Chronic pancreatitis （CP） is a common disease in clinical practice characterized by progressive inflammatory fibrosis of the pancreas. Gut microbiota， known as the “second genome” of humans， bidirectionally modulates the progression of fibrosis in CP via the gut-pancreas axis. This article systematically elaborates on the characteristics of gut microbiota during the progression of CP and its molecular mechanism in mediating pancreatic fibrosis through bacterial translocation， metabolites， immune regulatory networks， and microbe-pancreatic stellate cell interactions， with a focus on the pivotal role of short-chain fatty acids and inflammatory cytokine networks in pancreatic stellate cell activation and extracellular matrix deposition. In addition， this article explores the potential value of gut microbiota-targeted interventions in the prevention and treatment of CP fibrosis， such as probiotics， prebiotics， and fecal microbiota transplantation， and discusses the translational potential of using multi-omics technologies to identify diagnostic biomarkers and novel therapeutic targets for CP， in order to provide new ideas for the precise diagnosis and treatment of CP.

Purpose: To evaluate the clinical outcomes of endovascular treatment for ruptured vertebral artery dissecting aneurysms (VADAs), with a focus on endovascular protocols tailored to different anatomical subtypes. Materials and Methods: We retrospectively analyzed 44 consecutive patients with ruptured VADAs treated from December 2014 to October 2024. Treatment strategies were guided by aneurysm location: parent artery occlusion (PAO) was used for lesions in non-dominant VAs, while stent-assisted coiling (SAC) reconstruction was used for aneurysms in dominant VAs. Patients were stratified by modified Rankin Scale (mRS) scores at 3-month follow-up (favorable: mRS 0–2; unfavorable: mRS 3–6). Results: All procedures were technically successful, including 12 single SAC, 13 overlapping SAC, and 19 with PAO (2 involving posterior inferior cerebellar artery preservation). Immediate complete occlusion was achieved in 50.0% of single SAC cases, 76.9% overlapping SAC, and 100% in the PAO group. Six (13.6%) procedure-related complications occurred, including 2 hemorrhagic and 4 ischemic events. Thirty patients (68.2%) had favorable outcomes, and the unfavorable outcomes group showed a higher incidence of ischemic events (P=0.012). An initial poor Hunt–Hess grade (≥IV) was an independent risk factor for unfavorable outcomes (odds ratio 6.35, 95% confidence interval 1.24–32.59; P=0.027). Angiographic follow-up was performed for 34 aneurysms, with complete occlusion achieved in 32 (94.1%); the remaining 2 patients were retreated. Conclusion Endovascular management is safe and effective for ruptured VADAs. Anatomical stratification—PAO for non-dominant VA lesions and SAC for dominant VA aneurysms—may help achieve favorable outcomes.

Short-chain fatty acids （SCFA） are the main metabolic products generated by the fermentation of dietary fiber by gut microbiota. Studies have shown that SCFA not only play a role in energy metabolism， but also act as important signaling molecules， exhibiting a significant potential in alleviating liver and pancreatic fibrosis. The core mechanism of SCFA mainly involves the regulation of various key signaling pathways by activating G protein-coupled receptors and inhibiting the activity of histone deacetylase， thereby suppressing the activation and proliferation of hepatic stellate cell （HSC） and pancreatic stellate cell （PSC）， which is a key link in fibrosis formation. In addition， SCFA can effectively alleviate tissue inflammation response， improve intestinal barrier function， and regulate gut microbiota balance， thus indirectly preventing the process of fibrosis mediated by the “gut-liver/pancreas axis”. Compared with the research on SCFA in liver fibrosis， studies on their role in pancreatic fibrosis are limited. Given that HSC and PSC are highly homologous， the transcription factors and proteins that have been confirmed in liver fibrosis-related studies are also similarly expressed in PSC， suggesting that they may also influence the activation of PSC. This article systematically summarizes the recent advances in the research on SCFA in alleviating liver and pancreatic fibrosis， in order to provide new perspectives for exploring the mechanism of pancreatic fibrosis and developing related interventional strategies.

