Childhood simple obesity has become a significant public health issue in China. Modern medicine primarily relies on lifestyle interventions and often suffers from poor long-term compliance， while pharmacological options are limited and associated with potential adverse effects. Traditional Chinese Medicine （TCM） has a long history in the prevention and management of this condition， demonstrating eight distinct advantages， including systematic theoretical foundation， diversified therapeutic approaches， definite therapeutic efficacy， high safety profile， good patient compliance， comprehensive intervention strategies， emphasis on prevention， and stepwise treatment protocols. Additionally， TCM is characterized by six distinctive features： the use of natural medicinal substances， non-invasive external therapies， integration of medicinal dietetics， simple exercise regimens， precise syndrome differentiation， and diverse dosage forms. By combining internal and external treatments， TCM facilitates individualized regimen adjustment and holistic regulation， demonstrating remarkable effects in improving obesity-related metabolic indicators， regulating constitutional imbalance， and promoting healthy behaviors. However， challenges remain， such as inconsistent operational standards， insufficient high-quality clinical evidence， and a gap between basic research and clinical application. Future efforts should focus on accelerating the standardization of TCM diagnosis and treatment， conducting multicenter randomized controlled trials， and fostering interdisciplinary integration， so as to enhance the scientific validity and international recognition of TCM in the prevention and treatment of childhood obesity.

ObjectiveTo investigate the effect of mitochondrial calcium uniporter （MCU） on the cytoskeleton of pancreatic ductal epithelial cells in a mouse model of acute pancreatitis （AP） induced by caerulein （CAE）， to analyze the role of MCU in the development of AP， and to provide a theoretical basis for clinical treatment. MethodsIn the in vivo experiment， wild-type male C57BL6/J mice， aged 4 weeks， were randomly divided into control group and AP group， with 6 mice in each group. The mice in the AP group were given intraperitoneal injection of CAE to establish a model of AP， and those in the control group were given intraperitoneal injection of an equal volume of normal saline. Serum and pancreatic tissue samples were collected after 24 hours of modeling. HE staining was used to observe pancreatic histopathological changes； Western Blot was used to measure the expression levels of MCU， glutathione peroxidase 4 （GPX4）， and acyl-CoA synthetase long chain family member 4 （ASCL4）； kits were used to measure the serum level of amylase. In the in vitro experiment， the human pancreatic ductal epithelial cell line HPDE6-C7 was co-cultured with CAE for 24 hours to establish an in vitro AP model， and the cells were divided into control group， CAE group， RR （an MCU activity inhibitor） group， CAE+RR group， Fer-1 （an ferroptosis inhibitor） group， CAE+Fer-1 group， Erastin （an ferroptosis inducer） group， and CAE+Erastin group. CCK-8 assay was used to observe the influence of different agents on cell viability； Western Blot was used to measure the expression levels of MCU， GPX4， and ASCL4； immunofluorescence assay was used to measure reactive oxygen species （ROS）， actin cytoskeleton， and monolayer permeability； kits were used to measure the concentrations of malondialdehyde （MDA）， glutathione （GSH）， Fe²⁺， and total iron. 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 comparison between two groups. ResultsIn the in vivo experiment， compared with the control group， the AP group had significant increases in pancreatic histopathological score， the serum level of amylase， and the expression levels of MCU and ASCL4， as well as a significant reduction in the expression of GPX4 （all P<0.05）. In the in vitro experiment， compared with the control group， the CAE group had significant increases in the expression levels of MCU and ASCL4， a significant reduction in the expression of GPX4， and significant increases in the concentrations of Fe²⁺， total iron， and MDA， the green fluorescence intensity of ROS， and monolayer permeability， as well as a significant reduction in the concentration of GSH （all P<0.05）， with the presence of actin cytoskeleton disruption. Compared with the CAE group， the CAE+RR group had a significant increase in the expression level of GPX4， a significant reduction in the expression level of ASCL4， and significant reductions in the concentrations of Fe²⁺， total iron， and MDA， the green fluorescence intensity of ROS， and monolayer permeability and a significant increase in the concentration of GSH （all P<0.05）， with alleviation of actin cytoskeleton disruption. Compared with the CAE group， the CAE+Fer-1 group had significant reductions in the concentrations of Fe²⁺， total iron， and MDA， the green fluorescence intensity of ROS， and monolayer permeability and a significant increase in the concentration of GSH （all P<0.05）， with alleviation of actin cytoskeleton disruption. Compared with the CAE group， the CAE+Erastin group had significant increases in the concentrations of Fe²⁺， total iron， and MDA， the green fluorescence intensity of ROS， and monolayer permeability and a significant reduction in the concentration of GSH （all P<0.05）， with aggravation of actin cytoskeleton disruption. ConclusionDuring the onset of AP， MCU mediates oxidative stress-induced ferroptosis and leads to the disruption of the pancreatic ductal epithelial barrier， which may be one of the possible pathogeneses of AP.

