Angiogenesis， as a core mechanism for maintaining tissue perfusion and repairing ischemic injury， plays a crucial role in ischemic diseases such as coronary heart disease and peripheral arterial disease. Traditional Chinese medicine（TCM）， with its advantages of multi-target and synergistic regulation， provides a unique perspective for therapeutic angiogenesis. Based on this， this article intends to delve into the synergistic effects of key signaling pathways， including vascular endothelial growth factor（VEGF）/VEGF receptor（VEGFR）， Notch， phosphoinositide 3-kinase/ protein kinase B/mammalian target of rapamycin（PI3K/Akt/mTOR）， and angiopoietin/endothelial TEK tyrosine kinase（Ang/Tie2）， and elucidate the driving mechanisms of endothelial cell metabolic reprogramming and exosome-mediated intercellular communication within this process. Based on existing literature， it summarizes the microenvironment-dependent and bidirectional regulatory characteristics of natural active components of TCM（such as terpenes， tanshinones， and flavonoids） on angiogenesis. Furthermore， it systematically discusses how classical TCM formulas achieve blood vessel formation and functional maturation by protecting the neurovascular units， recruiting pericytes， and remodeling the microenvironment. Current evidence highlights the advantages of multi-target synergy and temporal regulation in TCM， but also reveals challenges such as high heterogeneity and a lack of functional evaluations and high-quality clinical trials. Future efforts should integrate multi-omics to decipher network mechanisms， optimize formula compatibility， and conduct multicenter studies to promote the development of innovative preparations. This review highlights the academic value of TCM in angiogenesis， provides an evidence base for treating ischemic diseases， and supports multidisciplinary integration and innovation.

Objective: To explore the relationship of social anxiety and emotion regulation strategy with short video addiction among college students, so as to provide reference for alleviating social anxiety, improving the level of emotion regulation and preventing short video addiction. Methods: From May to June 2024, 2 172 college students from a university in Guangzhou were selected by multistage random cluster sampling method. The Interaction Anxiousness Scale, Emotion Regulation Questionnaire and Short Video Addiction Scale were used as the measurement tools. The potential profile was used to analyze the potential categories of social anxiety and emotion regulation strategy. The Chi square test was used to analyze the characteristics of the distribution of potential profile categories of college students with different demographic characteristics. Multiple linear regression analysis was used to analyze the relationship between social anxiety, emotion regulation strategy and short video addiction. Results: The potential categories of social anxiety and emotion regulation strategy in college students were divided into adaptive regulation type (784 cases, 36.10 %), low anxiety-expression type (623 cases, 28.68%), inhibition-anxiety type (478 cases, 22.01%), high anxiety-disorder type (287 cases, 13.21%). There were statistically significant differences in the distribution of various potential categories of social anxiety and emotion regulation strategy among cadres of different gender, family residence, class cadres or not ( χ 2=42.55, 17.86 , 39.05, all P <0.01). Multiple linear regression analysis showed that after controlling the confounding factors such as demographic variables, the potential categories of social anxiety and emotion regulation strategy of college students (low anxiety-expression type, inhibition-anxiety type, high anxiety-disorder type) were the important related factors of short video addiction ( β =0.15,0.25,0.35, all P <0.05). Conclusions Social anxiety and emotion regulation strategy of college students exhibit distinct categorical characteristics, and its varying latent categories are associated with short video addiction. Schools should implement targeted intervention measures for different categories of college students to promote their comprehensive mental health development.