ObjectiveType I interferon (IFN-I) signaling is essential for antiviral innate immunity, yet its sustained or excessive activation contributes to the pathogenesis of several autoimmune diseases and interferonopathies, such as systemic lupus erythematosus and Aicardi-Goutières syndrome. Current strategies targeting this pathway, exemplified by JAK inhibitors, act mainly on downstream signal transduction and provide limited direct control over upstream IFN-I production, while also carrying the risk of broad immunosuppression. Phyllanthus emblica L. has long been used in traditional medicine for inflammatory disorders, but the bioactive constituent responsible for its regulation of IFN-I signaling and the underlying molecular mechanism have not been clearly defined. This study aimed to identify the active anti-inflammatory component of P. emblica and to characterize its mechanism of action on the IFN-I pathway in macrophages. MethodsActive components ofP. emblica and their candidate targets were screened by network pharmacology using the TCMSP and DrugBank databases (oral bioavailability≥30%, drug-likeness≥0.18) and intersected with inflammation-related genes retrieved from public databases. The predicted interaction between EGCG and IFN-I pathway proteins (TBK1, IRF3, STAT1) was evaluated by molecular docking, with BX795 and GSK8612 used as reference TBK1 inhibitors. Mechanistic experiments were performed in THP-1-derived macrophages and primary bone marrow-derived macrophages (BMDM). Upstream signaling was activated by transfection of the nucleic acid analogs poly(I∶C) and poly(dA∶dT) or by lipopolysaccharide (LPS) stimulation, whereas downstream signaling was activated by exogenous IFN-β. An siRNA-mediated TREX1 knockdown model was used to mimic endogenous nucleic acid-driven interferonopathy. Expression of IFN-β1 and interferon-stimulated genes (ISGs) was measured by RT-qPCR, protein phosphorylation by Western blot, and IFN-β secretion by ELISA. Cellular thermal shift assay (CETSA) and drug affinity responsive target stability (DARTS) were used to probe the interactionbetween EGCG and IRF3. ResultsNetwork pharmacology identified (-)-epigallocatechin-3-gallate (EGCG) as a candidate IFN-I-suppressive constituent of P. emblica, with predicted binding to TBK1, IRF3, and STAT1. Molecular docking yielded binding energies of -9.2, -7.2, and -8.2 kcal/mol for TBK1, IRF3, and STAT1, respectively, indicating an affinity for TBK1 comparable to that of the reference inhibitors BX795 (-5.7 kcal/mol) and GSK8612 (-6.4 kcal/mol). EGCG suppressed IFN-β1 and ISG mRNA expression under poly (I∶C), poly (dA∶dT), and LPS stimulation in both THP-1 macrophages and BMDM. At the protein level, EGCG reduced the phosphorylation of TBK1 and IRF3 without affecting the levels of the upstream sensors cGAS and RIG-I, and lowered IFN-β secretion in a concentration-dependent manner. CETSA and DARTS showed that EGCG did not enhance the thermal stability or protease resistance of IRF3, indicating that its effect on IRF3 is indirect. Following IFN-β stimulation, prolonged EGCG treatment reduced STAT1 phosphorylation in a time-dependent manner without an apparent change in IRF9, and partially attenuated ISG transcription; this effect was not monotonicly concentration-dependent, and CXCL10 showed the most consistent suppression. In TREX1-knockdown cells, the elevated mRNA levels of ISG15, ISG56, and CXCL10 were reduced by EGCG. ConclusionEGCG suppresses IFN-I responses by concurrently inhibiting TBK1-IRF3-dependent IFN‑β production and JAK-STAT1-mediated downstream transcription. These in vitro findings provide a mechanistic basis for the anti-inflammatory use of P. emblica in traditional medicine and identify EGCG as a candidate for further evaluation in interferon-driven autoimmune disease models.

