Objective: To analyze the trends in incidence and mortality of colorectal cancer in Jinhua City, Zhejiang Province from 2016 to 2024, and to predict the incidence and mortality from 2025 to 2027, so as to provide the evidence for improving regional colorectal cancer prevention and control strategies. Methods: Data on incidence and mortality of colorectal cancer in Jinhua City from 2016 to 2024 were collected through the Zhejiang Chronic Disease Surveillance Information Management System. The crude incidence and crude mortality were calculated, and standardized using the data from the Sixth National Population Census in 2010. Trends in incidence and mortality of colorectal cancer from 2016 to 2024 were analyzed using the average annual percent change (AAPC). A grey Markov model was constructed to predict the incidence and mortality of colorectal cancer from 2025 to 2027. Results: From 2016 to 2024, the crude incidence and standardized incidence of colorectal cancer in Jinhua City were 46.90/100 000 and 30.69/100 000, respectively, showing upward trends (AAPC=4.594% and 2.051%, both P<0.05). The crude mortality and standardized mortality were 17.47/100 000 and 10.36/100 000, respectively, and the trends were not statistically significant (both P>0.05). The standardized incidence and standardized mortality of colorectal cancer in males were higher than those in females (35.38/100 000 vs. 25.68/100 000, 11.96/100 000 vs. 8.57/100 000, both P<0.05). The crude incidence and crude mortality of colorectal cancer in the ≥80 years age group were the highest, at 220.04/100 000 and 186.86/100 000, respectively. From 2016 to 2024, the standardized incidence of colorectal cancer in males and females showed upward trends (AAPC=5.069% and 3.965%, both P<0.05), while the trends in standardized mortality were not statistically significant (all P>0.05). The crude incidence in the 70-<80 years age group showed an upward trend (AAPC=1.320%, P<0.05), and the crude mortality in the 40-<50 years age group showed a downward trend (AAPC=-3.756%, P<0.05). Trends in other age groups were not statistically significant (all P>0.05). The prediction results of the grey Markov model showed that the predicted values of crude incidence and crude mortality of colorectal cancer in the whole population would increase from 58.20/100 000 and 20.04/100 000 in 2025 to 61.70/100 000 and 21.26/100 000 in 2027. Conclusions From 2016 to 2024, the incidence of colorectal cancer in Jinhua City showed upward trends, while the mortality trend was stable. Males and the elderly aged ≥80 years are high-risk populations for colorectal cancer incidence and mortality. It is predicted that both crude incidence and crude mortality will increase from 2025 to 2027.

Objective To investigate and analyze the occupational stress levels and influencing factors among radiation workers in China, and provide a reference for alleviating occupational stress and promoting mental health. Methods Using the general situation questionnaire, Effort-Reward Imbalance questionnaire, and radiation protection knowledge questionnaire, a convenience sampling method was adopted to investigate the occupational stress of 243 radiation workers in Liaoning, Fujian, Guangdong, and Xinjiang provinces. The independent samples t-test, one-way analysis of variance, chi-square test, and binary logistic regression were used to analyze the influencing factors. Results The average score of Effort-Reward Imbalance was 0.97 ± 0.22, and 100 (41.15%) radiation workers had occupational stress. There were significant differences in the detection rate of occupational stress among radiation workers of different ages, working years in radiation positions, monthly incomes, daily sleep durations, and daily working hours (P < 0.05). Logistic regression analysis identified daily working hours as a factor contributing to occupational stress. Conclusion The occupational stress among radiation workers in China is relatively severe. It is recommended to pay attention to the associated risks and implement targeted intervention measures to reduce the impact of occupational stress.

