This paper systematically reviews the current status of integrated traditional Chinese and western medicine in the treatment of Helicobacter pylori （Hp） infection， as well as recent progress in clinical and basic research both in China and internationally. It summarizes the advantages of traditional Chinese medicine （TCM） in Hp infection management， including improving Hp eradication rates， enhancing antibiotic sensitivity， reducing antimicrobial resistance， decreasing drug-related adverse effects， and ameliorating gastric mucosal lesions. These advantages are particularly evident in patients who are intolerant to bismuth-containing regimens， those with refractory Hp infection， and individuals with precancerous gastric lesions. An integrated， whole-process management approach and individualized， staged comprehensive treatment strategies combining TCM and western medicine are proposed for Hp infection. Future prevention and control of Hp infection should adopt an integrative Chinese-western medical strategy， emphasizing prevention， strengthening primary care， implementing proactive long-term monitoring， optimizing screening strategies， and advancing the development of novel technologies and mechanistic studies of Chinese herbal interventions. These efforts aim to provide a theoretical basis and practical pathways for the establishment and improvement of Hp infection prevention and control systems.

Objective To evaluate the value of serum Mac-2 binding protein (M2BP) for assessment of the severity of schisto somiasis-induced liver fibrosis, so as to provide insights into non-invasive diagnosis and disease surveillance of liver fibrosis caused by schistosomiasis. Methods A total of 234 individuals with a history of Schistosoma japonicum infection were sampled from Xinhua Village, Lushan City, Jiangxi Province from 2019 to 2020, and 234 serum samples were collected from all participants. All participants received B-ultrasound examinations of the liver. Serum samples were categorized into four groups (grades 0, Ⅰ, Ⅱ and Ⅲ schistosomiasis-induced liver fibrosis groups) according to B-ultrasound examination results, and then, each group was randomly divided into a receiver operating characteristic (ROC) curve group and an efficacy assessment group at a ratio of 7∶3. Serum M2BP concentration was measured in four groups using the enzyme-linked immunosorbent assay (ELISA), and differences in serum M2BP concentrations were compared with analysis of variance and Spearman correlation analysis. Serum M2BP concentration was subjected to ROC curve analysis among individuals with different grades of schistosomiasis-induced liver fibrosis in the ROC curve group to determine the optimal diagnostic threshold of M2BP concentration at different fibrosis grades, and the area under the ROC curve (AUC) was calculated to evaluate the diagnostic performance. The diagnostic accuracy was verified by comparing the accordance rate and Kappa consistency test in the efficacy assessment group. Results Among 234 serum samples, there were 79 samples with grade 0 schistosomiasis-induced liver fibrosis, 87 samples with Grade Ⅰ, 46 samples with Grade Ⅱ and 22 samples with Grade Ⅲ according to the B-ultrasound examinations. The mean serum M2BP concentrations were (0.40 ± 0.31) [95% confidence interval (CI): (0.33, 0.47)], (0.64 ± 0.48) [95% CI: (0.53, 0.74)], (1.76 ± 0.58) [95% CI: (1.59, 1.93)] μg/mL and (2.56 ± 0.93) [95% CI: (2.14, 2.97)] μg/mL in the four groups, respectively (F = 150.796, P < 0.001), and the severity of schistosomiasis-induced liver fibrosis significantly positively correlated with serum M2BP concentration (rs = 0.715, P < 0. 001). The sample sizes of grades 0, Ⅰ, Ⅱ and Ⅲ schistosomiasis-induced liver fibrosis sera were randomly allocated as follows: 55 versus 24, 61 versus 26, 32 versus 14, and 15 versus 7 in the ROC curve and efficacy assessment groups, respectively, and the serum M2BP concentrations were (0.39 ± 0.29) μg/mL and (0.42 ± 0.36) μg/mL (F = 0.196, P > 0.05), (0.59 ± 0.47) μg/mL and (0.75 ± 0.51) μg/mL (F = 1.967, P > 0.05), (1.73 ± 0.59) μg/mL and (1.85 ± 0.57) μg/mL (F = 0.417, P > 0.05), and (2.46 ± 0.64) μg/mL and (2.76 ± 1.41) μg/mL (F = 0.491, P > 0.05), respectively. ROC curve analysis showed that the optimal diagnostic thresholds of serum M2BP concentration were 0.347 86 μg/mL (AUC = 0.635, P < 0.05), 1.188 83 μg/mL (AUC = 0.938, P < 0.000 1) and 2.021 21 μg/mL (AUC = 0.821, P < 0.000 1) for grade Ⅰ, Ⅱ and Ⅲ schistosomiasis-induced liver fibrosis. In addition, the accordance rates between the optimal diagnostic threshold of serum M2BP and B-ultrasound examinations for predicting grade Ⅰ, Ⅱ and Ⅲ schistosomiasis-induceed liver fibrosis were 69.23%, 85.71% and 71.43% (χ2 = 1.340, P > 0.05), and the overall Kappa consistency test showed moderate consistency [Kappa = 0.608, 95% CI: (0.428, 0.788); Z = 6.609, P < 0.000 1]. Conclusions Serum M2BP may serve as a potential biomarker for assessing moderate to advanced schistosomiasis-induced liver fibrosis; however, its diagnostic value for early-stage schistosomiasis-induced liver fibrosis remains limited.

