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Objective This study evaluated the predictive value of serum homocysteine (HcY) and potassium ion (K + ) for short-term prognosis of patients with acute cerebral infarction (ACI) undergoing intravenous thrombolysis with recombinant tissue plasminogen activator (rt-PA). Methods Totally, 140 ACI patients receiving intravenous thrombolysis using rt-PA were finally included and classified into early neurological deterioration (END) and non-END groups. Serum levels of HcY and electrolytes were detected. The 90-day prognosis of patients after thrombolysis was analyzed. Influencing factors for END and poor short-term prognosis in rt-PA-treated ACI patients were identified using stepwise regression models. Correlations of serum HcY and K + with modified Rankin scale (mRS) scores were analyzed, and values of serum HcY and K + in assessing END and poor prognosis of ACI patients were determined. Results The END group had higher age, atrial fibrillation, neutrophil ratio, CysC, FIB, FPG, TNF-ɑ, IL-6 and HcY levels, and National Institutes of Health Stroke Scale scores on admission but lower serum calcium ion and K + concentrations than the non-END group. In ACI patients, serum HcY and K + levels significantly correlated with mRS scores. Serum HcY and K + levels were independent influencing factors for END and poor short-term prognosis of rt-PA-treated ACI patients. Combination of serum HcY and K + could assist in predicting END and poor short-term prognosis in ACI patients. Conclusion Serum HcY and K + levels are closely linked to END and short-term prognosis in ACI patients after intravenous thrombolysis using rt-PA and can be used as novel biomarkers for short-term prognosis in ACI patients.

Vascular cognitive impairment (VCI) is a prevalent form of cognitive dysfunction. Resting-state functional magnetic resonance imaging (rs-fMRI) could serve as a potential biomarker for early detection. This study employed activation likelihood estimation (ALE) meta-analysis to investigate specific neural abnormalities in VCI patients. We systematically searched PubMed, Embase, and Web of Science for rs-fMRI studies on VCI that reported amplitude of low-frequency fluctuation (ALFF), regional homogeneity (ReHo), or functional connectivity (FC). Sixteen eligible fMRI studies were included in the ALE meta-analysis. Compared to healthy controls (HCs), VCI patients exhibited the following rs-fMRI alterations. For ALFF, there was an increase in the left anterior cingulate (AC) and left inferior frontal gyrus, possibly a compensatory over - activation. Decreases were seen in regions like the bilateral precuneus and medial frontal gyri (mFG), linked to cognitive deficits. ReHo increased in the left claustrum and insula, suggesting enhanced local synchronization, but decreased in the right sub - gyral region and middle temporal gyru (MTG), which may relate to language issues. FC was enhanced in areas related to complex cognitive processes, yet reduced in regions crucial for memory. VCI patients exhibited distinct functional abnormalities in specific brain regions, reflecting their diverse cognitive impairments. These region-specific alterations may serve as potential biomarkers for early diagnosis and targeted intervention in VCI.

Corporate social responsibility (CSR) in the food industry has received increasing attention in recent years. Many scholars have paid attention to case studies and other empirical analyses in this field, but there is no systematic or scientific literature review. The purpose of this study is to quantitatively evaluate the knowledge structure, research hotspots, and development history in CSR in the food industry. After searching, screening, and commenting, 498 articles were left for citation analysis, co-citation analysis, and co-word analysis. The main findings of the research are as follows: (1) The overall development status of the research in the field. The analysis of the three fields that constitute the knowledge structure. (2) Research in this field has become a hot spot, but the research is rather scattered, and the scholars and experts do not have a special research core. (3) The keywords’ cluster results in 9 clustering tags, which are further grouped into 7 groups. The research of the scholars focuses on the food supply chain, consumer perception, and social media communication. (4) The research topics in this field focus on environmental responsibility, nutrition and health, and food safety. The research results show that future research should be more in-depth and reflect the new characteristics of the Internet, digitalization, and big data.