OBJECTIVE To investigate the influence of CYP2C19 gene polymorphism on platelet function and inflammatory cytokines in elderly patients with ischemic stroke， and to analyze potential factors associated with poor prognosis. METHODS A retrospective study was conducted on elderly patients with ischemic stroke admitted to our hospital from June 2024 to June 2025， wh o underwent CYP2C19 genotype testing and received antiplatelet therapy with clopidogrel. The levels of platelet function indicators and inflammatory cytokines before and after treatment were compared among patients with different metabolic phenotypes. Based on the prognosis at 6 months post-treatment， patients were divided into poor prognosis group and good prognosis group. Univariate analysis was performed on general data， metabolic phenotype， the levels of platelet function indicators and inflammatory cytokines. Variables with P ＜0.05 and the levels of inflammatory cytokines before treatment were included in a multivariate Logistic regression analysis to identify independent risk factors for poor prognosis. Multiple linear regression was used to further analyze the relationship between metabolic phenotypes and inflammatory cytokines. RESULTS A total of 448 elderly patients with ischemic stroke were included； among them， 162 cases were normal metabolic phenotype， 218 were intermediate metabolic phenotype， and 68 were poor metabolic phenotype. No rapid or ultrarapid metabolic phenotypes were observed. After treatment， platelet aggregation rate， the levels of P-selectin and platelet activated complex-1 （PAC-1）， high-sensitivity C-reactive Protein （hs-CRP）， interleukin-1β （IL-1β）， IL-6 and tumor necrosis factor-α （TNF-α） in the normal metabolic phenotype group， intermediate metabolic phenotype group， and poor metabolic phenotype group （except for platelet aggregation rate， and the levels of P-selectin and PAC-1 in the poor metabolic phenotype group） were significantly lower than those before treatment in the same group. Moreover， the above indicators in the normal metabolic phenotype group were significantly lower than those in the intermediate and poor metabolic phenotype groups at the corresponding time， and the levels of platelet function indicators in the intermediate metabolic phenotype group were significantly lower than those in the poor metabol ic phenotype group at the corresponding time （ P ＜0.05）. Univariate and multivariate Logistic regression analyses showed that combined with hypertension， combined with diabetes mellitus， and intermediate or poor metabolic genotypes were independent risk factors for poor prognosis in elderly patients with ischemic stroke （ P ＜0.05）. Multiple linear regression analysis showed that serum levels of hs-CRP， IL-1β， IL-6 and TNF-α before treatment were significantly higher in patients with intermediate and poor metabolic genotypes compared to those with normal metabolic genotype （ P ＜0.05）， with a greater magnitude of increase in inflammatory cytokines observed in the patients with poor metabolic genotype. CONCLUSIONS The elderly ischemic stroke patients with CYP2C19 intermediate and poor metabolic genotypes have poor inhibition effect on platelet and higher levels of inflammatory cytokines than normal metabolic genotype； CYP2C19 gene polymorphism， and in combination with hypertension and diabetes， can be used as independent predictors of poor prognosis.

