Objective: To investigate the trends in incidence and mortality of thyroid cancer in Nantong City, Jiangsu Province from 2013 to 2022, so as to provide a basis for optimizing comprehensive regional prevention and control strategies. Methods: Data on incidence and mortality of thyroid cancer in Nantong City from 2013 to 2022 were collected via the Nantong Cancer Registration Reporting System. Crude incidence and mortality were calculated. The Chinese population-standardized incidence and Chinese population-standardized mortality were calculated using the standard age structure from the Fifth National Population Census in 2000. The average annual percent change (AAPC) was used to analyze the trends in incidence and mortality of thyroid cancer across different genders, age groups, and urban-rural areas from 2013 to 2022. Results: The crude incidence and Chinese population-standardized incidence in Nantong City rose from 5.79/100 000 and 4.36/100 000 in 2013 to 34.87/100 000 and 30.40/100 000 in 2022, respectively (AAPC=22.226%, 24.139%, both P<0.05). The crude mortality increased from 0.39/100 000 to 1.07/100 000 (AAPC=10.469%, P<0.05), while the trend for Chinese population-standardized mortality was not statistically significant (P>0.05). The Chinese population-standardized incidence and Chinese population-standardized mortality for females were 20.41/100 000 and 0.30/100 000, respectively, which were 3.28 times and 1.50 times those of males. The Chinese population-standardized incidence showed upward trends for both males and females (AAPC=22.840%, 24.592%, both P<0.05), while the trends for Chinese population-standardized mortality were not statistically significant (both P>0.05). From 2013 to 2022, the crude incidence in the age groups of 15-<45, 45-<65, and 65-<85 years, and the crude mortality in the age group of 65-<85 years showed upward trends (AAPC=27.808%, 21.756%, 13.365%, and 8.030%, all P<0.05), while trends in other age groups were not statistically significant (all P>0.05). The Chinese population-standardized incidence in urban areas was 16.96/105, which was 1.40 times that of rural areas. The Chinese population-standardized mortality in rural areas was 0.27/105, which was 1.29 times that of urban areas. From 2013 to 2022, the Chinese population-standardized incidence in both urban and rural areas and Chinese population-standardized mortality in rural areas showed upward trends (AAPC=17.264%, 27.758%, 6.387%, all P<0.05), while trend in Chinese population-standardized mortality in urban areas was not statistically significant (P>0.05). Conclusions From 2013 to 2022, the crude incidence, Chinese population-standardized incidence, and crude mortality of thyroid cancer in Nantong City all showed upward trends in the total population, males, and females, while the trend in Chinese population-standardized mortality was stable. There were differences in mortality trends between urban and rural areas: the trend in urban areas was stable, whereas the trend in rural areas was upward.

ObjectiveTo analyze the comorbidity patterns of chronic metabolic diseases and their influencing factors among residents aged 35‒75 years old in Nantong City of Jiangsu Province, and to provide theoretical support for the prevention and control of comorbidities. MethodsThe permanent residents aged 35‒75 years from the Comprehensive Prevention and Control Project of Cardiovascular and Cerebrovascular Diseases in Nantong City from 2021 to 2024 were selected as the research subjects. Clustering analysis and association rule were used to investigate the comorbidity patterns of chronic metabolic diseases, and their influencing factors were identified through logistic regression analyses. ResultsThe prevalence of comorbidity of chronic metabolic diseases among residents aged 35‒75 years in Nantong City was 47.40%. Among comorbidity patterns based on disease counts, the prevalence of hypertension+dyslipidemia was highest in binary comorbidity patterns (6.25%), while that of hypertension+dyslipidemia+obesity was highest in ternary comorbidity patterns (4.01%). Association rules showed that in both binary and ternary comorbidity patterns, the confidence level was highest for obesity+hypertension (72.70%) and obesity+dyslipidemia+hypertension (74.54%). Renal insufficiency formed an independent cluster in cluster analyses. Logistic regression analyses revealed that, compared with the non-comorbidity group, males (OR=2.22, 95%CI: 1.69‒2.91), advanced age (45‒54 years, OR=1.38, 95%CI: 1.02‒1.88; 55‒64 years, OR=1.59, 95%CI: 1.14‒2.23; 65‒75 years, OR=2.34, 95%CI: 1.58‒3.47), and low physical activity (OR=1.26, 95%CI: 1.10‒1.65) were influencing factors for metabolic disease comorbidity. ConclusionIn the comorbidity patterns of chronic metabolic diseases among residents aged 35‒75 years in Nantong City, hypertension, diabetes mellitus, and dyslipidemia interact with each other. Individuals with obesity are more prone to diseases such as hypertension and dyslipidemia. Prevention and control of chronic metabolic diseases should be strengthened for males, individuals with low physical activity and advanced age.

