.5 estimates. PM2.5 exposure and PA's effect on type 2 diabetes were assessed by cohort‐stratified Cox proportional hazards models, individually and in combination. Results In 488,166 person‐years of follow‐up, 5487 incident type 2 diabetes cases were observed. The association between PA and type 2 diabetes was modified by PM2.5. Compared with the lowest quartile of PA volume, the highest quartile was associated with reduced type 2 diabetes risk in low PM2.5 stratification (≤65.02 µg/m3) other than in high PM2.5 stratification (>65.02 µg/m3), with the hazard ratio (HR) of 0.75 (95% confidence interval [CI]: 0.66–0.85) and 1.10 (95% CI: 0.99–1.22), respectively. Similar results were observed for PA intensity. High PM2.5 exposure combined with the highest PA levels increased the risk of type 2 diabetes the most (HR = 1.79, 95% CI: 1.59–2.01 for PA volume; HR = 1.82, 95% CI: 1.64–2.02 for PA intensity). Conclusion PA could reduce type 2 diabetes risk in low‐pollution areas, but high PM2.5 exposure may weaken or even reverse the protective effects of PA. Safety and health benefits of PA should be thoroughly assessed for long‐term polluted residents.

Abstract Systemic lupus erythematosus (SLE), a chronic autoimmune disease, is marked by impaired immune tolerance and heightened activity in both innate and adaptive immune systems. Hallmarks of SLE include elevated type I interferons and autoantibody production, though the exact causes of SLE remain elusive despite advances in research techniques. Crucial to SLE research is understanding its pathogenesis and developing effective diagnostic and therapeutic methods. Recent studies have highlighted a significant link between mitochondrial abnormalities and SLE's development and progression. Mitochondrial dysfunction plays a key role in SLE pathogenesis through various mechanisms such as mitochondrial DNA mutations, oxidative stress, immune metabolic reprogramming, and cellular death. These factors collectively contribute to the loss of self‐tolerance, increased autoantibody production, and impaired clearance of immune complexes, leading to their deposition. This triggers sustained inflammatory responses and damages multiple organs. This review focuses on the diagnostic and therapeutic approaches related to mitochondrial abnormalities in SLE. Targeting mitochondrial pathways presents a promising strategy for treating SLE, potentially improving prognosis and quality of life for those affected. Future research should further investigate the role of mitochondria in the onset and progression of SLE, providing new avenues for understanding and managing this complex disease.

Abstract The overactivated immune cells in the infectious lesion may lead to irreversible organ damages under severe infections. However, clinically used immunosuppressive anti‐inflammatory drugs will usually disturb immune homeostasis and conversely increase the risk of infections. Regulating the balance between anti‐inflammation and anti‐infection is thus critical in treating certain infectious diseases. Herein, considering that hydrogen peroxide (H2O2), myeloperoxidase (MPO), and neutrophils are upregulated in the inflammatory microenvironment and closely related to the severity of appendectomy patients, an inflammatory‐microenvironment‐responsive nanomedicine is designed by using poly(lactic‐co‐glycolic) acid (PLGA) nanoparticles to load chlorine E6 (Ce6), a photosensitizer, and luminal (Lum), a chemiluminescent agent. The obtained Lum/Ce6@PLGA nanoparticles, being non‐toxic within normal physiological environment, can generate cytotoxic single oxygen via bioluminescence resonance energy transfer (BRET) in the inflammatory microenvironment with upregulated H2O2 and MPO, simultaneously killing pathogens and excessive inflammatory immune cells in the lesion, without disturbing immune homeostasis. As evidenced in various clinically relevant bacterial infection models and virus‐induced pneumonia, Lum/Ce6@PLGA nanoparticles appeared to be rather effective in controlling both infection and inflammation, resulting in significantly improved animal survival. Therefore, the BRET‐based nanoparticles by simultaneously controlling infections and inflammation may be promising nano‐therapeutics for treatment of severe infectious diseases.

