四川大学学报(医学版)最新文献

Objective: To investigate the perspectives and consensus among high-level medical professionals in China regarding critical thinking skills, identify key factors influencing the cultivation of critical thinking skills among medical students, propose optimization strategies, and provide both theoretical and practical guidance for standardizing mechanisms of critical thinking training within the medical education system.

Methods: A mixed-methods approach was employed. Semi-structured in-depth interviews were conducted with 22 core personnel involved in critical thinking training from multiple medical universities, hospitals, and clinical research teams across China between March 2023 and June 2023. Grounded theory was applied to explore the influencing factors, and the decision-making trial and evaluation laboratory (DEMATEL) method was applied to construct a structural model of the influencing factors. Centrality and causality analyses were conducted to examine the interrelationships among factors.

Results: The grounded theory analysis revealed a shared conceptual understanding of critical thinking skills among the participants, who emphasized that the development of critical thinking skills was influenced by multiple factors, including individual traits, teaching methods, and institutional environments. According to the DEMATEL analysis, 13 core factors influencing the development of critical thinking skills in high-level medical professionals were identified. Among these, knowledge foundation was the most important influencing factor, exhibiting the highest centrality (22.35). Curriculum design was the second most important influencing factor.

Conclusion: The cultivation of critical thinking skills in medical education exhibits a multi-level interactive structure that encompasses individual, organizational, and institutional dimensions. Future efforts should focus on reinforcing the cognitive scaffolding role of knowledge construction and interdisciplinary curriculum design.

Objective: To investigate the effect of obstructive sleep apnea (OSA) on behavioral problems in children and the association between them.

Methods: A simple random sampling method was used to select 100 children aged 4 to 12 years for the case group. All of them were diagnosed with OSA through overnight polysomnography at the Sleep Medicine Center, West China Fourth Hospital, Sichuan University between October 2022 and October 2023. An additional 100 children without snoring symptoms and clinically evaluated and confirmed as not having OSA were enrolled as the control group. General demographic data of the participants were collected. The Caregiver Report Form of the Achenbach Child Behavior Checklist (CBCL) was used for behavioral problem assessment, and polysomnography data were collected. The chi-square/t test was used to analyze the inter-group differences in general data, the total score of behavioral problems, and scores for each dimension. Linear regression was performed to analyze the relationship between OSA and the total score for children's behavioral problems and those for the different dimensions. Logistic regression was applied to analyze the relationship between the obstructive apnoea-hypopnea index (OAHI) and behavioral problems in children with OSA. A logistic regression model integrating the OAHI × sex interaction term was constructed to evaluate the moderating effect of sex on the association between OAHI and behavioral problems.

Results: No significant differences were observed in general demographic data between the case and control groups. The total score for behavioral problems and those for each dimension were higher in the case group than those in the control group, with the total score of the case group being 24.60 ± 1.55 and that of the control group being 8.85 ± 0.75 (P < 0.001). The results of the linear regression analysis showed a positive association between OSA and both the total score for behavioral problems (b = 16.01; 95% CI, 12.56-19.47) and those for each dimension. The results of the logistic regression analysis showed that, after adjusting for covariates, OAHI was a risk factor for behavioral problems in children with OSA (odds ratio [OR] = 1.17; 95% CI, 1.04-1.31). After stratification by sex and adjustment for covariates, the OR value of the effect of OAHI on behavioral problems was slightly higher in female participants (1.57) than that in male participants (1.21). The interaction effect analysis showed that sex moderated the association between OAHI and behavioral problems (OR = 1.64; 95% CI, 1.02-2.64; P = 0.04).

Conclusion: Children with OSA are prone to developing behavioral problems. OAHI is a risk factor for behavioral problems in children with OSA, with a potentially greater effect observed in girls.