BACKGROUND: Alpha-glucosidase inhibitors or dipeptidyl peptidase-4 inhibitors are both hypoglycemia agents that specifically impact on postprandial hyperglycemia. We compared the effects of acarbose and sitagliptin add on to metformin on time in range (TIR) and glycemic variability (GV) in Chinese patients with type 2 diabetes mellitus through continuous glucose monitoring (CGM). METHODS: This study was a randomized, open-label, active-con-trolled, parallel-group trial conducted at 15 centers in China from January 2020 to August 2022. We recruited patients with type 2 diabetes aged 18-65 years with body mass index (BMI) within 19-40 kg/m 2 and hemoglobin A1c (HbA1c) between 6.5% and 9.0%. Eligible patients were randomized to receive either metformin combined with acarbose 100 mg three times daily or metformin combined with sitagliptin 100 mg once daily for 28 days. After the first 14-day treatment period, patients wore CGM and entered another 14-day treatment period. The primary outcome was the level of TIR after treatment between groups. We also performed time series decomposition, dimensionality reduction, and clustering using the CGM data. RESULTS: A total of 701 participants received either acarbose or sitagliptin treatment in combination with metformin. There was no statistically significant difference in TIR between the two groups. Time below range (TBR) and coefficient of variation (CV) levels in acarbose users were significantly lower than those in sitagliptin users. Median (25th percentile, 75th percentile) of TBR below target level <3.9 mmol/L (TBR 3.9 ): Acarbose: 0.45% (0, 2.13%) vs . Sitagliptin: 0.78% (0, 3.12%), P = 0.042; Median (25th percentile, 75th percentile) of TBR below target level <3.0 mmol/L (TBR 3.0 ): Acarbose: 0 (0, 0.22%) vs . Sitagliptin: 0 (0, 0.63%), P = 0.033; CV: Acarbose: 22.44 ± 5.08% vs . Sitagliptin: 23.96 ± 5.19%, P <0.001. By using time series analysis and clustering, we distinguished three groups of patients with representative metabolism characteristics, especially in GV (group with small wave, moderate wave and big wave). No significant difference was found in the complexity of glucose time series index (CGI) between acarbose users and sitagliptin users. By using time series analysis and clustering, we distinguished three groups of patients with representative metabolism characteristics, especially in GV. CONCLUSIONS: Acarbose had slight advantages over sitagliptin in improving GV and reducing the risk of hypoglycemia. Time series analysis of CGM data may predict GV and the risk of hypoglycemia. TRIAL REGISTRATION Chinese Clinical Trial Registry: ChiCTR2000039424.