Objective: To analyze the trends in incidence and mortality of prostate cancer in Jinhua City, Zhejiang Province from 2016 to 2024, so as to provide the evidence for the improvement of prostate cancer prevention and control measures. Methods: The incidence and mortality data of prostate cancer in Jinhua City from 2016 to 2024 were collected from the Chronic Disease Surveillance Information Management System of Zhejiang Province, and the crude incidence and mortality were calculated. The Chinese Sixth National Population Census in 2010 was used to calculate standardized incidence and mortality. The trends in incidence and mortality of prostate cancer were evaluated using average annual percent change (AAPC). Results: A total of 8 357 cases of prostate cancer were diagnosed in Jinhua City from 2016 to 2024. The crude incidence and standardized incidence were 37.36/100 000 and 21.17/100 000, respectively, showing upward trends (AAPC=16.275%, 12.511%, both P<0.05). There were 1 615 deaths of prostate cancer, and the crude mortality was 7.22/100 000, showing an upward trend (AAPC=5.451%, P<0.05). The standardized mortality was 3.49/105, and the trend showed no statistically significant (P>0.05). There were 28 cases of prostate cancer in individuals under 50 years old, accounting for 0.34%. The crude incidence and crude mortality of patients aged ≥50 years increased with age (both P<0.05). From 2016 to 2024, the crude incidence of prostate cancer in the 50-<60, 60-<70, 70-<80, and ≥80 age groups showed upward trends (AAPC=17.849%, 14.704%, 12.654% and 8.081%, all P<0.05), and the 50-<60 age group increased more quickly. There was no significant change in the crude mortality of prostate cancer among different age groups (all P>0.05). Conclusion From 2016 to 2024, the incidence of prostate cancer in Jinhua City showed an upward trend and had a trend of becoming younger, while the mortality remained relatively stable.

BACKGROUND: Children's respiratory health demonstrates particular sensitivity to air pollution. Existing evidence investigating the association between short-term ozone (O₃) exposure and childhood pneumonia remains insufficient and inconsistent, especially in low- and middle-income countries (LMICs). METHOD: To provide more reliable and persuasive evidence, we implemented a multi-city, time-stratified case-crossover design with a large sample size, using data from seven representative children's hospitals across major geographical regions in China. To avoid the impact of the COVID-19 pandemic, individual-level medical records of inpatient children under 6 years of age diagnosed with pneumonia during 2016-2019 were collected. Conditional logistic regression models were fitted for each city, and city-specific estimates were pooled through a meta-analysis using a random-effects model. RESULTS: In total, the study included 137,470 pediatric pneumonia hospital admissions. The highest pooled estimate for O₃ occurred at lag0-1, with a 10 µg/m³ increase in O₃ associated with a 1.57% (95% CI: 0.67%-2.48%) higher risk of pediatric pneumonia hospital admissions. Stratified analyses indicated that the effects of O₃ were robust across different sexes, age groups, and admission seasons. We also observed a statistically significant increase in risk associated with O₃ concentrations exceeding the World Health Organization Air Quality Guidelines (WHO-AQGs). CONCLUSIONS This study revealed a significant positive association between O₃ and pediatric pneumonia hospital admissions. Our findings substantially strengthen the evidence base for the adverse health impacts of O₃, underscoring the importance of O₃ pollution control and management in reducing the public health burden of pediatric pneumonia.
Humans ; Ozone/analysis* ; China/epidemiology* ; Pneumonia/chemically induced* ; Child, Preschool ; Male ; Female ; Infant ; Cross-Over Studies ; Air Pollutants/analysis* ; Hospitalization/statistics & numerical data* ; Child ; Cities/epidemiology* ; Air Pollution/adverse effects* ; Infant, Newborn ; Environmental Exposure/adverse effects*

ObjectiveThe human angiotensin converting enzyme2 （hACE2） transgenic mouse model was used to clarify the antiviral efficacy of BD-77 against a novel coronavirus SARS-CoV-2 and explore the action mechanism of BD-77 against SARS-CoV-2. MethodSARS-CoV-2 Omicron and Delta variant strains-infected VeroE6 cell models were established and administered with BD-77 to observe the antiviral effect of BD-77 in vitro. A kit was used to detect the effect of BD-77 in vitro on the binding of spike S protein of SARS-CoV-2 virus （Delta/Omicron） to angiotensin converting enzyme2 （ACE2）. Chromatography was adopted to detect the binding of BD-77 to the S protein and N protein of the novel coronavirus. hACE2 transgenic C57BL/6 mice were divided into a blank control group， SARS-CoV-2 infection group， BD-77 administration groups of 37.5 mg·kg^-1 and 75 mg·kg^-1， with eight mice in each group. The pneumonia model of SARS-CoV-2-infected hACE2 transgenic mice was built to observe the survival of the mice， detect the virus titer of the lung tissue of the mice， and observe the lesions in the lung tissue. ResultBD-77 had a certain inhibitory effect on Omicron and Delta variant strains in vitro， with median inhibitory concentration （IC₅₀） of 526.3 mg·L^-1 and 653.0 mg·L^-1， respectively. BD-77 had no significant inhibitory effect on the binding of the S protein of WT， Omicron， and Delta variant strains of SARS-CoV-2 to ACE2 and had no binding effect with the S protein and N protein of the novel coronavirus. No mice in the blank group died， while the mortality rate of SARS-CoV-2-infected mice was 75%. There was a large amount of virus replication in the lung tissue of the mice and large areas of inflammatory infiltration in the lung tissue and interstitium. Compared with the model group， BD-77 administration groups of 37.5 mg·kg^-1 and 75 mg·kg^-1 could reduce the mortality of mice， significantly lower the virus titer in the lung tissue of mice （P<0.05）， and improve lung lesions. ConclusionBD-77 demonstrated significant inhibitory effects against SARS-CoV-2 virus in vitro and in vivo. However， its mechanism of action did not involve direct inhibition of the virus itself or intervention in the virus-host binding process. This finding suggests that the mechanism of action of BD-77 needs to be thoroughly investigated and elucidated by further experiments.

