Hypertension ranks among the most prevalent chronic non-communicable diseases worldwide, with its prevalence rising steadily and exerting substantial impacts on the demographic composition of voluntary blood donors and the safety of blood supply. The eligibility of hypertensive individuals for safe blood donation and the relevant screening and management strategies have long remained controversial in transfusion medicine. This article systematically reviews the epidemiological characteristics of hypertension, donation-related physiological alterations and underlying risk mechanisms. By synthesizing evidence from international multicenter studies and regulatory practices across major nations, it conducts a comprehensive analysis of blood donation safety and donor admission criteria for hypertensive patients. Available evidence demonstrates that for hypertensives with well-stabilized blood pressure and no severe cardiac, cerebral or renal complications or target organ damage, the overall incidence of adverse reactions following blood donation is comparable to that in healthy donors, and no definitive correlation has been identified between blood pressure levels and vasovagal responses. Current mainstream international management frameworks are gradually shifting from screening reliant on a single blood pressure cutoff value toward an integrated strategy combining stratified risk classification and individualized dynamic assessment, with core focus on long-term blood pressure control, consistency of medication regimens and complication status. Meanwhile, emerging technologies including artificial intelligence, ambulatory blood pressure monitoring and wearable devices have opened innovative avenues for blood donation risk evaluation and full-cycle donor management. In light of existing clinical evidence, future efforts should further refine the multi-dimensional risk stratification system, facilitate the implementation of intelligent screening and continuous monitoring technologies, and scale up health education and follow-up management for hypertensive populations. Such measures aim to appropriately expand the pool of eligible blood donors while safeguarding donation safety, ultimately achieving coordinated improvement in blood safety and blood supply capacity.

Hepatocellular carcinoma (HCC) imposes a major health and economic burden worldwide, with disproportionate effects in low- and middle-income countries (LMICs). Surveillance in high-risk populations, typically using semiannual ultrasound and alpha-fetoprotein testing, has been shown to be cost-effective by enabling earlier detection and improving survival. Yet, its overall value is reduced by poor adherence and the limited sensitivity of ultrasound, particularly in patients with metabolic-associated steatotic liver disease. Emerging approaches—including abbreviated magnetic resonance imaging, multi-biomarker models (e.g., gender, age, AFP, AFP-L3, and DCP), and liquid biopsy assays such as methylated DNA markers—demonstrate greater diagnostic accuracy and potential economic advantages compared with conventional methods. Integration of artificial intelligence into imaging may further enhance efficiency and reduce downstream costs. Moving toward precision surveillance, guided by individualized risk stratification that incorporates etiology, fibrosis stage, and molecular profiles, can optimize allocation of resources and maximize cost-effectiveness at the population level. Interventions to improve adherence, including mailed outreach and behavioral economic incentives, have shown both clinical benefit and cost savings, underscoring the role of implementation science. Because socioeconomic disparities influence both access and outcomes, economic models must explicitly address equity to achieve sustainable impact. Future research should prioritize prospective trials that evaluate not only clinical performance but also the real-world cost-effectiveness of novel technologies and stratified surveillance strategies. For LMICs, adapting proven models into affordable, context-appropriate programs is essential. By combining prevention, precision risk assessment, innovative technologies, and equitable implementation, HCC surveillance can deliver both clinical and economic value, reducing the global burden of disease.