ObjectiveTo investigate the effects of prostaglandin E₂ （PGE₂） microinjection into the median preoptic nucleus （MnPO） on core body temperature in female mice， and to clarify its underlying mechanism. MethodsMicroinjection cannula were implanted into the MnPO of female mice using stereotaxic surgery.Subsequently， a multi-channel temperature acquisition system was used to simultaneously monitor rectal and brown adipose tissue （BAT） temperatures before and after intra-MnPO injections of different reagents.To investigate the thermoregulatory effects of the microinjection of PGE₂ into the MnPO， 12 female C57BL/6 mice were randomly divided into a saline group （n=6） and a PGE₂ group （n=6）， which were injected with 0.1 μL saline and PGE₂ （2.8 mmol/L）， respectively.To determine whether E-series prostaglandin receptor （EP）1， EP3， and EP4 receptors mediate the thermoregulatory effects of PGE₂， 15 female C57BL/6 mice were randomly divided into 3 groups （n=5 per group）.Mice in each group first received an injection of 0.1 μL PGE2 （2.8 mmol/L） into the MnPO. After their body temperature returned to baseline levels， they were subsequently injected with a mixture of either EP1， EP3 or EP4 antagonist （ant） （20 mmol/L） + PGE2 （2.8 mmol/L）. ResultsCompared with baseline level， the rectal temperature （P<0.01） and BAT temperature （P<0.001） of female mice both increased significantly after microinjection of PGE₂ into the MnPO.Compared with the saline group， the increases in rectal temperature （P<0.001） and BAT temperature （P<0.000 1） were significantly greater in the PGE₂ group of mice.Furthermore， following the injection of PGE₂ into MnPO， the increase in BAT temperature was found to be significantly greater than that in rectal temperature in mice （P<0.001）.Compared to the administration of PGE₂ alone， co-injection of an EP3 ant + PGE₂ into the MnPO of mice resulted in a significantly smaller increase in both rectal temperature （P<0.001） and BAT temperature （P<0.001）.In contrast， the increases in rectal and BAT temperatures following MnPO injection of either EP1 ant + PGE₂ or EP4 ant + PGE₂ were not statistically significant （P>0.05）. ConclusionInjection of PGE₂ into the MnPO elevates BAT and core body temperature in female mice via the EP3 receptor.

ObjectiveTo investigate the relationship between solute carrier family 7 member 11 （SLC7A11） expression in esophageal squamous cell carcinoma （ESCC） and clinical prognosis， and to determine its effects on ESCC cell growth， migration， and other biological activities. MethodsSLC7A11 protein expression was measured in 310 ESCC tissues and 259 adjacent normal tissues using immunohistochemistry to statistically assess the association of SLC7A11 with clinicopathologic characteristics and prognosis in ESCC patients. The expression of SLC7A11 in ESCC cell lines was suppressed through siRNA-mediated knockdown. The specific effects of SLC7A11 knockdown on proliferation and migration were evaluated using CCK-8， clonogenic assay， and Transwell assays. Adenosine triphosphate （ATP）， lactic acid and pyruvate assays were used to measure ESCC metabolism. ResultsSLC7A11 protein expression was localized predominantly in the cytoplasm of ESCC tissues. Significantly higher SLC7A11 expression levels were observed in ESCC tissues compared to adjacent normal tissues （P<0.001）. High SLC7A11 expression was associated with poorer differentiation in patients （P<0.01）. Kaplan-Meier survival analysis demonstrated significantly shorter overall survival in patients with high SLC7A11 expression compared to those with low expression （P<0.05）. CCK-8 and colony formation assays demonstrated that the knockdown of SLC7A11 expression significantly suppressed the proliferative capacity of tumor cells （P<0.001）. Furthermore， Transwell assays revealed a marked decline in tumor cell migration capacity following SLC7A11 suppression （P<0.001）. Critically， SLC7A11 knockdown also reduced intracellular levels of ATP， lactate， and pyruvate， demonstrating that SLC7A11 modulated metabolic activity in ESCC cells（P<0.001）. ConclusionThe expression level of SLC7A11 is relatively high in ESCC and is strongly associated with poor prognosis. Silencing SLC7A11 significantly inhibits esophageal cancer cell growth and migration. SLC7A11 has the ability to regulate glucose， lactic acid and ATP metabolism levels in ESCC， thereby affecting the metabolic microenvironment of ESCC.

Histone lactylation is a recently identified post-translational modification, wherein lactate mediates the enzymatic addition of lactyl groups to lysine residues on histones. Since its discovery, extensive research has demonstrated that histone lactylation is widely present in human tissues and plays a pivotal role in regulating the transcription of specific genes. Subsequent studies have further established this modification as a widespread epigenetic mark with significant physiological implications. With advancing research, accumulating evidence confirms that lactylation at distinct histone sites elicits diverse biological effects—such as promoting cell proliferation, driving inflammatory responses, and enhancing fibrosis—all of which profoundly influence disease progression and serve as key drivers of disease onset and development. Conversely, inhibiting histone lactylation can alter disease outcomes, positioning histone lactylation as a promising therapeutic target. Moreover, studies have revealed crosstalk between histone lactylation and other post-translational modifications, such as acetylation and methylation, which collectively regulate disease progression. Notably, lactylation occurs not only on histones but also on non-histone proteins. Histone lactylation activates specific gene transcription and reshapes metabolic epigenetics, while non-histone lactylation directly modulates enzyme activity, signal transduction, and protein stability. These two facets form a synergistic network through shared lactate pools, common modifying enzyme systems, and pathway crosstalk, thereby constructing a multi-dimensional regulatory framework—namely, the “histone lactylation-metabolism hub-non-histone lactylation” axis. This architecture bridges metabolism and epigenetics, and deciphering its topological structure may provide novel targets for precise intervention in diseases driven by lactate-mediated signaling hijacking. Traditional Chinese medicine (TCM), grounded in clinical practice, has been shown to regulate histone lactylation by modulating lactate metabolism and lactylation-related enzymes, thereby influencing disease progression. Moreover, certain TCM formulations exhibit potential as alternative therapies for drug-resistant diseases, underscoring the significance of further exploring TCM-mediated regulation of histone lactylation in future therapeutic strategies. This review aims to elucidate the mechanisms underlying histone lactylation, systematically delineate the associations between site-specific histone lactylation and various diseases, present a comprehensive landscape of the “lactate-histone lactylation and functional protein lactylation” axis, and summarize the mechanistic basis and research advances in TCM-mediated regulation of histone lactylation for disease treatment. Additionally, we discuss current challenges in histone lactylation research and propose future directions, ultimately aiming to deepen understanding and broaden perspectives on the roles and therapeutic potential of histone lactylation in disease.