ObjectiveTo observe the therapeutic effect of BD-77 by nebulized inhalation on animal models of various respiratory viral infections and investigate the mechanism of broad-spectrum antiviral action of BD-77 using proteomics. MethodThe influenza virus H1N1/FM1 experiment used ICR mice and divided them into a normal group， model group， Tamiflu group， and BD-77 groups of 75 and 37.5 g·L^-1 for inhalation of 20 min and 25 min. Human coronavirus 229E and OC43 experiment divided the BALB/c mice into a normal group， model group， chloroquine phosphate group， and BD-77 groups of 75， 37.5， 18.75， and 9.375 g·L^-1， with 10 mice in each group. Influenza virus H1N1/FM1 and human coronaviruses 229E and OC43 infection-induced pneumonia models were used to detect mouse lung index， and real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to detect the viral load in lung tissue. Enzyme-linked immunosorbent assay （ELISA） was used to detect related inflammatory factors in lung tissue， and proteomics analysis was performed on the lung tissue of OC43-infected mice. ResultCompared with that in the normal group， the lung index of mice in each infection group was significantly increased （P<0.01）， and viral nucleic acid could be detected in the lung tissue of mice infected with human coronaviruses 229E and OC43. The levels of interleukin-6 （IL-6）， IL-10， and tumor necrosis factor-α （TNF-α） in the lung tissue of mice infected with human coronavirus 229E were all significantly increased （P<0.01）. BD-77 could significantly reduce the lung index of mice infected with influenza virus H1N1/FM1 and human coronaviruses 229E and OC43 （P<0.05， P<0.01）， cut down the viral load in the lungs of mice infected with human coronaviruses 229E and OC43 （P<0.01）， and lower the contents of IL-6， IL-10， and TNF-α in the lung tissue of mice infected with human coronavirus 229E （P<0.01）. Proteomics analysis of the lung tissue of OC43-infected mice showed that BD-77 regulated the AMPK signaling pathway， TNF signaling pathway， NOD-like signaling pathway， IL-17 signaling pathway， Forkhead box protein O （FoxO） signaling pathway， transforming growth factor-β （TGF-β） signaling pathway， and other signaling pathways. ConclusionNebulized inhalation of BD-77 is effective in treating pneumonia caused by influenza virus H1N1/FM1 and human coronaviruses 229E and OC43 infection in mice and may exert its antiviral effects by regulating the balance of cellular metabolism， enhancing the immune function of the host， and attenuating inflammatory responses.

Pyroptosis, an inflammatory caspase-dependent programmed cell death, plays a vital role in maintaining tissue homeostasis and activating inflammatory responses. Orthodontic tooth movement (OTM) is an aseptic force-induced inflammatory bone remodeling process mediated by the activation of periodontal ligament (PDL) progenitor cells. However, whether and how force induces PDL progenitor cell pyroptosis, thereby influencing OTM and alveolar bone remodeling remains unknown. In this study, we found that mechanical force induced the expression of pyroptosis-related markers in rat OTM and alveolar bone remodeling process. Blocking or enhancing pyroptosis level could suppress or promote OTM and alveolar bone remodeling respectively. Using Caspase-1^-/- mice, we further demonstrated that the functional role of the force-induced pyroptosis in PDL progenitor cells depended on Caspase-1. Moreover, mechanical force could also induce pyroptosis in human ex-vivo force-treated PDL progenitor cells and in compressive force-loaded PDL progenitor cells in vitro, which influenced osteoclastogenesis. Mechanistically, transient receptor potential subfamily V member 4 signaling was involved in force-induced Caspase-1-dependent pyroptosis in PDL progenitor cells. Overall, this study suggested a novel mechanism contributing to the modulation of osteoclastogenesis and alveolar bone remodeling under mechanical stimuli, indicating a promising approach to accelerate OTM by targeting Caspase-1.
Animals ; Humans ; Mice ; Rats ; Bone Remodeling/physiology* ; Caspase 1 ; Periodontal Ligament ; Pyroptosis ; Tooth Movement Techniques

