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The exposure of advanced glycation end products (AGEs) can induce chronic inflammation, oxidative stress, and accelerated aging, contributing the onset and progression of many diseases especially diabetic complications. Therefore, the searching of antiglycative foods is of practical significance, which may serve as a strategy in the attenuation of AGEs-associated diseases. In this study, we evaluated the antiglycative potential of some beans and bean sprouts that were common in our daily life. The results revealed that sprouting enhanced the antiglycative activity of beans, with black soybean sprouts demonstrating the highest efficacy (4.92-fold higher than the unsprouted beans). To assess practical implications, we examined the antiglycative activity of black soybean sprouts in pork soup, a popular food model that incorporates sprouts. Our findings confirmed the inhibitory effect on a dose-dependent manner. Through open column fractionation, we identified isoflavones and soyasaponin Bb as the candidates responsible for these effects. Additionally, compare to the unsprouted black soybeans, we found significant increases in the levels of antioxidative properties (2.51-fold), total phenolics (7.28-fold), isoflavones, and soyasaponin Bb during the sprouting process. Further studies determined that genistein, genistin, and daidzin were the major antiglycative compounds in black soybean sprouts. Collectively, this study emphasizes the benefits of sprouted beans and offers foundation for the development of functional sprouting foods.

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To understand the current saturation of emergency nurses' risk perception and its influencing factors, and to explore the correlation between emergency nurses' risk perception and nurse's safety behavior. This study is a cross-sectional study. From January 2024 to February 2024 using the questionnaire star online survey method. The convenience sampling method was used to survey nurses in the emergency departments of 5 hospitals in China. Male and female emergency nurses (n = 189) from China were included in the final sample. Nursing risk perception questionnaire and nurses safety behavior scale were used for evaluation. The collected data were comprehensively analyzed using various statistical methods, including descriptive analysis, 2 independent samples t-test mean comparison, 1-way analysis of variance for differences, multiple linear regression analysis to identify influencing factors, and Pearson correlation analyze correlations. All analyses were performed using SPSS version 26.0, and P < .05 was considered statistically significant (2-sided). The emergency nurses score was (87.08 ±â€…20.18) on the risk perception scale, scoring rate 62.2%. The results of multiple regression showed that age, marital status, education level, professional title, monthly income level, and safety behaviors were the main factors influencing the risk perception of emergency nurses (P < .05). The results of correlation analysis showed a positive correlation between the dimensions of nurses' risk perception and safety behaviors (R = 0.636, P < .01). Age, marriage, education level, years of work experience, professional title, duties. engagement type, monthly income level, participation in teaching work, safety training, and no adverse events were the influencing factors of risk perception. The research results emphasize that risk perception of emergency nurses has a positive prediction effect on safe behavior. It is suggested that nursing managers should optimize nursing workflow and human resource allocation, strategically add occupational risk training to vocational training, and strengthen nurses' safety behaviors.

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Non-alcoholic fatty liver disease (NAFLD) is a pressing global health concern that is associated with metabolic syndrome and obesity. On the basis of the insights provided by Jiang et al, this editorial presents an exploration of the potential of mesenchymal stem cells (MSCs) for NAFLD treatment. MSCs have numerous desirable characteristics, including immunomodulation, anti-inflammatory properties, and tissue regeneration promotion, rendering them attractive candidates for NAFLD treatment. Recent preclinical and early clinical studies have highlighted the efficacy of MSCs in improving liver function and reducing disease severity in NAFLD models. However, MSC heterogeneity, long-term safety concerns, and unoptimized therapeutic protocols remain substantial challenges. Addressing these challenges through standardized protocols and rigorous clinical trials is essential to the safe and successful application of MSCs in NAFLD management. Continued research into MSC mechanisms and therapeutic optimization is required to improve treatments for NAFLD and related liver diseases.

