OBJECTIVE To systematically evaluate risk prediction models for chemotherapy-induced myelosuppression in pediatric patients with malignant tumors， evaluate their modeling strategies， key predictors， and predictive performance， and provide evidence-based references for clinical decision-making and research. METHODS A literature search was conducted across 11 databases， including CNKI， Wanfang Data， and PubMed， for relevant studies published before April 2025. Two reviewers independently performed literature screening and data extraction， and the risk of bias and applicability of the models were evaluated using the PROBAST tool. RESULTS Ultimately， seven studies were selected， of which four were English articles and three were Chinese articles， involving 12 risk prediction models. Although model discrimination was good （AUC 0.748-0.981）， only two models underwent external validation； furthermore， calibration was inadequately reported in three studies. PROBAST indicated that all models exhibited a high risk of bias， with major issues including a predominance of retrospective designs， inadequate sample representativeness， and lack of blinding. However， in terms of applicability， all models received favorable evaluations. In terms of modeling methods， most studies employed traditional logistic regression approaches to construct models， while only a minority introduced machine learning algorithms and conducted systematic comparisons among multiple algorithms. Models developed using machine learning methods significantly outperformed those constructed with traditional statistical methods. CONCLUSIONS The existing risk prediction models for myelosuppression after chemotherapy in children with malignant tumors demonstrate potential in clinical risk early warning. However， they generally suffer from design and methodological limitations， such as a predominance of retrospective single-center designs， few events per variable， opaque handling of missing data， and inconsistent reporting of model coefficients. Future studies should adopt prospective designs， incorporate machine learning with key clinical predictors， and follow TRIPOD reporting guidelines to enhance scientific rigor and clinical utility.

Intervertebral disc degeneration (IVDD) is the predominant pathological contributor to chronic low back pain, a pervasive musculoskeletal condition affecting over 630 million people globally and imposing tremendous socioeconomic and public health burdens. The etiopathogenesis of IVDD is remarkably complex and multifactorial, involving intricate crosstalk among chronic inflammatory responses, extracellular matrix (ECM) catabolism, cellular senescence, aberrant programmed cell death (including apoptosis, pyroptosis, and ferroptosis), mitochondrial dysfunction, and oxidative damage. Compelling evidence indicates that the inflammatory microenvironment acts as a decisive driving force throughout the entire degenerative course of IVDD. Among the diverse inflammatory mediators, interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) serve as core pro-inflammatory cytokines that initiate and perpetuate the degenerative cascade. These two pivotal cytokines collectively activate an array of canonical intracellular signaling pathways, including nuclear factor-κB (NF-κB), mitogen-activated protein kinase (MAPK), nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3) inflammasome, and the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) cascade. Such interconnected signaling networks trigger a self-reinforcing positive feedback loop, which exacerbates inflammatory reactions, disrupts the anabolic-catabolic homeostasis of the ECM, promotes oxidative stress and mitochondrial injury, induces multiple forms of disc cell death, and ultimately leads to progressive structural collapse and functional deterioration of the intervertebral disc. Conventional therapeutic strategies, dominated by nonsteroidal anti-inflammatory drugs and surgical interventions, are limited by systemic adverse reactions, suboptimal long-term efficacy, and the risk of adjacent segment degeneration. In contrast, traditional Chinese medicine (TCM) exhibits prominent advantages in the prevention and treatment of IVDD by virtue of its holistic regulation, syndrome differentiation, and multi-component, multi-target, multi-pathway pharmacological properties. This review systematically elucidates the molecular mechanisms by which inflammation-associated signaling pathways modulate disc cell fate and ECM metabolic homeostasis, and comprehensively summarizes the experimental progress over the past five years on TCM monomers and compound formulas for intervening in IVDD. Accumulating studies have confirmed that numerous natural active ingredients isolated from herbal medicines (ferulic acid, mangiferin, paeonol, astragaloside IV) and representative TCM compound prescriptions (Bushen Huoxue Formula, Shensuitongzhi Formula, Fuzi Decoction) exert synergistic protective effects by coordinately targeting core signaling hubs. These TCM agents demonstrate potent anti-inflammatory, antioxidant, anti-apoptotic, anti-pyroptotic, anti-ferroptotic, ECM-protective, and autophagy-regulating bioactivities, thereby effectively decelerating the pathological progression of IVDD. Despite remarkable progress, current investigations are still confronted by several critical limitations. Most studies are restricted to validating the regulatory effects of single TCM components on individual signaling pathways, leaving the systematic, dynamic, and synergistic mechanisms of TCM compound formulas within multi-pathway regulatory networks largely unexplored. Furthermore, clinical translation of TCM is severely hampered by the lack of efficient targeted drug delivery systems, unclear pharmacokinetic profiles, suboptimal local bioavailability, and incomplete long-term safety assessments. Therefore, future research should adopt an interdisciplinary paradigm integrating multi-omics technologies, artificial intelligence, organoid models, and organ-on-chip systems to systematically decipher the scientific basis of TCM against IVDD. Concurrently, the development of intelligent, site-specific delivery systems (hydrogels, nanoparticles, exosome-based carriers) is urgently needed to enhance the local accumulation and sustained release of TCM ingredients. By deepening mechanistic exploration and accelerating translational research, TCM is expected to evolve into safe, effective, and personalized precision therapeutic regimens for IVDD, offering novel and reliable solutions for the clinical management of chronic low back pain.

