Objective To investigate the effects of low-dose ionizing radiation on the thyroid status and hormone levels of radiation workers. Methods Radiation workers who underwent occupational health examinations at a hospital in Guangzhou from 2015 to 2022 were selected as the subjects of this study. The levels of FT3, FT4 and TSH were analyzed, and the thyroid abnormality status of radiation workers in different groups were compared. Results A total of 1152 participants were included in this study, consisting of 885 (76.82%) males and 267 (23.18%) females, with an average age of (35.26 ± 10.16) years. The prevalence of thyroid abnormalities was 9.38%, which was significantly higher in females (13.86%) than in males (8.02%) (P < 0.05). The TSH level of females [(2.15 ± 1.29) mIU/L] was higher than that of males [(1.85 ± 1.20) mIU/L], while the levels of FT3 [(5.10 ± 0.64) pmol/L] and FT4 [(15.84 ± 2.32) pmol/L] in females were lower than those in males [(5.23 ± 0.63) pmol/L and (16.61 ± 2.75) pmol/L, P < 0.05]. The FT3 of industrial workers [(5.25 ± 0.63) pmol/L] was higher than that of medical workers [(5.10 ± 0.63) pmol/L], while the TSH of industrial workers [(1.80 ± 1.12) mIU/L] was lower than that of medical workers [(2.15 ± 1.37) mIU/L]. FT4 levels decreased with increasing age and duration of occupational exposure. Multivariable logistic regression analysis revealed that sex was a significant independent predictor of thyroid abnormalities among radiation workers. Female workers were more likely to experience thyroid abnormalities (β = −0.62, P < 0.05). Conclusion Low-dose ionizing radiation may have a certain impact on the thyroid status of radiation workers, especially for female workers, which requires further attention and research.

Background: Nasopharyngeal carcinoma (NPC) is characterized by high programmed death-ligand 1 (PD-L1) expression and abundant infiltration of non-malignant lymphocytes, which renders patients potentially suitable candidates for immune checkpoint blockade therapies. Palate, lung, and nasal epithelium clone (PLUNC) inhibit the growth of NPC cells and enhance cellular apoptosis and differentiation. Currently, the relationship between PLUNC (as a tumor-suppressor) and PD-L1 in NPC is unclear. Methods: We collected clinical samples of NPC to verify the relationship between PLUNC and PD-L1. PLUNC plasmid was transfected into NPC cells, and the variation of PD-L1 was verified by western blot and immunofluorescence. In NPC cells, we verified the relationship of PD-L1, activating transcription factor 3 (ATF3), and β-catenin by western blot and immunofluorescence. Later, we further verified that PLUNC regulates PD-L1 through β-catenin. Finally, the effect of PLUNC on β-catenin was verified by co-immunoprecipitation (Co-IP). Results: We found that PLUNC expression was lower in NPC tissues than in paracancer tissues. PD-L1 expression was opposite to that of PLUNC. Western blot and immunofluorescence showed that β-catenin could upregulate ATF3 and PD-L1, while PLUNC could downregulate ATF3/PD-L1 by inhibiting the expression of β-catenin. PLUNC inhibits the entry of β-catenin into the nucleus. Co-IP experiments demonstrated that PLUNC inhibited the interaction of DEAD-box helicase 17 (DDX17) and β-catenin. Conclusions PLUNC downregulates the expression of PD-L1 by inhibiting the interaction of DDX17/β-catenin in NPC.

