Objective: To analyze the etiological surveillance results of influenza-like illness (ILI) cases in Jiangsu Province, and investigate the distribution characteristics of different influenza virus types, so as to provide the evidence for improving influenza prevention and control measures. Methods: Influenza laboratory testing data for sentinel surveillance of ILI cases in Jiangsu Province from 2019 to 2024 were collected through the China Influenza Surveillance Information System. The positive detection rate of influenza virus was calculated, and descriptive analysis was performed to characterize the distribution of different influenza virus types. Using the farthest neighbor linkage method, influenza virus positive detection rates clustering was analyzed by year and week. Clusters were defined based on inter-cluster distance, and the intensity of the positive detection rate was visualized through color gradients in the clustering heatmap. Results: From 2019 to 2024, a total of 183 878 ILI specimens were collected in Jiangsu Province. Among them, 20 059 specimens tested positive for influenza virus, corresponding to an overall positive detection rate of 10.91%, and an average annual positive detection rate of 10.89%. The primary circulating influenza virus types were influenza A H3N2 subtype, accounting for 40.92%, followed by influenza B Victoria linage at 34.00%, and influenza A H1N1 subtype at 24.80%. Influenza B Yamagata linage was not detected throughout the five-year period. Influenza A H3N2 subtype predominated during two distinct periods: from January to March 2019, and from June 2022 to December 2023. Influenz B Victoria linage was the dominant type from April 2019 to May 2022 and again from January to April 2024. Influenza A H1N1 subtype emerged as the primary type from May to December 2024. Year-based clustering analysis grouped the annual positive detection rates from 2019 to 2024 into three clusters. The closest cluster distance was observed between 2019 and 2024. The highest annual positive detection rate occurred in 2023. Both influenza A H3N2 and H1N1 subtype each formed a single cluster, with their peak positive detection rates also recorded in 2023. Influenza B Victoria lineage was separated into two clusters, with its highest positive detection rate occurring in 2020. Week-based clustering analysis revealed that influenza virus detection was concentrated in weeks 47 to 52 and weeks 1 to 15. More specifically, the positive detection rates for influenza A H3N2 subtype peaked during weeks 30 to 34 and weeks 42 to 52; for influenza A H1N1 subtype, during weeks 9 to 15 and weeks 51 to 52; and for influenza B Victoria lineage, during weeks 1 to 11 and weeks 50 to 52. Conclusions From 2019 to 2024, the average annual positive detection rate of influenza virus in Jiangsu Province remained relatively low. Influenza activity characterized by the alternating circulation of influenza A H1N1 subtype, influenza A H3N2 subtype, and influenza B Victoria linage. It is necessary to maintain the surveillance sensitivity for the influenza B Yamagata lineage.

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

Objective To explore the biological function and downstream mechanism of ETS1 in glioma.Methods Bioinformatics and immunohistochemistry were used to analyze the differential expression characteristics of ETS1 in gliomas;qRT-PCR was employed to detect the expression level of ETS1 mRNA and lncRNA X-inactive specific transcript(XIST).CCK-8 and 5-ethyl-2′-deoxyuridine experiments were conducted to detect cell growth.Western blot was used to detect the expression of apoptosis-related proteins(Bax,Bak,Bcl-2).PROMO database was utilized to predict the binding sites between ETS1 and XIST promoter.Dual-luciferase reporter gene assay and chromatin immunoprecipitation-quantitative polymerase chain reaction assays were performed to verify the binding relationship between ETS1 and the XIST promoter region.cBioPortal database was used to analyze the correlation between the expression of ETS1 mRNA and XIST in glioma tissues.Results The expression levels of ETS1 mRNA and protein were significantly upregulated in glioma(P<0.05).The depletion of ETS1 significantly inhibited the proliferation of glioma cells and promoted cell apoptosis(P<0.05).ETS1 could target and bind with the XIST promoter and promote the expression of XIST(P<0.05).The overexpression of XIST reversed the effects of ETS1 on the proliferation of glioma cells and the promotion of cell apoptosis(P<0.05).Conclusion ETS1 is highly expressed in glioma tissues.It could promote the expression of lncRNA XIST,boost the proliferation of glioma cells,and inhibit cell apoptosis.

Objective: To investigate the effects of plateau environment exposure on the reproductive system of male rats, so as to provide the reference for mechanisms of reproductive damage in plateau environment. Methods: Sixty SPF-grade 12-week-old male Wistar rats were randomly divided into the plain-exposed group, the 1 day-, 3 day-, 7 day-, 14 day- and 28 day- plateau-exposed groups. The rats in the plain-exposed group were raised under normal conditions for 28 days, while the rats in the plateau-exposed groups were raised in a simulated high-altitude plateau chamber. After the completion of the designated feeding periods, the rats were sacrificed under anesthesia, and testicular tissue and abdominal aortic blood were collected to detect the testicular index and evaluate sperm quality. Histological and cellular morphologies of the testicular tissue were analyzed. Additionally, the levels of malondialdehyde (MDA), superoxide dismutase (SOD) and reactive oxygen (ROS) in the testicular tissue were determined, along with serum levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH) and testosterone (T). Conclusions Plateau environment may cause a decrease in testicular index and sperm quality, impair mitochondrial function, induce oxidative stress, and thus affect reproductive system of male rats. However, there are signs of self-repair in the reproductive system with the increase of exposure duration.

[摘 要] 目的：研究芳香烃受体（AHR）在乳腺癌中的表达及其对乳腺癌细胞增殖、凋亡和药物敏感性的调控机制。方法：通过GEPIA数据库数据分析乳腺癌组织及癌旁组织中AHR的表达水平，探讨其与患者生存期的关联。利用基因敲低和过表达技术构建AHR表达变化的乳腺癌细胞，采用CCK-8实验、细胞计数和流式细胞分析等方法评估AHR对细胞增殖、凋亡和药物敏感性的影响，通过免疫印迹法验证相关分子机制。此外，利用AHR激动剂6-甲酰基吲哚并[3,2-B]咔唑（FICZ）研究外源性激活AHR对乳腺癌细胞多柔比星（DOX）敏感性的影响。结果：GEPIA数据库数据分析结果显示，乳腺癌组织中AHR呈明显低表达（P < 0.05）；对155例乳腺癌患者的生存期进行统计分析也显示AHR低表达与不良预后呈正相关（P < 0.05）。敲低AHR促进细胞增殖（P < 0.05），过表达则能抑制其增殖（P < 0.05）并促进其凋亡（P < 0.05）。外源激活AHR能增强乳腺癌细胞对DOX的敏感性（P < 0.05）。AHR可与MYC基因启动子结合，抑制MYC表达（P < 0.05），从而影响乳腺癌的进展。结论：AHR在乳腺癌中通过调控MYC表达影响细胞增殖和凋亡，外源激活AHR可能成为提高乳腺癌细胞对DOX敏感性的治疗策略。

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.

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.