This paper primarily reviews the current research status of passive and active monitoring methods for interventional radiology personnel, encompassing the types and wearing positions of personal dosimeters, simulation results versus measured outcomes, and discrepancies between different simulation results. By reviewing domestic and international literature, it lists effective dose estimation formulas for single- and dual-dosimeter systems developed by various researchers worldwide. Recommendations are proposed based on the current dosimeter wearing practices among interventional radiology staff, providing reference for the formulation of relevant standards.

OBJECTIVE To observe the clinical efficacy of evolocumab combined with atorvastatin in the treatment of patients with borderline coronary heart disease （CHD）. METHODS In this retrospective cohort study， 342 hospitalized patients diagnosed with borderline CHD were enrolled in the First Affiliated Hospital of Nanyang Medical College from August 2021 to June 2024， and divided into control group （treated with atorvastatin， 190 cases） and trial group （treated with evolocumab combined with atorvastatin， 152 cases） according to therapeutic regimen. Blood lipid indexes， high-sensitivity C-reactive protein （hs-CRP） and intravascular ultrasound of the coronary artery at baseline and after 1 year of treatment， and incidence of cardiovascular adverse events were compared after propensity score matching. RESULTS A total of 295 patients （158 in control group and 137 in trial group） were finally included in the analysis. One year after the treatment， compared with control group， total cholesterol， triglycerides， low-density lipoprotein cholesterol and hs-CRP levels were decreased significantly in trial group （ P ＜0.05）， whereas high-density lipoprotein cholesterol level was increased significantly （ P ＜0.05）. The lumen diameter， lumen area， and the minimum lumen area were significantly increased （ P ＜0.05）， while plaque area and plaque burden were significantly decreased （ P ＜0.05）. Overall incidence of adverse events in trial group was significantly lower than that in control group （ P ＜0.05）. CONCLUSIONS Evolocumab combined with atorvastatin can significantly improve coronary luminal narrowing and reduce plaque burden， as well as reduce the incidence of cardiovascular adverse events in patients with borderline CHD.

Diabetic sarcopenia (DS) is a common but often ignored skeletal muscle complication in individuals with diabetes mellitus. It is characterized by progressive loss of skeletal muscle mass, reduced muscle strength, and impaired physical performance, which may further increase the risk of falls, disabilities, metabolic disorders, and adverse clinical outcomes. Traditionally, DS has been attributed mainly to hyperglycemia, insulin resistance, aging-related muscle decline, and chronic complications of diabetes. However, increasing evidence suggests that lipid metabolic disturbance and pathological lipid metabolic reprogramming are not merely secondary consequences of diabetes, but may actively participate in the initiation and progression of DS. Under diabetic conditions, impaired fatty acid uptake, transport, oxidation, and storage disrupt skeletal muscle metabolic homeostasis, leading to ectopic lipid deposition and accumulation of lipotoxic intermediates. These lipid-derived metabolites can aggravate insulin resistance, impair mitochondrial energy production, enhance oxidative stress, activate chronic low-grade inflammation, and disturb protein synthesis and degradation balance, thereby accelerating skeletal muscle atrophy and functional decline. Lipid metabolic dysregulation may also interact with multiple pathological processes involved in DS, including mitochondrial dysfunction, inflammatory signaling, oxidative damage, impaired autophagy, and gut microbiota imbalance. These mechanisms do not occur independently; instead, they form a complex bidirectional vicious cycle with diabetes-related metabolic disorders. Specifically, mitochondrial dysfunction reduces fatty acid oxidative capacity, which further promotes lipid accumulation and lipotoxicity. Inflammatory activation can impair insulin signaling and muscle protein metabolism, while lipid overload may in turn amplify inflammatory responses. Similarly, gut microbiota dysbiosis and altered microbial metabolites may influence systemic inflammation, lipid metabolism, and skeletal muscle homeostasis. Therefore, lipid metabolic reprogramming provides an important mechanistic perspective for understanding the progression of DS from metabolic disturbance to structural and functional muscle impairment. Exercise intervention is an effective and clinically feasible non-pharmacological strategy for the prevention and management of DS. Both aerobic exercise and resistance training have been shown to improve insulin sensitivity, enhance fatty acid oxidation, increase mitochondrial biogenesis, reduce ectopic lipid deposition, and attenuate lipotoxic metabolite accumulation. These adaptations not only improved glucose and lipid metabolism, but also increased the preservation of muscle mass, muscle strength, and physical function. Moreover, combined exercise strategies may provide complementary benefits by integrating the metabolic advantages of aerobic exercise with the anabolic and functional effects of resistance training. Based on analyses of publicly available datasets and literature evidences, this review systematically summarizes the role of lipid metabolic disorders in the pathogenesis of DS, with particular attention to the molecular mechanisms linking lipid dysregulation to insulin resistance, chronic inflammation, oxidative stress, mitochondrial dysfunction, and gut microbiota disturbance. Furthermore, this review discusses the potential mechanisms by which exercise intervention improves DS through the regulation of lipid metabolic reprogramming, and outlines exercise prescription strategies in terms of modality, intensity, frequency, and duration. Understanding the interaction between lipid metabolism and skeletal muscle dysfunction may provide new theoretical evidence for early identification, mechanistic research, and precision exercise therapy in DS. Overall, targeting pathological lipid metabolic reprogramming through exercise intervention represents a promising and clinically actionable approach for improving muscle health and prognosis in individuals with DS.

