Objective To conduct a comprehensive survey of the resource allocation and radiological diagnosis frequency in radiological diagnosis and treatment institutions in Shaanxi Province, and provide scientific evidence for optimizing regional medical resource allocation and formulating radiation protection strategies. Methods In 2022, a cross-sectional survey was conducted on 1564 radiological diagnosis and treatment institutions in Shaanxi Province (excluding dental clinics and military/armed police force hospitals). Data on equipment configuration, personnel distribution, and number of diagnostic examinations were collected. Results There were a total of 8798 radiation workers engaged in radiological diagnosis and 3617 X-ray diagnostic units in Shaanxi Province. Moreover, 35.8% (3151) of the radiation workers and 21.9% (792) of the radiological diagnostic units were in tertiary hospitals. There were 91.5 X-ray diagnostic units per million population, including 53.2 X-ray radiography units and 17.1 computed tomography (CT) units per million population. In 2022, the total number of X-ray diagnostic examinations was 21 303 635, primarily including 10 812 197 (50.8%) X-ray radiography examinations and 8 969 358 (42.1%) CT examinations. Analysis of equipment utilization intensity showed that the average annual number of examinations per unit of radiological diagnostic equipment in tertiary hospitals reached 10 506.1, with CT equipment bearing the most prominent workload (13 248.7 examinations/unit). The overall radiological diagnosis frequency was 538.8 examinations/thousand population (273.4 X-ray radiography and 226.8 CT examinations/thousand population). Tertiary, secondary, and primary and below institutions accounted for 39.1%, 44.0%, and 16.9% of the total number of examinations, respectively. Conclusion The radiological diagnosis frequency in Shaanxi Province (538.8 examinations/thousand population) was below the United Nations Scientific Committee on the Effects of Atomic Radiation (UNSCEAR) Healthcare Level I (823 examinations/thousand population). Issues such as uneven resource distribution and CT equipment overload should be addressed by digital upgrading, hierarchical diagnosis and treatment systems, and enhanced equipment maintenance.

Lung cancer constitutes the most prevalent and lethal malignant tumor in China. Approximately 85% of lung cancer diagnoses correspond to the non-small cell histological subtype [non-small cell lung cancer (NSCLC)]. Despite surgery being the mainstay for early-stage disease, postoperative recurrence remains high and adjuvant chemotherapy offers limited benefit. In recent years, targeted therapy has demonstrated substantial advantages in driver mutation-positive NSCLC. To this end, the Lung Cancer Medical Education Committee of the Chinese Medical Education Association developed guidelines based on a systematic review of evidence through November 2025, using the Grading of Recommendations, Assessment, Development and Evaluations (GRADE) approach and a modified Delphi method. Focusing on epidermal growth factor receptor (EGFR) and anaplastic lymphoma kinase (ALK), and addressing ROS proto-oncogene 1 (ROS1), B-Raf proto-oncogene serine/threonine kinase (BRAF) V600E mutation, and mesenchymal-epithelial transition factor (MET) exon 14 (METex14) skipping, the guideline covers molecular testing, neoadjuvant/adjuvant therapy, perioperative strategies, minimal residual disease monitoring, and postoperative surveillance. It defines testing requirements, specifies stage-directed and subtype-specific treatments, and standardizes minimal residual disease monitoring. These recommendations emphasize precision and feasibility to improve survival and quality of life.