Eight compounds were isolated and purified from the ethyl acetate part of 70% acetone extract of Rehmannia glutinosa by various chromatographic techniques such as silica gel, MCI gel CHP-20, ODS, Toyopearl HW-40C, combined with TLC and semi-preparative HPLC. Their structures were elucidated by modern spectroscopy techniques (NMR, MS, UV, IR), and identified as neomartynoside A (1), osmanthuside B₆ (2), martynoside (3), isomartynoside (4), (E)-p-hydroxycinnamic acid (5), caffeic acid (6), ferulic acid (7), and methyl caffeate (8). Compound 1 is a new phenylethanol glycoside, which was identified as neomartynoside A. Compound 2 was isolated from Rehmannia glutinosa for the first time. In addition, compounds 2, 6 and 7 significantly increased relative glucose consumption, showing potential hypoglycemic activity.

[Objective] To evaluate the participation rate of voluntary blood donation among college students in China by meta-analysis. [Methods] CNKI, Wan Fang Data, VIP, Pub Med, Web of science and Embase databases were searched to collect cross-sectional studies on the participation rate of voluntary blood donation among college students from the establishment of the database to August 10, 2024. Two researchers independently screened the literature, extracted the data and assessed the risk of bias of the included studies, and then used Stata16.1 software for meta-analysis. [Results] Finally, 36 articles were included, with a total of 37 348 research subjects and 11 541 college students participating in voluntary blood donation. The meta-analysis results showed that the participation rate of college students in voluntary blood donation in China was 34.0% [95% CI (31.0,37.0)]. The sub group analysis results showed that the participation rate of college students in voluntary blood donation in different regions was 36.1% [95% CI (24.1, 48.1)] in the eastern region, 30.2% [95% CI (26.8, 33.6)] in the central region, and 35.1% [95% CI (31.0, 39.3)] in the western region, with the eastern region higher than the central and western regions (P<0.001); The participation rate of college students in voluntary blood donation during different research periods was 32.0% before 2020 [95% CI (31.4, 32.6)] and 27.1% after 2020 [95% CI (26.3, 27.9)], with before 2020 higher than after 2020 (P<0.001); The participation rate of voluntary blood donation among college students of different genders is 36.8% for males [95% CI (32.8, 40.9)] and 28.5% for females [95% CI (24.8, 32.2)], with males higher than females (P<0.001); The participation rate of college students in voluntary blood donation among different academic backgrounds was 26.8% for associate degree students [95% CI (23.1, 30.5)], 26.4% for undergraduate students and above [95% CI (22.9, 29.8)], with no statistically significant difference (P>0.05); The participation rate of college students in voluntary blood donation among different majors is 46.4% [95% CI (34.4, 58.4)] for medical majors and 29.1% [95% CI (22.1, 36.0)] for non-medical majors, with medical majors higher than non-medical majors (P<0.001); The participation rate of college students in voluntary blood donation among different grades is 27.7% [95% CI (24.3, 31.2)] for second grade and below, 33.7% [95% CI (26.4, 40.9)] for third grade and above, with the latter higher than the former (P<0.001); The participation rate of college students in voluntary blood donation among different household registrations is 24.7% in urban areas [95% CI (21.5, 27.8)] and 26.8% in rural areas [95% CI (22.1, 31.4)], with no statistically significant difference (P>0.05); The participation rate of college students in voluntary blood donation among different family attitudes was 43.3% in support [95% CI (18.5, 68.2)] and 37.8% in non support [95% CI (26.6, 48.9)], with no statistical difference (P>0.05); The participation rate of college students in voluntary blood donation was 35.7% [95% CI (27.8, 43.5)] among those who were aware of the blood donation policies, and 24.7% [95% CI (13.7, 35.7)] among those who were not aware, with the former higher than the latter (P<0.001); The participation rate of voluntary blood donation among college students was 47.8% [95% CI (34.5, 61.0)] among those who were aware of blood donation knowledge and 38.0% [95% CI (22.1, 53.9) among those who were not aware, with the former higher than the latter (P<0.001). [Conclusion] There is still room for improvement in the rate of voluntary blood donation among college students, and the government should plan the overall situation of blood collection, and cooperate with colleges and universities to play the main role of donation publicity, and correctly identify potential donors, so as to improve the participation rate of voluntary blood donation among college students and promote the development of voluntary blood donation.