ObjectiveTo screen a set of short tandem repeat (STR) markers covering rat chromosomes 1-20 and the X chromosome, with 2-4 markers on each chromosome, and establish a dedicated marker panel for genetic contamination detection and strain identification of 5 commonly used inbred rat strains. MethodsSix 6-8 week-old rats (half male and half female) were selected from F344, BN, DA, Lewis, and PVG strain, respectively. Genomic DNA was extracted from rat tail tissues. A total of 61 STR markers were selected, including 27 from the national standard GB 14923—2022 and 34 from the literature. Singleplex STR PCR amplification combined with capillary electrophoresis was used for genotyping of the 5 inbred rat strains, and genotype data were analyzed using GeneMapper ID v3.2 software. Based on the STR genotyping results, genetic distances between strains were calculated with GenAlEx 6.51b2 software, and a phylogenetic tree of the inbred rat strains was constructed using MEGA7 software. ResultsAmong the 61 STR markers, non-specific amplification was observed for D15mit3, while no specific amplification product was obtained for D3wox7. LCA, AGT, and D5Hmgc2 exhibited no inter-strain polymorphism across the 5 inbred strains, while the remaining 56 markers exhibited inter-strain polymorphism. These 56 markers covered rat chromosomes 1-20 and the X chromosome (2-4 markers per chromosome). Among them, 42 markers could be used for genetic contamination detection in inbred rat strains. The amplified product lengths of D7wox14, D15rat123, and D20wox3 differed among the 5 strains, which could be applied for strain identification. The phylogenetic tree showed that the number of STR allelic differences between BN and F344 strains was 49, with a genetic distance of 1.775, both of which were the highest among all strain pairs. This indicated that the two strains exhibited the highest level of genetic differentiation and were the most distantly related. Among the 5 strains, F344, DA, and PVG clustered together, indicating their relatively close genetic distance, while BN and Lewis formed another cluster, indicating a relatively close genetic distance between them. The genetic relationships among the 5 strains were consistent with previous reports. ConclusionThis study successfully screened a set of STR markers for molecular genetic detection of 5 commonly used inbred rat strains, including F344, BN, DA, Lewis, and PVG, and established specific marker combinations for genetic contamination detection and strain identification, respectively.

Gastroesophageal varices （GOV） bleeding is a severe complication of portal hypertension with a high mortality rate. Animal models are indispensable tools for investigating its pathogenesis and developing novel therapeutic strategies. This article systematically reviews the methods for establishing various GOV models， with a particular focus on their efficacy in simulating the key pathological processes such as an increase in hepatic venous pressure gradient and the risk of bleeding， and it also proposes targeted strategies for model selection. Finally， this article discusses the application prospects of emerging techniques in the era of precision medicine， such as organoids and gene editing， in order to provide model selection and a theoretical reference for exploring the mechanism and clinical translation of GOV.

Multidrug-resistant (MDR) bacterial infections have emerged as a serious challenge of global public health crisis. The overuse and misuse of conventional antibiotics have dramatically accelerated the emergence, evolution and worldwide spread of drug-resistant bacterial strains, necessitating urgent exploration of novel antibacterial strategies. Bacteriophages serve as natural bacterial predators offering distinct advantages including high host specificity, autonomous self-replication capabilities and cost-effective large-scale production. However, wild-type phages present significant clinical limitations due to their narrow host ranges, susceptibility to rapid immune clearance and poor penetration of bacterial biofilms, which severely restrict their therapeutic applications. The convergence of synthetic biology, nanotechnology and advanced gene editing technologies has accelerated the development of engineered bacteriophage platforms, providing programmable, scalable and clinically translatable pathways to overcome these inherent biological constraints. Here, we systematically delineate four fundamental strategies for engineered bacteriophage development. Chemical modification utilizes reactive functional groups such as amino, carboxyl and thiol moieties on capsid proteins through esterification, amidation or click chemistry reactions to achieve precise drug conjugation and surface functionalization. In vivo editing encompasses ultraviolet or chemical mutagenesis for random mutation induction, homologous recombination for targeted genetic alterations, recombineering methodologies including electroporation-mediated bacteriophage recombination engineering, and CRISPR-Cas systems for precise genome editing to enable exact genetic reconstruction and host range reprogramming. In vitro synthesis leverages genome engineering platforms where intact phage genomes are transferred into yeast or host bacteria to facilitate highly efficient homologous recombination, enabling large DNA fragment assembly and cross-gene host range expansion without bacterial toxicity constraints. Directed evolution combines artificial selection through mutation library screening with rational design approaches involving chimeric receptor binding protein construction or site-specific mutagenesis, effectively balancing the discovery of unknown adaptive pathways with targeted host specificity modification. Moreover, we comprehensively discuss therapeutic applications across diverse clinical scenarios. Engineered bacteriophage effectively disrupt bacterial biofilms through sophisticated functionalized delivery platforms including nanozyme-conjugated phages, phage-liposome nanoconjugates and bio-responsive hydrogels, demonstrating significantly enhanced bactericidal efficiency compared to unmodified free phages. These bioengineered vectors attenuate bacterial virulence and resensitize pathogens to antibiotics by delivering CRISPR-Cas systems or base editors to disrupt critical virulence factors such as pili, capsule synthesis machineries and quorum sensing systems, or by inactivating antibiotic resistance determinants including beta-lactamase genes. As an intelligent nanomedicine delivery platform, engineered bacteriophage enable precise pathogen elimination an through photocatalytic reactive oxygen species generation, immunomodulatory interventions, or controlled release of antibacterial drugs. Furthermore, oral administration of engineered bacteriophage facilitates microbiota modulation, which selectively eliminate intestinal pathogens while preserve beneficial commensal microbiota, thereby restoring microbial community balance and preventing complications associated with dysbiosis. Finally, we critically analyze persistent challenges including host strain matching complexity, evolution of bacterial resistance mechanisms, pharmacokinetic optimization requirements, optimal administration route selection, large-scale production quality control standards and clinical dosing determination protocols. Through multidisciplinary integration of synthetic biology, infectious disease medicine and immunology, future translational medicine studies of bacteriophage should establish comprehensive technical platforms encompassing rapid phage screening, intelligent rational design, rigorous in vivo evaluation and standardized clinical validation processes, ultimately advancing engineered bacteriophage from laboratory innovations to clinically approved therapeutics for effectively combating MDR bacterial infections.