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BACKGROUND & AIMS: Frailty is associated with multiple morbidities. However, its effect on chronic liver diseases remains largely unexplored. This study evaluated the association of frailty with the risk of incident metabolic dysfunction-associated steatotic liver disease (MASLD), cirrhosis, liver cancer, and liver-related mortality. METHODS: A total of 339,298 participants without prior liver diseases from the UK Biobank were included. Baseline frailty was assessed by using physical frailty and the frailty index, categorizing participants as nonfrail, prefrail, or frail. The primary outcome was MASLD, with secondary outcomes, including cirrhosis, liver cancer, and liver-related mortality, confirmed through hospital admission records and death registries. RESULTS: During a median follow-up of 11.6 years, 4,667 MASLD, 1,636 cirrhosis, 257 liver cancer, and 646 liver-related mortality cases were identified. After multivariable adjustment, the risk of MASLD was found to be higher in participants with prefrailty (physical frailty: HR = 1.66, 95% CI = 1.40-1.97; frailty index: HR = 2.01, 95% CI = 1.67-2.42) and frailty (physical frailty: HR = 3.32, 95% CI = 2.54-4.34; frailty index: HR = 4.54, 95% CI = 3.65-5.66) than in those with nonfrailty. Similar results were also observed for cirrhosis, liver cancer, and liver-related mortality. Additionally, the frail groups had a higher risk of MASLD, which was defined as magnetic resonance imaging-derived liver proton density fat fraction > 5%, than the nonfrail group (physical frailty: OR = 1.64, 95% CI = 1.32-2.04; frailty index: OR = 1.48, 95% CI = 1.30-1.68). CONCLUSIONS: Frailty was associated with an increased risk of chronic liver diseases. Public health strategies should target reducing chronic liver disease risk in frail individuals. IMPACT AND IMPLICATIONS: While frailty is common and associated with a poor prognosis in people with MASLD and advanced chronic liver diseases, its impact on the subsequent risk of these outcomes remains largely unexplored. Our study showed that frailty was associated with the increased risks of MASLD, cirrhosis, liver cancer, and liver-related mortality. This finding suggests that assessing frailty may help identify a high-risk population vulnerable to developing chronic liver diseases. Implementing strategies that target frailty could have major public health benefits for liver-related disease prevention.

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Viruses are dependent on the host factors for their replication and survival. Therefore, identification of host factors that druggable for antiviral development is crucial. The actin cytoskeleton plays an important role in the virus infection. The dynamics change of actin and its function are regulated by multiple actin-associated proteins (AAPs). However, the role and mechanism of various AAPs in the life cycle of virus are still enigmatic. In this study, we analyzed the roles of actin and AAPs in the replication of pseudorabies virus (PRV). Using a library of compounds targeting AAPs, our data found that multiple AAPs, such as Rho-GTPases, Rock, Myosin and Formin were involved in PRV infection. Besides, our result demonstrated that the actin-binding protein Drebrin was also participated in PRV infection. Further studies are necessary to elucidate the molecular mechanism of AAPs in the virus life cycle, in the hope of mining host factors for antiviral developments.

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Background: Artesunate (ART), a natural compound derived from Artemisia annua, has shown promising clinical potentials in the treatment of various tumors, but the exact mechanism is unclear. Choroidal melanoma (CM) is a major malignant ocular tumor in adults, known for its significant malignancy and poor prognosis, with limited efficacy in current treatments. This study explored the anti-CM effects and mechanisms of ART using a combination of network pharmacology, molecular docking and experimental validation. Methods: Potential targets of ART were screened in PubChem, Swiss Target Prediction and Traditional Chinese Medicine Systems Pharmacology (TCMSP) Database Analysis Platform databases, while target genes related to CM prognosis were selected from Online Mendelian Inheritance in Man (OMIM), GeneCards and DisGeNET databases. The intersection of these two groups of datasets yielded the target genes of ART involved in CM. Protein-protein interaction (PPI) network analysis of the intersecting targets, as well as Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, were conducted to identify core targets and critical pathways. Molecular docking methods were performed to predict the binding interactions between ART and core targets. The effects of ART on CM were evaluated through CCK8, colony formation, transwell, as well as flow cytometry assays to detect apoptosis, cell cycle, reactive oxygen species (ROS). Western blot (WB) assays were conducted to investigate the impact of ART on key proteins and pathways associated with CM. Finally, in vivo assays were conducted to further validate the effects of ART on subcutaneous tumors in nude mice. Results: Research has shown that key pathways and core targets for ART in treating CM were identified through a network pharmacology approach. Molecular docking results verified the strong binding affinity between ART and these core targets. The analysis and predicted results indicated that ART primarily exerted its effects on CM through various tumor-related pathways like apoptosis. The assays in vitro confirmed that ART significantly inhibited the proliferation and migration of CM cells. This was achieved by promoting apoptosis through activation of the p53 signaling pathway, causing cell cycle arrest at the G0/G1 phase by inhibiting the PI3K/AKT/mTOR signaling pathway and increasing the intracellular level of ROS by activating the NRF2/HO-1 signaling pathway. Additionally, the assays in vivo further validated the significant proliferation-inhibitory effect of ART on CM. Conclusion: This study, making the initial exploration, illustrated through network pharmacology combined with molecular docking and in vitro/in vivo assays, confirmed that ART exerted potential anti-cancer effects on CM by promoting apoptosis, inducing cell cycle arrest and increasing intracellular levels of ROS. These findings suggested that ART held significant therapeutic potential for CM.

