Objective: To investigate the influencing factors for cognitive function among aluminum workers, so as to provide the basis for intervention and prevention of cognitive function among aluminum-exposed populations. Methods: From July to August 2019, male aluminum workers in the electrolytic aluminum workshop of an aluminum factory in Shanxi Province were selected using the cluster sampling method. Demographic information, prevalence of chronic diseases, lifestyle behaviors, night shifts, and sleep quality were collected through questionnaire surveys. Blood aluminum levels were measured using inductively coupled plasma-mass spectrometry. Cognitive function was investigated using the Montreal Cognitive Assessment. Factors affecting cognitive function among aluminum workers were analyzed by a quantile regression model. Results: A total of 142 aluminum workers were surveyed, including 57 workers aged 20 to <40 years (40.14%) and 85 workers aged 40 to 60 years (59.86%). The median blood aluminum level was 38.23 (interquartile range, 21.82) μg/L. The median cognitive function score was 24.00 (interquartile range, 3.00) points. Quantile regression analysis revealed that older age (βQ5=-0.186, 95%CI: -0.269 to -0.102), lower educational level (βQ5=1.933, 95%CI: 1.029 to 2.838; βQ10=1.743, 95%CI: 0.480 to 3.006; βQ50=1.038, 95%CI: 0.141 to 1.935; βQ75=1.006, 95%CI: 0.437 to 1.575; βQ90=1.111, 95%CI: 0.291 to 1.930), smoking (βQ5=-2.056, 95%CI: -3.264 to -0.849), alcohol consumption (βQ5=-1.821, 95%CI: -3.247 to -0.396) and higher blood aluminum level (βQ5=-0.075, 95%CI: -0.110 to -0.040; βQ10=-0.078, 95%CI: -0.127 to -0.029; βQ50=-0.075, 95%CI: -0.110 to -0.040; βQ75=-0.057, 95%CI: -0.079 to -0.035; βQ90=-0.067, 95%CI: -0.099 to -0.035) were associated with cognitive function decline among aluminum workers. Conclusions Educational level and blood aluminum level are the main factors affecting the cognitive function among aluminum workers. Among those with lower cognitive function scores, age, smoking and alcohol consumption are also associated with cognitive function.

China is a high-incidence region for gastric cancer globally. The disease is characterized by a high morbidity rate, low early diagnostic rate, and poor long-term outcomes, imposing a significant burden on both patients and society. Therefore, exploring the pathogenesis of gastric cancer, developing novel therapeutic strategies, and identifying new drug targets is of great importance. Telomerase expression is broadly associated with cancer cell targeting, and its up-regulation is one of the key factors driving the initiation and progression of gastric cancer. Additionally, telomerase is intricately involved in the regulation of autophagy and autophagy-associated cell death. While autophagy can induce chemoresistance, excessive autophagy may lead to cell death, which also constitutes one of the mechanisms of chemotherapy. Telomerase not only directly contributes to gastric cancer pathogenesis but also indirectly influences its development and treatment by modulating autophagy and autophagic cell death. Therefore, telomerase holds promise as a novel therapeutic target in gastric cancer.
Humans ; Stomach Neoplasms/genetics* ; Telomerase/genetics* ; Autophagy/physiology*

Glioma is the most common primary malignant tumor of the central nervous system in adults. Despite the standard treatment of surgery combined with radiotherapy and chemotherapy, the prognosis for high-grade glioma patients remains poor, highlighting the urgent need to further explore its pathogenesis and develop new therapeutic strategies. This article reviews the research progress in the field of glioma in China in 2024, covering tumorigenesis mechanisms, tumor immune microenvironment composition, advances in imaging techniques and novel imaging agents, improvements in surgical approaches, mechanisms of radio- and chemoresistance, and explorations of new therapeutic modalities. These studies provide a solid theoretical foundation for advancing clinical diagnosis and treatment of gliomas and may offer new opportunities to improve patient outcomes.