Nasojejunal feeding tubes are widely used in surgical, intensive care, and older patients. Manual blind insertion of nasojejunal feeding tubes is technically challenging, associated with a high failure rate, and prone to complications. The primary causes of suboptimal placement outcomes are the uncertainty and weak controllability of the interaction forces during the coordination between manual posterior advancement and the patient's physiological state. While current auxiliary techniques such as X-ray, ultrasound, and endoscopy can improve the success rate of nasojejunal tube placement and reduce complications to some extent, the accuracy and safety of placement remain constrained by challenges in controlling insertion forces and achieving precise positional localization. Robotic technology holds promise for addressing the uncertainties and controllability issues inherent in the placement process. By leveraging precise sensing, real-time navigation, and efficient control, robots can achieve intelligent positioning and precise control over the direction and location of the catheter tip during nasojejunal intubation. However, current research on robotic applications for nasojejunal feeding tube placement is still in an early stage, facing challenges such as high costs, operational complexity, and concerns over safety and reliability. Herein, we analyzed the limitations and causes of failure in existing placement methods and explored the application prospects of robotic technologies for precise control and intelligent positioning in nasojejunal feeding tube placement. The paper provides new insights for developing nursing techniques that enable safer and more effective, comfortable, and rapid intubation. Future efforts should focus on deepening the integration of artificial intelligence and robotics, optimizing drive technologies, and accelerating the translation of these technologies from the laboratory to clinical practice. This will drive the advancement of nasojejunal feeding tube placement techniques towards intelligent, precise, and accessible solutions.

Objective: To investigate the potential therapeutic effects of trifolin on hypertension-induced renal injury, as well as the key targets and pathways involved.

Methods: The mRNA transcriptional profiles of peripheral blood clinical samples from hypertensive patients were analyzed using Gene Expression Omnibus (GEO), a high-throughput gene expression database. The network pharmacology method was employed to screen key targets of trifolin in treating hypertension-induced renal injury. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were conducted. NRK-52E cells, a rat renal proximal tubular cell line, were used to construct an angiotensin Ⅱ (Ang Ⅱ)-stimulated cell model. Flow cytometry was performed to assess cell apoptosis rates and Western blotting was performed to determine the expression levels of apoptosis-related proteins, including Bax, Bcl-2, cleaved caspase-3, and caspase-3, and the phosphorylation and total protein levels of the key MAPK pathway proteins, including ERK, p38 MAPK, and JNK.

Results: Analysis of the dataset GSE75360 revealed that, compared with healthy controls, 3331 genes were upregulated and 3197 genes were downregulated in peripheral blood mononuclear cells of hypertensive patients. According to network pharmacology analysis, 472 potential targets of trifolin were identified, including CASP3 and MAPK1. Protein-protein interaction network analysis showed that these targets were closely associated with apoptosis regulatory signaling pathways. GO and KEGG pathway enrichment analyses indicated that trifolin was significantly enriched in pathways associated with negative regulation of apoptosis, apoptotic signaling pathways, and the MAPK signaling pathway. The in vitro experiments confirmed that, compared with the Ang Ⅱ group, trifolin intervention inhibited apoptosis in Ang Ⅱ-stimulated NRK-52E cells, suppressed the expression of Bax and cleaved caspase-3, promoted Bcl-2 expression, and inhibited the phosphorylation of p38 MAPK, ERK, and JNK (P < 0.05).

Conclusion: Trifolin may exert its protective effect against hypertension-induced renal injury by inhibiting Ang Ⅱ-induced NRK-52E cell apoptosis and regulating the MAPK signaling pathway, representing an important mechanism underlying its therapeutic action.

Objective: To investigate the effects of low background radiation environments in deep underground settings on the biological behavior of NP69 human nasopharyngeal epithelial cells (NP69 cells) and the underlying molecular mechanisms.

Methods: A parallel control experimental design was adopted and NP69 cells were synchronously cultured in settings of three underground depths at the China in situ Deep-Underground Facility & Life Observatory (DeUFO)-ground level (DeUFO-0 m), 1000 m underground (DeUFO-1000 m), and 1500 m underground (DeUFO-1500 m). Changes in cell proliferation and migration capabilities were assessed using the Cell Counting Kit-8 (CCK-8) assay and scratch assay, respectively. High-throughput RNA sequencing (RNA-Seq) was performed to identify differentially expressed genes (DEGs). Functional annotation and pathway enrichment analysis of the DEGs were performed using the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases.