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Fluorescent solvatochromic dyes that are sensitive to the nature of local microenvironmental, have been explored as probes in applications ranging from the imaging biomolecules to understanding of basic biomolecule functions. To expand the scope of fluorescent solvatochromic dyes for G-quadruplex (G4) DNA structures, and to illustrate the relationship between structure and properties, three newly designed D-π-A type fluorescent dyes were synthesized by introducing diarylimidazole to carbazole skeleton linked to benzene, furan or thiophene π-conjugated bridge and connected with pyridinium acceptor, respectively. Their structural characteristics, optical properties, and G4 DNA binding properties were discussed in detail. In general, the incorporation of furan and thiophene as π-conjugated bridges leads the better conjugation and molecular coplanarity with more efficient intramolecular charge transfer (ICT) effect compared with benzene bridge. The fluorescence intensities induced upon interaction were found that TP-6 with thiophene π-conjugated bridge had the strongest response toward G4 DNAs. In addition, the application of this dye as a fluorescent agent for living cell imaging was also demonstrated.

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Advancements in assisted driving technologies are expected to enable future passengers to use a wide range of multimedia applications in electric vehicles (EVs). To address the bandwidth demands for high-resolution and immersive videos during peak traffic, this study introduces a bandwidth-management algorithm to support differentiated streaming services in heterogeneous vehicle-to-everything (V2X) networks. By leveraging cellular 6G base stations, along with Cell-Free (CF) Massive Multi-Input Multi-Output (mMIMO) Wi-Fi 7 access points, the algorithm aims to provide a high-coverage, high-speed, and low-interference V2X network environment. Additionally, Li-Fi technology is employed to supply extra bandwidth to vehicles with limited connectivity via V2V communication. Importantly, the study addresses the urgency and prioritization of different applications to ensure the smooth execution of emergency applications and introduces a pre-downloading mechanism specifically for non-real-time applications. Through simulations, the algorithm's effectiveness in meeting EV users' bandwidth needs for various multimedia streaming applications is demonstrated. During peak-bandwidth-demand periods, users experienced an average increase in bandwidth of 47%. Furthermore, bandwidth utilization across the V2X landscape is significantly improved.

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Heart failure (HF) remains a significant burden on global healthcare systems, necessitating innovative approaches for its management. This manuscript critically evaluates the role of remote monitoring and telemedicine in revolutionizing HF care delivery. Drawing upon a synthesis of current literature and clinical practices, it delineates the pivotal benefits, challenges, and personalized strategies associated with these technologies in HF management. The analysis highlights the potential of remote monitoring and telemedicine in facilitating timely interventions, enhancing patient engagement, and optimizing treatment adherence, thereby ameliorating clinical outcomes. However, technical intricacies, regulatory frameworks, and socioeconomic factors pose formidable hurdles to widespread adoption. The manuscript emphasizes the imperative of tailored interventions, leveraging advancements in artificial intelligence and machine learning, to address individual patient needs effectively. Looking forward, sustained innovation, interdisciplinary collaboration, and strategic investment are advocated to realize the transformative potential of remote monitoring and telemedicine in HF management, thereby advancing patient-centric care paradigms and optimizing healthcare resource allocation.