Quantum dots (QDs), nanoscale semiconductor crystals, have emerged as a revolutionary class of nanomaterials with unique optical and electrochemical properties, making them highly promising for applications in disease diagnosis and treatment. Their tunable emission spectra, long-term photostability, high quantum yield, and excellent charge carrier mobility enable precise control over light emission and efficient charge utilization, which are critical for biomedical applications. This article provides a comprehensive review of recent advancements in the use of quantum dots for disease diagnosis and therapy, highlighting their potential and the challenges involved in clinical translation. Quantum dots can be classified based on their elemental composition and structural configuration. For instance, IB-IIIA-VIA group quantum dots and core-shell structured quantum dots are among the most widely studied types. These classifications are essential for understanding their diverse functionalities and applications. In disease diagnosis, quantum dots have demonstrated remarkable potential due to their high brightness, photostability, and ability to provide precise biomarker detection. They are extensively used in bioimaging technologies, enabling high-resolution imaging of cells, tissues, and even individual biomolecules. As fluorescent markers, quantum dots facilitate cell tracking, biosensing, and the detection of diseases such as cancer, bacterial and viral infections, and immune-related disorders. Their ability to provide real-time, in vivo tracking of cellular processes has opened new avenues for early and accurate disease detection. In the realm of disease treatment, quantum dots serve as versatile nanocarriers for targeted drug delivery. Their nanoscale size and surface modifiability allow them to transport therapeutic agents to specific sites, improving drug bioavailability and reducing off-target effects. Additionally, quantum dots have shown promise as photosensitizers in photodynamic therapy (PDT). When exposed to specific wavelengths of light, quantum dots interact with oxygen molecules to generate reactive oxygen species (ROS), which can selectively destroy malignant cells, vascular lesions, and microbial infections. This targeted approach minimizes damage to healthy tissues, making PDT a promising strategy for treating complex diseases. Despite these advancements, the translation of quantum dots from research to clinical application faces significant challenges. Issues such as toxicity, stability, and scalability in industrial production remain major obstacles. The potential toxicity of quantum dots, particularly to vital organs, has raised concerns about their long-term safety. Researchers are actively exploring strategies to mitigate these risks, including surface modification, coating, and encapsulation techniques, which can enhance biocompatibility and reduce toxicity. Furthermore, improving the stability of quantum dots under physiological conditions is crucial for their effective use in biomedical applications. Advances in surface engineering and the development of novel encapsulation methods have shown promise in addressing these stability concerns. Industrial production of quantum dots also presents challenges, particularly in achieving consistent quality and scalability. Recent innovations in synthesis techniques and manufacturing processes are paving the way for large-scale production, which is essential for their widespread adoption in clinical settings. This article provides an in-depth analysis of the latest research progress in quantum dot applications, including drug delivery, bioimaging, biosensing, photodynamic therapy, and pathogen detection. It also discusses the multiple barriers hindering their clinical use and explores potential solutions to overcome these challenges. The review concludes with a forward-looking perspective on the future directions of quantum dot research, emphasizing the need for further studies on toxicity mitigation, stability enhancement, and scalable production. By addressing these critical issues, quantum dots can realize their full potential as transformative tools in disease diagnosis and treatment, ultimately improving patient outcomes and advancing biomedical science.

Streptococcus equinus is a zoonotic disease that can cause illness in various animals under specific environmental condi-tions.No reports have described isolation of this bacterium from the liver in affected sheep.This study successfully isolated and identi-fied a strain of Streptococcus equinus through bacterial isolation and culture,Gram staining,drug sensitivity testing,mouse sensitivity testing,bacterial biochemical testing,and whole genome sequencing.The strain was found to have pathogenicity toward Kunming white mice,and to be sensitive to four antibiotics(penicillin,ampicillin,ceftiofur sodium,and ceftriaxone sodium)but resistant to four antibiotics(streptomycin,amoxicillin,tetracycline,and gentamicin).On the basis of drug sensitivity testing,targeted treatment of the affected sheep flock with ceftiofur sodium effectively controlled the disease within 2 days,and no new cases occurred.This study provides a reference for biological characterization of ovine Streptococcus equinus;public health;and the investigation of disease pre-vention,control,and epidemiology.