Humans ; Metformin/therapeutic use* ; Sitagliptin Phosphate/therapeutic use* ; Acarbose/therapeutic use* ; Diabetes Mellitus, Type 2/blood* ; Middle Aged ; Male ; Female ; Adult ; Blood Glucose/drug effects* ; Hypoglycemic Agents/therapeutic use* ; Aged ; Glycated Hemoglobin/metabolism* ; Adolescent ; Young Adult ; China ; East Asian People

BACKGROUND: Asthma is a common chronic inflammatory airway disease and intermittent hypoxia is increasingly recognized as a factor that may impact disease progression. The present study investigated whether intermittent hypoxia (IH) could aggravate asthma by promoting hypoxia-inducible factor-1α (HIF-1α)/nucleotide-binding oligomerization domain (NOD)-like receptor pyrin domain-containing protein 3 (NLRP3)/interleukin (IL)-1β-dependent pyroptosis and the inflammatory response and further elucidated the underlying molecular mechanisms involved. METHODS: A total of 49 patients diagnosed with severe bronchial asthma and diagnosed by polysomnography were enrolled at Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, between January 2022 and December 2022, and their general data and induced sputum were collected. BEAS-2B cells were treated with IL-13 and subjected to IH. An ovalbumin (OVA)-treated mouse model was also used to assess the effects of chronic intermittent hypoxia (CIH) on asthma. Pyroptosis, the inflammatory response, and related signalling pathways were assessed in vivo and in vitro . RESULTS: In this study, as the apnoea and hypopnea index (AHI) increased, the proportion of patients with uncontrolled asthma increased. The proportions of neutrophils and the levels of IL-6, IL-8, HIF-1α and NLRP3 in induced sputum were related to the AHI. NLRP3-mediated pyroptosis, which could be mediated by the HIF-1α signalling pathway, was activated in IL-13 plus IH-treated BEAS-2B cells and in the lungs of OVA/CIH mice. HIF-1α downregulation significantly reduced lung pyroptosis and ameliorated neutrophil inflammation by modulating the NLRP3/IL-1β pathway both in vitro and in vivo . Similarly, pretreatment with LW6, an inhibitor of HIF-1α, effectively blocked the generation of inflammatory cytokines in neutrophils. In addition, administration of the NLRP3 activator nigericin obviously increased lung neutrophil inflammation. CONCLUSIONS Obstructive sleep apnoea-hypopnea syndrome (OSAHS) is a risk factor for asthma exacerbation. IH aggravates neutrophil inflammation in asthma via NLRP3/IL-1β-dependent pyroptosis mediated by the HIF-1α signalling pathway, which should be considered a potential therapeutic target for the treatment of asthma with OSAHS.
NLR Family, Pyrin Domain-Containing 3 Protein/metabolism* ; Humans ; Asthma/metabolism* ; Animals ; Pyroptosis/physiology* ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism* ; Mice ; Signal Transduction/physiology* ; Male ; Hypoxia/metabolism* ; Female ; Interleukin-1beta/metabolism* ; Adult ; Inflammation/metabolism* ; Middle Aged ; Mice, Inbred C57BL

BACKGROUND: Epoxyeicosatrienoic acids (EETs), which are metabolites of arachidonic acid catalyzed by cytochrome P450 epoxygenase, are degraded into inactive dihydroxyeicosatrienoic acids by soluble epoxide hydrolase (sEH). Many studies have revealed that sEH gene deletion exerts protective effects against diabetes. Vascular calcification is a common complication of diabetes, but the potential effects of sEH on diabetic vascular calcification are still unknown. METHODS: The level of aortic calcification in wild-type and Ephx2-/- C57BL/6 diabetic mice induced with streptozotocin was evaluated by measuring the aortic calcium content through alizarin red staining, immunohistochemistry staining, and immunofluorescence staining. Mouse vascular smooth muscle cell lines (MOVAS cells) treated with β-glycerol phosphate (0.01 mol/L) plus advanced glycation end products (50 mg/L) were used to investigate the effects of sEH inhibitors or sEH knockdown and EETs on the calcification of vascular smooth muscle cells, which was detected by Western blotting, alizarin red staining, and Von Kossa staining. RESULTS: sEH gene deletion significantly inhibited diabetic vascular calcification by increasing levels of EETs in the aortas of mice. EETs (especially 11,12-EET and 14,15-EET) efficiently prevented the osteogenic transdifferentiation of MOVAS cells by decreasing nidogen-2 (NID2) expression. Interestingly, suppressing sEH activity by small interfering ribonucleic acid or specific inhibitors did not block osteogenic transdifferentiation of MOVAS cells induced by β-glycerol phosphate and advanced glycation end products. NID2 overexpression significantly abolished the inhibitory effect of sEH gene deletion on diabetic vascular calcification. Moreover, NID2 overexpression mediated by adeno-associated virus 9 vectors markedly increased insulin-like growth factor 2 (IGF2) and phospho-ERK1/2 expression in MOVAS cells. Overall, sEH gene knockout inhibited diabetic vascular calcification by decreasing aortic NID2 expression and, then, inactivating the downstream IGF2-ERK1/2 signaling pathway. CONCLUSIONS sEH gene deletion markedly inhibited diabetic vascular calcification through repressed osteogenic transdifferentiation of vascular smooth muscle cells mediated by increased aortic EET levels, which was associated with decreased NID2 expression and inactivation of the downstream IGF2-ERK1/2 signaling pathway.