Objective To analyze the epidemic characteristics of scarlet fever in Pudong New Area, Shanghai from 2010 to 2023, and to grasp the incidence of scarlet fever in time. Methods The information on the registration of scarlet fever in Pudong New Area, Shanghai from January 1, 2010 to December 31, 2023 was collected through the China Disease Prevention and Control Information System, and descriptive epidemiological methods and Joinpoint regression model were used for data analysis. Results From 2010 to 2023, a total of 5 669 cases of scarlet fever were reported in Pudong New Area, Shanghai, and no deaths were reported. The annual reported incidence rate was 7.2/100 000, and the overall trend was decreasing year by year. In terms of time distribution, the incidence peaks were in spring and winter. The incidence rate in males was higher than that in females, and it mainly affected children, especially those aged 2 to 10 years. Joinpoint regression model analysis showed that the annual percentage change (APC) and average annual percentage change (AAPC) of the reported incidence rate of scarlet fever from 2010 to 2023 showed that the incidence rate was fluctuating, and the incidence rate decreased significantly from 2019 to 2023 (APC was -53.7%). Conclusion The reported incidence rate of scarlet fever in Pudong New Area in Shanghai has decreased year by year from 2010 to 2023, and children remain the focus of prevention and control.

Prostate cancer is one of the most common malignant tumors of male genitourinary system. Prostate cancer has the following characteristics： insidious onset， early asymptomatic or not obvious symptoms， complex etiology and pathogenesis， long incubation period and so on. Therefore， the realization of its early diagnosis and treatment is of great significance to the prognosis of patients. Prostate-specific membrane antigen （PSMA） is a type 2 transmembrane glycoprotein that is highly expressed on the membrane of almost all primary and metastatic prostate cancer cells， and is an ideal target for prostate cancer imaging and treatment. In recent years， with the approval of urea-containing small molecule PET （positron emission computed tomography） radiopharmaceutical based on PSMA （⁶⁸Ga-PSMA-11， ¹⁸F-PSMA-1007）， PET-CT （positron emission computed tomography/computed tomography） has shown new potential for early diagnosis and accurate staging of prostate cancer patients. This review mainly summarizes the research progress of urea-containing PSMA PET imaging agents and finds that they have defects such as uptake in non-target tissues like the kidneys， lacrimal glands， and salivary glands. Thus， further optimizing their structure to reduce the uptake in non-target tissues， providing provide convenience for the labeling of therapeutic radiopharmaceuticals， thereby achieving the goal of integrated diagnosis and treatment， is an important development direction in this field.

Objective To investigate the temporal changes in pathological damage and macrophage polarization in liver and spleen tissues of mice infected with Angiostrongylus cantonensis, and to preliminarily unravel the peripheral immune responses during the early stage of A. cantonensis infection. Methods Forty female BALB/c mice at ages of 6 to 8 weeks were randomly divided into four groups, including the control group and 7-, 14-, and 21-day infection groups, with 10 mice in each group. Each mouse in the infection groups was inoculated with 30 third-stage (L3) larvae of A. cantonensis by oral gavage, and five mice were randomly selected from each infection group on days 7, 14, and 21 post-infection, while mice in the control group were given the same volume of physiological saline and five mice were randomly selected from the control