With the continuous deepening of the concept of precision diagnosis and treatment for lung cancer, how to achieve higher efficiency and accuracy in the screening, diagnosis, and treatment pathways in clinical practice has become an important issue that urgently needs to be overcome. The current clinical difficulty lies in the fact that despite continuous advancements in imaging and molecular diagnostic technologies, there are still limitations in manual efficiency and subjective experience when it comes to massive data analysis and multi-scale feature extraction. Artificial intelligence (AI), especially algorithm systems based on deep learning, is an innovative technology capable of deeply empowering medical big data. This method utilizes algorithms such as convolutional neural networks, combined with radiomics, pathomics, and multi-modal data fusion analysis, demonstrating immense potential in early precise detection and benign-malignant differentiation of pulmonary nodules, digital pathological subtype recognition and non-invasive prediction of driver genes, precise 3D surgical planning and automatic delineation of radiotherapy target volumes, as well as dynamic risk warning during follow-up. This innovative technology provides a brand-new solution for realizing intelligent and individualized lung cancer diagnosis and treatment models. This consensus, based on the latest evidence from evidence-based medicine and combined with the development trends in the AI field and real-world clinical needs, was ultimately formed by gathering the consensus opinions of multidisciplinary experts in radiology, pathology, thoracic surgery, and other fields. The main content covers the application specifications of AI in the three core scenarios of lung cancer screening, diagnosis, and treatment, the technical standards for data collection and algorithm validation, as well as the ethical and regulatory challenges faced at the current stage. It aims to clarify the applicable boundaries of AI as a clinical auxiliary decision support tool, providing scientific guidance and standardized exploration directions for peers currently engaged in or planning to carry out AI-assisted clinical diagnosis, treatment, and translation of lung cancer.

IgG4-related sclerosing cholangitis (IgG4-SC) is an IgG4-related disease charac-terized by bile duct wall thickening and luminal stricture. Its pathogenesis involves complex multi-dimensional regulation, including immune imbalance, genetic epigenetic regulation, microbial ecolo-gical abnormalities, and activation of fibrotic pathways. Due to the lack of specificity in clinical mani-festations, IgG4-SC is easily misdiagnosed as biliary tract diseases such as cholangiocarcinoma and primary sclerosing cholangitis in the early stage, leading to diagnostic difficulties. At present, gluco-corticoids are the preferred treatment option. Although most patients can quickly recover in the early stages, high recurrence rates and hormone dependence limit the long-term effectiveness of treatment. The authors combine the latest research progress at home and abroad to deeply analyze the pathogenesis, clinical manifestations, and diagnosis of IgG4-SC, focusing on treatment strategies and cutting-edge advances, in order to provide reference and inspiration for clinical practice.

Objective To explore the mechanism of Glaucocalyxin A(GLA)in inhibiting ovalbumin(OVA)-induced airway remodeling in asthmatic mice through the topoisomerase Ⅱ α(TOP2A)/cyclin-dependent kinase 1(CDK1)signaling pathway.Methods Forty Balb/c mice were randomly divided into 5 groups:the control group,the model group,the low-dose GLA group,the high-dose GLA group and the Dexamethasone group,with 8 mice in each group.The effect of GLA on airway remodeling was examined by immunohistochemical staining,ELISA and other methods,and bioinformatics methods were used to predict new targets of GLA.The action targets of TOP2A were screened using the STRING database,and the interaction relationship between the two was verified by co-immunoprecipitation.In vitro,GLA and siRNA were used to interfere with interleukin-4(IL-4)-stimulated human airway epithelial cells BEAS-2B.The expressions of TOP2A,epidermal growth factor receptor(EGFR),Integrin β1,focal adhesion kinase(FAK),β-catenin,CDK1 and DRP1 were detected by Western Blot.Results GLA intervention could significantly reduce OVA-induced asthma airway remodeling,airway smooth muscle thickening,collagen deposition around the airway,the number of eosinophils in alveolar lavage fluid,the expression of pro-inflammatory cytokines such as IL-4,and the level of serum IgE.The new target of GLA screened out was TOP2A,which was highly expressed in the lung tissue of the asthma airway remodeling model.GLA intervention could down-regulate its expression.In vitro,intervention with GLA and si-TOP2A could significantly down-regulate the expressions of IL-4-induced TOP2A,EGFR,Integrin β1,FAK and β-catenin.Further studies have found that TOP2A had an interaction relationship with CDK1.si-TOP2A could downregulate the expression of CDK1,and knockdown of CDK1 could significantly down-regulate the expression of phosphorylated DRP1.Conclusion GLA may alleviate asthma airway remodeling by targeting the TOP2A/CDK1 signaling pathway,providing experimental evidence for the clinical diagnosis and treatment of asthma airway remodeling in asthma.