Animals ; Mice ; Vascular Calcification/metabolism* ; Mice, Inbred C57BL ; Epoxide Hydrolases/metabolism* ; Diabetes Mellitus, Experimental/genetics* ; Male ; Gene Deletion ; MAP Kinase Signaling System/genetics* ; Cell Line ; Immunohistochemistry ; Muscle, Smooth, Vascular/metabolism* ; Signal Transduction/genetics* ; Mice, Knockout

Objective: To analyze the characteristics and safety risks of preservatives and sweeteners in beverages sold near schools in Anshun City, so as to provide a evidence for formulating targeted regulatory strategies in campus. Methods: From December 2023 to July 2024, 834 beverage samples were collected from sales points near primary and secondary schools in Xixiu District and four surrounding townships of Anshun City by a stratified random sampling method. High performance liquid chromatography was used to detect three preservatives (sorbic acid, benzoic acid and dehydroacetic acid) and four sweeteners (sodium saccharin, acesulfame-K, aspartame, and neotame). Differences were analyzed using the Chi-square test. Results: The overall exceedance rate of preservative was 8.6% (72 samples), with dehydroacetic acid showing the highest exceedance rate (7.0%, 58 samples), significantly higher than sorbic acid (0.6%, 5 samples) and benzoic acid (0.4%, 3 samples) ( χ 2=90.85, P <0.01). The overall exceedance rate of sweetener was 10.4% (87 samples), with sodium saccharin having the highest exceedance rate ( 6.2 %, 52 samples),significantly higher than neotame (2.8%, 23 samples), acesulfame-K (0) and aspartame (0) ( χ 2=262.04, P <0.01). Potential risks were identified due to the co occurrence of multiple additive exceedances, including 0.7% (6 samples) for mixed preservatives and 1.6% (13 samples) for mixed sweetener. No statistically significant differences were found in preservative (7.2%, 26 samples) or sweetener (12.3%, 44 samples) exceedance rates between micro enterprises and large, medium and small enterprises ( χ 2=2.67, 5.16, both P >0.05). Conclusion Systemic misuse risk of food additives in beverages sold near school necessitates a risk traceability based regulatory framework, with emphasis on standardizing enterprise production practices and strengthening oversight of sales outlets near campuses.