Background and purpose Vascular cognitive impairment (VCI) is strongly linked to blood-brain barrier (BBB) dysfunction. This study investigated whether Tubuloside B (Tub-B), a primary bioactive compound of Cistanche tubulosa, ameliorates cognitive deficits by protecting BBB integrity through inhibition of tricellulin (TRIC) ubiquitination and degradation. Methods The main plasma metabolites of total glycosides of Cistanche (TCGs) were identified by UPLC-QQQ-MS. A bilateral common carotid artery occlusion (BCCAO) rat model was used to induce chronic cerebral hypoperfusion (CCH). Cognitive function was assessed using the Morris water maze, and BBB permeability was evaluated by Evans blue extravasation. The concentrations of inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-10, and transforming growth factor-β (TGF-β), in the rat hippocampal tissues were quantified using ELISA kits. TRIC expression and ubiquitination were analyzed by Western blot, co-immunoprecipitation, and immunohistochemistry. An in vitro oxygen-glucose deprivation (OGD) model in brain microvascular endothelial cells was used to validate the effects on barrier function. Results Tub-B was identified as the major circulating metabolite, accounting for 52.3% ± 2.1% of plasma components. In CCH rats, Tub-B (20 mg/kg) significantly improved spatial memory, increasing platform crossings (3.00 ± 0.58 vs. CCH, P <  0.05) and reducing Evans blue leakage (0.038 ± 0.007 µg/g tissue vs. 0.15 ± 0.02 µg/g in CCH, P <  0.001). Furthermore, Tub-B treatment dose-dependently suppressed pro-inflammatory cytokines (TNF-α, IL-1β) and concomitantly enhanced anti-inflammatory cytokines (IL-10, TGF-β) in the hippocampus. It also attenuated the downregulation of TRIC and suppressed its ubiquitination. In OGD-injured endothelial cells, Tub-B enhanced barrier integrity and inhibited TRIC ubiquitination. Conclusion Tub-B attenuates CCH-induced BBB disruption and cognitive impairment by inhibiting TRIC ubiquitination and degradation, likely via interference with VEGF signaling. These results highlight its potential as a therapeutic agent for VCI.

Customer participation in brand environmental responsibility is necessary for enterprises and consumers to co-create value. However, it is not yet clear why some corporate social responsibility (CSR) communications are more effective in attracting higher customer participation in a digitally transparent environment. Based on signal theory and social identity theory, this study examines the impact of the interactive effect of CSR strategy (proactive vs. reactive) and transparency signals (high vs. low) on customer trust (perceived integrity and perceived competence), customer–brand identification, and participation intention in brand environmental responsibility. We conduct a 2 × 2 study with 140 respondents. The findings reveal a significant interaction effect of CSR strategy and transparency signals on perceived integrity, perceived competence, and participation intention in brand environmental responsibility. Mediation analysis reveals that the impact of CSR strategy on participation intention is serially mediated via perceived trust and customer–brand identification and varies across different transparency levels.