Background Some studies have suggested that exposure to multiple metals is closely linked to the development of metabolic syndrome (MS) in the populations, but the effect of aluminum exposure on MS remains unclear. Objective To analyze the prevalence and influencing factors of MS among employees with aluminum exposure in Shanxi Province. Methods Cluster sampling was employed to survey male frontline workers in an aluminum factory in Shanxi Province. Data on general demographic information, lifestyle, occupational history, medical history, and family history of chronic diseases were collected through questionnaires. The concentration of fasting blood glucose was determined using the glucose oxidase technique, and blood lipid levels were determined using the peroxidase method. Serum aluminum levels were detected using inductively coupled plasma-mass spectrometry (ICP-MS), and blood biochemical indicators were measured using the peroxidase method. Based on the China's 2020 diagnostic criteria for MS, the participants were and divided into an MS group anda non-MS group. Variables with statistical significance in univariate analysis were included to construct a logistic regression model. Results A cohort of 312 workers participated in this research, with 84 individuals diagnosed with MS, yielding a prevalence rate of 26.92%. The logistic regression model revealed that body mass index (BMI)≥24.0 kg·m⁻² (OR=1.967, 95%CI: 1.057, 3.659), alcohol consumption (OR=1.883, 95%CI: 1.063, 3.336), experiencing major life event (OR=3.886, 95%CI: 1.509, 10.008), family history of hypertension (OR=2.112, 95%CI: 1.162, 3.837), serum aluminum concentration (OR=1.024, 95%CI: 1.012, 1.035), alanine aminotransferase (ALT) level (OR=1.032, 95%CI: 1.011, 1.054), and white blood cell (WBC) count (OR=1.210, 95%CI: 1.001, 1.465) were significant influencing factors for MS. Conclusion BMI≥24.0 kg·m⁻², alcohol consumption, experiencing major life event, family history of hypertension, elevated serum aluminum concentration, increased ALT level, and elevated WBC count are risk factors for MS among occupationally aluminum-exposed workers.

Background In vitro-in vivo extrapolation (IVIVE) is an approach utilizing in vitro experimental data to predict in vivo phenomena. It is a promising tool for chemical risk assessment. Objective To learn the hotspots, evolution path, and trend of IVIVE in risk assessment by literature search and bibliometric analysis, and provide reference and data support for subsequent research. Methods PubMed and Web of Science Core Collection were selected as foreign databases to search for literature about IVIVE applied in risk assessment published by December 31, 2023. The number of relevant documents in CNKI and Wanfang database was too small, so the Chinese databases were not included in this study. This study employed bibilometric analysis using VOSviewer and CiteSpace for visualizing networks categorized by author, institution, country, journal, keyword, and co-citation. Results A total of 189 articles were included in this study. The first article was published in 2006, and since then the number of publications overall showed an upward trend and increased significantly after 2016. The institution with the most publications was the United States Environmental Protection Agency (28 articles). The United States was the most productive country (87 articles), and had a close cooperation with the United Kingdom. The journal with the most publications and the highest number of citations per article was Archives of Toxicology (19 articles). The keyword co-occurrence analysis suggested that research on IVIVE in risk assessment mainly studied the methods and models of IVIVE and prediction of chemical toxicity, and toxicity, in vitro, and models were the research hotspots in this field. Keyword timeline cluster analysis suggested that the assessment objects gradually expanded from drugs to environmental chemicals, organic chemicals and food additives. The co-citation analysis suggested that articles about IVIVE in risk assessment mostly cited journals in the environment, food, and drug fields, and these articles were mainly methodological studies followed by literature reviews. Conclusion The research of IVIVE in risk assessment has developed rapidly. With the improvement of prediction models and the expansion of application scope, animal experiments in risk assessment may be greatly reduced and the efficiency of risk assessment can be increased. At present, the United States has a leading position in this field, while China has few relevant studies and needs to actively carry out international cooperation to improve the level of applied research of IVIVE. In the future, it is hoped that the IVIVE method can be further refined to improve its application and expand its research fields.

