Objective: To explore the longitudinal association between weight trajectories and physical fitness test composite scores among primary school students, so as to provide empirical evidence for school based weight management and physical health promotion. Methods: A total of 2 112 students from a primary school in Beijing who participated in physical fitness assessments annually from 2008 to 2023 were included and classified into different body weight trajectory groups based on body mass index (BMI) threshold: "normal/overweight-obese". Group based trajectory model was used to identify distinct weight trajectories. Generalized estimating equation and Cox regression were used to analyze the associations between weight trajectories and changes in physical fitness test scores, as well as event risks. Robustness checks were conducted. Results: The prevalence of overweight and obesity among primary school students was 26.50%. BMI showed a significant negative correlation with physical fitness composite scores ( r=-0.19, P <0.01). Four types of weight trajectories were identified: persistent normal group (64.5%, 1 362), persistent overweight- obese group (18.2%, 385), normal to overweight-obese group (14.0%, 296), and overweight-obese to normal group (3.3%, 69). Compared to the persistent normal group, both the normal to overweight-obese and persistent overweight-obese groups showed significantly higher risks of failing the physical fitness test ( HR =4.23, 4.60), and the speed of achieving excellent was slower ( HR = 0.52, 0.40) (all P <0.05). Robustness tests confirmed the stability of the findings. Conclusions Body weight trajectories have a long term impact on physical fitness performance among primary school students. Students with persistent or progressive overweight-obese trajectories have limited score improvement and a higher risk of failure; primary school students with persistent or progressive overweight and obesity should be a key focus.

Objective To investigate CBX2 and TIM3 in salivary adenoid cystic carcinoma(SACC)tissue and their relationship with clinical pathological features and prognosis.Methods 80 patients with SACC who underwent surgical treatment in the First Affiliated Hospital of Hebei North University from January 2016 to January 2020 were selected.Immunohistochemistry was used to measure CBX2 and TIM3 in tissues.The relationship between CBX2 and TIM3 in SACC tissue and prognosis was discussed though Kaplan-Meier method.The factors influencing the prognosis of SACC were discussed using multivariate Cox regression.Results The positive rates of CBX2 and TIM3 in SACC tissues were clearly higher than those in normal glandular tissues adjacent to cancer(χ2=11.237,8.229,P<0.05).The CBX2 and TIM3 were associated with nerve invasion and distant metastasis(P<0.05).After a 5-year follow-up,26 cases died and 54 cases survived,with an overall 5-year survival rate of 67.50%(54/80).The death group had higher positive rates of CBX2 and TIM3 in SACC tissues than the survival group(P<0.05).Patients with positive CBX2 and TIM3 in SACC tissues had clearly lower 5-year survival rate than patients with negative CBX2 and TIM3(Log Rank χ2=6.564,5.197,P<0.05).CBX2,TIM3 positivity,nerve invasion,and distant metastasis were risk factors affecting prognosis(P<0.05).Conclusion The positive expression of CBX2 and TIM3 in SACC tissues is closely related to the clinical pathological features and prognosis of patients.

Hepatocellular carcinoma(HCC)is one of the most common malignant tumors.Tyrosine kinase inhibitors have been used in the mainstream treatment of HCC for many years,but their therapeutic efficacy is limited and the prognosis of patients is very poor.In recent years,the rapid rise of immunotherapy has provided a new direction for tumor treatment.In particular,immune checkpoint inhibitors have shown excellent clinical effect in the treatment of various solid tumors,including HCC.This article reviews various immune checkpoint inhibitors related to HCC and their clinical practice and research progress,aiming to provide a relevant reference and theoretical basis for the immunotherapy of HCC.

Tumor immunotherapy,recognized as the fourth major treatment modality alongside surgery,radiotherapy,and chemotherapy,fundamentally relies on mobilizing and enhancing the body's intrinsic immune system to achieve the precise targeting and elimination of neoplastic lesions.In this therapeutic framework,macrophages derived from blood monocyte differentiation serve as critical components of the innate immune defense system and exert profound impacts within the tumor microenvironment(TME).As the dominant inflammatory cell population infiltrating the TME,tumor-associated macrophages(TAMs)not only perform a key function in immune regulation but also serve as a paradigm for the connection between inflammation and tumors.Therapeutic strategies targeting TAMs aim to reverse the immunosuppressive milieu of the TME through multifaceted regulatory mechanisms,including cellular depletion or functional reprogramming,thereby effectively impeding tumor progression.This review systematically analyzes the intricate immune regulatory mechanisms of macrophages in tumor immunotherapy and synthesizes research advancements in major therapeutic agents targeting TAMs,aiming to provide researchers in the field of tumor immunotherapy and developers of macrophage-modulating pharmaceuticals with novel theoretical insights and practical guidelines.