Objective: To explore the association between daytime outdoor physical activity (OPA) and oral health indicators among primary school students, aiming to provide evidence for developing oral health intervention strategies based on natural exposure. Methods: In October 2023, based on the "Tianchang Children s Light Exposure and Growth Development Cohort", 799 second and third grades children were recruited from two primary schools in Tianchang, Chuzhou City, Anhui Province. Physical activity intensity and light exposure were objectively monitored for 24 hours over 5 consecutive days using triaxial accelerometers synchronized with portable illuminance meters. Standardized oral examinations were performed to record dental caries, gingivitis, and malocclusion. Demographics, lifestyle variables, and household socioeconomic data were collected via questionnaires. Multiple linear regression (for the number of carious teeth) and Logistic regression (for gingivitis risk) were used to analyze the relationship between daytime outdoor moderate to vigorous physical activity (MVPA) and oral health outcomes. Results: The average daytime outdoor MVPA was (0.76±0.35)h, with (0.95±0.40)h on weekdays and (0.49±0.47)h on weekends. The detection rates for dental caries, gingivitis, and malocclusion were 31.0%, 4.6%, and 59.7%, respectively. Compared with children with good oral health, the duration of outdoor MVPA on school days was reduced in children with caries or gingivitis ( Z =-11.4, -5.01, both P <0.01). Multiple regression analysis showed that after adjusting for factors such as gender, age, body mass index, oral hygiene behaviors, an increase in daytime outdoor MVPA duration was associated with a decrease in the number of dental caries ( β=-0.64, 95%CI =-0.93 to -0.35) and a reduced risk of gingivitis ( OR= 0.58 , 95%CI =0.34-0.98) in primary school students (both P <0.05). The association was primarily observed on school days ( β=-0.72, 95%CI = -1.07 to -0.37; OR=0.42, 95%CI =0.21-0.85) (both P < 0.05). Conclusions Daytime outdoor MVPA on weekdays is significantly associated with a lower number of carious teeth and a reduced risk of gingivitis in primary school students. Increasing daytime outdoor activities on weekdays may serve as a promising and potential strategy for promoting children s oral health.

