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Purpose: The aim of this study is to develop a deep learning model capable of discriminating between pancreatic plasma cystic neoplasms (SCN) and mucinous cystic neoplasms (MCN) by leveraging patient‐specific clinical features and imaging outcomes. The intent is to offer valuable diagnostic support to clinicians in their clinical decision‐making processes. Methods: The construction of the deep learning model involved utilizing a dataset comprising abdominal magnetic resonance T2‐weighted images obtained from patients diagnosed with pancreatic cystic tumors at Changhai Hospital. The dataset comprised 207 patients with SCN and 93 patients with MCN, encompassing a total of 1761 images. The foundational architecture employed was DenseNet‐161, augmented with a hybrid attention mechanism module. This integration aimed to enhance the network's attentiveness toward channel and spatial features, thereby amplifying its performance. Additionally, clinical features were incorporated prior to the fully connected layer of the network to actively contribute to subsequent decision‐making processes, thereby significantly augmenting the model's classification accuracy. The final patient classification outcomes were derived using a joint voting methodology, and the model underwent comprehensive evaluation. Results: Using the five‐fold cross validation, the accuracy of the classification model in this paper was 92.44%, with an AUC value of 0.971, a precision rate of 0.956, a recall rate of 0.919, a specificity of 0.933, and an F1‐score of 0.936. Conclusion: This study demonstrates that the DenseNet model, which incorporates hybrid attention mechanisms and clinical features, is effective for distinguishing between SCN and MCN, and has potential application for the diagnosis of pancreatic cystic tumors in clinical practice. [ABSTRACT FROM AUTHOR]

Esophageal squamous cell carcinoma (ESCC) is one of the gastrointestinal malignancies with high prevalence and poor prognosis. Previous reports suggested that circular ribose nucleic acids might exert regulatory functions in ESCC. This study aims to explore the role of circ_0000592 in ESCC progression, providing novel insights into the diagnosis and therapeutic avenues for ESCC. The GSE131969 data set was utilized to assess circ_0000592 expression in ESCC. The validation was performed in the tumorous tissues of ESCC patients (n = 80) and human‐immortalized ESCC cell lines. The correlation between circ_0000592 expression and prognosis was analyzed. The impact of circ_0000592 on ESCC cell activity was evaluated through downregulating circ_0000592, as well as encompassing cell viability, migration, and invasion abilities. The downstream pathway of circ_0000592 was explored by binding site prediction from the TargetScan database, followed by in vitro and in vivo experiments. An in vivo xenograft tumor model was established to highlight the role of circ_0000592 in ESCC. Patients with ESCC exhibited higher circ_0000592 expression levels compared to noncancerous patients, which were associated with reduced survival time, higher TNM stage, and increased lymph node metastasis. The circ_0000592 downregulation suppressed cell viability, migration, and invasion abilities in vitro. Mechanistically, circ_0000592 countered the inhibitory effects on the target gene Frizzled 5 (FZD5) through interactions with miR‐155‐5p. The overexpression of miR‐155‐5p curtailed the luciferase activity of circ_0000592 in ESCC cells, inhibiting downstream molecule FZD5 protein expression and subsequently mitigating the detrimental consequences of escalated circ_0000592 expression in ESCC cells. Consistently, circ_0000592 downregulation curbed proliferation and metastasis of ESCC tumors in vivo. In summary, circ_0000592 promoted the progress of ESCC by counteracting the inhibitory impact on FZD5 through its interaction with miR‐155‐5p. Together, our findings highlighted circ_0000592 as a prospective therapeutic target for ESCC. [ABSTRACT FROM AUTHOR]

Background and Aims: The use of corticosteroids in chronic drug‐induced liver injury (DILI) is an important issue. Our previous randomized controlled trial showed that patients with chronic DILI benefited from a 48‐week steroid stepwise reduction (SSR) regimen. However, it remains unclear whether a shorter course of therapy can achieve similar efficacy. In this study, we aimed to assess whether a 36‐week SSR can achieve efficacy similar to that of 48‐week SSR. Methods: A randomized open‐label trial was performed. Eligible patients were randomly assigned to the 36‐ or 48‐week (1:1) SSR group. Liver biopsies were performed at baseline and at the end of treatment. The primary outcome was the proportion of patients with relapse rate (RR). The secondary outcomes were improvement in liver histology and safety. Results: Of the 90 participants enrolled, 84 (87.5%) completed the trial, and 62 patients (68.9%) were women. Hepatocellular damage was observed in 53.4% of the cohort. The RR was 7.1% in the 36‐week SSR group but 4.8% in the 48‐week SSR group, as determined by per‐protocol set analysis (p = 1.000). Significant histological improvements in histological activity (93.1% vs. 92.9%, p = 1.000) and fibrosis (41.4% vs. 46.4%, p =.701) were observed in both the groups. Biochemical normalization time did not differ between the two groups. No severe adverse events were observed. Conclusions: Both the 36‐ and 48‐week SSR regimens demonstrated similar biochemical response and histological improvements with good safety, supporting 36‐week SSR as a preferable therapeutic choice (ClinicalTrials.gov, NCT03266146). [ABSTRACT FROM AUTHOR]