Intervertebral disc degeneration (IVDD) is the predominant pathological contributor to chronic low back pain, a pervasive musculoskeletal condition affecting over 630 million people globally and imposing tremendous socioeconomic and public health burdens. The etiopathogenesis of IVDD is remarkably complex and multifactorial, involving intricate crosstalk among chronic inflammatory responses, extracellular matrix (ECM) catabolism, cellular senescence, aberrant programmed cell death (including apoptosis, pyroptosis, and ferroptosis), mitochondrial dysfunction, and oxidative damage. Compelling evidence indicates that the inflammatory microenvironment acts as a decisive driving force throughout the entire degenerative course of IVDD. Among the diverse inflammatory mediators, interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) serve as core pro-inflammatory cytokines that initiate and perpetuate the degenerative cascade. These two pivotal cytokines collectively activate an array of canonical intracellular signaling pathways, including nuclear factor-κB (NF-κB), mitogen-activated protein kinase (MAPK), nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3) inflammasome, and the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) cascade. Such interconnected signaling networks trigger a self-reinforcing positive feedback loop, which exacerbates inflammatory reactions, disrupts the anabolic-catabolic homeostasis of the ECM, promotes oxidative stress and mitochondrial injury, induces multiple forms of disc cell death, and ultimately leads to progressive structural collapse and functional deterioration of the intervertebral disc. Conventional therapeutic strategies, dominated by nonsteroidal anti-inflammatory drugs and surgical interventions, are limited by systemic adverse reactions, suboptimal long-term efficacy, and the risk of adjacent segment degeneration. In contrast, traditional Chinese medicine (TCM) exhibits prominent advantages in the prevention and treatment of IVDD by virtue of its holistic regulation, syndrome differentiation, and multi-component, multi-target, multi-pathway pharmacological properties. This review systematically elucidates the molecular mechanisms by which inflammation-associated signaling pathways modulate disc cell fate and ECM metabolic homeostasis, and comprehensively summarizes the experimental progress over the past five years on TCM monomers and compound formulas for intervening in IVDD. Accumulating studies have confirmed that numerous natural active ingredients isolated from herbal medicines (ferulic acid, mangiferin, paeonol, astragaloside IV) and representative TCM compound prescriptions (Bushen Huoxue Formula, Shensuitongzhi Formula, Fuzi Decoction) exert synergistic protective effects by coordinately targeting core signaling hubs. These TCM agents demonstrate potent anti-inflammatory, antioxidant, anti-apoptotic, anti-pyroptotic, anti-ferroptotic, ECM-protective, and autophagy-regulating bioactivities, thereby effectively decelerating the pathological progression of IVDD. Despite remarkable progress, current investigations are still confronted by several critical limitations. Most studies are restricted to validating the regulatory effects of single TCM components on individual signaling pathways, leaving the systematic, dynamic, and synergistic mechanisms of TCM compound formulas within multi-pathway regulatory networks largely unexplored. Furthermore, clinical translation of TCM is severely hampered by the lack of efficient targeted drug delivery systems, unclear pharmacokinetic profiles, suboptimal local bioavailability, and incomplete long-term safety assessments. Therefore, future research should adopt an interdisciplinary paradigm integrating multi-omics technologies, artificial intelligence, organoid models, and organ-on-chip systems to systematically decipher the scientific basis of TCM against IVDD. Concurrently, the development of intelligent, site-specific delivery systems (hydrogels, nanoparticles, exosome-based carriers) is urgently needed to enhance the local accumulation and sustained release of TCM ingredients. By deepening mechanistic exploration and accelerating translational research, TCM is expected to evolve into safe, effective, and personalized precision therapeutic regimens for IVDD, offering novel and reliable solutions for the clinical management of chronic low back pain.