Early neurological deterioration (END) significantly worsens outcomes in patients with acute ischemic stroke (AIS) receiving intravenous thrombolysis, yet clinicians lack reliable tools to identify high-risk patients who need intensified monitoring and preemptive interventions. This study aimed to develop and validate a high-performance machine learning model for END prediction that enables personalized risk-stratified management of patients with AIS after thrombolysis. This multicenter study analyzed 1927 patients with AIS who were treated with intravenous thrombolysis in 3 hospitals, comprising a development cohort (n=1361) from Lianyungang Clinical Medical College and an external validation cohort (n=566) from 2 independent hospitals. We systematically evaluated 27 clinical parameters using multiple machine learning algorithms to develop ENDRAS (Early Neurological Deterioration Risk Assessment Score), a prediction model based on 6 readily available clinical variables. Model performance was assessed through comprehensive metrics (area under the receiver operating characteristic curve, accuracy, precision, recall, F1-score) in both internal and external validation cohorts. The XGBoost-based ENDRAS showed promising predictive performance (area under the receiver operating characteristic curve=0.988, 95% CI 0.983-0.993) using 6 readily available parameters: Trial of ORG 10172 in Acute Stroke Treatment classification, intracranial artery stenosis severity, National Institutes of Health Stroke Scale score, systolic blood pressure, neutrophil count, and red blood cell distribution width. We established a dual-pathway management protocol for stratifying patients into low-risk (<29%) and high-risk (≥29%) groups, where high-risk patients receive intensive monitoring with hourly assessments and expedited imaging, while low-risk patients follow a resource-optimized protocol without compromising safety. Implemented as a web-based calculator with a <0.02-second computation time, ENDRAS enables real-time clinical decision support at the point of care. ENDRAS integrates END prediction into actionable clinical pathways, potentially improving postthrombolysis care through personalized monitoring strategies and targeted interventions. Its robust performance in merged cohorts, efficient computation time, and structured management framework address key challenges in stroke care while enhancing resource utilization. Further prospective validation across diverse populations is needed to fully establish ENDRAS as a standard clinical decision-support system, but its ability to identify high-risk patients early may significantly improve outcomes in AIS.

Enzyme-regulated biomineralization offers precise spatiotemporal control over tissue mineralization, overcoming key limitations of conventional regenerative therapies. This review systematically examines the underlying biological mechanisms, focusing on enzymatic regulation of phosphate metabolism, mineralization regulators, and matrix stabilization that orchestrate hierarchical mineral deposition. Organic matrices facilitate nanoconfinement-driven nucleation and spatially controlled mineralization through biochemical functionalization. These fundamental mechanisms have inspired the development of advanced enzyme-functionalized biomaterials, such as covalently immobilized hydrogels, physically entrapped nanocomposites, bioaffinity scaffolds, and stimuli-responsive 3D-printed constructs, which enable precisely tunable in situ mineralization. In clinical applications, such biomaterial systems demonstrate significant therapeutic potential, with critical-sized bone defects showing accelerated healing through biomimetic mineral-collagen alignment and enzyme-mediated enamel restoration achieving both hardness recovery and reduced secondary caries incidence. Current limitations primarily involve enzymatic stability, immunogenicity, and manufacturing scalability. Emerging solutions focus on gene-enzyme hybrid platforms and intelligent responsive systems for personalized regenerative approaches. The synergistic integration of biological principles with materials science provides a transformative foundation for developing next-generation therapeutic strategies. Schematic illustration of enzyme-mediated mineralization processes. This diagram outlines key aspects of enzyme-regulated biomineralization, including immobilization strategies (physical encapsulation, covalent conjugation, and advanced carrier systems), the physiological roles of mineralization-related enzymes, and the development of enzyme-functionalized biomaterials such as engineered scaffolds, hydrogels, and 3D-bioprinted constructs. This integrated approach synergistically combines biochemical regulation with material design to facilitate biomimetic tissue repair and regeneration in bone and dental applications [Display omitted] •Enzymatic mineralization provides precise control, overcoming the limits of traditional grafts for tissue regeneration.•Enzyme-based biomaterials enable tunable mineralization, enhancing bone and dental regeneration via biomimetic alignment.•Stability and scalability challenges drive innovation toward smart, gene-enzyme hybrid platforms for personalized therapies.

Between 2022 and 2024, a severe branch dieback disease was observed affecting over 6% of sweet cherry trees of the ‘Tieton’ cultivar in commercial greenhouses in southern Liaoning Province, China. Symptoms primarily occurred at the top of young branches. At the early stage of disease onset, the lesions appeared as dark brown, irregularly shaped areas with a moist surface; as the disease progressed, these lesions turned dry and rotten, leading to tree decline symptoms in sweet cherry trees. Disease diagnosis was carried out in sweet cherry greenhouses across Liaoning Province, where 24 diseased samples were collected and 14 fungal isolates were obtained therefrom. Based on morphological traits, cultural characteristics, and multi-locus phylogenetic analyses of the internal transcribed spacer (ITS) region, beta-tubulin (TUB2) gene, and translation elongation factor 1-α (TEF1) gene, these isolates were identified as Botryosphaeria dothidea. Two representative isolates, namely zdcy-1 and zdcy-2, were selected for pathogenicity assays. Both mycelial plug and spore suspension inoculation methods confirmed the pathogenicity of the pathogen. The biological characteristic assays revealed that the optimal temperature range for the pathogen’s mycelial growth on PDA medium was 25–28 °C, and the optimal pH range was 6.0–8.0. This study improves the understanding of branch dieback disease in sweet cherry orchards in China, enriches the knowledge regarding the geographical distribution, host range, and infection sites of the pathogen, and provides novel insights for the management of sweet cherry diseases.