Hepatocellular carcinoma(HCC)is one of the most common malignant tumors.Tyrosine kinase inhibitors have been used in the mainstream treatment of HCC for many years,but their therapeutic efficacy is limited and the prognosis of patients is very poor.In recent years,the rapid rise of immunotherapy has provided a new direction for tumor treatment.In particular,immune checkpoint inhibitors have shown excellent clinical effect in the treatment of various solid tumors,including HCC.This article reviews various immune checkpoint inhibitors related to HCC and their clinical practice and research progress,aiming to provide a relevant reference and theoretical basis for the immunotherapy of HCC.

Tumor immunotherapy,recognized as the fourth major treatment modality alongside surgery,radiotherapy,and chemotherapy,fundamentally relies on mobilizing and enhancing the body's intrinsic immune system to achieve the precise targeting and elimination of neoplastic lesions.In this therapeutic framework,macrophages derived from blood monocyte differentiation serve as critical components of the innate immune defense system and exert profound impacts within the tumor microenvironment(TME).As the dominant inflammatory cell population infiltrating the TME,tumor-associated macrophages(TAMs)not only perform a key function in immune regulation but also serve as a paradigm for the connection between inflammation and tumors.Therapeutic strategies targeting TAMs aim to reverse the immunosuppressive milieu of the TME through multifaceted regulatory mechanisms,including cellular depletion or functional reprogramming,thereby effectively impeding tumor progression.This review systematically analyzes the intricate immune regulatory mechanisms of macrophages in tumor immunotherapy and synthesizes research advancements in major therapeutic agents targeting TAMs,aiming to provide researchers in the field of tumor immunotherapy and developers of macrophage-modulating pharmaceuticals with novel theoretical insights and practical guidelines.

Stem cells are a kind of cells with the ability of self-renewal and differentiation, which can differentiate into melanocytes to fill the areas of pigment loss in damaged skin, fight against the apoptosis of melanocytes caused by autoimmunity and oxidative stress damage, and improve repigmentation rates in combination with traditional therapies. Studies have shown significant efficacy of stem cell therapy in the repigmentation of vitiligo. This review summarizes the latest advances in the basic and clinical research on the application of stem cells in the treatment of vitiligo.

Ulcerative colitis(UC)is a chronic inflammatory bowel disease affecting the colon(particularly the descending colon and sigmoid)and rectum.UC primarily presents with persistent or recurrent diarrhea,abdominal pain,bloody stools,and other symptoms.The primary pathological mechanism of UC involves intestinal barrier injury.When the intestinal barrier function is compromised,characterized by loss of epithelial layer integrity,thinning of the mucus layer,and microbiota dysregulation,pathogenic microorganisms can infiltrate the lamina propria from the intestinal lumen through the damaged barrier,triggering and exacerbating the intestinal inflammatory response.Current treatments for UC are limited by high costs,numerous adverse reactions,and a high likelihood of relapse.Consequently,there is an urgent need for the development of new drugs that can effectively and safely treat UC.Natural products have become significant research targets in treating various diseases due to their broad biological activity,multiple action targets,low toxicity,and easy availability.They play a crucial role in the targeted repair of the intestinal barrier,with potential mechanisms including enhancing intes-tinal epithelial cells and their secreted proteins,regulating gut microbiota and its metabolism,and balancing immune cell subsets.Additionally,it is essential to consider the synergistic effects,bioavailability,and safety of natural products.This paper summarizes the natural products reported in the past five years for their anti-UC properties by repairing the intestinal barrier,providing a theoretical basis for the development and application of natural products in anti-UC drugs.