ABSTRACT Purpose To compare the efficacy of first‐line regimens based on programmed cell death (or ligand) [PD‐(L)1] blockade in extensive‐stage small‐cell lung cancer (ES‐SCLC) patients with or without liver metastases (LM), and to identify optimal treatment strategies. Methods Network meta‐analysis of randomized controlled trials (RCTs) comparing chemo‐immunotherapy (CIT) and chemotherapy (CT) in ES‐SCLC patients stratified by LM. Overall survival (OS) and progression‐free survival (PFS) were evaluated using hazard ratios (HRs) and 95% confidence intervals (CIs). Results Seven RCTs involving 3658 ES‐SCLC patients (1243 with LM, 2415 without LM) were analyzed. For patients with LM, the combination therapies of anti‐PD‐1 + CT (HR, 0.67; 95% CI, 0.54%–0.82%; p

Abstract Complete removal of all tumor tissue with a wide surgical margin is essential for the treatment of osteosarcoma (OS). However, it's difficult, sometimes impossible, to achieve due to the invisible small satellite lesions and blurry tumor boundaries. Besides, intraoperative frozen‐section analysis of resection margins of OS is often restricted by the hard tissues around OS, which makes it impossible to know whether a negative margin is achieved. Any unresected small tumor residuals will lead to local recurrence and worse prognosis. Herein, based on the high expression of B7H3 in OS, a targeted probe B7H3‐IRDye800CW is synthesized by conjugating anti‐B7H3 antibody and IRDye800CW. B7H3‐IRDye800CW can accurately label OS areas after intravenous administration, thereby helping surgeons identify and resect residual OS lesions (

Abstract Conductive polymer hydrogels exhibit unique electrical, electrochemical, and mechanical properties, making them highly competitive electrode materials for stretchable high‐capacity energy storage devices for cutting‐edge wearable electronics. However, it remains extremely challenging to simultaneously achieve large mechanical stretchability, high electrical conductivity, and excellent electrochemical properties in conductive polymer hydrogels because introducing soft insulating networks for improving stretchability inevitably deteriorates the connectivity of rigid conductive domain and decreases the conductivity and electrochemical activity. This work proposes a distinct confinement self‐assembly and multiple crosslinking strategy to develop a new type of organic–inorganic hybrid conductive hydrogels with biphase interpenetrating cross‐linked networks. The hydrogels simultaneously exhibit high conductivity (2000 S m−1), large stretchability (200%), and high electrochemical activity, outperforming existing conductive hydrogels. The inherent mechanisms for the unparalleled comprehensive performances are thoroughly investigated. Elastic all‐hydrogel supercapacitors are prepared based on the hydrogels, showing high specific capacitance (212.5 mF cm−2), excellent energy density (18.89 µWh cm−2), and large deformability. Moreover, flexible self‐powered luminescent integrated systems are constructed based on the supercapacitors, which can spontaneously shine anytime and anywhere without extra power. This work provides new insights and feasible avenues for developing high‐performance stretchable electrode materials and energy storage devices for wearable electronics.

Abstract Background Leukemia is the tenth most common cause of cancer death worldwide and one of the most important causes of disability. To understand the current status and changing trends of the disease burden of leukemia at the global, regional, and national levels, and to provide a scientific basis for the development of leukemia prevention and treatment strategies. Methods Based on open data from the Global Burden of Disease Study 2019 (GBD 2019), R software was used to calculate estimated annual percentage changes to estimate trends in the age‐standardized incidence (ASIR) and the age‐standardized disability‐adjusted life years (DALY) rate due to leukemia and its major subtypes from 1990 to 2019. Results In 2019, globally, the number of incidences and DALYs of leukemia were 643.6 × 103 (587.0 × 103, 699.7 × 103) and 11,657.5 × 103 (10529.1 × 103, 12700.7 × 103), respectively. The ASIR (estimated annual percentage change (EAPC) = −0.37, 95%UI −0.46 to −0.28) and the age‐standardized DALY rate (EAPC = −1.72, 95%UI −1.80 to −1.65) of leukemia showed a decreasing trend from 1990 to 2019. The APC model analysis showed that the age effect of leukemia risk was a “U”‐shaped distribution of relative risk (RR) with increasing age from 1990 to 2019, globally. The time effect was an increase in incidence rate with increasing years but a decrease in DALY rate with increasing years. The cohort effects of both incidence and DALY rates tended to increase and then decrease with the development of the birth cohort. In 1990 and 2019, smoking, high body‐mass index, occupational exposure to benzene, and occupational exposure to formaldehyde were risk factors for DALY in leukemia, especially in areas with high SDI. Conclusions From 1990 to 2019, the disease burden of leukemia showed a decreasing trend, but it is worth noting that its overall severity is still very high. The disease burden of leukemia varies greatly from region to region, and exclusive strategies for the prevention and treatment of leukemia should be developed according to the economic and cultural development of each region.