Background: Nasopharyngeal carcinoma (NPC) is characterized by high programmed death-ligand 1 (PD-L1) expression and abundant infiltration of non-malignant lymphocytes, which renders patients potentially suitable candidates for immune checkpoint blockade therapies. Palate, lung, and nasal epithelium clone (PLUNC) inhibit the growth of NPC cells and enhance cellular apoptosis and differentiation. Currently, the relationship between PLUNC (as a tumor-suppressor) and PD-L1 in NPC is unclear. Methods: We collected clinical samples of NPC to verify the relationship between PLUNC and PD-L1. PLUNC plasmid was transfected into NPC cells, and the variation of PD-L1 was verified by western blot and immunofluorescence. In NPC cells, we verified the relationship of PD-L1, activating transcription factor 3 (ATF3), and β-catenin by western blot and immunofluorescence. Later, we further verified that PLUNC regulates PD-L1 through β-catenin. Finally, the effect of PLUNC on β-catenin was verified by co-immunoprecipitation (Co-IP). Results: We found that PLUNC expression was lower in NPC tissues than in paracancer tissues. PD-L1 expression was opposite to that of PLUNC. Western blot and immunofluorescence showed that β-catenin could upregulate ATF3 and PD-L1, while PLUNC could downregulate ATF3/PD-L1 by inhibiting the expression of β-catenin. PLUNC inhibits the entry of β-catenin into the nucleus. Co-IP experiments demonstrated that PLUNC inhibited the interaction of DEAD-box helicase 17 (DDX17) and β-catenin. Conclusions PLUNC downregulates the expression of PD-L1 by inhibiting the interaction of DDX17/β-catenin in NPC.

Background Air pollution remains a critical public health issue, with persistent exposure to air pollutants continuing to pose significant health risks. Currently, research investigating the association between air pollution and myocardial infarction mortality in Shenzhen remains inadequate. Objective To quantitatively assess the association between air pollutants and myocardial infarction mortality in residents. Methods Based on the mortality surveillance system of Shenzhen Center for Disease Control and Prevention, we conducted a time-stratified case-crossover study of 10089 permanent residents who died from myocardial infarction in Shenzhen between 2013 and 2022. Using residential address information, we obtained individual-level exposure data for air pollutants from the China High Air Pollutants dataset and meteorological factors from the China Meteorological Administration Land Data Assimilation System. A time-stratified case-crossover study design was employed to construct a conditional logistic regression model to assess the association between short-term exposure to air pollutants and myocardial infarction mortality. The exposure-response relationship was visualized, and a comprehensive health risk assessment was performed. Results This study included a total of 10 089 cases of myocardial infarction deaths in Shenzhen. The median [interquartile range (IQR)] concentrations of fine particulate matter (PM_2.5), inhalable particulate matter (PM₁₀), sulfur dioxide (SO₂), nitrogen dioxide (NO₂), carbon monoxide (CO), and ozone (O₃) in Shenzhen from 2013 to 2022 were 24.59 (20.19) μg·m⁻³, 42.85 (28.42) μg·m⁻³, 8.53 (3.39) μg·m⁻³, 29.47 (13.56) μg·m⁻³, 0.77 (0.27) mg·m⁻³, and 86.53 (51.39) μg·m⁻³, respectively. The moving average concentrations of PM_2.5 and PM₁₀ over the current day and the previous 2 days (lag02) showed the highest risk of myocardial infarction mortality, with an odds ratio (OR) and 95% confidence interval (95%CI) of 1.004 (1.001, 1.007) and 1.004 (1.002, 1.006), respectively. At lag05, SO₂ demonstrated the strongest association with the risk of myocardial infarction mortality, with an OR (95%CI) of 1.042 (1.019, 1.065). The exposure-response relationships of PM_2.5, PM₁₀, and SO₂ with myocardial infarction mortality were approximately linear, whereas NO₂ exhibited a nonlinear relationship. At lag05, the highest risk of myocardial infarction mortality associated with NO₂ exposure was observed when the NO₂ concentration was ≤21.92 μg·m⁻³, with an OR (95% CI) of 1.024 (1.003, 1.046). The health risk assessment indicated that, using the WHO Air Quality Guidelines as the reference, the local PM_2.5 and NO₂ exposure led to an excess mortality of 398 and 298 cases, respectively. The sensitivity analysis revealed that after adjusting for O₃ and restricting the study period to 2013—2019, the effect estimates for PM_2.5, PM₁₀, NO₂, and SO₂ on myocardial infarction mortality slightly increased. Conclusion Short-term exposure to air pollutants, including PM_2.5, PM₁₀, NO₂, and SO₂, could increase the risk of myocardial infarction mortality. This study provides important scientific evidence for environmental health risk assessment and environmental management in Shenzhen.