BACKGROUND:Hippocampal injury caused by aortic coarctation has been poorly studied,and combined detection of tumor necrosis factor α,nuclear factor κB and ionized calcium binding adaptor molecule-1 expression in aortic dissection has not been reported.OBJECTIVE:To observe histomorphologic changes in the hippocampus of a mouse model of aortic dissection and investigate the expression and significance of tumor necrosis factor alpha,nuclear factor kappaB and ionized calcium binding adaptor molecule-1 in the hippocampus of aortic dissection mice.METHODS:Sixteen healthy 3-week-old male C57BL/6 mice were randomly divided into two groups:control group and aortic dissection group,with eight mice in each group.In the aortic dissection group,mice were given β-aminopropionitrile monofumarate as drinking water for 4 weeks,and the angiotensin Ⅱ microinfiltration pump was then implanted to establish an animal model of aortic dissection.Mice in the control group were given normal diet and water.After the model was established,the maximum diameter of the ascending aorta was measured,hematoxylin-eosin staining and EVG staining were performed to evaluate the model formation rate,and the levels of inflammatory factors tumor necrosis factor α and interleukin 6 in serum were detected by enzyme-linked immunosorbent assay.The hippocampus was dissected and stained with hematoxylin-eosin to observe the pathological changes of the hippocampus in brain sections.The protein expression of tumor necrosis factor α,nuclear factor κB and ionized calcium binding adaptor molecule-1 was detected by western blot analysis.RESULTS AND CONCLUSION:(1)Compared with the control group,the maximum diameter of the ascending aorta in the aortic dissection group was significantly enlarged.(2)Hematoxylin-eosin staining of the aorta showed obvious thickening of the middle aorta and destruction and disorder of the aortic wall structure in mice.Neurons in the CA1 and CA3 regions of mice were sparsely arranged,reduced in size,and showed pyknosis with deeply stained nuclei.(3)Serum levels of inflammatory factors tumor necrosis factor α and interleukin 6 were increased in the aortic dissection group compared with the control group(P＜0.01).(4)The expression levels of tumor necrosis factor α,nuclear factor κB,phosphorylated nuclear factor κB,and ionized calcium binding adaptor molecule-1 in the hippocampus were increased in the aortic dissection group compared with the control group(P＜0.05).To conclude,microglial activation and increased expression of tumor necrosis factor α and nuclear factor κB may be involved in hippocampal neuron injury in aortic dissection mice.

Objective To explore the clinical factors influencing complete response in patients with locally advanced rectal cancer (LARC) after neoadjuvant chemoradiotherapy (nCRT). Methods Clinical data of LARC patients treated in the Department of Radiation Oncology at Beijing Shijitan Hospital between January 2013 and December 2024 were retrospectively collected. All patients received nCRT, after which surgery or a watch-and-wait approach was adopted based on treatment response. Univariable and multivariable logistic regression analyses were performed to identify prognostic factors influencing complete response. A clinical prediction model was constructed based on the multivariable analysis results, and its predictive performance was evaluated using the receiver operating characteristic curve. Results A total of 113 eligible patients were included. After nCRT, 19 patients (16.8%) achieved complete response, including 3 with clinical complete response and 16 with pathological complete response. Univariable analysis indicated that pretreatment clinical N stage, extramural venous invasion, carcinoembryonic antigen level, and neoadjuvant treatment regimen were associated with complete response after nCRT (P<0.05). Multivariable logistic regression analysis identified pretreatment extramural venous invasion, carcinoembryonic antigen level, and neoadjuvant treatment regimen as independent influencing factors for complete response (P<0.05). A prediction model incorporating these independent factors yielded an area under the receiver operating characteristic curve of 0.813 (95% confidence interval: 0.713-0.913), with a sensitivity of 89.5% and a specificity of 60.6%, demonstrating good predictive performance. Conclusion Pretreatment extramural venous invasion, carcinoembryonic antigen level, and neoadjuvant treatment regimen are independent factors influencing complete response after nCRT in LARC patients. The prediction model combining these factors may assist in evaluating treatment efficacy following nCRT in LARC patients.