This study was aimed at determining the molecular characteristics of Yersinia pestis in the natural plague foci around Qinghai Lake through single nucleotide polymorphism technology,to lay a foundation for molecular epidemiological and source-tracing analysis of Y.pestis in this area.Using the whole genome sequencing technology,we obtained the whole genome sequences of 84 representative Y.pestis strains.Using the sequences of Y.pestis and Yersinia pseudotuberculosis IP32953 from the NCBI database as references,we compared and analyzed the 2 298 SNP loci of these strains.From 1957 to 2020,84 representative strains of Y.pestis from the natural plague foci around Qinghai Lake were divided into two clades:1.IN2 and 3.ANT1.The 1.IN2 clade was the characteristic population of Y.pestis throughout all epidemic years in this area.Additionally,analysis of the SNP distribution and hosts in the region indicated that the 1.IN2 clade was located in five counties except Wulan,whereas the 3.ANT1 clade was isolated from Himalayan marmot and dog in two counties.In conclusion,the population structure of SNP of Y.pestis in the natural plague foci around Qinghai Lake is relatively simple,and SNP analysis of Y.pestis provided a scientific basis for tracing plague epidemic sources and formulating plague prevention and control measures in this area.

Objective:To assess the predictive value for the risk of cardiogenic stroke (CS) in patients with paroxysmal atrial fibrillation (PAF) using quantification of left atrial appendage early blood stasis (LAA-BS) signs derived from left atrium-pulmonary vein CT examination.Methods:A retrospective analysis of 187 patients with PAF, who were confirmed to have LAA-BS by left atrium-pulmonary vein CT examinations, was conducted at Second Affiliated Hospital of Nantong University from January 2019 to December 2021. The ratio of LAA-BS CT values to ascending aorta (AA) CT values (HU BS/HU AA) and the ratio of LAA-BS volume to LAA volume (V BS/V LAA) were measured at the peak time of AA enhancement, which were used as characteristic quantitative indicators of LAA-BS. Using the median values of HU BS/HU AA and V BS/V LAA as cut-off points for grouping, the differences between the high-ratio and low-ratio groups were compared in terms of general information, clinical characteristics, and imaging characteristics. All enrolled patients were followed up with the primary outcome event of CS occurrence. The differences in the proportion of CS occurrence between the high-ratio and low-ratio groups were compared. The risk stratification analysis of the occurrence of CS in PAF patients was performed using Kaplan-Meier curves. Additionally, the predictive value of HU BS/HU AA, V BS/V LAA and other imaging indices for the risk of CS occurrence was assessed using Cox proportional risk regression models. Results:The incidence of hypertension and the proportion of patients with atrial fibrillation-stroke risk score (CHA 2DS 2-VASc)≥3 in the high V BS/V LAA group were higher than that in the low V BS/V LAA group, and the difference was statistically significant ( P=0.041, P=0.011). The left atrial volume (LAV) in patients in the low HU BS/HU AA group was greater than in the high HU BS/HU AA group, and the difference was statistically significant ( P=0.040). Kaplan-Meier analysis showed a higher incidence of CS in the low HU BS/HU AA group than in the high HU BS/HU AA group ( P=0.012). Similarly, the high V BS/V LAA group had a higher incidence of CS compared with the low V BS/V LAA group ( P=0.019). Subgroup analysis revealed a significantly higher incidence of CS in the subgroup with low HU BS/HU AA and high V BS/V LAA compared to other subgroups (all P<0.05). The Cox proportional hazards regression model, adjusting for confounding factors, identified low HU BS/HU AA and high V BS/V LAA as independent risk factors for CS occurrence in PAF patients ( P=0.005 and P=0.029). Conclusion:The HU BS/HU AA and V BS/V LAA quantified using left atrium-pulmonary vein CT imaging are predictive factors for CS occurrence in patients with PAF. These ratios synergistically contribute to the risk assessment of CS.