Objective To compare the long-term survival of elderly patients with esophageal squamous cell carcinoma (ESCC) treated with surgical versus non-surgical treatment. Methods A retrospective analysis was conducted on the clinical data of elderly patients aged ≥70 years with ESCC who underwent esophagectomy or radiotherapy/chemotherapy at Sichuan Cancer Hospital from January 2009 to September 2017. Patients were divided into a surgical group (S group) and a non-surgical group (NS group) according to the treatment method. The propensity score matching method was used to match the two groups of patients at a ratio of 1∶1, and the survival of the two groups before and after matching was analyzed. Results A total of 726 elderly patients with ESCC were included, including 552 males and 174 females, with 651 patients aged ≥70-80 years and 75 patients aged ≥80-90 years. There were 515 patients in the S group and 211 patients in the NS group. The median follow-up time was 60.8 months, and the median overall survival of the S group was 41.9 months [95%CI (35.2, 48.5)], while that of the NS group was only 24.0 months [95%CI (19.8, 28.3)]. The 1-, 3-, and 5-year overall survival rates of the S group were 84%, 54%, and 40%, respectively, while those of the NS group were 72%, 40%, and 30%, respectively [HR=0.689, 95%CI (0.559, 0.849), P<0.001]. After matching, 138 patients were included in each group, and there was no statistical difference in the overall survival between the two groups [HR=0.871, 95%CI (0.649, 1.167), P=0.352]. Conclusion Compared with conservative treatment, there is no significant difference in the long-term survival of elderly patients aged ≥70 years who undergo esophagectomy for ESCC. Neoadjuvant therapy combined with surgery is still an important choice to potentially improve the survival of elderly patients with ESCC.

Neoadjuvant therapy for hepatocellular carcinoma is the frontier and hot topic in the current field of liver cancer research.The fundamental purpose is to reduce the risk of postoperative recurrence through standardized preoperative treatment methods.From the attempts of Transcatheter Arterial Chemoembolization monotherapy for neoadjuvant therapy for hepatocellular carcinoma to systematic treatment represented by"targeted combined with immunotherapy",the latter has become the most promising neoadjuvant strategy due to its high objective response rate and potential to induce pathological complete remission.However,the field still faces challenges such as lack of evidence of overall survival benefit in Phase Ⅲ randomized controlled trials,treatment-related adverse reactions that may lead to delay in surgery,optimal population screening,and timing of surgery.This article aims to briefly discuss the current research status of the application of neoadjuvant therapy in resectable hepatocellular carcinoma,explore relevant diagnosis and treatment concepts,and further understand neoadjuvant therapy.