Background and purpose:Despite Radiation-induced lymphopenia has been associated with poor survival outcomes in certain solid tumors,there is limited evidence for small cell lung cancer(SCLC).The purpose of this study was to investigate whether the absolute lymphocyte count before and after radiotherapy could predict the clinical outcomes for limited-stage SCLC(LS-SCLC)patients.Methods:This was a single-center,retrospective cohort study.A retrospective analysis of patients evaluated at Fudan University Shanghai Cancer Center from January 2007 to December 2017 was conducted.Inclusion criteria:⑴ pathologically confirmed small-cell lung cancer;⑵ limited-stage disease defined by positron emission tomography and computed tomography(PET/CT)and contrast-enhanced brain magnetic resonance imaging(MRI)[American Joint Committee on Cancer(AJCC)8th edition TNM stage M0];⑶ receipt of definitive chemoradiotherapy;⑷ availability of complete blood counts before,during and within 1 month after radiotherapy;⑸ complete survival,relapse,and last-follow-up information retrievable.Exclusion criteria:⑴ distant metastasis at baseline(AJCC 8th edition TNM stage M1,including any distant nodal,visceral,or bone-marrow involvement);⑵ total radiotherapy dose＜50 Gy[calculated as an equivalent biological dose at 2 Gy/fraction,i.e.,a biological effective dose(BED)＜40 Gy];⑶ incomplete laboratory data at any scheduled time point;⑷ inability to ascertain survival or relapse status or insufficient follow-up records.The study protocol was approved by the ethics committee of Fudan University Shanghai Cancer Center(approval number:2303271-15),and the requirement for informed consent was waived.Clinical data extracted comprised age,sex,Eastern Cooperative Oncology Group performance status(ECOG PS)score,smoking history,TNM stage,chemotherapy regimen and number of cycles,radiotherapy dose and fractionation schedule,use of concurrent chemoradiotherapy and administration of prophylactic cranial irradiation(PCI).Laboratory data comprised serial absolute lymphocyte counts obtained within 1 month before,during and after radiotherapy;lymphopenia was graded according to the Common Terminology Criteria for Adverse Events(CTCAE)version 4.0.Progression-free survival(PFS)and overall survival(OS)were estimated using the Kaplan-Meier method and compared with the log-rank test.Results:A total of 170 patients were included.The median age of the patients was 57 years,with 77.6%being male.The median radiation therapy dose was 60 Gy(range:45-66 Gy).For the entire cohort,the median PFS was 22.0 months,the 5-year PFS rate was 31.3%,and the 10-year PFS rate was 19.8%.The median OS was 38.0 months,the 5-year OS rate was 37.5%,and the 10-year OS rate was 24.2%.Before radiation therapy,14 patients(8.2%)had grade 1-2 lymphocytopenia.During radiation therapy,the number of patients with grade 1,2,3 and 4 lymphocytopenia was 7(4.1%),22(12.9%),111(65.3%),and 24(14.1%),respectively.One month after radiation therapy,the number of patients with grade 1,2,3 and 4 lymphocytopenia was 36(21.2%),36(21.2%),11(6.5%)and 1(0.6%),respectively.There were no significant differences in PFS and OS among patients with different grades of lymphocytopenia before,during,or after radiation therapy.Conclusion:Before immunotherapy,radiotherapy-induced lymphopenia did not appear to affect the prognosis of patients with LS-SCLC.