Pyroptosis,an inflammatory caspase-dependent programmed cell death,plays a vital role in maintaining tissue homeostasis and activating inflammatory responses.Orthodontic tooth movement(OTM)is an aseptic force-induced inflammatory bone remodeling process mediated by the activation of periodontal ligament(PDL)progenitor cells.However,whether and how force induces PDL progenitor cell pyroptosis,thereby influencing OTM and alveolar bone remodeling remains unknown.In this study,we found that mechanical force induced the expression of pyroptosis-related markers in rat OTM and alveolar bone remodeling process.Blocking or enhancing pyroptosis level could suppress or promote OTM and alveolar bone remodeling respectively.Using Caspase-1-/-mice,we further demonstrated that the functional role of the force-induced pyroptosis in PDL progenitor cells depended on Caspase-1.Moreover,mechanical force could also induce pyroptosis in human ex-vivo force-treated PDL progenitor cells and in compressive force-loaded PDL progenitor cells in vitro,which influenced osteoclastogenesis.Mechanistically,transient receptor potential subfamily V member 4 signaling was involved in force-induced Caspase-1-dependent pyroptosis in PDL progenitor cells.Overall,this study suggested a novel mechanism contributing to the modulation of osteoclastogenesis and alveolar bone remodeling under mechanical stimuli,indicating a promising approach to accelerate OTM by targeting Caspase-1.

Pyroptosis,an inflammatory caspase-dependent programmed cell death,plays a vital role in maintaining tissue homeostasis and activating inflammatory responses.Orthodontic tooth movement(OTM)is an aseptic force-induced inflammatory bone remodeling process mediated by the activation of periodontal ligament(PDL)progenitor cells.However,whether and how force induces PDL progenitor cell pyroptosis,thereby influencing OTM and alveolar bone remodeling remains unknown.In this study,we found that mechanical force induced the expression of pyroptosis-related markers in rat OTM and alveolar bone remodeling process.Blocking or enhancing pyroptosis level could suppress or promote OTM and alveolar bone remodeling respectively.Using Caspase-1-/-mice,we further demonstrated that the functional role of the force-induced pyroptosis in PDL progenitor cells depended on Caspase-1.Moreover,mechanical force could also induce pyroptosis in human ex-vivo force-treated PDL progenitor cells and in compressive force-loaded PDL progenitor cells in vitro,which influenced osteoclastogenesis.Mechanistically,transient receptor potential subfamily V member 4 signaling was involved in force-induced Caspase-1-dependent pyroptosis in PDL progenitor cells.Overall,this study suggested a novel mechanism contributing to the modulation of osteoclastogenesis and alveolar bone remodeling under mechanical stimuli,indicating a promising approach to accelerate OTM by targeting Caspase-1.

Pyroptosis,an inflammatory caspase-dependent programmed cell death,plays a vital role in maintaining tissue homeostasis and activating inflammatory responses.Orthodontic tooth movement(OTM)is an aseptic force-induced inflammatory bone remodeling process mediated by the activation of periodontal ligament(PDL)progenitor cells.However,whether and how force induces PDL progenitor cell pyroptosis,thereby influencing OTM and alveolar bone remodeling remains unknown.In this study,we found that mechanical force induced the expression of pyroptosis-related markers in rat OTM and alveolar bone remodeling process.Blocking or enhancing pyroptosis level could suppress or promote OTM and alveolar bone remodeling respectively.Using Caspase-1-/-mice,we further demonstrated that the functional role of the force-induced pyroptosis in PDL progenitor cells depended on Caspase-1.Moreover,mechanical force could also induce pyroptosis in human ex-vivo force-treated PDL progenitor cells and in compressive force-loaded PDL progenitor cells in vitro,which influenced osteoclastogenesis.Mechanistically,transient receptor potential subfamily V member 4 signaling was involved in force-induced Caspase-1-dependent pyroptosis in PDL progenitor cells.Overall,this study suggested a novel mechanism contributing to the modulation of osteoclastogenesis and alveolar bone remodeling under mechanical stimuli,indicating a promising approach to accelerate OTM by targeting Caspase-1.