The aim of this study was to improve understanding of the impacts of low-light stress induced by branch-bagged shading on photosynthetic physiology and biochemical composition. Eight-year-old ‘Tieton’ sweet cherry leaves and white parchment bags with a 23% shading rate were selected to cover ten 50 cm long branches for 10 d, 20 d, and 30 d followed by 10 d light restoring. The results indicated that when shading for 30 d, the net photosynthetic rate (PN) of the leaves, including stomatal conductance (gs), transpiration rate (E), intercellular CO2 concentration (Ci), superoxide dismutase (SOD), peroxide (POD), catalase (CAT), starch, and sugar contents were lower, whereas chlorophyll (Chl) and malondialdehyde (MDA) concentrations were higher than those in CK leaves. After 10-10 treatments, leaf parameters including SOD, POD, CAT, starch, and sugar levels were almost the same as those in control (CK; no shading) leaves; the opposite was true for Chl and MDA. However, after 10 d of no bag following 20 and 30 d of shading, the PN, Ci, E, and SOD, CAT, glucose, sorbitol, sucrose and starch levels were lower than those in CK leaves, whereas MDA levels were higher. At 20-10, there was no difference in leaf fructose levels compared to those in CK leaves; the Chl levels were higher. At 30-10, leaf fructose levels were reduced compared with those in CK leaves; Chl levels showed no difference. Therefore, sweet cherry leaves have robust recovery abilities; however, prolonged low-light stress can impede physiological restoration.

Background: A recent study disclosed that ferroptosis was an important myocyte death style in myocardial infarction (MI). However, the diagnostic value of ferroptosis regulators and correlated underlying mechanisms in acute myocardial infarction (AMI) remain unknown. Methods: Bioinformatical analyses were conducted to identify the candidate biomarkers for AMI, and the collected local samples were used to validate the findings via real-time quantitative PCR. Bioinformatical analysis and luciferase reporter assay were implemented to identify the transcriptional factor. Transient transfection and ferroptosis characteristic measurement, including glutathione peroxidase 4, malondialdehyde, iron, and glutathione, was performed to verify the ability of the candidate gene to regulate the ferroptosis of cardiomyocytes. A meta-analysis was conducted in multiple independent cohorts to clarify the diagnostic value. Results: A total of 121 ferroptosis regulators were extracted from previous studies, and aldo-keto reductase family 1 member C3 (AKR1C3) was significantly downregulated in the peripheral blood samples of AMI cases from the analysis of GSE48060 and GSE97320. HOXB4 served as a transcriptional activator for AKR1C3 and could suppress the ferroptosis of the H9C2 cells treated with erastin. Besides this, peripheral blood samples from 16 AMI patients and 16 patients without coronary atherosclerotic disease were collected, where AKR1C3 and HOXB4 both showed a high diagnostic ability. Furthermore, a nomogram including HOXB4 and AKR1C3 was established and successfully validated in six independent datasets. A clinical correlation analysis displayed that AKR1C3 and HOXB4 were correlated with smoking, CK, CK-MB, and N-terminal-pro-B-type natriuretic peptide. Conclusion: Taken together, this study demonstrates that AKR1C3 and HOXB4 are promising diagnostic biomarkers, providing novel insights into the ferroptosis mechanisms of AMI.