Objective To investigate the changes and clinical significance of pyroptosis and inflammation in children with acute lymphoblastic leukemia after chemotherapy.Methods A retrospective analysis was con-ducted on the clinical data of 98 children with acute lymphoblastic leukemia who received chemotherapy in the pediatrics and hematology and oncology departments of the hospital from May 2023 to August 2024.Accord-ing to the results of blood culture,the selected children were divided into the Gram-positive bacteria group,the Gram-negative bacteria group,the fungal group and the non-bloodstream infection group,and drug sensitivity tests were conducted.After chemotherapy,the children were divided into the granulocytosis group and the non-granulocytosis group according to the granulocyte level.The relevant indicators were detected and com-pared by methods such as blood routine,flow microsphere array technology,enzyme-linked immunosorbent assay(ELISA),and Western blot.Results After chemotherapy,the pyroptosis related indicators caspase-1,caspase-4,caspase-5,caspase-11,interleukin(IL)-1 β,IL-18,the proportion of pyroptosis cells and the relative expression level of GSDMD protein in children of each infection type were significantly increased compared with those before chemotherapy(P＜0.05).After chemotherapy,the levels of IL-4,IL-6,IL-10 and interfer-on-γ(IFN-γ)in the granulocytosis group were significantly higher than those in the non-granulocytosis group(P＜0.05),and the granulocyte level was negatively correlated with the levels of IL-4,IL-6,IL-10 and IFN-γ(P＜0.05).There were statistically significant differences in the levels of IL-4,IL-6,IL-10 and IFN-γ in dif-ferent infection states after chemotherapy(P＜0.05).Conclusion The number of granulocytes and the levels of serum cytokines can serve as potential indicators of infection in children with leukemia.The regulation of pyroptosis may provide new strategies for the treatment of childhood leukemia.

With the rapid development of population aging in various countries around the world,the health and elderly care industry has been paid high attention.The standardization of smart health and elderly care technology and services is particularly important.This paper firstly reviewed the policies related to healthy elderly care in China.By analyzing the industrial standards and provincial standards issued,this paper focused on the policies proposed by the Shanghai Municipal Government for the standardization of smart health and elderly care,as well as the researches on the standard system and the construction of standard families.Shanghai group standards in the field of smart health and elderly care were summarized,including the guidelines for the construction of standard systems,elderly care service platforms,community elderly cafeterias,portable health monitoring terminals,indoor sports services,and home-based elderly care safety monitoring.A series of case analyses of the standardized implementation of the above aspects were also provided.Through standardization research and practice in recent years,it has been fully demonstrated that the standard research plays an important leading role in the field of smart health and elderly care.

The placenta is a regulator of maternal-fetal circulation，regulating nutrient and waste exchange，endocrine function，and immune response. The placental vascular structure is the basis of the placental exchange function and the key to maternal-fetal circulation. Placental vascular changes may affect fetal growth and cardiovascular development，and even the origin of postnatal health and disease. The placenta is crucial in fetal growth and development and future health，but our understanding of placental vascular structure is still insufficient. This article reviews the imaging methods and progress of placental imaging，focusing on the placental microvascular imaging technology，which aims to provide a method reference for prenatal evaluation and monitoring of placental vascular structure by realizing the visualization of placental vascular structure. Based on this new technology，it is expected to provide new ideas for the study of the hemodynamic mechanisms of fetal growth and cardiovascular development in the future.

With advancements in prenatal diagnostic technology and postnatal clinical rescue，the survival rate of children with congenital heart disease（CHD）has significantly improved. However，neurodevelopmental delay or disorder has become the most common complication，profoundly affecting the quality of life throughout their lifetime. The risk factors and pathogenic mechanisms underlying CHD associated neurodevelopmental abnormalities remain unclear. This paper focus on the current status of neurodevelopmental outcomes in children with CHD and the potential risk factors，summarize prenatal and postnatal imaging methods for neurodevelopmental assessment，explore possible pathogenic mechanisms，and outline an integrated prenatal and postnatal neurodevelopmental evaluation framework for CHD patients. This review aims to provide comprehensive literature support for both scientific research and clinical evaluation of neurodevelopment in children with CHD.