Background: Nasopharyngeal carcinoma (NPC) is characterized by high programmed death-ligand 1 (PD-L1) expression and abundant infiltration of non-malignant lymphocytes, which renders patients potentially suitable candidates for immune checkpoint blockade therapies. Palate, lung, and nasal epithelium clone (PLUNC) inhibit the growth of NPC cells and enhance cellular apoptosis and differentiation. Currently, the relationship between PLUNC (as a tumor-suppressor) and PD-L1 in NPC is unclear. Methods: We collected clinical samples of NPC to verify the relationship between PLUNC and PD-L1. PLUNC plasmid was transfected into NPC cells, and the variation of PD-L1 was verified by western blot and immunofluorescence. In NPC cells, we verified the relationship of PD-L1, activating transcription factor 3 (ATF3), and β-catenin by western blot and immunofluorescence. Later, we further verified that PLUNC regulates PD-L1 through β-catenin. Finally, the effect of PLUNC on β-catenin was verified by co-immunoprecipitation (Co-IP). Results: We found that PLUNC expression was lower in NPC tissues than in paracancer tissues. PD-L1 expression was opposite to that of PLUNC. Western blot and immunofluorescence showed that β-catenin could upregulate ATF3 and PD-L1, while PLUNC could downregulate ATF3/PD-L1 by inhibiting the expression of β-catenin. PLUNC inhibits the entry of β-catenin into the nucleus. Co-IP experiments demonstrated that PLUNC inhibited the interaction of DEAD-box helicase 17 (DDX17) and β-catenin. Conclusions PLUNC downregulates the expression of PD-L1 by inhibiting the interaction of DDX17/β-catenin in NPC.

Tumor cells use glycolysis to provide material and energy under hypoxic conditions to meet the energy requirements for rapid growth and proliferation， namely the Warburg effect. Even under aerobic conditions， tumor cells mainly rely on glycolysis to provide energy. Therefore， glucose transporter protein 1（GLUT1）， which is involved in the process of glucose metabolism， plays an important role in tumorigenesis， development and drug resistance， and is considered to be one of the important targets in the treatment of malignant tumors. In recent years， research on tumor glucose metabolism has gradually become a hot spot. It has been shown that various factors are involved in the regulation of tumor energy metabolism， among which the role of GLUT1 is the most critical. In this paper， the authors reviewed the latest research progress of GLUT1-targeted traditional Chinese medicine（TCM） active ingredient nano-delivery system in tumor therapy， aiming to reveal the feasibility and effectiveness of this system in the delivery of chemotherapeutic drugs. The GLUT1-targeted TCM active ingredient nano-delivery system can overcome the bottleneck of the traditional targeting strategy as well as the high-permeability long retention（EPR） effect. In summary， the authors believe that the GLUT1-targeted TCM active ingredient nano-delivery system provides a new strategy for targeted treatment of tumors and has a broad application prospect in tumor prevention and treatment.

Globally, the incidence of early-onset colorectal cancer (EOCRC) among individuals younger than 50 is escalating. Compared to late-onset colorectal cancer, EOCRC exhibits distinct clinical, pathological, and molecular features, with a higher prevalence in the left colon and rectum. However, the occurrence and development of EOCRC is a multi-factor and multi-stage evolution process, which is the result of the mutual effect of environmental, genetic and biological factors, and involves the multi-level regulation mechanism of other organisms. With the development and improvement of high-throughput sequencing technology, the application of multi-omics analysis has become an important development direction to resolve the pathogenesis of complex diseases and individualized treatment plans. This article aims to review the research progress of EOCRC at the multi-omics level, providing a theoretical foundation for earlier diagnosis and more precise treatment of this diseases.