ObjectiveDonkey hide is the sole legally designated raw material for the preparation of the traditional Chinese medicine Ejiao. The quality stability of donkey hide during preservation directly determines the efficacy and safety of Ejiao. This study focuses on the dynamic succession of microbial communities during the preservation of donkey hides from different origins, aiming to clarify the correlation between microbial biodiversity difference and the degradation profiles of hide collagen and critical biochemical components, thereby providing a theoretical foundation for developing targeted preservation strategies based on microbial regulation. MethodsDonkey hides originating from four different regions were subjected to an accelerated microbial aging assay to simulate the spoilage process. The microbial community succession was analyzed using high-throughput sequencing. Microstructure changes and pore structure characteristics were assessed by scanning electron microscopy and mercury intrusion porosimetry, respectively. Additionally, the content of major components, including lipids, proteins, and sugars were determined by biochemical methods. ResultsAfter 96 h of aging, the collagen fiber structure in Africa donkey hides (ADH) exhibited significant degradation and collapse, followed by Xinjiang donkey hides (XDH). Instead, the microstructure of Dong’e black donkey hides (DDH) and Peru donkey hides (PDH) remained relatively intact. The porosities of DDH, XDH, PDH, and ADH increased from 27.9%, 15.7%, 30.3%, and 46.2% to 36.5%, 52.6%, 42.8%, and 57.7%, respectively, during the aging process, which suggested that the originally compact fiber structure was disrupted by microbial aging. Fourier transform infrared spectrometer analysis revealed the amide bands in XDH exhibited relatively weak intensity, and no collagen amide I band was observed in ADH. Meanwhile, the lipid and protein contents decreased in all four types of donkey hides, indicating that these components served as the primary nutrient sources for the growth of microorganism. Notably, the most severe collagen degradation was observed in XDH and ADH. A substantial increase was detected in the total soluble sugar in PDH aging solution and hydroxyproline in the ADH aging solution, respectively. These results indicated that donkey hides exhibit distinct patterns of structural degradation and nutrient utilization. Furthermore, the viable cells number of donkey hides increased sharply after 48 h of aging. Metagenomic analysis revealed that the relative abundance of Euryarchaeota in ADH, PDH and XDH declining from initial 93.19%, 97.73% and 30.08% to 0.79%, 1.43% and 0.02% after 96 h, respectively. Conversely, a significantly increase was observed in the abundance of Bacillota, with a marked increase in ADH, peaking at 92.75%. Additionally, the abundance of Pseudomonadota in PDH increased from 0.10% to 87.84%, suggesting that Bacillota and Pseudomonadota may be key factors exacerbating donkey hide spoilage. Unlike the other three types of donkey hides, the dominant bacterial phylum in DDH shifted from Pseudomonadota to Bacteroidota, characterized by a substantial abundance increase of Bacteroidota from 0.13% to 44.22%. ConclusionRegional variation in origin significantly influence the microbial aging of donkey hides, leading to distinct patterns of structural deterioration and differential nutrient utilization. Therefore, implementing origin-specific preservation strategies, through the precisely controlling environmental factors to suppress harmful phyla such as Bacillota and Pseudomonadota, is crucial for enhancing the storage quality of donkey hides.