Purpose To investigate the clinicopathological features,diagnosis,and molecular genetic characteris-tics of central nervous system(CNS)high-grade neuroepithelial tumors with BCOR alterations.Methods Five cases of CNS high-grade neuroepithelial tumors harboring BCOR alterations were collected.Using immunohistochemistry and molecular detection to analyze its clinical and histological characteristics,and review relevant literatures.Results A-mong the 5 patients,3 cases with EP300 ∷ BCOR tumor(male-to-female ratio 2∶1).These tumors were located in supratentorial regions(right temporal lobe,right frontotemporal lobe,and right frontal lobe).The 2 patients with BCOR-ITD tumors were younger,both with tumors located in the left cerebellum.Imaging studies revealed well-defined large mass lesions in all cases.Histologically,all 5 cases tumor exhibited ependymoma-like or oligodendroglioma-like morphology,featuring uniformly oval or round cells.Focal areas showed increased cellular density,nuclear enlarge-ment,and readily identifiable mitotic figures indicative of anaplastic features.A rich capillary network was frequently observed in the stroma.Palisading necrosis,microcystic changes,and microcalcifications were present in 3 cases.Im-munohistochemically,all 5 cases consistently expressed vimentin and CD56,focal Olig-2 positivity,variable S-100 ex-pression,and were uniformly negative for GFAP.BCOR immunostaining was weakly positive in 1 case with an EP300∷ BCOR fusion and strongly positive in 2 cases with BCOR-ITD.NGS identified an EP300 ∷ BCOR fusion in 3 cases,and Sanger sequencing confirmed the ITD in exon 15 of BCOR gene in 2 cases.During a follow-up period of 8 to 77 months,one pediatric patient with a BCOR-ITD tumor died,while the remaining four patients were alive with no evi-dence of recurrence or metastasis.Conclusion BCOR-ITD and EP300 ∷ BCOR fusion tumors are similar in morphology and immunophenotype,and the incidence rate of BCOR fusion tumors may be underestimated.NGS sequencing based on DNA and RNA and DNA methylation spectrum analysis are helpful for accurate diagnosis of this type of tumor.

ObjectiveTo observe the effect of Yifei Jianpi prescription on the of signal transducer and activator of transcription protein 1 （STAT1）/interferon regulatory factor 3 （IRF3） signaling pathway in a pneumonia model induced by lipopolysaccharide （LPS） and to explore the mechanism of Yifei Jianpi prescription in improving lung immune and inflammatory responses. MethodsSixty male SPF SD rats were used in this study. Ten rats were randomly assigned to the normal control group， and the remaining 50 were instilled with LPS in the trachea to establish a pneumonia model. After successful modeling， the rats were randomly divided into the model group， dexamethasone group （0.5 mg·kg^-1）， and Yifei Jianpi prescription high-dose （12 mg·kg^-1）， medium-dose （6 mg·kg^-1）， and low-dose （3 mg·kg^-1） groups， with 10 rats in each group. Treatment was administered once daily， and the normal control and model groups received the same volume of normal saline. After 14 days， flow cytometry was used to detect the classification of whole blood lymphocytes. Enzyme-linked immunosorbent assay （ELISA） was used to measure serum levels of immunoglobulin G （IgG）， immunoglobulin A （IgA）， immunoglobulin M （IgM）， and the content of tumor necrosis factor-α （TNF-α）， interleukin-8 （IL-8）， interleukin-6 （IL-6）， and interleukin-10 （IL-10） in alveolar lavage fluid （BALF）. Hematoxylin-eosin （HE） staining was used to observe lung tissue pathology and score the damage. Thymus weight， spleen weight， and wet-to-dry weight ratio （W/D） were recorded. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect the mRNA expression of STAT1， IRF3， IL-6， and interferon-alpha （IFN-α） in lung tissues， while Western blot was performed to assess the protein expression of STAT1， IRF3， IL-6， and IFN-α. ResultsCompared with the normal control group， the model group showed significantly increased proportion of B lymphocytes in peripheral blood， decreased proportions of NK cells and CD4⁺/CD8⁺ （P<0.05， P<0.01）， decreased serum levels of IgG and IgA， significantly increased IgM levels （P<0.01）， significantly elevated content of TNF-α， IL-6， and IL-8 in BALF， and significantly decreased IL-10 levels （P<0.01）. Lung tissue damage was evident， with significant increases in thymus and spleen weights and a higher W/D ratio （P<0.01）. The mRNA and protein expression of STAT1， IRF3， IFN-α， and IL-6 in lung tissues was significantly upregulated （P<0.05，P<0.01）. Compared with the model group， the Yifei Jianpi prescription groups showed significantly reduced proportions of B lymphocytes in peripheral blood， increased proportions of NK cells and CD4⁺/CD8⁺ ratios （P<0.05， P<0.01）， significantly increased serum levels of IgG and IgA， significantly decreased IgM levels （P<0.05， P<0.01）， significantly reduced levels of TNF-α， IL-6， and IL-8 in BALF， and significantly increased IL-10 levels （P<0.01）. Lung tissue damage was alleviated， thymus and spleen weights were significantly reduced， and the W/D ratio was markedly decreased （P<0.01）. The mRNA and protein expression of STAT1， IRF3， IFN-α， and IL-6 in lung tissues was significantly downregulated （P<0.05， P<0.01）. ConclusionYifei Jianpi prescription can alleviate lung tissue damage and improve immune and inflammatory responses in LPS-induced pneumonia rats. The mechanism may be related to the inhibition of STAT1/IRF3 signaling pathway activation.