This study aimed to investigate the mechanism of liquiritin (LQ) in the improvement of ventricular remodeling (VR) after acute myocardial infarction (AMI). Molecular docking was used to predict the binding affinity of liquiritin to thioredoxin-interacting protein (TXNIP). After 2 weeks of modeling, the rats were randomly divided into a model group, a low-dose liquiritin group (20 mg/kg LQ), and a high-dose liquiritin group (40 mg/kg LQ). Liquiritin was administered by gavage once a day, and the sham group and model group were given the same volume of 0.5% sodium carboxymethylcellulose (CMC-Na), with intervention of 4 consecutive weeks. Echocardiography was employed to detect the cardiac function, HE staining was used to observe cardiological changes, ELISA was used to detect the activity of serum creatine kinase-MB (CK-MB) activity, and the colorimetric method was adopted to detect serum malondialdehyde (MDA), total superoxide dismutase (T-SOD) and catalase (CAT) activities. RT-qPCR was used to detect the gene expressions of TXNIP, thioredoxin (TRX) and NACHT, LRR, and PYD domains-containing protein 3(NLRP3). Western blot was used to detect the protein expressions of TXNIP, TRX and NLRP3 in rat myocardial tissue. Molecular docking results showed that liquiritin had a good binding affinity to TNXIP target. After 20 and 40 mg/kg liquiritin intervention, the levels of ejection fraction (EF) and fractional shortening (FS) were significantly increased (P<0.01), and the levels of LVIDs, LVIDd, LVESV, and LVEDV were decreased (P<0.01). The myocardial structure was significantly improved, the cell arrangement tended to be regular, and the area of inflammatory cell infiltration and necrosis was reduced. Liquiritin significantly reduced the level of CK-MB (P<0.01), decreased the activity of MDA, and increased the activities of CAT and T-SOD (P<0.01). Liquiritin effectively inhibited the overexpression of TXNIP and NLRP3 genes and proteins, and enhanced the expression of TRX genes and proteins in the myocardial tissues of AMI rats. In conclusion, liquiritin has a regulatory effect on the TXNIP/TRX signaling pathway, inhibits the activation of the NLRP3 inflammasome, and thus improves ventricular remodeling after acute myocardial infarction.

The Type III Secretion System (T3SS) serves as a pivotal virulence apparatus for numerous Gram-negative bacterial pathogens, enabling them to infect both animal and plant hosts. Functioning as a molecular syringe, the T3SS directly translocates bacterial effector proteins from the bacterial cytoplasm into the interior of eukaryotic host cells. These effectors are central weapons that precisely manipulate a wide spectrum of host cellular physiological processes, ranging from cytoskeletal dynamics to immune signaling, to establish a favorable niche for bacterial survival and proliferation. Among the diverse arsenal of T3SS effectors, the YopJ family constitutes a critical group of virulence factors. Members of this family are characterized by a conserved catalytic triad structure—a hallmark of the CE clan of cysteine proteases that has been evolutionarily repurposed to confer acetyltransferase activity. A defining and intriguing feature of these enzymes is their stringent dependence on a host-derived eukaryotic cofactor, inositol hexakisphosphate (IP₆), for allosteric activation. This requirement acts as a sophisticated molecular safeguard, ensuring enzymatic activity only within the appropriate host environment, thereby preventing detrimental effects on the bacterium itself. While seminal studies on individual members such as Yersinia’s YopJ and Salmonella’s AvrA have provided deep mechanistic insights, a systematic and integrative understanding of the structure-function relationships across the entire family remains fragmented. Key questions persist regarding how a conserved catalytic core has diverged to recognize distinct host substrates in different kingdoms of life. To address this gap, this article provides a systematic review of the YopJ family, focusing on three interconnected aspects: their structural features, their catalytic mechanism, and their divergent immunosuppressive strategies in animal versus plant hosts. By conducting a comparative analysis of the sequences and resolved three-dimensional structures of three representative members (e.g., HopZ1a, PopP2, AvrA), we elucidate regions of significant variation embedded within the conserved core catalytic architecture. These variable regions, often involving surface loops and substrate-binding interfaces, are crucial determinants of target specificity and functional specialization. The functional divergence of this effector family is most apparent when comparing their modes of action in different hosts. In animal hosts, YopJ-family effectors primarily sabotage innate immune signaling pathways. They achieve this by acetylating key serine and threonine residues within the activation loops of critical kinases in the MAPK and NF‑κB pathways. This post-translational modification blocks the phosphorylation and subsequent activation of these kinases, leading to potent suppression of inflammatory cytokine production. Conversely, in plant hosts, the strategy broadens to dismantle the two-tiered plant immune system. YopJ homologs target a more diverse set of substrates, including immune-associated receptor-like cytoplasmic kinases (RLCKs), microtubule networks via tubulin acetylation (which disrupts cellular trafficking and signaling), and transcription factors central to defense gene regulation. This multi-target approach effectively suppresses both Pattern-Triggered Immunity (PTI) and Effector-Triggered Immunity (ETI). In conclusion, this synthesis aims to deepen the mechanistic understanding of YopJ family-mediated pathogenesis by integrating structural biology with cellular function across host kingdoms. Elucidating the precise molecular basis for substrate selection—how conserved platforms achieve target diversity—is a major frontier. Furthermore, this knowledge provides a vital theoretical foundation for developing novel anti-virulence strategies. Targeting the conserved IP₆-binding pocket or the catalytic acetyltransferase activity itself represents a promising avenue for designing broad-spectrum inhibitors that could disarm this critical family of bacterial effectors, potentially offering new therapeutic approaches against a range of pathogenic bacteria.