Objective In this paper,CiteSpace(V6.3.R1)was used to sort out and summarize the experimental study on the mechanism and development trend of acupuncture intervention in Alzheimer's disease(AD),so as to provide basis and suggestions for subsequent research.Methods Relevant literatures on the mechanism of acupuncture intervention in AD were retrieved from CNKI database from March 1997 to March 2024.CiteSpace(V6.3.R1)software was used to visually display keywords,draw corresponding maps,and discuss the hot spots of acupuncture intervention mechanism in AD.Results After screening,a total of 397 articles were included in this study.The mechanism of acupuncture intervention in AD mainly focuses on the regulation of synaptic plasticity,regulation of neurotransmitter release,regulation of neuroinflammation,regulation of apoptosis,influence on mitochondrial autophagy,anti-oxidative stress and so on.Conclusion Acupuncture intervention in AD has developed rapidly,involving Notch1/Hes signaling pathway,Shh signaling pathway,NF-κB signaling pathway,PI3K/Akt signaling pathway and other signaling pathways.The research heat of TCM acupuncture intervention in AD continues to rise,and various research teams have harvested rich research results,diversified research hotspots,and in-depth exploration of acupuncture treatment of AD has rich clinical value.

Objective:To explore the correlation between metabolic syndrome (MS), serum high-sensitivity C-reactive protein (hs-CRP) levels, their combination and the risk of digestive system malignancies.Methods:A prospective cohort study was conducted in the participants from the Kailuan cohort who took health examination in July 2006. Anthropometric parameters, epidemiological information, and laboratory test results were collected. Incidence and mortality of digestive system malignant tumors were collected through biennial health examinations and questionnaires. The follow-up period ended on December 31, 2021.According to MS status and hs-CRP levels (hs-CRP≤3 or >3 mg/L), the cohort was divided into 4 groups, induding MS -hs-CRP -, MS -hs-CRP +, MS + hs-CRP -, and MS + hs-CRP + group. Chi-squared test, one analysis of variance, and the Kruskal-Wallis H test were used for inter-group comparison among groups. Kaplan-Meier method was used to calculate the cumulative incidence of digestive system malignant tumors, and log-rank test was performed to compare the cumulative incidence among groups. Multivariable Cox proportional hazards regression models were used to evaluate the effects of MS and hs-CRP levels on the overall risk of digestive system malignant tumors, as well as the effects of their combination on the risk of digestive system malignant tumors of different site, and relevant confounding factors were adjusted.A sensitivity analysis was conducted by excluding individuals diagnosed with digestive system malignancies within one year of follow-up, as well as those taking antihypertensive, antidiabetic, or lipid-lowering medications. Results:A total of 92 916 participants were included in this study. Among them, 57 933 cases were in the MS -hs-CRP - group, 10 949 cases in the MS -hs-CRP + group, 18 412 cases in the MS + hs-CRP - group, and 5 622 cases in the MS + hs-CRP + group.The median follow-up period was 15.01 years (14.66 to 15.20 years). By the end of follow-up, these were 1 992 cases of new-onset digestive system malignant tumors. The cumulative incidence rates of digestive system malignant tumors of MS -hs-CRP -, MS -hs-CRP +, MS + hs-CRP -, and MS + hs-CRP + groups were 2.0%(1 164/57 933), 2.3%(249/10 949), 2.4%(440/18 412), and 2.5%(139/5 622), respectively. The difference in the cumulative incidence among the 4 groups was statistically significant ( χ2=14.09, P=0.003).The results of multivariate Cox analysis showed that, after hs-CRP level and other confounding factors were adjusted, the risk of developing digestive system malignant tumors in participants with MS was 21.4% higher than that in those without MS ( HR=1.214 (95% confidence interval (95% CI): 1.086 to 1.340), P<0.001). After MS status and other confounding factors were adjusted, the risk of developing digestive system malignant tumors in participants with high hs-CRP level (>3 mg/L) was 17.2% higher than those with low hs-CRP level (≤3 mg/L) ( HR=1.172 (95% CI: 1.042 to 1.303), P=0.008). After relevant confounding factors were adjusted, the risks of developing digestive system malignant tumors in the MS -hs-CRP +, MS + hs-CRP -, and MS + hs-CRP + groups increased by 17.2%, 21.4%, and 35.9%, respectively, as compared with that of the MS -hs-CRP - group ( HR=1.172 (95% CI: 1.017 to 1.399), P=0.028; HR=1.214 (95% CI: 1.074 to 1.356), P=0.002; HR=1.359 (95% CI: 1.135 to 1.635), P=0.001). Among the 4 groups, the overall risk of developing digestive system malignant tumors of MS + hs-CRP + group was the highest. After relevant confounding factors were adjusted, the risks of colorectal cancer, liver cancer, and pancreatic cancer of the MS + hs-CRP + group increased by 46.2%, 35.7%, and 88.3%, respectively, as compared with those of the MS -hs-CRP - group ( HR=1.462 (95% CI: 1.088 to 1.956), HR=1.357 (95% CI: 1.132 to 2.089), HR=1.883 (95% CI: 1.052 to 3.342)), suggesting that MS combined with high hs-CRP was a significant risk factor for increased incidences of colorectal cancer, liver cancer, and pancreatic cancer ( P=0.012, 0.016 and 0.033). After participants diagnosed with new digestive system malignancies within one year of follow-up and those taking antihypertensive, antidiabetic, or lipid-lowering medications (108 cases, 10 680 cases, 2 344 cases, 906 cases) were excluded, the results of sensitivity analysis indicated the increased risk of digestive system malignant tumors in the MS -hs-CRP +, MS + hs-CRP -, and MS + hs-CRP + groups were 12.1%, 21.4%, 28.7%; 18.2%, 21.4%, 24.8%; 16.4%, 21.4%, 32.2%; 17.3%, 20.4%, 35.8%. Among the 3 groups, the increased risk of developing digestive system malignant tumors of MS + hs-CRP + group was the highest. Conclusion:MS and hs-CRP >3 mg/L are both independent risk factors for developing digestive system malignant tumors, and their combination further increases the risk of developing digestive system malignant tumors.