Lithium‐ion batteries (LIBs) have gained widespread attention due to their numerous advantages, including high energy density, prolonged cycle life, and environmental friendliness. Nevertheless, their electrochemical performance deteriorates rapidly under extreme temperature conditions, accompanied by a series of safety issues. Electrolyte optimization has emerged as a crucial and feasible strategy to expand the operational temperature range of LIBs. This review comprehensively summarizes the challenges, advances, and characterization methodologies of electrolytes at both subzero and elevated temperatures. Initially, it discusses the degradation mechanisms of different types of electrolytes at extreme temperatures, integrates recent advances, and offers insights into future research directions. Subsequently, various experimental techniques are systematically presented to evaluate the fundamental physical properties, stability, and dynamic behaviors of electrolytes in non‐ambient environments. Finally, it also provides relevant computational methods across the electronic, molecular, and macroscopic scales, and explores the application of high‐throughput techniques in this field. This review offers valuable guidance for breaking the working temperature limits of electrolytes and promoting the development of next‐generation LIBs. [ABSTRACT FROM AUTHOR]

Helianthus annuus seed byproduct is a residual product obtained after seed oil extraction. The present study investigated the preventive and repair effects of the H. annuus seed byproduct ethanol extract (HSE) on ultraviolet radiation (UVR)‐induced injury in human immortalized keratinocytes (HaCaTs) and human skin fibroblasts (HSFs). Results revealed that the total phenolic acid and oligosaccharide content in HSE was >50%. HSE had a stronger preventive effect on UVR‐induced injury than the repair effect. Moreover, phenolic acids were the main active component of HSE mediating the preventative effect. In HaCaTs and HSFs, HSE prevented UVR‐induced injury by inhibiting excessive ROS production. It reduced the secretion of tumor necrosis TNF‐α, IL‐1α, IL‐1β, IL‐6, and IL‐8 by inhibiting the level of ROS, thus reducing inflammation‐mediated injury to skin cells. In addition, HSE inhibited the expression of various mRNA kinases in the MAPK–ERK/p38/JNK pathway. This downregulated the expression of activator protein‐1 (AP‐1) mRNA and further reduced the secretion of matrix metalloproteinase (MMP)‐1, MMP‐3, and MMP‐9 as well as reduced UVR‐induced injury to the cells. In conclusion, HSE is a broad‐spectrum, natural UV filter with high efficiency and low toxicity that has the potential to be used in sunscreen products. [ABSTRACT FROM AUTHOR]

Background: Organoid technology is an emerging and rapidly growing field that shows promise in studying organ development and screening therapeutic regimens. Although organoids have been proposed for a decade, concerns exist, including batch‐to‐batch variations, lack of the native microenvironment and clinical applicability. Main body: The concept of organoids has derived patient‐derived tumour organoids (PDTOs) for personalized drug screening and new drug discovery, mitigating the risks of medication misuse. The greater the similarity between the PDTOs and the primary tumours, the more influential the model will be. Recently, 'tumour assembloids' inspired by cell‐coculture technology have attracted attention to complement the current PDTO technology. High‐quality PDTOs must reassemble critical components, including multiple cell types, tumour matrix, paracrine factors, angiogenesis and microorganisms. This review begins with a brief overview of the history of organoids and PDTOs, followed by the current approaches for generating PDTOs and tumour assembloids. Personalized drug screening has been practised; however, it remains unclear whether PDTOs can predict immunotherapies, including immune drugs (e.g. immune checkpoint inhibitors) and immune cells (e.g. tumour‐infiltrating lymphocyte, T cell receptor‐engineered T cell and chimeric antigen receptor‐T cell). PDTOs, as cancer avatars of the patients, can be expanded and stored to form a biobank. Conclusion: Fundamental research and clinical trials are ongoing, and the intention is to use these models to replace animals. Pre‐clinical immunotherapy screening using PDTOs will be beneficial to cancer patients. Key Points: The current PDTO models have not yet constructed key cellular and non‐cellular components.PDTOs should be expandable and editable.PDTOs are promising preclinical models for immunotherapy unless mature PDTOs can be established.PDTO biobanks with consensual standards are urgently needed. [ABSTRACT FROM AUTHOR]