Abstract Cancer stands as a leading global cause of death, with its etiology characterized by complexity and multifaceted factors. Growing research indicates a strong correlation between environmental factors and cancer incidence, underscoring the critical importance of intervening in environmental risk factors to mitigate cancer occurrence. Despite this, specialized research institutions focusing on the intersection of environment and cancer remain scarce, with global investment in cancer prevention significantly trailing behind efforts in diagnosis and treatment. Against the backdrop of rapid global climate change, industrialization, urbanization, aging populations, and the globalization of lifestyles, we proposed the concept of Environmental Oncology (EO) to address these challenges. We discussed the rationale and necessity of developing EO and presented a comprehensive research framework focusing on cancer prevention and treatment. Future EO research will aim to identify cancer causes and implement early prevention strategies using advanced scientific technologies and methods. By emphasizing multidisciplinary collaboration and integrating molecular biology at the micro level, EO will explore the relationship between external and internal environments and cancer. EO will identify potential therapeutic targets by studying the pathways through which environmental exposures lead to carcinogenesis. EO will develop early warning systems and disseminate research findings by collecting big data, employing robust statistical models, and establishing research centers.

Abstract MicroRNAs (miRNAs) can regulate several physiological processes of cells after transcription, such as cell proliferation, differentiation, and apoptosis. In this study, we found that 500 μM of palmitic acid (PA) could significantly induce the apoptosis of porcine subcutaneous preadipocytes (p

Abstract The high uncertainty of wind power output greatly affects the rapid reactive power optimization of power systems. This paper proposes a neural network‐based comprehensive reactive power optimization method for large‐scale wind power grids, effectively addressing the challenges of rapid reactive power optimization in power systems. Firstly, by constructing typical wind‐power‐load scenarios, the generalization ability of the neural network is improved. Then, focusing on the comprehensive reactive power optimization problem after integrating typical wind‐power‐load scenarios into the system, the improved Harris hawks optimization algorithm (HHO) is compared with the particle swarm optimization algorithm and traditional HHO algorithm, highlighting its advantages. Finally, HHO is utilized for solving, thereby constructing a comprehensive reactive power optimization strategy tag set. Furthermore, through deep fitting of the neural network between the power grid operating state and the comprehensive reactive power optimization strategy, the computational complexity and decision‐making time of reactive power optimization are reduced.

Abstract The safe operation of oil‐immersed transformers is critical to the safety and stability of the power grid. As the operating time increases, the failure rate of oil‐immersed transformers shows an increasing trend, posing serious challenges to safe operation. It is necessary to investigate the internal state of the oil‐immersed transformer to improve the digital degree and achieve digitalisation and intelligent operation and maintenance. A physics‐informed neural network (PINN) for oil‐immersed transformers was introduced to reconstruct the temperature distribution inside the transformer. According to the approach, the loss function of the network would be optimised by incorporating physical constraint loss terms including heat transfer equations, initial conditions and boundary conditions. The results show that the method proposed can be used to reconstruct and predict the temperature field of transformers in a few seconds with satisfactory accuracy. In conclusion, the PINN proposed outperforms deep neural networks in terms of accuracy, reliability and interpretability, especially in data‐poor cases.

Abstract Relapse remains the main cause of treatment failure in patients with myeloid malignancies even after allogeneic hematopoietic stem cell transplantation (allo‐HSCT). We observed a particularly low incidence of relapse in patients prepared with fludarabine, busulfan and melphalan in our previous study and this multicenter retrospective analysis aimed to confirm the feasibility of the regimen and to identify the potential prognostic factors. This study was performed using registry data from adults patients with myeloid malignancies who underwent their first allo‐HSCT following fludarabine(≥100 mg/m2), busulfan (≥3.2 mg/kg) and melphalan (≥100 mg/m2) based conditioning at nine transplantation centers in China between Jan. 2020 and Mar. 2022. A total of 221 consecutive patients (AML n = 171, MDS‐IB‐1 or 2 n = 44, CMML n = 6) with median age of 46 were enrolled in this study. The median follow‐up was 507 days for survivors. The 2‐year NRM, CIR, OS and DFS were 10.6% ± 2.2%, 14.8% ± 3.3%, 79.4% ± 3.7% and 74.6% ± 3.7%, respectively. In multivariate analyses, high HCT‐CI (≥3) was the only independent factor for higher NRM [hazard ratio (HR), 2.96; 95% confidence interval (CI), 1.11 to 7.90; p = 0.030] and ECOG score ≥2 was the only independent factor for inferior OS (HR, 2.43; 95%CI, 1.15 to 5.16; p = 0.020) and DFS (HR, 2.12; 95%CI, 1.13 to 4.02; p = 0.020). AML diagnosis and positive measurable residual disease (MRD) at transplantation were predictors for higher CIR (HR = 7.92, 95%CI 1.05‐60.03, p = 0.045; HR = 3.64, 95%CI 1.40‐9.44, p = 0.008; respectively), while post‐transplantation cyclophosphamide based graft‐versus‐host disease prophylaxis was associated with lower CIR (HR = 0.24 95%CI 0.11‐0.54, p = 0.001). The intensity of conditioning regimen did not impact CIR, NRM, DFS and OS. These results supported that double alkylating agents of busulfan and melphalan based conditioning regimens were associated with low relapse rate and acceptable NRM in adult patients with myeloid malignancies. The optimal dose remained to be confirmed by further prospective studies.