BACKGROUND:Bone relies on the close connection between blood vessels and bone cells to maintain its integrity.Bones are in a physiologically hypoxic environment.Therefore,the study of angiogenesis and osteogenesis in hypoxic environment is closer to the microenvironment in vivo. OBJECTIVE:To explore the influence of Wenshen Tongluo Zhitong(WSTLZT)formula on H-type bone microvascular endothelial cell/bone marrow mesenchymal stem cell co-culture system in hypoxia environment and its related mechanism. METHODS:Enzyme digestion method and flow sorting technique were used to isolate and identify H-type bone microvascular endothelial cells.Mouse bone marrow mesenchymal stem cells were isolated and obtained by bone marrow adhesion method.H-type bone microvascular endothelial cell/bone marrow mesenchymal stem cell hypoxic co-culture system was established using Transwell chamber and anoxic culture workstation.WSTLZT formula powder was used to intervene in each group at a mass concentration of 50 and 100 μg/mL.The angiogenic function of H-type bone microvascular endothelial cells in the co-culture system was evaluated by scratch migration test and tube formation test.The osteogenic differentiation ability of bone marrow mesenchymal stem cells in the co-cultured system was evaluated by alkaline phosphatase staining and alizarin red staining.The protein and mRNA expression changes of PDGF/PI3K/AKT signal axis related molecules in H-type bone microvascular endothelial cells in the co-cultured system were detected by Western Blotting and q-PCR,respectively. RESULTS AND CONCLUSION:(1)Compared with the normal oxygen group,the scratch mobility and new blood vessel length of H-type bone microvascular endothelial cells were significantly higher(P<0.05);the osteogenic differentiation capacity of bone marrow mesenchymal stem cells was higher(P<0.05);the expression of PDGF/PI3K/AKT axis-related molecular protein and mRNA increased(P<0.05)in the hypoxia group.(2)Compared with the hypoxia group,scratch mobility and new blood vessel length were significantly increased in the H-type bone microvascular endothelial cells(P<0.05);bone marrow mesenchymal stem cells had stronger osteogenic function(P<0.05);the expression of PDGF/PI3K/AKT axis-related molecular proteins and mRNA further increased(P<0.05)after treatment with different dose concentrations of WSTLZT formula.These findings conclude that H-type angiogenesis and osteogenesis under hypoxia may be related to the PDGF/PI3K/AKT signaling axis,and WSTLZT formula may promote H-type vasculo-dependent bone formation by activating the PDGF/PI3K/AKT signaling axis,thereby preventing and treating osteoporosis.

Objective: To investigate the role of STAT3 phosphorylation in ferroptosis regulation and its impact on cisplatin resistance mechanisms in human osteosarcoma cells． Methods: Human osteosarcoma HOS cells and cispl- atin-resistant HOS / DDP cells were treated with cisplatin ( 0. 5，1，2，4，8，16，32 mg / L) ，the ferroptosis inducer Erastin ( Era) ( 2 μmol / L) ，and / or the ferroptosis inhibitor Ferrostatin-1 ( Fer1) ( 10 μmol / L) ．Cell viability and proliferation were assessed using the Cell Counting Kit-8 ( CCK-8) and colony formation assays，and cell migration was evaluated via a scratch assay．Reactive oxygen species ( ROS) ，intracellular ferrous iron levels，mitochondrial membrane potential，mitochondrial function，malondialdehyde ( MDA) levels，and the reduced glutathione / oxi- dized glutathione ( GSH / GSSG) ratio were measured using commercial kits．The mRNA expression of ferroptosis- related genes was analyzed by quantitative reverse transcription polymerase chain reaction ( RT-qPCR) ．The protein levels of glutathione peroxidase 4 ( GPX4) ，solute carrier family 7 member 11 ( SLC7A11) ，phosphorylated STAT3 ( p-STAT3) ，and total STAT3 were determined by Western blot． Results: With cisplatin treatment，HOS cells ex- hibited decreased cell viability，mitochondrial membrane potential，and GSH / GSSG ratio ( P＜0. 01) ，along with elevated levels of ROS，ferrous ion，and MDA content ( P ＜0. 01) ． The protein levels of GPX4 ( P ＜0. 01) ， SLC7A11，and p-STAT3 also decreased ( P ＜0. 05) ．Coadministration with the ferroptosis inhibitor Ferrostatin-1 ( Fer-1) reversed these aforementioned effects ( P ＜0. 05) ．In HOS / DDP cells，the mRNA levels of ferroptosis- suppressive genes ( GPX4，FTH1，SLC7A11，and AIFM2) were significantly higher than those in HOS cells ( P < 0. 05) ，whereas the expression of ferroptosis-promoting genes ( ACSL4 and PTGS2) was significantly lower ( P < 0. 05) ．The cisplatin-induced reductions in cell viability and mitochondrial membrane potential，as well as the in- creases in ROS，ferrous ion，and MDA levels，were less pronounced in HOS / DDP cells than in HOS cells．The SLC7A11 protein level showed no significant change． However，combined treatment with the ferroptosis inducer Erastin ( Era) resulted in significant decreases in viability，mitochondrial membrane potential，and the GSH / GSSG ratio in HOS / DDP cells ( P＜0. 05) ．Furthermore，the protein levels of p-STAT3，GPX4，and SLC7A11 were also markedly reduced ( P＜0. 05) ． Conclusion The activation of ferroptosis mediated by p-STAT3 enhances cisplatin sensitivity in HOS / DDP cells．