Conventional RGB‐T salient object detection treats RGB and thermal modalities equally to locate the common salient regions. However, the authors observed that the rich colour and texture information of the RGB modality makes the objects more prominent compared to the background; and the thermal modality records the temperature difference of the scene, so the objects usually contain clear and continuous edge information. In this work, a novel mirror‐complementary Transformer network (MCNet) is proposed for RGB‐T SOD, which supervise the two modalities separately with a complementary set of saliency labels under a symmetrical structure. Moreover, the attention‐based feature interaction and serial multiscale dilated convolution (SDC)‐based feature fusion modules are introduced to make the two modalities complement and adjust each other flexibly. When one modality fails, the proposed model can still accurately segment the salient regions. To demonstrate the robustness of the proposed model under challenging scenes in real world, the authors build a novel RGB‐T SOD dataset VT723 based on a large public semantic segmentation RGB‐T dataset used in the autonomous driving domain. Extensive experiments on benchmark and VT723 datasets show that the proposed method outperforms state‐of‐the‐art approaches, including CNN‐based and Transformer‐based methods. The code and dataset can be found at https://github.com/jxr326/SwinMCNet. [ABSTRACT FROM AUTHOR]

Global climate change is becoming an increasingly serious issue. China, the largest carbon emitter, has a long way towards its sustainable development goals (SDGs) and take on its carbon reduction responsibility, especially in the industrial sector. In this vein, industrial intelligence, a key driver in the "Industry 4.0 era", offers an opportunity in this carbon reduction campaign. This paper seeks to examine the influences of industrial intelligence on carbon emissions, their heterogeneous characteristics and transmission mechanisms, and the moderating role of human capital. Therefore, we properly probed theoretical aspects, and then we used China's provincial data from 2006 to 2019 and a number of tests, namely the fixed effect model, the two‐stage test, and the moderating effect model, to test the relevant assumptions. We first unfolded that industrial intelligence can significantly mitigate carbon emissions. Specifically, the heterogeneous analysis found that carbon reduction efforts are more pronounced in China's central and western regions and resource‐based regions. We further highlight the mechanism identification, which reveals that industrial structure upgrading and technological innovation are the main channels for industrial intelligence to abate CO2 emissions. Importantly, we pinpoint the role of human capital, which positively moderates the relationship between industrial intelligence and carbon emissions and can well amplify the industrial structure effect of industrial intelligence. These results are conducive to accurately assessing the environmental benefits of industrial intelligence and providing policy enlightenment for China to alleviate carbon emissions, and they will also offer a reference for other developing countries to learn from. [ABSTRACT FROM AUTHOR]

Soil salinity can adversely affect crop growth and yield, and an improved understanding of the genetic factors that confer salt tolerance could inform breeding strategies to engineer salt‐tolerant crops and improve productivity. Here, a group of K+‐preferring HKT transporters, TaHKT8, TaHKT9 and TaHKT10, were identified and negatively regulate the wheat shoot K+ accumulation and salt tolerance. A genome‐wide association study (GWAS) and candidate gene association analysis further revealed that TaHKT9‐B substantially underlies the natural variation of wheat shoot K+ accumulation under saline soil conditions. Specifically, an auxin responsive element (ARE) within an 8‐bp insertion in the promoter of TaHKT9‐B is strongly associated with shoot K+ content among wheat accessions. This ARE can be directly bound by TaARF4 for transcriptional activation of TaHKT9‐B, which subsequently attenuates shoot K+ accumulation and salt tolerance. Moreover, the tae‐miR390/TaTAS3/TaARF4 pathway was identified to regulate the salt‐induced root development and salt tolerance in wheat. Taken together, our study describes the genetic basis and accompanying mechanism driving phenotypic variation in wheat shoot K+ accumulation and salt tolerance. The identified tae‐miR390/TaTAS3/TaARF4/TaHKT9‐B module is an important regulator in wheat subjected to salt stress, which provides the potentially important genetic resources for breeders to improve wheat salt tolerance. Summary statement: Here, a genome‐wide association study and candidate gene association analysis revealed that TaHKT9‐B substantially underlies the natural variation of wheat shoot K+ accumulation under saline soil conditions. In addition, this study provides the first evidence of which we are aware showing that the tae‐miR390/TaTAS3/TaARF4/TaHKT9‐B module is a key regulator of root growth in salt‐stressed wheat, providing a genetic basis for enhancing salt tolerance in wheat and other crops. [ABSTRACT FROM AUTHOR]