Polycystic ovary syndrome （PCOS） is a common endocrine and metabolic disorder among women of reproductive age. Hyperandrogenism （HA）， one of its core pathological features， is closely associated with the clinical manifestations and metabolic complications of the disease. Current western medical treatments for PCOS-HA mainly include anti-androgen therapy and ovulation induction， such as short-acting oral contraceptives like Diane-35 and Yasmin. However， long-term use of these medications may result in adverse reactions like increasing the risk of liver dysfunction and exacerbating lipid metabolism disorders， with unsatisfactory long-term efficacy when used alone. Traditional Chinese medicine offers unique advantages in the treatment of PCOS-HA due to its holistic approach and multi-target regulatory mechanisms. In the view of traditional Chinese medicine， PCOS-HA is classified under the categories such as "delayed menstruation"， "amenorrhea"， and "infertility"， with kidney deficiency as the root， as well as liver stagnation and spleen deficiency as the manifestations. Phlegm and blood stasis are considered to be intertwined throughout the disease course. Modern studies have shown that traditional Chinese medicine is significantly effective in improving the androgen levels， restoring ovulation， and improving insulin resistance in PCOS-HA patients. Representative prescriptions， such as Erxian Tang， Jiawei Xiaoyaosan， Guizhi Fulingwan， and Cangfu Daotantang， exert therapeutic effects through various mechanisms including regulation of the hypothalamic-pituitary-ovarian axis， reduction of ovarian androgen synthase activity， improvement of insulin signaling pathways， and inhibition of inflammation and oxidative stress， which demonstrates the characteristics of comprehensive treatment with traditional Chinese medicine. Based on the perspectives of etiology and pathogenesis of traditional Chinese medicine， modern medical cognition， typical prescriptions， and action mechanisms， this paper reviewed the research progress of traditional Chinese medicine in the treatment of PCOS-HA， aiming to provide a reference for in-depth research and clinical applications in this field.

Polycystic ovary syndrome （PCOS） is a common endocrine and metabolic disorder among women of reproductive age. Hyperandrogenism （HA）， one of its core pathological features， is closely associated with the clinical manifestations and metabolic complications of the disease. Current western medical treatments for PCOS-HA mainly include anti-androgen therapy and ovulation induction， such as short-acting oral contraceptives like Diane-35 and Yasmin. However， long-term use of these medications may result in adverse reactions like increasing the risk of liver dysfunction and exacerbating lipid metabolism disorders， with unsatisfactory long-term efficacy when used alone. Traditional Chinese medicine offers unique advantages in the treatment of PCOS-HA due to its holistic approach and multi-target regulatory mechanisms. In the view of traditional Chinese medicine， PCOS-HA is classified under the categories such as "delayed menstruation"， "amenorrhea"， and "infertility"， with kidney deficiency as the root， as well as liver stagnation and spleen deficiency as the manifestations. Phlegm and blood stasis are considered to be intertwined throughout the disease course. Modern studies have shown that traditional Chinese medicine is significantly effective in improving the androgen levels， restoring ovulation， and improving insulin resistance in PCOS-HA patients. Representative prescriptions， such as Erxian Tang， Jiawei Xiaoyaosan， Guizhi Fulingwan， and Cangfu Daotantang， exert therapeutic effects through various mechanisms including regulation of the hypothalamic-pituitary-ovarian axis， reduction of ovarian androgen synthase activity， improvement of insulin signaling pathways， and inhibition of inflammation and oxidative stress， which demonstrates the characteristics of comprehensive treatment with traditional Chinese medicine. Based on the perspectives of etiology and pathogenesis of traditional Chinese medicine， modern medical cognition， typical prescriptions， and action mechanisms， this paper reviewed the research progress of traditional Chinese medicine in the treatment of PCOS-HA， aiming to provide a reference for in-depth research and clinical applications in this field.