Objective:To investigate the predictive value of serum neutrophil gelatinase-associated lipocalin(NGAL),calcitonin gene-related peptide(CGRP),and neutrophil-to-lymphocyte ratio(NLR)for the prognostic regression of elderly patients with stroke complicated with pulmonary infection(SCPI).Methods:This study was a retrospective single-center study,149 elderly patients with SCPI who were admitted to Inner Mongolia Baogang Hospital from June 2020 to June 2024 were selected,they were divided into poor prognosis group(n=56)and good prognosis group(n=93)according to the prognosis.Baseline data and laboratory test indicators were collected,and NLR was calculated.Serum NGAL and CGRP levels were measured by ELISA.Influencing factors of poor prognosis of elderly patients with SCPI were analyzed by Multivariate logistic regression.Predicts value was analyzed by Receiver operating characteristic(ROC)curve.Results:Compared with good prognosis group,the poor prognosis group had higher of aged ≥ 70 years,incidence of hemorrhagic stroke,serum creatinine,white blood cell count,national institute of health stroke scale(NIHSS),platelet count,C-reactive protein,NGAL,and NLR levels,longer nerosurgery intensive care unit(NICU)stay,and lower CGRP levels(P＜0.05).Higher CGRP level was an independent protective factor of poor prognosis of elderly patients with SCPI(OR＜1,P＜0.05).Age ≥ 70 years,hemorrhagic stroke,longer NICU stay,higher NIHSS score,higher NGAL level and higher NLR were independent risk factors of poor prognosis of elderly patients with SCPI(OR＞1,P＜0.05).The area under the curve(AUC)for predicting the prognostic regression of elderly patients with SCPI used NGAL,CGRP,and NLR alone or in combination was 0.777,0.771,0.786,and 0.927,respectively,with the combination of three factors showed the highest predictive power(P＜0.05).Conclusion:Age ≥70 years,hemorrhagic stroke,longer NICU stay,higher NIHSS score,higher NGAL level and higher NLR are independent risk factors of poor prognosis of elderly patients with SCPI,while higher CGRP level is an independent protective factor.The combination detection of NGAL,CGRP and NLR can improve the predictive value of prognostic regression in elderly patients with SCPI.

In recent years, the incidence of liver metastasis from colorectal cancer has continued to rise, posing a significant threat to human health and life.Although traditional treat-ments such as surgery and chemotherapy have shown some efficacy in certain patients, options remain limited for those who are not surgical candidates or are resistant to chemotherapy.Yttrium-90 microsphere selective internal radiation therapy, as an innovative local treatment, has fully demons-trated its effectiveness and safety in treating colorectal cancer liver metastasis patients. The authors review the research background, mechanisms, and principles of yttrium-90 microsphere selective internal radiation therapy in the field of colorectal cancer liver metastasis, and to explore its applica-tion progress in clinical practice, aiming to provide clinical doctors with more comprehensive and detailed reference information, with the goal of improving treatment outcomes and quality of life for colorectal cancer liver metastasis patients.

Objective:To analyze the research status of family management for children with cancer, explore research hotspots and development trends, so as to provide reference for subsequent research and clinical practice in family management for children with cancer.Methods:Literature related to family management for children with cancer was retrieved from the Web of Science Core Collection Database. The search period was from January 31, 2014 to December 31, 2024. CiteSpace 6.4.R1 was employed for bibliometric analysis.Results:A total of 647 articles were included. The annual publication volume showed an overall trend of first decreasing, then increasing, and fluctuating upward. The authors conducting the study on family management for children with cancer formed a distinct core team. The United States and the University of Pennsylvania were the top countries and institutions in terms of publications, with close collaboration and exchange among institutions. Research focuses on recurrence treatment, social support systems, and deepening precision interventions for Ewing sarcoma. The development of technology driven management tools, cross-cultural research, and the integration of policy and ethical studies represent a future trend.Conclusions:Research focuses on key areas such as recurrence treatment, social support systems, and precision interventions for Ewing sarcoma, emphasizing family management practices, building social support networks, and identifying therapeutic targets. In the future, technology driven management tools should be developed to achieve intelligence, cross-cultural research should be deepened, and a humanized management model should be constructed by combining policy and ethical research, in order to improve the efficiency and effectiveness of subsequent related research and clinical practice for family management for children with cancer.