Objective: To investigate the clinical potential and safety of Moluodan to reverse gastric precancerous lesions. Methods: Patients aged 18–70 years diagnosed with moderate‐to‐severe atrophy and/or moderate‐to‐severe intestinal metaplasia, with or without low‐grade dysplasia, and negative for Helicobacter pylori were recruited in this randomized, double‐blind, parallel‐controlled trial. The primary outcome was the improvement of global histological diagnosis at 1‐year follow‐up endoscopy using the operative link for gastritis assessment, the operative link for gastric intestinal metaplasia assessment, and the disappearance rate of dysplasia. Results: Between November 3, 2017 and January 27, 2021, 166 subjects were randomly assigned to the Moluodan group, 168 to the folic acid group, 84 to the combination group, and 84 to the high‐dose Moluodan group. The improvement in global histological diagnosis was achieved in 60 (39.5%) subjects receiving Moluodan, 59 (37.8%) receiving folic acid, 26 (32.1%) receiving the combined drugs, and 36 (47.4%) receiving high‐dose Moluodan. Moluodan was non‐inferior to folic acid (95% confidence interval: −9.2 to 12.5; P = 0.02). High‐dose Moluodan had a trend for better protective efficacy, though there was no statistical significance. The disappearance rate of dysplasia was 82.8% in the Moluodan group, which was superior to folic acid (53.9%; P = 0.006). No drug‐related serious adverse events were observed. Conclusions: One pack of Moluodan three times daily for 1 year was safe and effective in reversing gastric precancerous lesions, especially dysplasia. Doubling its dose showed a better efficacy trend. [ABSTRACT FROM AUTHOR]

Background: Paclitaxel (PTX) resistance has become a notable clinical concern of Non‐small cell lung cancer (NSCLC). Our study aim is to investigate the effects of Resveratrol (RES) on NSCLC cells that have developed resistance to PTX. The NSCLC cell line A549 was employed in this investigation to establish a PTX‐resistant NSCLC cell line, denoted as A549/PTX, and established tumor transplantaton model. The presence of miR‐671‐5p, Stomatin‐like protein 2 (STOML2), and mitophagy biomarkers was evaluated using quantitative teal‐time PCR (qRT‐PCR) and western blot, The assessment of cell proliferation and apoptosis was conducted through the utilisation of colony formation and flow cytometry assays. The investigation of mitochondrial autolysosomes was conducted using transmission electron microscopy (TEM). Our results showed that the application of RES therapy resulted in a substantial improvement in the sansitivity of A549/PTX cells. RES exhibited an augmentation of apoptosis and a suppression of mitophagy in A549/PTX cells. RES induced an upregulation in the expression of miR‐671‐5p. This, in turn, leaded to the inhibition of STOML2, a protein that directly interacts with PINK1. In summary, our research indicates that RES improved the susceptibility of A549/PTX cells to PTX through miR‐671‐5p‐mediated STOML2 inhibition. [ABSTRACT FROM AUTHOR]

Both human and animal experiments have demonstrated that energy metabolism dysfunction in neurons after seizures is associated with an imbalance in mitochondrial fusion/fission dynamics. Effective neuronal mitochondrial dynamics regulation strategies remain elusive. Nicotinamide mononucleotide (NMN) can ameliorate mitochondrial functional and oxidative stress in age‐related diseases. But whether NMN improves mitochondrial energy metabolism to exert anti‐epileptic effects is unclear. This study aims to clarify if NMN can protect neurons from pentylenetetrazole (PTZ) or Mg2+‐free‐induced mitochondrial disorder and apoptosis via animal and cell models. We established a continuous 30‐day PTZ (37 mg/kg) intraperitoneal injection‐induced epileptic mouse model and a cell model induced by Mg2+‐free solution incubation to explore the neuroprotective effects of NMN. We found that NMN treatment significantly reduced the seizure intensity of PTZ‐induced epileptic mice, improved their learning and memory ability, and enhanced their motor activity and exploration desire. At the same time, in vitro and in vivo experiments showed that NMN can inhibit neuronal apoptosis and improve the mitochondrial energy metabolism function of neurons. In addition, NMN down‐regulated the expression of mitochondrial fission proteins (Drp1 and Fis1) and promoted the expression of mitochondrial fusion proteins (Mfn1 and Mfn2) by activating the SIRT1‐PGC‐1α pathway, thereby inhibiting PTZ or Mg2+‐free extracellular solution‐induced mitochondrial dysfunction, cell apoptosis, and oxidative stress. However, combined intervention of SIRT1 inhibitor, Selisistat, and PGC‐1α inhibitor, SR‐18292, eliminated the regulatory effect of NMN pre‐treatment on mitochondrial fusion and fission proteins and apoptosis‐related proteins. Therefore, NMN intervention may be a new potential treatment for cognitive impairment and behavioral disorders induced by epilepsy, and targeting the SIRT1‐PGC‐1α pathway may be a promising therapeutic strategy for seizures. [ABSTRACT FROM AUTHOR]