Objective To explore the number of peripheral blood regulatory T cells (Treg) in patients with chronic kidney disease (CKD) and its correlation with vascular calcification. Methods This was a single-center, cross-sectional, and observational study. Non-dialysis patients with CKD treated at Zhongshan Hospital, Fudan University from March 2021 to March 2022 were enrolled. Abdominal aortic calcification (AAC) was assessed using lateral abdominal X-ray. Number of Treg and cytokine levels were measured by flow cytometry. Logistic regression analysis was performed to evaluate the related factors for AAC in CKD patients. Results A total of 83 patients were included, aged 17–86 years, with 57 males (68.7%). The distribution of CKD stages was as follows: stage G1 in 7 patients (8.4%), stage G2 in 17 patients (20.5%), stage G3 in 21 patients (25.3%), stage G4 in 19 patients (22.9%), and stage G5 in 19 patients (22.9%). No AAC was observed in patients with stages G1 and G2, while the prevalence of AAC in patients with stages G3, G4, and G5 was 23.8%, 21.1%, and 26.3%, respectively. Compared with stage G1 patients, those with stages G3–5 showed decreased number of peripheral blood Treg and elevated levels of interleukin (IL)-6 and IL-17F (P＜0.05). The area under the receiver operating characteristic curve for number of peripheral blood Treg in predicting AAC in CKD patients was 0.766 (95%CI 0.652–0.879, P＝0.002). Logistic regression analysis showed that decreased number of Treg was related factor for AAC in CKD patients (OR＝0.957, 95%CI 0.922–0.992, P＝0.018). Conclusion As CKD progresses, number of peripheral blood Treg significantly decreases, which is correlated with AAC in CKD patients.

BACKGROUND:Hippocampal injury caused by aortic coarctation has been poorly studied,and combined detection of tumor necrosis factor α,nuclear factor κB and ionized calcium binding adaptor molecule-1 expression in aortic dissection has not been reported.OBJECTIVE:To observe histomorphologic changes in the hippocampus of a mouse model of aortic dissection and investigate the expression and significance of tumor necrosis factor alpha,nuclear factor kappaB and ionized calcium binding adaptor molecule-1 in the hippocampus of aortic dissection mice.METHODS:Sixteen healthy 3-week-old male C57BL/6 mice were randomly divided into two groups:control group and aortic dissection group,with eight mice in each group.In the aortic dissection group,mice were given β-aminopropionitrile monofumarate as drinking water for 4 weeks,and the angiotensin Ⅱ microinfiltration pump was then implanted to establish an animal model of aortic dissection.Mice in the control group were given normal diet and water.After the model was established,the maximum diameter of the ascending aorta was measured,hematoxylin-eosin staining and EVG staining were performed to evaluate the model formation rate,and the levels of inflammatory factors tumor necrosis factor α and interleukin 6 in serum were detected by enzyme-linked immunosorbent assay.The hippocampus was dissected and stained with hematoxylin-eosin to observe the pathological changes of the hippocampus in brain sections.The protein expression of tumor necrosis factor α,nuclear factor κB and ionized calcium binding adaptor molecule-1 was detected by western blot analysis.RESULTS AND CONCLUSION:(1)Compared with the control group,the maximum diameter of the ascending aorta in the aortic dissection group was significantly enlarged.(2)Hematoxylin-eosin staining of the aorta showed obvious thickening of the middle aorta and destruction and disorder of the aortic wall structure in mice.Neurons in the CA1 and CA3 regions of mice were sparsely arranged,reduced in size,and showed pyknosis with deeply stained nuclei.(3)Serum levels of inflammatory factors tumor necrosis factor α and interleukin 6 were increased in the aortic dissection group compared with the control group(P＜0.01).(4)The expression levels of tumor necrosis factor α,nuclear factor κB,phosphorylated nuclear factor κB,and ionized calcium binding adaptor molecule-1 in the hippocampus were increased in the aortic dissection group compared with the control group(P＜0.05).To conclude,microglial activation and increased expression of tumor necrosis factor α and nuclear factor κB may be involved in hippocampal neuron injury in aortic dissection mice.