Abstract Objective Efgartigimod, a neonatal Fc receptor antagonist, facilitates antibody degradation including pathogenic IgGs. The ADAPT study demonstrated the tolerability and efficacy of efgartigimod in the treatment of generalized myasthenia gravis (gMG). However, very limited evidence is available for the Chinese population, and it remains inconclusive about which kind of patients are selected to preferentially receive efgartigimod in real‐world settings. Methods This multicenter cohort study included gMG patients treated at 14 neuromuscular reference centers in China. The Myasthenia Gravis Activities of Daily Living (MG‐ADL) score, immunosuppressants, and the incidence of treatment‐emergent adverse events (TEAEs) were prospectively collected. Results Of the 1640 gMG admitted between September and December 2023, 61 (3.7%) received efgartigimod for at least one treatment cycle. Among them, 56 cases (92%) were anti‐AChR antibody‐positive, 4 were anti‐MuSK antibody‐positive, and 1 was seronegative. Thymoma‐associated myasthenia gravis accounted for most cases (44%, 27 out of 61). The principal causes of efgartigimod initiation included MG acute exacerbation (MGAE) (48%, 29 out of 61) and myasthenic crisis (MC) (15%, 9 out of 61). Clinically meaningful improvement was rapidly achieved in 97% (58 out of 61) of patients at 1.3 ± 0.7 weeks. By week 12, the MG‐ADL score reduced to 3.8 ± 4.1 (baseline:10.5 ± 5.2) for all participants, while it reduced to 4.0 ± 4.7 for MGAE and 3.8 ± 4.2 for MC, respectively. All but one TMG patient required no additional rescue therapies after efgartigimod initiation. 11.5% (7 out of 61) reported ≥1 TEAEs. Interpretation This multicenter cohort study demonstrated the efficacy of efgartigimod in rapid control of gMG. Patients with MGAE or MC would benefit from efgartigimod treatment.

Abstract Karyopherin α 2 (KPNA2, importin α1), a transport factor shuttling between the nuclear and cytoplasmic compartments, is involved in the nuclear import of proteins and participates in cellular processes such as cell cycle regulation, apoptosis, and transcriptional regulation. However, it is still unclear which signaling regulates the nucleocytoplasmic distribution of KPNA2 in response to cellular stress. In this study, we report that oxidative stress increases nuclear retention of KPNA2 through alpha serine/threonine‐protein kinase (AKT1)‐mediated reduction of serine 62 (S62) phosphorylation. We first found that AKT1 activation was required for H2O2‐induced nuclear accumulation of KPNA2. Immunoprecipitation and quantitative proteomic analysis revealed that the phosphorylation of KPNA2 at S62 was decreased under H2O2‐induced oxidative stress. We showed that cyclin‐dependent kinase 1 (CDK1), a kinase responsible for KPNA2 S62 phosphorylation, contributes to the localization of KPNA2 in the cytoplasm. AKT1 knockdown increased KPNA2 S62 phosphorylation and inhibited CDK1 activation. Furthermore, H2O2‐induced AKT1 activation promoted nuclear KPNA2 interaction with nucleophosmin 1 (NPM1), resulting in attenuation of NPM1‐mediated cyclin D1 gene transcription. Thus, we infer that the AKT1‐CDK1 axis regulates the nucleocytoplasmic shuttling and function of KPNA2 through spatiotemporal regulation of KPNA2 S62 phosphorylation under oxidative stress conditions.