Results: CCK-8 assay revealed that, after 72 h of culture, the absorbance value of the DeUFO-0 m group was 1.35 times and 1.27 times those of the those of the DeUFO-1000 m and DeUFO-1500 m groups, respectively (both P < 0.0001). After 96 h of culture, the absorbance value of the DeUFO-0 m group was 1.52 times and 1.41 times those of the DeUFO-1000 m and DeUFO-1500 m groups, respectively (both P < 0.0001). Colony formation assays revealed that the number of cell colonies in the DeUFO-0 m group was 1.59 times and 1.27 times those in the DeUFO-1000 m group and DeUFO-1500 m group, respectively (both P < 0.001). The scratch assay revealed that the 36-hour wound healing rate of the DeUFO-0 m group was 2.22 times and 4.00 times those of the DeUFO-1000 m group and DeUFO-1500 m group, respectively (both P < 0.0001). Transwell assays revealed that the number of migrating cells in the DeUFO-0 m group was 2.08 times and 2.56 times those in the DeUFO-1000 m group and DeUFO-1500 m group, respectively (both P < 0.0001). Transcriptome sequencing analysis revealed consistent upregulation of CELF2, CELF4, CGB8, GRHL2, and DMRTA2 genes in the DeUFO-1000 m and DeUFO-1500 m groups. Pathway enrichment analysis indicated significant enrichment of extracellular matrix (ECM) remodeling-associated pathways and gene expression regulation pathways in the experimental groups (false discovery rate [FDR] < 0.05).

Conclusion: The low background radiation environment in deep underground settings suppresses the proliferation and migration activities of NP69 cells by mediating ECM remodeling and post-transcriptional regulatory mechanisms through the regulation of target genes such as the CELF family. This study provides experimental evidence for establishing a dose-response relationship between environmental radiation and cellular effects.

Objective: To analyze the molecular epidemiology of Candida tropicalis (C. tropicalis) isolates from bloodstream infections, and to investigate preliminarily the underlying mechanisms of fluconazole resistance.

Methods: Clinical C. tropicalis isolates were collected from bloodstream infections at West China Hospital, Sichuan University and other hospitals in Sichuan Province. All the collected isolates were identified using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry, and the antifungal susceptibility test was performed by the broth microdilution method. Multilocus sequence typing (MLST) was conducted using the first generation sequencing technique. Genes associated with drug-resistance were sequenced and the mutation sites were identified. The relative expression levels of genes associated with drug-resistance were analyzed using reverse transcription-quantitative polymerase chain reaction (RT-qPCR).

Results: A total of 39 C. tropicalis isolates from bloodstream infections were collected. The MLST phylogenetic tree showed that most of the strains clustered in the phylogenetic tree shared identical or similar minimal inhibitory concentrations (MICs). All MLST types were not matched with the isolates in the PubMLST database, representing new diploid sequence types (DSTs). A total of 3 sense mutations, including Ser154Phe, Tyr132Phe, and Tyr257His were identified in ERG11, and were present only in drug-resistant strains. UPC2 contained 4 sense mutations, including Ala251Thr, Gln289Leu, Ser279Glu, and Gln313His, which were also present only in drug-resistant strains. Ser279Glu and Gln313His were previously unreported. There were two sense mutations in ERG3, namely Ser112Gly and Ala48Ser, both being previously unreported, and Ser112Gly was found only in drug-resistant strains. The expression levels of ERG11 (14.48 vs 7.109, P = 0.003) and UPC2 (1.922 vs 0.832, P = 0.04) in non-sensitive group (MIC > 2 mg/L) were higher than those in sensitive group (MIC ≤ 2 mg/L), and the difference was statistically significant.

Conclusion: There may be a unique genetic relationship among C. tropicalis isolates from Sichuan province, and the MICs of fluconazole against C. tropicalis are associated with molecular typing. ERG11 mutations were the major mechanism underlying fluconazole resistance in C. tropicalis isolates. The upregulation of ERG11 and UPC2 was associated with fluconazole resistance in C. tropicalis.

Objective: To investigate the effects of individual social capital on depressive symptoms among older couples across different socioeconomic statuses (SES) using the actor-partner interdependence model (APIM).

Methods: A cross-sectional survey was conducted using a staged sampling method, involving 245 older couples from communities in Chengdu, China. Data on household SES, individual social capital, and depression levels were collected. Pearson correlation analysis was performed to examine the relationships among these variables, and the APIM was applied to analyze the actor and partner effects of individual social capital on depression across different SES groups.