group on the day of oral gavage. Mouse liver and spleen tissues were sampled. The histopathological changes of mouse liver and spleen tissues were observed using hematoxylin and eosin (HE) staining, and the percentage of positive staining area and the co-localization positive rates of the macrophage surface antigens F4/80, CD86, and CD206 were quantified in mouse liver and spleen tissues using immunohistochemical and immunofluorescence staining. In addition, five mice were collected from each infection group on days 7, 14, and 21 post-infection, and five mice were collected from the control group on the day of oral gavage. Mouse liver and spleen tissues were sampled for detection of macrophage markers CD86 and CD206 and macrophage phenotyping using flow cytometry, and the expression of M1 macrophage markers, including inducible nitric oxide synthase (Nos2), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and M2 markers, including arginase 1 (Arg1), mannose receptor C-type 1 (Mrc1) and chitinase-like protein 3 (Chil3) was quantified in mouse liver and spleen tissues using real-time quantitative PCR (RT-qPCR) assay. Results Proliferative lesions of the hepatocyte were observed in mouse liver tissues and the follicular structures of the mouse spleen white pulp were disrupted 21 days post-infection with A. cantonensis. Immunohistochemical staining showed that there were significant differences in the percentages of F4/80, CD86 and CD206 positive staining areas in the liver and spleen tissues among the four groups of mice (F = 242.40, 197.14, 183.19, 157.65, 242.35 and 146.24; all P values < 0.001), and the percentages of positive staining in the liver and spleen tissues of mice in the 14-day infection group [(4.45 ± 0.51)%, (3.74 ± 0.67)%, (8.32 ± 0.72)%, (16.56 ± 1.14)%, (11.62 ± 0.52)%, and (8.29 ± 0.72)%, respectively] and the 21-day infection group [(3.70 ± 0.11)%, (3.22 ± 0.43)%, (11.53 ± 1.03)%, (12.59 ± 1.05)%, (9.02 ± 0.83)%, and (11.67 ± 1.10)%, respectively] were higher than in the control group [(0.35 ± 0.16)%, (0.40 ± 0.02)%, (0.93 ± 0.05)%, (2.78 ± 0.26)%, (2.33 ± 0.20)%, and (1.85 ± 0.20)%, respectively] (all P values < 0.05). Immunofluorescence staining showed significant differences in the positive rates of F4/80 co-localization with CD86 and CD206 in mouse liver and spleen tissues among the four groups (F = 24.42, 25.28, 54.51 and 130.55; all P values < 0.001). Flow cytometry detected significant differences in the proportions of CD86⁺ and CD206⁺ macrophages in mouse liver and spleen tissues among the four groups (F = 67.98, 18.41, 29.77, 172.80; all P values < 0.001), and the proportions of CD206⁺ macrophages in the liver and spleen of the 21-day infection group were significantly higher than those in the control group [(9.25 ± 2.55)% vs (3.83 ± 0.72)%, and (4.22 ± 0.56)% vs (0.47 ± 0.18)%, respectively] (both P values < 0.05). In addition, RT-qPCR assay quantified significant differences in the relative mRNA expression of M1 macrophage markers (IL-1β, TNF-α and Nos2) and M2 macrophage markers (Arg1, Chil3 and Mrc1) in mouse liver and spleen tissues among the four groups (F = 41.30, 31.82, 199.33, 19.96, 62.01, 119.76, 23.67, 95.90, 72.27, 82.59, 123.41 and 29.75; all P values < 0.05). Conclusions A. cantonensis infection may cause progressive pathological damage in mouse liver and spleen tissues, accompanied by dynamic temporal changes in macrophage polarization. M1 macrophage polarization predominates at the early stage of A. cantonensis infection and shifts towards M2 polarization at the later stages, suggesting that M2 polarization may participate in immune regulation at late stages of A. cantonensis infection by suppressing excessive inflammatory responses and promoting tissue repair.