Drug clinical trials constitute a critical link in new drug development and an essential means to verify the safety and efficacy of pharmaceuticals. The protection of participants’ rights and interests and the prevention of risks directly affect the scientific ethics and social credibility of the trials. Vulnerable groups， due to restricted autonomous decision-making capacities or special social status， are more susceptible to safety risks. Children are a typical representative of vulnerable groups. Their physiological particularities， cognitive limitations， and dependence collectively epitomize the universal protection demands of vulnerable research participants. Taking children as an instance， this paper analyzes the current weak links in the protection of pediatric research participants. Integrating advanced international experience with domestic practical demands， it comprehensively identified protection risk points at every stage and constructed a multi-stakeholder collaborative mechanism for the full-process protection of pediatric research participants. This mechanism incorporated seven main entities， including drug regulatory authorities， sponsors， researchers， and ethics committees， covering the pre-trial， intra-trial， and post-trial phases to meet the requirements of full-chain and multi-dimensional protection. It provided references for the subsequent establishment of a systematic protection mechanism for vulnerable populations.

Background Exposure to benzo[a]pyrene (BaP) may impair lung function through various mechanisms; however, it remains uncertain whether BaP induces ferroptosis in lung tissue cells, resulting in lung function impairment. Objective To investigate the ferroptosis of lung tissue cells triggered by subchronic BaP exposure in mice and its correlation with lung injury, and to explore the function of ferroptosis in BaP-induced lung tissue damage. Method Seventy-two healthy 3-weeks-old male C57BL/6J mice were acclimatized for 1 week and then randomly divided into six groups: control group (corn oil 10 mL·kg⁻¹), low-dose BaP group (2.5 mg·kg⁻¹), medium-dose BaP group (5 mg·kg⁻¹), high-dose BaP group (10 mg·kg⁻¹), BaP+ferrostatin-1 (Fer-1) group (10 mg·kg⁻¹+1 mg·kg⁻¹), and Fer-1 group (1 mg·kg⁻¹), with 12 mice each group. Corn oil and BaP were administered via gavage every other day, followed by an intraperitoneal injection of Fer-1 the subsequent day, throughout a period of 90 d. Whole-body plethysmography was applied to detect lung function; hematoxylin-eosin staining (HE) and Masson staining were used to observe lung tissue injury and fibrosis; microscopy of alveolar epithelial cells was conducted to reveal mitochondrial morphology; biochemical assays were used to measure the content of tissue iron, malondialdehyde (MDA), and glutathione (GSH), as well as the activity of glutathione peroxidase (GSH-Px); Western blotting and real-time quantitative PCR (RT-qPCR) analyses were performed to reveal the protein and mRNA expression of ferroptosis markers. Results Compared to the control group, the high-dose BaP group showed a significant increase in expiration time (Te) (P<0.01), and a significant decrease in ratio rate of achieving peak expiratory flow (Rpef), tidal volume (TVb), peak inspiratory flow (PIF), minute volume (MVb), and peak expiratory flow (PEF) (P<0.05 or 0.01). Based on the results of HE and Masson staining, partial destruction of alveolar structures, thickening of alveolar walls, infiltration of inflammatory cells, significant thickening of tracheal walls and a large deposition of collagen fibers in lung tissue were observed in the medium- and high-dose BaP groups. By microscopy, the alveolar epithelial cells exposed to low-dose BaP showed condensed chromatin, and the mitochondria exposed to medium and high-dose BaP showed wrinkles, increased mitochondrial membrane density, and diminished mitochondrial cristae. Compared to the control group, in the medium- and high-dose BaP groups, the lung tissue iron content and the expression levels of ACSL4 protein and mRNA significantly elevated (P<0.01 or 0.05), while the mRNA expression level of SLC7A11 significantly decreased (P<0.05); in the high-dose BaP group, the MDA content, COX2 protein, and PTGS2 mRNA expression levels significantly increased (P<0.05 or 0.01), GSH content and GSH-Px activity, GPX4 protein and mRNA expression levels, and the expression level of SLC7A11 protein significantly decreased (P<0.01 or 0.05). The ferroptosis inhibitor Fer-1 markedly reversed respiratory function, morphology, mitochondrial alterations, and the aforementioned ferroptosis-related biochemical indicators. Conclusion Subchronic exposure to BaP can induce ferroptosis in mice lung tissue cells, resulting in compromised lung function.