Objective To investigate the expression of PCI Domain Containing 2(PCID2)in gastric cancer,its effect on gastric cancer cell cycle and proliferation and the possible molecular mechanisms.Methods We examined PCID2 expression levels in gastric cancer and adjacent tissues from 100 patients undergoing radical gastrectomy in our hospital between January,2012 and December,2016,and analyzed the correlation of PCID2 expression level with cancer progression and postoperative 5-year survival rate of the patients.GO enrichment analysis was performed to identify the possible pathways that mediated the effect of PCID2 in gastric cancer progression.The effects of lentivirus-mediated PCID2 knockdown and overexpression on cell proliferation and cell cycle were analyzed in gastric cancer MGC-803 cells and in nude mice.Results PCID2 was highly expressed in gastric cancer tissues and positively correlated with peripheral blood levels of CA19-9 and CEA(P<0.01).In gastric cancer patients,a high PCID2 expression was associated with a significantly lowered postoperative 5-year survival rate(P<0.001)as an independent risk factor for postoperative survival(HR:2.987,95%CI:1.616-5.519).The sensitivity,specificity,and area under the curve of PCID2 for predicting postoperative 5-year survival were 76.74%,75.44%,and 0.755(P<0.001),respectively.GO enrichment analysis suggested that PCID2 was associated with gastric cancer cell cycle progression.PCID2 overexpression in MGC-803 cells significantly promoted cell proliferation,G1/S phase transition,expressions of cyclin D1 and CDK6,and the growth of transplanted xenograft in nude mice(P<0.05).The expressions of p27 and p16 were significantly lowered in gastric cancer tissues,and their expression levels were negatively regulated by PCID2 expression in MGC-803 cells(P<0.05).Conclusion PCID2 is highly expressed in gastric cancer tissues in close correlation with poor prognosis of the patients.High PCID2 expression promotes gastric cancer proliferation and cell cycle progression by inhibiting the expression of p27 and p16.

Objective To investigate the expression level of Kruppel-like transcription factor family member KLF11 in intestinal mucosal tissues of Crohn's disease (CD) and its regulatory effect on intestinal inflammation in CD-like colitis. Methods We examined KLF11 expression levels in diseased and normal colon mucosal tissues from 12 CD patients and 12 patients with colorectal cancer using immunofluorescence staining. KLF11 expression was also detected in the colon mucosal tissues of a mouse model of 2,4,6-trinitrobenesulfonic acid (TNBS)-induced colitis. A recombinant adenoviral vector was used to upregulate KLF11 expression in the mouse models and the changes in intestinal inflammation was observed. A Caco-2 cell model with stable KLF11 overexpression was constructed by lentiviral infection. The effect of KLF11 overexpression on expressions of JAK2/STAT3 signaling pathway proteins was investigated using immunoblotting in both the mouse and cell models. The mouse models were treated with coumermycin A1, a JAK2/STAT3 signaling pathway agonist, and the changes in intestinal inflammatory responses were observed. Results The expression level of KLF11 was significantly lowered in both the clinical specimens of diseased colon mucosal tissues and the colon tissues of mice with TNBS-induced colitis (P<0.05). Adenovirus-mediated upregulation of KLF11 significantly improved intestinal inflammation and reduced the expression levels of inflammatory factors in the intestinal mucosa of the colitis mouse models (P<0.05). Overexpression of KLF11 significantly inhibited the expression levels of p-JAK2 and p-STAT3 in intestinal mucosal tissues of the mouse models and in Caco-2 cells (P<0.05). Treatment with coumermycin A1 obviously inhibited the effect of KLF11 upregulation for improving colitis and significantly increased the expression levels of inflammatory factors in the intestinal mucosa of the mouse models (P<0.05). Conclusion KLF11 is downregulated in the intestinal mucosa in CD, and upregulation of KLF11 can improve intestinal inflammation and reduce the production of inflammatory factors probably by inhibiting the JAK2/STAT3 signaling pathway.

Objective To investigate the expression of PCI Domain Containing 2(PCID2)in gastric cancer,its effect on gastric cancer cell cycle and proliferation and the possible molecular mechanisms.Methods We examined PCID2 expression levels in gastric cancer and adjacent tissues from 100 patients undergoing radical gastrectomy in our hospital between January,2012 and December,2016,and analyzed the correlation of PCID2 expression level with cancer progression and postoperative 5-year survival rate of the patients.GO enrichment analysis was performed to identify the possible pathways that mediated the effect of PCID2 in gastric cancer progression.The effects of lentivirus-mediated PCID2 knockdown and overexpression on cell proliferation and cell cycle were analyzed in gastric cancer MGC-803 cells and in nude mice.Results PCID2 was highly expressed in gastric cancer tissues and positively correlated with peripheral blood levels of CA19-9 and CEA(P<0.01).In gastric cancer patients,a high PCID2 expression was associated with a significantly lowered postoperative 5-year survival rate(P<0.001)as an independent risk factor for postoperative survival(HR:2.987,95%CI:1.616-5.519).The sensitivity,specificity,and area under the curve of PCID2 for predicting postoperative 5-year survival were 76.74%,75.44%,and 0.755(P<0.001),respectively.GO enrichment analysis suggested that PCID2 was associated with gastric cancer cell cycle progression.PCID2 overexpression in MGC-803 cells significantly promoted cell proliferation,G1/S phase transition,expressions of cyclin D1 and CDK6,and the growth of transplanted xenograft in nude mice(P<0.05).The expressions of p27 and p16 were significantly lowered in gastric cancer tissues,and their expression levels were negatively regulated by PCID2 expression in MGC-803 cells(P<0.05).Conclusion PCID2 is highly expressed in gastric cancer tissues in close correlation with poor prognosis of the patients.High PCID2 expression promotes gastric cancer proliferation and cell cycle progression by inhibiting the expression of p27 and p16.