ObjectiveTo investigate the therapeutic effect of sitravatinib on carbon tetrachloride （CCl₄）-induced liver fibrosis in mice. MethodsA total of 30 male C57BL/6J mice， aged 8 weeks， were randomly divided into control group， CCl₄ model group， and low- （5 mg/kg）， middle- （10 mg/kg）， and high-dose （20 mg/kg） sitravatinib groups. All mice except those in the control group were given intraperitoneal injection of CCl₄ for 4 consecutive weeks to induce liver fibrosis， and since the first day of modeling， the mice in the low-， middle-， and high-dose sitravatinib groups were given sitravatinib at the corresponding dose by gavage every day. The serum levels of total cholesterol （TC）， triglyceride （TG）， and alanine aminotransferase （ALT） were measured for the mice in each group； hepatic hydroxyproline content was measured； HE staining， Masson staining， and Sirius Red staining were used to observe liver histopathological changes； quantitative real-time PCR and Western blot were used to measure the mRNA and protein expression levels of α-smooth muscle actin （α-SMA） and collagen type I alpha 1 （Col1a1） in liver tissue. The therapeutic effect of sitravatinib was assessed based on the above results. A one-way analysis of variance was used for comparison of continuous data between multiple groups， and the least significant difference t-test was used for further comparison between two groups. ResultsCompared with the control group， the model group had significant increases in the levels of TC， TG， and ALT （all P<0.05）， and there were no significant differences in the levels of TC， TG， and ALT between the model group and the low-， middle-， and high-dose sitravatinib groups （all P>0.05）. Hepatic hydroxyproline content decreased after sitravatinib intervention， with a significant difference between the middle-/high-dose sitravatinib groups and the CCl₄ model group （both P<0.05）. Histopathological staining showed that the sitravatinib treatment groups had a reduction in collagen deposition， along with thinning and fragmentation of fibrous septa， and in the high-dose sitravatinib group， 4 mice had a fibrosis stage of S0—S1 and 2 mice had a fibrosis stage of S2—S3， suggesting a certain degree of alleviation of liver fibrosis degree compared with the CCl₄ model group （mainly S3—S4）. The measurement of related molecules showed that sitravatinib downregulated the mRNA and protein expression levels of α-SMA and Col1a1 （all P<0.05）. ConclusionSitravatinib can effectively alleviate CCl₄-induced liver fibrosis in mice， possibly by inhibiting hepatic stellate cell activation and collagen synthesis.

Objective To investigate the value of 3.0 T MRI in-phase/opposed-phase (IP-OP) imaging features in the quantitative assessment of hepatic steatosis after liver transplantation. Methods Clinical data of 115 patients who underwent liver transplantation and completed MRI IP-OP examination and liver biopsy within 3 months were retrospectively collected. According to the gold standard of pathological results, patients were divided into the steatosis group (n=18) and the non-steatosis group (n=97). The relative signal intensity of hepatic parenchyma was measured on MRI IP-OP sequences, and the hepatic fat fraction (HFF) was calculated. Differences in clinical data and imaging features between the two groups were compared, and the efficacy of HFF in the diagnosis of graft hepatic steatosis was evaluated using the receiver operating characteristic (ROC) curve. Results Among the 115 recipients, 18 cases were diagnosed with hepatic steatosis by liver biopsy, including 13 cases of mild steatosis, 3 cases of moderate steatosis and 2 cases of severe steatosis. Compared with the non-steatosis group, the steatosis group had a lower proportion of hepatitis B virus (HBV)-related hepatocellular carcinoma, higher proportions of HBV-related liver failure and alcoholic liver cirrhosis, and higher platelet levels (all P<0.05). There were statistically significant differences in hepatic imaging features between the two groups (all P<0.05). The ROC curve showed that the area under the curve (AUC) of the quantitative value calculated by IP-OP in the diagnosis of graft hepatic steatosis was 0.925 (95% confidence interval 0.870-0.980). Conclusions 3.0 T MRI IP-OP sequence may accurately and non-invasively quantitatively assess the severity of hepatic steatosis after liver transplantation, which is of great value for the early detection of graft hepatic steatosis and the guidance of clinical intervention.