Objective To analyze the clinical and immunological characteristics of a rare case of CHARGE syndrome,we summarize the genotype and phenotype in the Chinese patient population,and explore the underlying immunopathogenic mechanisms.Methods Clinical data from a pediatric patient with CHARGE syndrome were collected and analyzed.A comprehensive analysis of the Chinese patient population was conducted.Gene analysis and immunological characterization were performed using flow cytometry,deep sequencing,and quantitative PCR.Results The proband was a premature female infant whose primary clinical manifestations included congenital heart disease,recurrent respiratory infections,respiratory failure,airway dysplasia,hearing impairment,and bilateral choroidal coloboma.Whole-exome sequencing revealed a de novo heterozygous nonsense mutation in the CHD7 gene,c.5122C＞T(p.Gln1708Ter),classified as pathogenic according to ACMG criteria.Immunological studies indicated impaired thymic output of T cells,significant alterations in the number and proportion of CD8+T cell subsets,increased apoptosis,and defective activation and production of key effector cytokines such as IFN-γ by CD8+T cells.However,no significant abnormalities were observed in peripheral lymphocyte proliferation.Conclusion CHARGE syndrome is a rare autosomal dominant genetic disorder primarily caused by mutations in the CHD7 gene.The main clinical features include ocular defects,cardiac disease,choanal atresia/cleft lip and palate,growth retardation,gonadal hypoplasia,and ear anomalies.This case study suggests that CHARGE syndrome is associated with abnormalities in the development,apoptosis,and effector functions of immune cells.

AIM To investigate the effects of Yiqi Juanbi Formula on chondrocyte pyroptosis in rat models of collagen-induced arthritis(CIA).METHODS Fifty rats were subcutaneously injected at the tail base with an emulsion containing equal volumes of bovine type Ⅱ collagen and incomplete Freund's adjuvant(IFA)to establish the CIA models.These rats were then randomly assigned to the model group,the methotrexate group(0.35 mg/kg),and the low-dose,medium-dose,and high-dose Yiqi Juanbi Formula groups(9.4,18.7,37.4 g/kg),in contrast to the ten intact rats serving in the normal control group.Following four weeks of intragastric administration,the rats had their general conditions observed;their joint swelling and arthritis indices measured;their ankle joint pathology assessed by HE staining;their serum levels of IL-1β,IL-18 and TNF-ɑ detected by ELISA;their mRNA expressions of NLRP3,Caspase-1,GSDMD,IL-1β,IL-18 and TNF-ɑ in ankle cartilage quantified by RT-qPCR;their protein expressions of NF-κB,NLRP3 and Caspase-1 in ankle cartilage analyzed by Western blot;and their NLRP3 and GSDMD positive expressions in ankle cartilage examined by immunohistochemistry.RESULTS Compared to the control group,the model group showed significantly increased joint swelling and arthritis indices(P＜0.01);elevated serum levels of IL-1 β,IL-18 and TNF-ɑ(P＜0.01);pathological changes including cartilage surface defects,reduced cell count,altered cellular morphology,irregular cell arrangement,and significant inflammatory cell infiltration in synovial tissue;upregulated mRNA expressions of NF-κB,NLRP3,Caspase-1,GSDMD,IL-1β,IL-18 and TNF-ɑ(P＜0.01)and increased protein expressions of NF-κB,NLRP3 and Caspase-1(P＜0.01)in ankle cartilage;enhanced positive expressions of NLRP3 and GSDMD in ankle cartilage(P＜0.01).Compared to the model group,the groups intervened with methotrexate or medium-or high-dose Yiqi Juanbi Formula exhibited reduced joint swelling and arthritis indices(P＜0.01);alleviated pathological damage in ankle joints;decreased serum levels of IL-1β,IL-18 and TNF-ɑ(P＜0.01);downregulated mRNA expressions of NF-κB,NLRP3,Caspase-1,GSDMD,IL-1β,IL-18 and TNF-ɑ(P＜0.05,P＜0.01),and reduced protein expressions of NF-κB,NLRP3 and Caspase-1(P＜0.05,P＜0.01)in ankle cartilage;and diminished positive expressions of NLRP3 and GSDMD in ankle cartilage(P＜0.01).CONCLUSION Yiqi Juanbi Formula alleviates inflammation in CIA rats,potentially by inhibiting the activation of the NF-κB/NLRP3/Caspase-1 signaling pathway,thereby suppressing chondrocyte pyroptosis.