BackgroundFear of progression is one of the typical psychological consequences in patients with chronic obstructive pulmonary disease （COPD）. The level of fear of progression is affected by the illness perception status， and the link between social support and fear of progression is acknowledged， whereas the mechanism underlying the three remains unclear due to the lack of empirical research evidence and needs to be further studied. ObjectiveTo explore the mediating role of social support in the relationship between illness perception and fear of progression in COPD patients， and to provide references for effectively alleviating fear in COPD patients. MethodsA total of 435 COPD patients admitted to the Department of Respiratory and Critical Care Medicine， the Affiliated Hospital of Southwest Medical University from March 9 to July 31， 2024 were selected as the study objects. The Chinese version of Fear of Progression Questionnaire-Short Form （FoP-Q-SF）， Chinese version of Brief Illness Perception Questionnaire （BIPQ） and Social Support Rate Scale （SSRS） were used for the evaluation. Pearson's coefficient was calculated to assess the correlation among above scales. Model 4 of the Process macro 3.4.1 for SPSS 25.0 was used to test the mediating effect of social support on the relationship between illness perception and fear of progression， with Bootstrapping used to evaluate the significance of mediating effect. ResultsA total of 412 patients （94.71%） completed this study.BIPQ score was positively correlated with FoP-Q-SF score （r=0.238， P<0.01）， and negatively correlated with SSRS score in COPD patients （r=-0.260， P<0.01）. FoP-Q-SF score was negatively correlated with SSRS score （r=-0.271， P<0.01）. Social support mediated the relationship between illness perception and fear of progression， with an indirect effect value of 0.025 （95% CI： 0.009~0.041）， accounting for 13.02% of the total effect. ConclusionIllness perception can affect the fear of progression in COPD patients both directly and indirectly through social support. ［Funded by Nursing Research Project of Sichuan Province （number， H22010）］

Sleep deprivation (SD) has emerged as a significant modifiable risk factor for Alzheimer’s disease (AD), with mounting evidence demonstrating its multifaceted role in accelerating AD pathogenesis through diverse molecular, cellular, and systemic mechanisms. SD is refined within the broader spectrum of sleep-wake and circadian disruption, emphasizing that both acute total sleep loss and chronic sleep restriction destabilize the homeostatic and circadian processes governing glymphatic clearance of neurotoxic proteins. During normal sleep, concentrations of interstitial Aβ and tau fall as cerebrospinal fluid oscillations flush extracellular waste; SD abolishes this rhythm, causing overnight rises in soluble Aβ and tau species in rodent hippocampus and human CSF. Orexinergic neurons sustain arousal, and become hyperactive under SD, further delaying sleep onset and amplifying Aβ production. At the molecular level, SD disrupts Aβ homeostasis through multiple converging pathways, including enhanced production via beta-site APP cleaving enzyme 1 (BACE1) upregulation, coupled with impaired clearance mechanisms involving the glymphatic system dysfunction and reduced Aβ-degrading enzymes (neprilysin and insulin-degrading enzyme). Cellular and histological analyses revealed that these proteinopathies are significantly exacerbated by SD-induced neuroinflammatory cascades characterized by microglial overactivation, astrocyte reactivity, and sustained elevation of pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) through NF‑κB signaling and NLRP3 inflammasome activation, creating a self-perpetuating cycle of neurotoxicity. The synaptic and neuronal consequences of chronic SD are particularly profound and potentially irreversible, featuring reduced expression of critical synaptic markers (PSD95, synaptophysin), impaired long-term potentiation (LTP), dendritic spine loss, and diminished neurotrophic support, especially brain-derived neurotrophic factor (BDNF) depletion, which collectively contribute to progressive cognitive decline and memory deficits. Mechanistic investigations identify three core pathways through which SD exerts its neurodegenerative effects: circadian rhythm disruption via BMAL1 suppression, orexin system hyperactivity leading to sustained wakefulness and metabolic stress, and oxidative stress accumulation through mitochondrial dysfunction and reactive oxygen species overproduction. The review critically evaluates promising therapeutic interventions including pharmacological approaches (melatonin, dual orexin receptor antagonists), metabolic strategies (ketogenic diets, and Mediterranean diets rich in omega-3 fatty acids), lifestyle modifications (targeted exercise regimens, cognitive behavioral therapy for insomnia), and emerging technologies (non-invasive photobiomodulation, transcranial magnetic stimulation). Current research limitations include insufficient understanding of dose-response relationships between SD duration/intensity and AD pathology progression, lack of long-term longitudinal clinical data in genetically vulnerable populations (particularly APOE ε4 carriers and those with familial AD mutations), the absence of standardized SD protocols across experimental models that accurately mimic human chronic sleep restriction patterns, and limited investigation of sex differences in SD-induced AD risk. The accumulated evidence underscores the importance of addressing sleep disturbances as part of multimodal AD prevention strategies and highlights the urgent need for clinical trials evaluating sleep-focused interventions in at-risk populations. The review proposes future directions focused on translating mechanistic insights into precision medicine approaches, emphasizing the need for biomarkers to identify SD-vulnerable individuals, chronotherapeutic strategies aligned with circadian biology, and multi-omics integration across sleep, proteostasis and immune profiles may delineate precision-medicine strategies for at-risk populations. By systematically examining these critical connections, this analysis positions sleep quality optimization as a viable strategy for AD prevention and early intervention while providing a comprehensive roadmap for future mechanistic and interventional research in this rapidly evolving field.