Objective To analyze the rates of drug resistance of carbapenem-resistant Klebsiella pneumoniae (CRKP) and extended-spectrum β-lactamase-producing Escherichia coli (ESBL-E.coli) in bronchoalveolar lavage fluid (BALF) of critically ill patients with severe pneumonia and artificial airway and risk factors of CRKP. Methods Patients with severe pneumonia and artificial airway treated in the Center of Emergency and Intensive Care Unit, Jinshan Hospital, Fudan University from May 2022 to May 2025 were selected. Klebsiella pneumoniae (K. pneumoniae) and Escherichia coli (E.coli) isolated and cultured from BALF of these patients were analyzed. The drug resistance rates of the two bacteria were compared. The multivariate logistic regression was used to analyze related risk factors for CRKP infection. Results A total of 384 patients were included, and 384 strains were cultured, including 330 strains (85.9%) of K. pneumoniae and 54 strains (14.1%) of E.coli. The infection rate of K. pneumoniae was higher. Compared with E.coli, the drug-resistant gene expression rate of K. pneumoniae was lower (37.3% vs 57.4%, P＜0.01). The resistance rates of CRKP to cefotaxime, cefepime, aztreonam, and imipenem were higher than those of ESBL-E.coli (P＜0.003). Both CRKP and ESBL-E.coli had high sensitivity to polymyxin and tigecycline. Multivariate logistic regression showed duration of mechanical ventilation ≥ 7 days, and combination of ≥ 2 antibiotics for over 7 days were independent risk factors for CRKP infection (P＜0.01). Conclusions For patients with severe pneumonia and artificial airway in ICU, K. pneumoniae is the main bacterial infection. CRKP and ESBL-E.coli in BALF exhibit different degrees of drug resistance to various antibacterial agents, both have the characteristic of multidrug resistance, and are sensitive to polymyxin and tigecycline. Prevention and control of risk factors related to CRKP should be formulated particularly.

Objective:To investigate the survival outcomes and prognostic factors in patients undergoing radical resection for pancreatic body and tail cancer.Methods:A retrospective case series study was conducted on 992 patients who underwent radical resection for pancreatic body and tail cancer at the Pancreatic Center of the First Affiliated Hospital of Nanjing Medical University from January 2016 to June 2024. In this study, 577 (58.2%) were male and 415 (41.8%) were female,with an age of (65±9) years (range: 26 to 86 years). Follow-up continued until June 2024. Survival rates were estimated using the Kaplan-Meier method,and prognostic factors were identified using univariate and multivariate Cox proportional hazards models.Results:Among 992 patients,open surgery was the predominant approach (89.1%, 884/992), and radical antegrade modular pancreatosplenectomy (RAMPS) was performed in 317 patients (32.0%). Combined organ resection,venous resection,and arterial resection were performed in 23.5%, 9.3%,and 11.2% of patients,respectively. The rates of R0, R1-1 mm, and R1-direct resections were 49.8% (494/992),41.5% (412/992), and 8.7% (86/992),respectively. Stage ⅡB was the most common TNM stage (32.2%,319/992). A total of 801 patients (80.8%) received adjuvant chemotherapy. The median follow-up period was 32.0(8.8) months(range:3.2 to 105.3 months),during which 508 patients (51.2%) died. The overall median survival (OS) was 26.4 months,with 1-,3-, and 5-year survival rates of 79.0%,40.0%, and 29.0%, respectively. In the recent five years (from 2020 to 2024), the median OS improved significantly to 34.1 months compared to 20.0 months from 2016 to 2019 ( P<0.01). Histological subtype analysis showed that the median OS time was 26.7 months for pancreatic ductal adenocarcinoma (PDAC, n=855),58.9 months for invasive intraductal papillary mucinous carcinoma (IPMC, n=32),and 15.7 months for adenosquamous carcinoma of pancreas (ASCP, n=73) ( P=0.001). Among PDAC patients, adjuvant chemotherapy significantly improved survival (29.1 months vs. 14.4 months, P<0.01);in IPMC patients, adjuvant chemotherapy also extended survival (65.7 months vs. 58.9 months, P=0.047). Although ASCP patients receiving chemotherapy had a longer median OS time than those without (18.8 months vs. 8.9 months),the difference was not statistically significant ( P=0.151). Multivariate Cox regression analysis in PDAC patients indicated that adjuvant chemotherapy, R0 resection, T stage,N stage,and tumor differentiation were independent prognostic factors ( P<0.01). The median OS time by TNM stage was:not reached for stage ⅠA, 51.6 months for ⅠB, 25.5 months for ⅡA, 23.7 months for ⅡB, 23.0 months for Ⅲ, and 14.4 months for Ⅳ. The median OS time for R0,R1-1 mm,and R1-direct resections was 34.1,24.7,and 15.7 months,respectively ( P<0.01). Conclusion:Adjuvant chemotherapy,R0 resection,tumor stage,and differentiation are independent prognostic factors for pancreatic body and tail cancer.