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A highly enantioselective Pd/Bim-catalyzed dearomative Michael reaction applying polycyclic tropones as non-benzenoid aromatic Michael acceptors and arylboronic acids as aryl pronucleophiles has been developed. The bridged biaryls bearing central and axial chirality, including pentacyclic cyclohepta[b]indoles and 6,7-dihydrodibenzo[a,c][7]annulen-5-ones, are generally generated in good to high yields and excellent enantioselectivities and can be readily transformed into useful derivatives.

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Porcine reproductive and respiratory syndrome (PRRS) is a globally prevalent contagious disease caused by the positive-strand RNA PRRS virus (PRRSV), resulting in substantial economic losses in the swine industry. Modifying the CD163 SRCR5 domain, either through deletion or substitution, can eff1ectively confer resistance to PRRSV infection in pigs. However, large fragment modifications in pigs inevitably raise concerns about potential adverse effects on growth performance. Reducing the impact of genetic modifications on normal physiological functions is a promising direction for developing PRRSV-resistant pigs. In the current study, we identified a specific functional amino acid in CD163 that influences PRRSV proliferation. Viral infection experiments conducted on Marc145 and PK-15 CD163 cells illustrated that the mE535G or corresponding pE529G mutations markedly inhibited highly pathogenic PRRSV (HP-PRRSV) proliferation by preventing viral binding and entry. Furthermore, individual viral challenge tests revealed that pigs with the E529G mutation had viral loads two orders of magnitude lower than wild-type (WT) pigs, confirming effective resistance to HP-PRRSV. Examination of the physiological indicators and scavenger function of CD163 verified no significant differences between the WT and E529G pigs. These findings suggest that E529G pigs can be used for breeding PRRSV-resistant pigs, providing novel insights into controlling future PRRSV outbreaks.

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The role of melatonin (MT), an essential phytohormone controlling the physiological and biochemical reactions of plants to biotic and abiotic stress, in alleviating pesticide phytotoxicity remains unclear. This study explores the effects of MT (0 and 200 mg/L) and six doses of fluroxypyr-meptyl (FLUME) (0-0.14 mg/L) on the physiological response of rice (Oryza sativa). FLUME exposure inhibited the growth of rice seedlings, with MT treatment ameliorating this effect. To determine the biochemical processes and catalytic events involved in FLUME breakdown in rice, six rice root and shoot libraries exposed to either FLUME or FLUME-MT were generated and then subjected to RNA-Seq-LC-Q-TOF-HRMS/MS analyses. The results showed that 1510 root genes and 139 shoot genes exhibited higher upregulation in plants treated with an ecologically realistic FLUME concentration and MT than in those treated with FLUME alone. Gene enrichment analysis revealed numerous FLUME-degradative enzymes operating in xenobiotic tolerance to environmental stress and molecular metabolism. Regarding the FLUME degradation process, certain differentially expressed genes were responsible for producing important enzymes, such as cytochrome P450, glycosyltransferases, and acetyltransferases. Four metabolites and ten conjugates in the pathways involving hydrolysis, malonylation, reduction, glycosylation, or acetylation were characterized using LC-Q-TOF-HRMS/MS to support FLUME-degradative metabolism. Overall, external application of MT can increase rice tolerance to FLUME-induced oxidative stress by reducing phytotoxicity and FLUME accumulation. This study provides insights into MT's role in facilitating FLUME degradation, with potential implications for engineering genotypes supporting FLUME degradation in paddy crops.