Objective:To analyze the correlation and predictive value of obesity measurement indicators and cerebrovascular function scores in healthy physical examination population.Methods:It was a cross-sectional analysis that employed a simple random sampling method to select 3 496 individuals who underwent healthy physical examinations and cerebrovascular function tests at the Physical Examination Center of the Affiliated Hospital of Guizhou Medical University from January to December 2022. The general information, physical examination data, biochemical examination results, human component analyses, and cerebrovascular function integral data were collected. Based on cerebrovascular function scores, the participants were divided into high-risk group (0-24 points, 70 cases), medium-risk group (25-49 points, 317 cases), low-risk group (50-74 points, 787 cases), and normal group (≥75 points, 2 322 cases). Spearman correlation analysis and receiver operating characteristic (ROC) curve analyses were utilized to assess the correlation and predictive value of obesity measurement indicators and cerebrovascular function integrals.Results:Among the 3 496 subjects included in the analysis, 2 018 were male and 1 478 were female, with an average age of (46.4±7.9) years. The age, systolic blood pressure, diastolic blood pressure, body mass index, waist-to-hip ratio, body fat ratio, body fat content, visceral fat area, fasting blood glucose, total cholesterol, low-density lipoprotein, homocysteine all exhibited an increasing trend as the cerebrovascular function integral value decreased (all P<0.05). The skeletal muscle content in the low-risk group was significantly higher than those in the high-risk group, medium-risk group, and normal group [45.00 (36.80, 50.60) vs 44.10 (36.98, 50.45), 44.50 (37.80, 50.20), and 42.75 (36.30, 48.60) kg, respectively] ( P<0.05). The triglyceride level in the medium-risk group was higher when compared to those in the high-risk group, low-risk group, and normal group[1.87 (1.29, 2.70) vs 1.71 (1.24, 2.80), 1.75 (1.18, 2.70), and 1.43 (1.00, 2.14) mmol/L] ( P<0.05). The high-density lipoprotein level in the normal group was higher than the high-risk group, medium-risk group, and low-risk group[1.26 (1.05, 1.51) vs 1.16 (0.94, 1.36), 1.15 (0.99, 1.39), and 1.16 (0.97, 1.39) mmol/L, respectively] ( P<0.05). The increases in systolic blood pressure, diastolic blood pressure, body mass index, and body fat content were all moderately negatively correlated with the cerebrovascular function score ( rs=-0.347, -0.335, -0.370, and -0.340, respectively, all P<0.05). The increase in age ( OR=1.012, 95% CI: 1.002-1.022), systolic blood pressure ( OR=1.027, 95% CI: 1.017-1.036), diastolic blood pressure ( OR=1.028, 95% CI: 1.014-1.042), body mass index ( OR=1.157, 95% CI: 1.083-1.237), body fat rate ( OR=1.021, 95% CI: 1.007-1.035), and fasting blood glucose ( OR=1.072, 95% CI: 1.020-1.127) were all positively correlated with the decrease of the cerebrovascular function score; conversely, the increase in skeletal muscle content ( OR=0.967, 95% CI: 0.951-0.982) was negatively correlated with the decrease in cerebrovascular function score (all P<0.05). The area under the curve for the combined prediction of cerebrovascular function integral value by age, systolic blood pressure, diastolic blood pressure, body mass index, body fat rate, skeletal muscle content, and fasting blood glucose was 0.754. Conclusions:As the body mass index and body fat content increase and the skeletal muscle content decreases in the healthy physical examination population, the likelihood of abnormal cerebrovascular function integral values rises; the combination of age, systolic blood pressure, diastolic blood pressure, body mass index, body fat percentage, skeletal muscle content, and fasting blood glucose indicators can predict the increased risk of cerebrovascular function integral values.