Background/Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression. Methods: USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes. Results: USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5. Conclusions USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.

Objective To establish baseline radiation dose data for computed tomography (CT) examinations in Shaanxi Province, China and to provide scientific evidence for optimizing medical radiation protection. Methods From 2020 to 2023, a multicenter cross-sectional study was conducted using 16 CT scanners across 9 hospitals (2 specialized pediatric hospitals and 7 general hospitals). Standardized registration forms were used to collect basic information (e.g., age and examination site), scanning parameters (e.g., tube voltage, tube current-time product, and scan length), and dosimetric parameters (volume CT dose index [CTDI_vol] and dose-length product [DLP]). Non-parametric tests were employed for intergroup comparisons. Results A significant positive correlation was observed between age and major CT scanning parameters. Both CTDI_vol and DLP increased significantly with age across all examination sites (P < 0.001). Abdominal CTDI_vol was significantly lower in specialized pediatric hospitals than in general hospitals (8.0 vs. 15.5 mGy, P < 0.001). The < 1-year age group showed higher abdominal CTDI_vol (13.2 vs. 8.6 mGy) but lower DLP (243.5 vs. 261.9 mGy·cm) compared to the 1- < 5-year group. Conclusion This study established the first baseline radiation dose database for CT examinations in Shaanxi Province, providing critical scientific support for developing regional diagnostic reference levels and optimizing radiological protection practices.

Background/Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression. Methods: USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes. Results: USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5. Conclusions USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.

Background/Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression. Methods: USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes. Results: USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5. Conclusions USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.

Megakaryocytes and hepatocytes are unique cells in mammals that undergo polyploidization through endomitosis in terminal differentiation. Many polyploidization regulators and underlying mechanisms have been reported, most of which are tightly coupled with development, organogenesis, and cell differentiation. However, the nature of endomitosis, which involves successful entry into and exit from mitosis without complete cytokinesis, has not yet been fully elucidated. We highlight that endomitosis is a new cell fate in the cell cycle, and tetraploidy is a critical stage at the bifurcation of cell fate decision. This review summarizes the recent research progress in this area and provides novel insights into how cells manipulate mitosis toward endomitosis. Endomitotic cells can evade the tetraploidy restrictions and proceed to multiple rounds of the cell cycle. This knowledge not only deepens our understanding of endomitosis as a fundamental biological process but also offers new perspectives on the physiological and pathophysiological implications of polyploidization.
Hepatocytes/physiology* ; Megakaryocytes/physiology* ; Humans ; Polyploidy ; Animals ; Cell Cycle/physiology* ; Cell Differentiation ; Mitosis/physiology*