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Papillary craniopharyngioma (PCP) and adamantinomatous craniopharyngioma (ACP) are distinct, slow growing tumors of the suprasellar region. Their location, composition and biology have historically evaded successful surgical, radiation, and medical therapy. Meanwhile compromise of critical structures either by tumor or treatments increase morbidity, impacting patient and carer quality of life. There has been a paradigm shift in the management of PCP, stemming from the discovery of BRAFV600E mutation in its tumorigenesis. Such a treatment breakthrough may soon be the case for ACP, changing the landscape of craniopharyngioma management. We use a case of ACP, partially responding to ERK inhibitor therapy to demonstrate chronicity of disease progression and discuss modern management strategies highlighting the importance of access to tumour agnostic clinical trials, and future directions.

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Pancreatic ductal adenocarcinoma (PDAC) is characterized by increasing fibrosis, which can enhance tumor progression and spread. Here, we undertook an unbiased temporal assessment of the matrisome of the highly metastatic KPC (Pdx1-Cre, LSL-KrasG12D/+, LSL-Trp53R172H/+) and poorly metastatic KPflC (Pdx1-Cre, LSL-KrasG12D/+, Trp53fl/+) genetically engineered mouse models of pancreatic cancer using mass spectrometry proteomics. Our assessment at early-, mid-, and late-stage disease reveals an increased abundance of nidogen-2 (NID2) in the KPC model compared to KPflC, with further validation showing that NID2 is primarily expressed by cancer-associated fibroblasts (CAFs). Using biomechanical assessments, second harmonic generation imaging, and birefringence analysis, we show that NID2 reduction by CRISPR interference (CRISPRi) in CAFs reduces stiffness and matrix remodeling in three-dimensional models, leading to impaired cancer cell invasion. Intravital imaging revealed improved vascular patency in live NID2-depleted tumors, with enhanced response to gemcitabine/Abraxane. In orthotopic models, NID2 CRISPRi tumors had less liver metastasis and increased survival, highlighting NID2 as a potential PDAC cotarget.

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Reprogramming of cellular energy metabolism, including deregulated lipid metabolism, is a hallmark of head and neck squamous cell carcinoma (HNSCC). However, the underlying molecular mechanisms remain unclear. Long-chain acyl-CoA synthetase 4 (ACSL4), which catalyzes fatty acids to form fatty acyl-CoAs, is critical for synthesizing phospholipids or triglycerides. Despite the differing roles of ACSL4 in cancers, our data showed that ACSL4 was highly expressed in HNSCC tissues, positively correlating with poor survival rates in patients. Knockdown of ACSL4 in HNSCC cells led to reduced cell proliferation and invasiveness. RNA sequencing analyses identified interferon-induced protein 44 (IFI44) and interferon-induced protein 44-like (IFI44L), encoded by two interferon-stimulated genes, as potential effectors of ACSL4. Silencing IFI44 or IFI44L expression in HNSCC cells decreased cell proliferation and invasiveness. Manipulating ACSL4 expression or activity modulated the expression levels of JAK1, tyrosine kinase 2 (TYK2), signal transducer and activator of transcription 1 (STAT1), interferon α (IFNα), IFNß, and interferon regulatory factor 1 (IRF1), which regulate IFI44 and IFI44L expression. Knockdown of IRF1 reduced the expression of JAK1, TYK2, IFNα, IFNß, IFI44, or IFI44L and diminished cell proliferation and invasiveness. Our results suggest that ACSL4 upregulates interferon signaling, enhancing IFI44 and IFI44L expression and promoting HNSCC cell proliferation and invasiveness. Thus, ACSL4 could serve as a novel therapeutic target for HNSCC.

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In this editorial we comment on the article published in a recent issue of the World Journal of Gastrointestinal Oncology. Characterized by high mortality rates and geographical variations in its incidence, esophageal cancer poses a major global health challenge. This editorial article synthesizes insights from the review of esophageal cancer conducted by Qu et al, which highlights the importance of tailored screening and treatment strategies. Key themes include the effect of regional disparities on screening protocols, advancements in early detection methodologies, and therapeutic management disparities between different regions. By embracing personalized approaches grounded in regional nuances and technological innovation, the article advocates for comprehensive and collaborative efforts to improve patient outcomes in esophageal cancer care.