Objective To evaluate the precision and effectiveness of ultrasound-guided visualization for nasojejunal tube placement with the"R(right reclining)-S(shoulder)-A(abdominal)"3-point positioning for critically ill patients.Methods A retrospective analysis was conducted on all critically ill patients who underwent nasojejunal tube placement in Department of Critical Medicine of a tertiary hospital in Chongqing from April 2022 to August 2023.According to the position of the catheter,they were divided into a control group and an observation group.The control group received ultrasound-guided nasojejunal tube insertion,while the observation group used the"R-S-A"3-point positioning (the patient were placed in a right lateral position,the nurse stood at the right shoulder of the patient,and the ultrasound operator stood on the right side of the abdomen in the operating direction)for ultrasound-guided nasojejunal tube insertion.And,the control group had no specific requirements for positioning during the procedure.After propensity matching,the time and success rate of catheter insertion and incidence of complications were compared between the 2 groups.Results The time of catheter insertion was significantly shorter (36.2±10.3 vs 42.3±8.3 min),and the success rate of insertion was obviously higher (95.2％ vs 66.7％)in the observation group when compared with the control group (P<0.05).The incidence of complication was 9.5％ in the observation group,and 28.6％ in the control group,but there was no statistical difference between the 2 groups.Conclusion Ultrasound-guided nasojejunal tube placement based on "R-S-A"3-point positioning has high precision and strong effectiveness in critically ill patients,which can shorten the time and improve the success rate of catheter insertion.

AIM:To investigate the effects of the compound ANBP on wound healing in diabetic rats and ex-plore its mechanism of action.METHODS:Ninety male SD rats were randomly divided into blank,model,compound ANBP,Beifuxin,and nicotinamide mononucleotide(NMN)groups,with 16 rats in each group.Wound healing in each group was observed and samples were taken on days 3,7 and 14 to analyze the wound healing rate.Local histopathological changes were observed using HE and Masson staining.The expressions of pyruvate dehydrogenase E1 subunit alpha 1(PDHA1),citrate synthase(CS),isocitrate dehydrogenase(IDH1)and oxoglutarate dehydrogenase(OGDH)were de-tected through immunofluorescence and Western blot.The number and morphology of mitochondria in the wound tissue were observed using transmission electron microscopy.RESULTS:Histomorphological changes revealed significant im-provement in diabetic wound healing in the blank and compound ANBP groups compared to that of the model group.The wound healing rates of the blank,compound ANBP,Beifuxin,and NMN groups were significantly increased on days 3,7,and 14(P<0.01).Compared to the model group,granulation tissue generation was higher in the other groups,cover-ing the wound defect and producing abundant collagen fibers.At 3,7,and 14 days after intervention,the blank,com-pound ANBP,Beifuxin,and NMN groups showed significantly enhanced fluorescence intensities of TCA cycling-related enzymes PDHA1,CS,IDH1,and OGDH indicating increased expression of these enzymes.The levels of the TCA cy-cling-related enzymes were significantly increased(P<0.01)in the compound ANBP,Beifuxin and NMN groups but were significantly decreased(P<0.01)in the model group.An increase in the number and density of mitochondria and a de-crease in the cavitation rate of mitochondria with improved morphology(P<0.05)was observed in the group treated with compound ANBP.CONCLUSION:Compound ANBP may increase the number of mitochondria,improve mitochondrial morphology and function,upregulate the expression levels of PDHA1,CS,IDH1,and OGDH proteins,and accelerate the regeneration of wound granulation tissue,thus promoting the healing of diabetic wounds in rats.

Globally, the incidence of early-onset colorectal cancer (EOCRC) among individuals younger than 50 is escalating. Compared to late-onset colorectal cancer, EOCRC exhibits distinct clinical, pathological, and molecular features, with a higher prevalence in the left colon and rectum. However, the occurrence and development of EOCRC is a multi-factor and multi-stage evolution process, which is the result of the mutual effect of environmental, genetic and biological factors, and involves the multi-level regulation mechanism of other organisms. With the development and improvement of high-throughput sequencing technology, the application of multi-omics analysis has become an important development direction to resolve the pathogenesis of complex diseases and individualized treatment plans. This article aims to review the research progress of EOCRC at the multi-omics level, providing a theoretical foundation for earlier diagnosis and more precise treatment of this diseases.