Objective To investigate the expression level of Kruppel-like transcription factor family member KLF11 in intestinal mucosal tissues of Crohn's disease (CD) and its regulatory effect on intestinal inflammation in CD-like colitis. Methods We examined KLF11 expression levels in diseased and normal colon mucosal tissues from 12 CD patients and 12 patients with colorectal cancer using immunofluorescence staining. KLF11 expression was also detected in the colon mucosal tissues of a mouse model of 2,4,6-trinitrobenesulfonic acid (TNBS)-induced colitis. A recombinant adenoviral vector was used to upregulate KLF11 expression in the mouse models and the changes in intestinal inflammation was observed. A Caco-2 cell model with stable KLF11 overexpression was constructed by lentiviral infection. The effect of KLF11 overexpression on expressions of JAK2/STAT3 signaling pathway proteins was investigated using immunoblotting in both the mouse and cell models. The mouse models were treated with coumermycin A1, a JAK2/STAT3 signaling pathway agonist, and the changes in intestinal inflammatory responses were observed. Results The expression level of KLF11 was significantly lowered in both the clinical specimens of diseased colon mucosal tissues and the colon tissues of mice with TNBS-induced colitis (P<0.05). Adenovirus-mediated upregulation of KLF11 significantly improved intestinal inflammation and reduced the expression levels of inflammatory factors in the intestinal mucosa of the colitis mouse models (P<0.05). Overexpression of KLF11 significantly inhibited the expression levels of p-JAK2 and p-STAT3 in intestinal mucosal tissues of the mouse models and in Caco-2 cells (P<0.05). Treatment with coumermycin A1 obviously inhibited the effect of KLF11 upregulation for improving colitis and significantly increased the expression levels of inflammatory factors in the intestinal mucosa of the mouse models (P<0.05). Conclusion KLF11 is downregulated in the intestinal mucosa in CD, and upregulation of KLF11 can improve intestinal inflammation and reduce the production of inflammatory factors probably by inhibiting the JAK2/STAT3 signaling pathway.

Objective:To conduct a scoping review on the application of sedentary behavior intervention in chronic disease patients and identify the delivery carriers, intervention time, intervention content and intervention results, so as to provide guidance for health care personnel to carry out relevant intervention research.Methods:Literature was systematically searched in PubMed, Embase, CINAHL, Cochrane Library, China National Knowledge Infrastructure and Wanfang data from establishment of the databases to June 15, 2023. The included literatures were screened, summarized and analyzed.Results:A total of 25 articles were included, among which the delivery carriers of sedentary behavior intervention included offline guidance, wearable device monitoring, telephone follow-up, mobile phone applications, email and website platform. The most common intervention implementers were rehabilitation therapists, followed by nurses, doctors and psychologists. Intervention durations ranged from 4 weeks to 3 years. Behavioral intervention strategies covered eight aspects, including providing information about behavioral consequences, goal setting, action planning, obstacle identification/problem-solving, behavioral feedback, exploring social support, motivational rewards and restructuring the physical environment. The types of outcome indicators for intervention included sedentary time, physical activity time, physiological indicators, psychological indicators, feasibility evaluation and safety evaluation. The results showed that sedentary behavior intervention not only reduced sedentary behavior in patients with chronic diseases, but also affected their quality of life and self-efficacy.Conclusions:Sedentary behavior intervention has positive effects on sedentary behavior, physical activity, physical health and mental health of patients with chronic diseases. Future research should strengthen the development and application of mobile phone applications and strengthen environmental intervention to further improve the intervention effect.