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Background: Myocardial bridging (MB) is a congenital coronary anomaly and an important cause of chest pain. The long-term effects of MB on cardiovascular events remain elusive. Methods: We used the National Health Insurance Research Database of Taiwan to conduct an analysis. All patients who had undergone coronary angiography were considered for inclusion. The primary endpoint was a composite of nonfatal myocardial infarction, nonfatal ischemic stroke, and cardiovascular death. Results: We identified 10,749 patients from 2008 to 2018 and matched them with an equal number of controls by propensity-score matching. The mean follow-up period was 5.78 years. In patients without coronary artery disease, MB increased the risk of the composite endpoint (hazard ratio [HR]: 1.57, 95% confidence interval [CI]: 1.44-1.72, p < 0.001), which was driven by increased risks of nonfatal myocardial infarction and cardiovascular death. In patients with significant coronary artery disease, MB did not increase the risk of major adverse cardiovascular events. MB was identical to insignificant coronary artery disease from the viewpoint of clinical outcomes. Conclusions: The presence of MB significantly increases cardiovascular risks in patients with normal coronary vessels. Atherosclerotic coronary artery disease mitigates the effect of MB on cardiovascular outcomes. MB can be considered an insignificant coronary artery disease equivalent.

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Diastolic dysfunction, a prevalent condition characterized by impaired relaxation and filling of the left ventricle, significantly contributes to heart failure with preserved ejection fraction (HFpEF). Galectin-3, a ß-galactoside-binding lectin, has garnered attention as a potential biomarker and mediator of fibrosis and inflammation in cardiovascular diseases. This comprehensive review investigates the impact of galectin-3 on diastolic dysfunction. We explore its molecular mechanisms, including its involvement in cellular signaling pathways and interaction with components of the extracellular matrix. Evidence from both animal models and clinical studies elucidates galectin-3's role in cardiac remodeling, inflammation, and fibrosis, shedding light on the underlying pathophysiology of diastolic dysfunction. Additionally, we examine the diagnostic and therapeutic implications of galectin-3 in diastolic dysfunction, emphasizing its potential as both a biomarker and a therapeutic target. This review underscores the significance of comprehending galectin-3's role in diastolic dysfunction and its promise in enhancing diagnosis and treatment approaches for HFpEF patients.

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Isoleucine-proline-proline (Ile-Pro-Pro, IPP) is a natural food source tripeptide that inhibits angiotensin-converting enzyme (ACE) activity. The aim of this study was to determine the central and peripheral roles of IPP in attenuating sympathetic activity, oxidative stress and hypertension. Male Sprague-Dawley rats were subjected to sham-operated surgery (Sham) or two-kidney one-clip (2K1C) surgery to induce renovascular hypertension. Renal sympathetic nerve activity and blood pressure were recorded. Bilateral microinjections of IPP to hypothalamic paraventricular nucleus (PVN) attenuated sympathetic activity (-16.1 ± 2.5%, P < 0.001) and hypertension (-8.7 ± 1.5 mmHg, P < 0.01) in 2K1C rats by inhibiting ACE activity and subsequent angiotensin II and superoxide production in the PVN. Intravenous injections of IPP also attenuated sympathetic activity (-15.1 ± 2.1%, P < 0.001) and hypertension (-16.8 ± 2.3 mmHg, P < 0.001) via inhibiting ACE activity and oxidative stress in both PVN and arteries of 2K1C rats. The duration of the effects of the intravenous IPP was longer than those of the PVN microinjection, but the sympatho-inhibitory effect of intravenous injections occurred later than that of the PVN microinjection. Intraperitoneal injection of IPP (400 pmol/day for 20 days) attenuated hypertension and vascular remodeling via inhibiting ACE activity and oxidative stress in both PVN and arteries of 2K1C rats. These results indicate that IPP attenuates hypertension and sympathetic activity by inhibiting ACE activity and oxidative stress. The sympathoinhibitory effect of peripheral IPP is mainly caused by the ACE inhibition in PVN, and the antihypertensive effect is related to the sympathoinhibition and the arterial ACE inhibition. Long-term intraperitoneal IPP therapy attenuates hypertension, oxidative stress and vascular remodeling.