Objective To evaluate the influence of the wearing position of dosimeters outside lead aprons on effective dose estimation for interventional radiology workers, analyze the differences between single and double dosimeter methods in effective dose estimation, and provide a reference for the personal dose monitoring of interventional radiology workers. Methods This study employed a combined approach of on-site monitoring and Monte Carlo simulation to evaluate the impact of the wearing position of dosimeters outside lead aprons on effective dose estimation, as well as the differences between effective doses measured using single and double dosimeters. Interventional radiology workers wore dosimeters at three positions: the neck outside the lead collar, the left chest outside the lead apron, and inside the lead apron. Effective doses were estimated using the single and double dosimeter methods specified in GBZ 128-2019 Specifications for individual monitoring of occupational external exposure, and the impact of different wearing positions on the estimation results was compared. Geant4 Monte Carlo simulations were used to model dose distributions at the neck outside the lead collar and at the left chest outside the lead apron for operators performing cardiovascular interventions under tube voltages of 70, 80, 90, and 100 kVp and exposure angles of posteroanterior (PA), anteroposterior (AP), and left anterior oblique 45° (LAO45°) positions. The study assessed the impact of dosimeter wearing position on effective dose estimation. Results Monte Carlo simulations demonstrated that neck doses consistently exceeded left chest doses across different tube voltages and exposure angles, with neck-to-chest dose ratios of 0.80-0.90. Under identical tube voltage conditions, AP showed the highest doses, followed by LAO45°, and PA demonstrated the lowest doses. The single and double dosimeter methods exhibited consistent patterns in effective dose estimation. Single dosimeter method generally yielded higher effective doses with relative deviations of 9.9% to 83%, though these deviations decreased under high tube voltages. Field monitoring data indicated that most interventional radiology workers maintained relative deviations between single and double dosimeter calculations below 6%, with neck-to-chest dose ratios of 0.95-1.1. The estimation patterns remained consistent across both methods, though single dosimeter method showed slightly higher results. Conclusion Under PA, AP, or LAO45°, the doses at the neck consistently exceeded those at the left chest. Therefore, when wearing lead protective equipment, the dosimeter should be properly positioned at the neck outside the lead collar to accurately reflect the radiation doses of surgeons. Some interventional radiology workers improperly positioned the dosimeter (intended at the neck outside the lead collar) at the left chest outside the lead apron, and this may result in an underestimation of the effective dose.

Objective:To observe the effect of combine treatment of butorphanol combined with esketamine in patients with remifentanil induced hyperalgesia after laparoscopic gynecological surgery.Methods:Based on randomized double-blind controlled trial,120 patients undergoing laparoscopic gynecological surgery in our hospital from April 2023 to October 2024 were divided into control group 1(received esketamine treatment,n=40),control group 2(received butorphanol treatment,n=40),and study group(received butorphanol combined with esketamine treatment,n=40).The awakening time,extubation time,mean arterial pressure(MAP),heart rate(HR),visual pain analog scale(VAS)score,ramsay sedation score,and incidence of adverse reactions among three groups were compared.Results:The awakening time and extubation time in the study group were shorter than those in the control group 1 and control group 2(P＜0.05).The MAP and HR in the study group were lower than those in the control group 1 and control group 2 at 30 minutes,60 minutes after extubation(P＜0.05).The VAS scores in the study group were lower than those in the control group 1 and control group 2 at 30 minutes,60 minutes after extubation(P＜0.05).The ramsay sedation scores in the study group were higher than those in the control group 1 and control group 2 at 30 minutes,60 minutes after extubation(P＜0.05).There was no significant difference in the incidence of postoperative adverse reactions among the three groups(P＞0.05).Conclusion:Butorphanol combined with esketamine can further alleviate remifentanil induced hyperalgesia after laparoscopic gynecological surgery,exert good sedative and analgesic effects,maintain hemodynamic stability,and have good safety.

Aim To investigate the antagonistic effect of Schizandrin A(SchA)on oxidative stress-induced endothelial dysfunction and its mechanism of action.Methods Human umbilical vein endothelial cells(HUVECs)were selected as the research subjects,and the effects of SchA on cell viability were detected by MTT assay;the content of ROS in the cells was detec-ted by flow cytometry;the content of MDA and CAT in the cells,and the content of NO and ET-1 in the cell supernatant were detected by kit assay;and the expres-sion of SOD1,p-eNOS/eNOS proteins,and ET-1 in the cell supernatant were detected by Western blot.Immu-nofluorescence experiments were performed to detect Nrf2 entry into the nucleus of cells.Results SchA re-versed the LPS-or hypoxia-induced increase in ROS and MDA content as well as the decrease in SOD1 and CAT content in HUVECs by activating the Nrf2/Keap1/HO-1 signaling pathway.SchA inhibited the decrease of p-eNOS and eNOS protein expression in HUVECs cells,as well as NO content in cell culture medium and the increase of ET-1 content induced by LPS.The Nrf2 inhibitor ML385 reversed the antagonis-tic effects of SchA on oxidative stress and endothelial dysfunction.Conclusions SchA antagonized LPS and hypoxia-induced oxidative stress,and SchA amelio-rated oxidative stress-induced endothelial dysfunction by up-regulating the Nrf2/Keap1/HO-1 signaling path-way.