Objective:To investigate the predictive value of different obesity indicators for colorectal cancer (CRC) risk in different gender populations.Methods:This observational study was conducted within the Kailuan Study (Registration Number: ChiCTR-TNC-11001489). From July 2006 to October 2007, a total of 101,510 employed and retired individuals underwent health examinations, including gastrointestinal disease screening, hematological tests, and questionnaires, at Kailuan General Hospital and its 10 affiliated hospitals. After excluding those with incomplete data, 93,606 participants were included in this study and divided into male (74 852) and female (18 754) groups. CRC incidence was collected through physical examinations and questionnaires every two years. Each participant's follow-up period began at the time of the questionnaire and ended upon CRC diagnosis, death, or December 31, 2021. Body Mass Index (BMI), waist circumference, waist-to-hip ratio (WHR), and waist-to-height ratio (WHtR) were quartiled (Q1, Q2, Q3, Q4), with Q1 serving as the control group. After adjusting for traditional risk factors such as age, total cholesterol, triglycerides, diabetes, hypertension, smoking status, alcohol consumption, and physical exercise, Cox regression models were used to calculate the correlations between BMI, waist circumference, WHR, WHtR, and CRC incidence in both male and female populations.Results:The age of all patients was (51±12) years, BMI was (25.06±3.49) kg/m 2, waist circumference was (86.94±9.97) cm, hip circumference was (97.30±8.81) cm, WHR was 0.89±0.07, and WHtR was 0.52±0.06.Female participants had significantly lower BMI, waist circumference, WHR, and WHtR compared to males, with statistically significant differences (all P<0.05). The mean follow-up duration for all participants was 15.01 (14.10±2.66) years, during which 718 CRC cases were identified, including 626 males (0.83%) and 92 females (0.49%). Cox proportional hazards models for males showed that CRC risk increased with waist circumference from Q3 (HR=1.43, 95%CI: 1.13-1.79, P=0.003) to Q4 (HR=1.45,95%CI: 1.14-1.82, P=0.002). Similarly, CRC risk increased with WHR from Q3 (HR=1.22, 95%CI: 1.01-1.53, P=0.007) to Q4 (HR=1.43, 95%CI: 1.14-1.79, P=0.002) and with WHtR from Q3 (HR=1.37, 95%CI: 1.08-1.74, P=0.009) to Q4 (HR=1.68, 95%CI: 1.33-2.12, P<0.001). For females, CRC risk increased with waist circumference from Q2 (HR=2.37, 95%CI: 1.20-4.67, P=0.012) to Q3 (HR=2.42, 95%CI: 1.21-4.84, P=0.013) but decreased in Q4 ( HR=2.08, 95%CI: 1.02-4.25, P=0.043). CRC risk increased significantly with WHR from Q2 (HR=2.20, 95%CI: 1.11-4.39, P=0.024) to Q3 (HR=2.89, 95%CI: 1.48-5.67, P=0.002) in females but was not statistically significant in Q4 ( P=0.074). Among females, CRC risk also increased significantly with WHtR in Q2 (HR=2.30, 95% CI: 1.16-4.56, P=0.017) and Q4 (HR=2.64, 95%CI: 1.32-5.29, P=0.006). There were no statistically significant differences in CRC risk associated with BMI in either male or female populations (both P>0.05). Conclusion:Waist circumference, WHR, and WHtR were better predictors of CRC risk than BMI in both male and female populations.