Results: The prevalence of depressive symptoms was 38.2%. Individual social capital of the husbands and wives was negatively correlated with their personal depression levels (actor effects among the husbands: r = －0.218, P < 0.01; those among the wives: r = －0.323, P < 0.01) and with the spouse's depression levels (partner effects: husband on wife, r = －0.185, P < 0.01; wife on husband: r = －0.183, P < 0.01). Among high-SES couples, the husband's social capital had a protective effect only on his own depression (β = －0.242, 95% CI: －0.462 to －0.054). In contrast, among low-SES couples, the wife's individual social capital exhibited a protective effect against depressive symptoms both for herself (β = －0.658, 95% CI: －0.848 to －0.456) and for the husband (β = －0.379, 95% CI: －0.630 to －0.143).

Conclusion: Individual social capital among older couples demonstrates both actor and partner effects on depression levels, with distinct pathways of influence observed across different levels of SES. These findings highlight the importance of considering socioeconomic status when designing interventions to enhance social capital and improve mental health outcomes in older couples.

Objective: To investigate the critical role of macrophage M1 polarization in mediating the effect of periodontitis on the progression of chronic obstructive pulmonary disease (COPD).

Methods: Alveolar lavage fluid samples were collected from COPD patients with comorbid periodontitis, and gene expression analysis was performed to validate the changes in the expression of M1 polarization-related genes. A mouse model of COPD, with experimentally induced periodontitis, were established. Hematoxylin and eosin (HE) staining of pathological sections was performed to observe the effect of periodontitis on COPD progression. Flow cytometry, immunofluorescence staining, and reverse transcription quantitative polymerase chain reaction (RT-qPCR) were performed to analyze the effect of periodontitis on macrophage M1 polarization and the expression of relevant genes in the alveolar lavage fluid and lung tissues.

Results: In clinical samples of alveolar lavage fluid from COPD patients with periodontitis, the expression of macrophage M1 polarization-related genes, including CD86, inducible nitric oxide synthase (iNOS), interleukin (IL)-1β, tumor necrosis factor (TNF)-α, IL-23, and IL-6, was upregulated compared with that of COPD patients without periodontitis. Analysis of a mouse disease model revealed that periodontitis affected the growth of COPD mice, with the final body mass of mice in the periodontitis and COPD comorbid group ([21.3 ± 0.52] g, day 34) lower than that of the COPD group ([23.93 ± 0.45] g, day 34). Pathological sections of the lung tissue showed that periodontitis exacerbated COPD progression, with more pronounced alveolar expansion and alveolar wall destruction observed in the periodontitis and COPD comorbid group. Flow cytometry revealed a higher proportion of M1-polarized macrophages in alveolar lavage fluid from COPD and periodontitis comorbid mice ([31.36 ± 2.51]%) compared with the COPD mice ([23.19 ± 1.07]%). Immunofluorescence assays indicated that periodontitis also promoted macrophage M1 polarization in the lung tissue of COPD mice. Gene expression analysis demonstrated that M1 polarization-related gene expression was significantly upregulated in both the alveolar lavage fluid and lung tissue of mice in the COPD and periodontitis co-morbid group compared to the COPD group.

Conclusion: Periodontitis exacerbates COPD progression by promoting macrophage M1 polarization in the lungs. Enhancing oral hygiene management and targeting the inhibition of macrophage M1 polarization may represent new therapeutic strategies for the clinical prevention and control of COPD.

Periodontal disease is one of the most common infectious diseases affecting the oral cavity, with dental plaque biofilm and dental calculus being the primary pathogenic factors. Periodontal disease represents one of the leading causes of tooth loss in adults. According to the Fourth National Oral Health Epidemiological Survey, the incidence of periodontal disease remains high in China. As an odontogenic lesion, periodontal disease is also one of the principal oral conditions that can aggravate or trigger systemic diseases. It is closely associated with the onset and progression of cardiovascular, respiratory, gastrointestinal, metabolic, and bone-related diseases, as well as adverse pregnancy outcomes and mental health problems. Periodontal disease is also among the oldest diseases afflicting humans, accompanying human evolution and development throughout history. Archaeological research on periodontal disease provides an in-depth understanding of the occurrence and characteristics of periodontal disease and dental calculus formation in ancient humans. Such studies also help elucidate the dietary structures, lifestyle habits, general health status, and the evolution of disease spectrum of ancient populations. Consequently, research on periodontal disease provides important historical evidence for the study of human evolution, the development of civilization, and strategies for the prevention and treatment of periodontal diseases at the population level.