Objective To summarize the clinical and genetic characteristics of children with sodium taurocholate co-transporting polypeptide(NTCP)deficiency.Methods Clinical data of children with NTCP deficiency diagnosed and treated at the First People's Hospital of Yunnan Province from July 2022 to March 2025 were retrospectively analyzed.Results A total of 14 children were included(6 males,8 females),all with normal growth and development.Reasons for initial consultation included elevated serum bile acids in 7 cases,jaundice in 4 cases,cholestatic hepatitis in 1 case,and one case each of pneumonia and cow's milk protein allergy.At the first visit,all patients had elevated serum total bile acids beyond the normal range,with a mean of 152.5 μmol/L.Elevated alanine aminotransferase was observed in 1 case,elevated aspartate aminotransferase in 2 cases,and elevated total bilirubin in 10 cases.Genetic sequencing revealed that all children carried the homozygous SLC10A1 variant c.800C>T(p.Ser267Phe),classified as likely pathogenic.Conclusions NTCP deficiency often lacks obvious clinical symptoms and signs.Some children present with transient hyperbilirubinemia,cholestasis,or other liver function abnormalities.Persistent isolated elevation of serum bile acids warrants suspicion for this disease.Biallelic pathogenic variants in SLC10A1 constitute the basis for definitive diagnosis.There is no specific treatment for this disease,and management is mainly symptomatic.

Mutations in the cyclin-dependent kinase-like 5 gene (CDKL5) cause a severe neurodevelopmental disorder, yet the impact of truncating mutations remains unclear. Here, we introduce the Cdkl5^492stop mouse model, mimicking C-terminal truncating mutations in patients. 492stop/Y mice exhibit altered dendritic spine morphology and spontaneous seizure-like behaviors, alongside other behavioral deficits. After creating cell lines with various Cdkl5 truncating mutations, we found that these mutations are regulated by the nonsense-mediated RNA decay pathway. Most truncating mutations result in CDKL5 protein loss, leading to multiple disease phenotypes, and offering new insights into the pathogenesis of CDKL5 disorder.
Animals ; Disease Models, Animal ; Mice ; Protein Serine-Threonine Kinases/deficiency* ; Mutation/genetics* ; Epileptic Syndromes/genetics* ; Humans ; Dendritic Spines/pathology* ; Spasms, Infantile/genetics* ; Male ; Seizures/genetics* ; Mice, Inbred C57BL

OBJECTIVE: Patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection frequently develop central nervous system damage, yet the mechanisms driving this pathology remain unclear. This study investigated the primary pathways and key factors underlying brain tissue damage induced by the SARS-CoV-2 beta variant (lineage B.1.351). METHODS: K18-hACE2 and C57BL/6 mice were intranasally infected with the SARS-CoV-2 beta variant. Viral replication, pathological phenotypes, and brain transcriptomes were analyzed. Gene Ontology (GO) analysis was performed to identify altered pathways. Expression changes of host genes were verified using reverse transcription-quantitative polymerase chain reaction and Western blot. RESULTS: Pathological alterations were observed in the lungs of both mouse strains. However, only K18-hACE2 mice exhibited elevated viral RNA loads and infectious titers in the brain at 3 days post-infection, accompanied by neuropathological injury and weight loss. GO analysis of infected K18-hACE2 brain tissue revealed significant dysregulation of genes associated with innate immunity and antiviral defense responses, including type I interferons, pro-inflammatory cytokines, Toll-like receptor signaling components, and interferon-stimulated genes. Neuroinflammation was evident, alongside activation of apoptotic and pyroptotic pathways. Furthermore, altered neural cell marker expression suggested viral-induced neuroglial activation, resulting in caspase 4 and lipocalin 2 release and disruption of neuronal molecular networks. CONCLUSION These findings elucidate mechanisms of neuropathogenicity associated with the SARS-CoV-2 beta variant and highlight therapeutic targets to mitigate COVID-19-related neurological dysfunction.
Animals ; COVID-19/genetics* ; Mice ; Brain/metabolism* ; Apoptosis ; Mice, Inbred C57BL ; SARS-CoV-2/physiology* ; Pyroptosis ; Gene Expression Profiling ; Transcriptome ; Male ; Female