Objective: To elucidate the biological basis of traditional Chinese medicine (TCM) syndromes from the perspective of “same syndrome, different diseases” in patients with chronic hepatitis B (CHB), liver cirrhosis (LC), and hepatocellular carcinoma (HCC), thereby providing a complementary approach for the diagnosis and treatment of chronic liver diseases (CLD). Methods: To investigate the dynamic characteristics of TCM syndromes in CLD, transcriptomic profiling of peripheral blood mononuclear cells (PBMCs) was performed from patients with CHB, LC, or HCC presenting with three TCM syndromes: liver gallbladder dampness heat syndrome (LGDHS), liver depression spleen deficiency syndrome (LDSDS), and liver kidney Yin deficiency syndrome (LKYDS). These participants were recruited at Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine between August 1, 2018 and December 31, 2021. Differentially expressed genes (DEGs) were identified using the random variance model (RVM) F test with false discovery rate (FDR) correction. Principal component analysis (PCA) and unsupervised hierarchical clustering were applied to visualize sample grouping. Dynamic network biomarkers (DNB) analysis was employed to detect critical transition stages during syndrome evolution, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses to characterize the functional roles and pathway involvement of the DNB members. Random forest (RF) analysis and the area under the receiver operating characteristic (ROC) curves (AUC) were used to rank the importance of candidate genes. External validation was performed using microarray data from an independent CLD cohort (GSE89377) and RNA-seq data from The Cancer Genome Atlas Liver Hepatocellular Carcinoma (TCGA-LIHC) dataset. Additionally, reverse transcription quantitative polymerase chain reaction (RT-qPCR) was performed on an independent cohort of LC patients to validate the expression levels of the candidate genes. Results: The study included a total of 132 participants. DNB analysis identified LDSDS stage as a critical tipping point during TCM syndrome evolution across CHB, LC, and HCC. The phosphoinositide 3-kinase/protein kinase B (PI3K-AKT) signaling pathway was consistently enriched in the DNB analysis across all three types of CLD, suggesting its potential involvement in the critical transition of TCM syndromes. Among the 24 core DNB members of the PI3K-AKT pathway, four genes—integrin subunit beta 1 (ITGB1), collagen type IV alpha 1 chain (COL4A1), collagen type IV alpha 2 chain (COL4A2), and DNA damage inducible transcript 3 (DDIT3)—were identified by RF analysis (Gini score > 1) and ROC analysis. ROC analysis demonstrated high discriminative ability for distinguishing LGDHS from LKYDS in CHB patients, with AUC of 0.7891 for ITGB1, 0.7070 for COL4A1, 0.7148 for COL4A2, and 0.8945 for DDIT3. In the independent CLD cohort (GSE89377), all four genes showed significant stepwise upregulation from normal to CHB, LC, and HCC (all P < 0.05). In the TCGA-LIHC dataset, their expression progressively increased with tumor stage. RT-qPCR validation in an independent LC cohort (30 LGDHS vs. 30 LKYDS) confirmed that ITGB1, COL4A2, and DDIT3 were significantly upregulated in LKYDS compared with LGDHS (P = 0.0152, 0.0186, and 0.0247, respectively), whereas COL4A1 showed a non-significant upward trend (P = 0.1201). Conclusion This study introduces a novel approach to understanding the molecular features underlying TCM syndrome evolution in CLD. The PI3K-AKT pathway and four identified genes (ITGB1, COL4A1, COL4A2, and DDIT3) play crucial roles in the transition from excess (LGDHS) to deficiency (LKYDS) via the critical LDSDS stage. These findings offer potential quantitative biomarkers and therapeutic targets for TCM syndrome differentiation and may help arrest syndrome progression in CLD.

Objective: To investigate the correlation between the color parameters (L^*, a^*, b^*, Eab^* values) of Polygoni Multiflori Radix Praeparata powder prepared by different processing techniques and the contents of 2,3,5,4’-tetrahydroxystilbene-2-O-β-D-glucopyranoside, emodin, physcion, emodin-8-O-β-D-glucopyranoside, physcion-8-O-β-D-glucopyranoside.
Methods: The L^*, a^*, b^* and Eab^* values of Polygoni Multiflori Radix Praeparata powder prepared by different processing techniques were determined by spectrophotometer, and the contents of the five components were determined by high performance liquid chromatography. Secondly, SPSS 26.0 software and Simca 14.1 software were used to analyze the correlation.