Chronic obstructive pulmonary disease （COPD）， as one of the three major causes of death， is a complex systemic disease with high prevalence， high mortality， high disability， frequent acute exacerbations， and a variety of pulmonary complications. The pathogenesis is complex. Western medicine has no effective specificity scheme for a complete cure. However， multiple-component and multiple-target characteristics of traditional Chinese medicine （TCM） demonstrate significant advantages in COPD treatment through multi-link， multi-pathway， and multi-mechanism intervention. Therefore， exploring the essence of COPD pathogenesis and discovering effective TCM treatment drugs through the application of TCM principles and prescriptions is a key focus of modern research. Animal models are of paramount importance in medical research. It is the first consideration to select appropriate animals， adopt reasonable modeling methods to replicate stable animal models that closely resemble the clinical manifestations and pathophysiological characteristics of COPD， and use appropriate evaluation methods to determine the success of COPD animal models in experimental research. The core of experimental research lies in observing the intervention effect of TCM on COPD animal models， exploring the specific pathways and regulatory mechanisms of TCM on COPD disease， and finding TCM monomers， single herbs， and TCM formulas with definite curative effects. At present， animal model research on COPD mainly involves model establishment， model evaluation， efficacy observation， mechanism exploration， and other aspects. In recent years， there has been no systematic organization， update， and reflection on the relevant research on TCM intervention in COPD animal models. This study reviewed the selection of animals for the COPD model， methods for establishing COPD animal models， model evaluation methods， and the intervention effects of TCM on COPD animal models. It aims to grasp the current research status and identify existing problems for further improvement， in order to provide evidence and support for scientific research and clinical treatment of COPD.

Chronic obstructive pulmonary disease （COPD）， as one of the three major causes of death， is a complex systemic disease with high prevalence， high mortality， high disability， frequent acute exacerbations， and a variety of pulmonary complications. The pathogenesis is complex. Western medicine has no effective specificity scheme for a complete cure. However， multiple-component and multiple-target characteristics of traditional Chinese medicine （TCM） demonstrate significant advantages in COPD treatment through multi-link， multi-pathway， and multi-mechanism intervention. Therefore， exploring the essence of COPD pathogenesis and discovering effective TCM treatment drugs through the application of TCM principles and prescriptions is a key focus of modern research. Animal models are of paramount importance in medical research. It is the first consideration to select appropriate animals， adopt reasonable modeling methods to replicate stable animal models that closely resemble the clinical manifestations and pathophysiological characteristics of COPD， and use appropriate evaluation methods to determine the success of COPD animal models in experimental research. The core of experimental research lies in observing the intervention effect of TCM on COPD animal models， exploring the specific pathways and regulatory mechanisms of TCM on COPD disease， and finding TCM monomers， single herbs， and TCM formulas with definite curative effects. At present， animal model research on COPD mainly involves model establishment， model evaluation， efficacy observation， mechanism exploration， and other aspects. In recent years， there has been no systematic organization， update， and reflection on the relevant research on TCM intervention in COPD animal models. This study reviewed the selection of animals for the COPD model， methods for establishing COPD animal models， model evaluation methods， and the intervention effects of TCM on COPD animal models. It aims to grasp the current research status and identify existing problems for further improvement， in order to provide evidence and support for scientific research and clinical treatment of COPD.