Results: Through the hierarchical cluster analysis (HCA), it was found that the steamed samples and black bean steamed samples could be obviously divided into two categories: raw products and processed products. The processed products could be further divided into 2-8 h and 12-48 h. Pearson correlation analysis showed that the content of stilbene glycoside was significantly positively correlated with L^*, a^* and b^* values (P<0.01). The a^* value was significantly positively correlated with the content of emodin and physcion (P<0.01). Emodin-8-O-β-D-glucoside was positively correlated with L^* value and b^* value, while physcion-8-O-β-D-glucoside was negatively correlated with a^* value. Partial least squares discriminant analysis (PLS) showed that 2,3,5,4’-tetrahydroxystilbene-2-O-β-D-glucoside (VIP=1.69) and emodin-8-O-β-D-glucoside (VIP=1.06) were the key variables affecting chromaticity characteristics (P<0.01).
Conclusion: The three processes of steaming, black bean steaming and black bean stewing are consistent in composition transformation and chromaticity variation, and stilbene glycoside can be used as a specific index component to characterize the processed color. Chromatic parameters can effectively reflect the processing progression and serve as quality monitoring indicators during production.

Background: High-mobility group box protein 1 (HMGB1) is a chromatin-binding protein involved in arthritis, ischemia, sepsis, atherosclerosis, neurodegenerative disorders, meningitis, and cancer. HMGB1 exhibits dual roles in cancer, acting as either a tumor suppressor or oncoprotein depending on context. Objective: This research aimed to elucidate HMGB1’s functional significance in cutaneous squamous cell carcinoma (cSCC). Methods: We overexpressed HMGB1 in cSCC cell lines using recombinant adenovirus and examined its effects on cell proliferation, colony formation, and cell migration. Results: Immunohistochemical analysis revealed elevated HMGB1 expression levels in cSCC tissue relative to normal epidermis. To assess the influence of HMGB1, we employed recombinant adenoviruses expressing HMGB1 to transduce SCC cell lines (SCC12 and SCC13). Enhanced HMGB1 expression significantly promoted cellular proliferation and colony formation capacity.Notably, HMGB1 overexpression elevated the levels of proliferation regulators, including P63, SOX2, CDK4 and CDK6. Furthermore, HMGB1 overexpression substantially enhanced tumor invasiveness, accompanied by upregulation of epithelial-mesenchymal transition (EMT) biomarkers. Mechanistically, overexpression of HMGB1 enhanced transforming growth factor-β signaling by increasing phosphorylation of SMAD2/3, the key mediators of EMT. Conclusion These data imply that HMGB1 acts as a tumor-promoting factor in cSCC.

Background: While observational studies have suggested a potential link between metabolic syndrome (MetS) and an increased risk of colon polyps, the causal nature of this association remains uncertain. This study used a two-sample Mendelian randomization (MR) approach to evaluate the relationship between MetS and colon polyps. Methods: A two-sample MR analysis was performed using data on MetS, its indicators, and colon polyps obtained from publicly available genome-wide association studies in the Integrative Epidemiology Unit (IEU) and MAGIC databases. Outliers were removed using Mendelian Randomization Pleiotropy RESidual Sum and Outlier (MR-PRESSO), followed by MR calculations and false discovery rate (FDR) correction. The primary analysis was conducted with the inverse variance-weighted (IVW) method. Results: The IVW results indicated no association between hypertension, hyperlipidemia, or diabetes and the risk of colon polyps. High-density lipoprotein cholesterol (HDL-C) (P=0.005), 2-hour glucose (P=0.004), glycated hemoglobin A1c (P=0.004), and the ratio of omega-6 to omega-3 fatty acids (P<0.001) were negatively associated with colon polyps. Conversely, body mass index (BMI) (P<0.001), body fat percentage (P=0.002), waist-to-hip ratio adjusted for BMI (P=0.001), total cholesterol (TC) (P=0.002), triglycerides (TG) (P<0.001), and both omega-3 (P<0.001) and omega-6 fatty acid levels (P=0.02) were positively associated with colon polyps. The relationships between these metabolic indicators and colon polyps remained significant after FDR correction. Conclusion Obesity-related traits, TC, and TG may increase the risk of colon polyps, while HDL-C may have a protective effect.