Objective: To create a prediction model for stroke risk among middle-aged and elderly populations, so as to provide a basis for early identification of high-risk population for stroke. Methods: From October to December 2023, residents aged ≥45 years in Chongchuan District, Nantong City, Jiangsu Province were selected using a multi-stage stratified random sampling method. The demographic information, life behavior, and chronic disease data were collected through a questionnaire survey. The standardized prevalence of stroke was calculated using data from the seventh National Population Census. The subjects were randomly divided into the training set and the internal validation set according to the ratio of 8∶2. The basic demographic information, life behavior, and chronic diseases of residents aged ≥45 years in Rugao City were collected from July to August 2023 as the external validation set. Predictive factors were selected using multivariable logistic regression model, and a nomogram for stroke among residents aged ≥45 years was established. The prediction effect was evaluated using the area under the curve (AUC) of the receiver operating characteristic (ROC), calibration curve, and Hosmer-Lemeshow goodness of fit test. Results: A total of 6 290 residents aged ≥45 years were included, including 2 975 males (47.30%) and 3 315 females (52.70%). The average age was (61.90±10.20) years. The prevalence of stroke was 3.80%, and the standardized prevalence was 3.36%. The multivariable logistic regression showed that age, smoking, hypertension, and hyperlipidemia were predictors of stroke risk among residents aged ≥45 years, and the prediction model was ln[p/(1-p)]=-4.619+0.046×age+0.383×smoking+0.887×hypertension+0.678×hyperlipidemia. The AUC values of the training set, internal validation set, and external validation set were 0.748, 0.755, and 0.738, respectively. The consistency indexes were 0.748, 0.755, and 0.738, respectively. The Hosmer-Lemeshow goodness of fit test showed a good fitting effect (P>0.05). Conclusion The prediction model based on age, smoking, hypertension, and hyperlipidemia has good discrimination and calibration, and can be used to predict the risk of stroke among middle-aged and elderly populations aged ≥45 years.

Objective: To investigate trends in incidence and mortality of colorectal cancer in Nantong City, Jiangsu Province from 2013 to 2022. Methods: Data on incidence and mortality of colorectal cancer from 2013 to 2022 in Nantong City were collected through the Nantong City cancer registry. The crude incidence, crude mortality, average age at onset, and average age at death of colorectal cancer were calculated. Chinese population-standardized incidence, Chinese population-standardized mortality, Chinese population-standardized average age at onset and Chinese population-standardized average age at death were calculated using the age structure of the standard population from the Fifth National Population Census in 2000. Trends in incidence and mortality of lung cancer from 2013 to 2022 were evaluated using average annual percent change (AAPC). Trends in the Chinese population-standardized average age at onset and Chinese population-standardized average age at death of lung cancer from 2013 to 2022 were evaluated using the linear regression model. Results: From 2013 to 2022, the crude incidence and Chinese population-standardized incidence of colorectal cancer in Nantong City increased from 33.63/105 and 16.05/105 to 53.82/105 and 19.62/105, respectively, showing upward trends (AAPC=5.665% and 2.467%, both P<0.05). The crude mortality increased from 15.99/105 in 2013 to 25.65/105 in 2022, also showing an upward trend (AAPC=5.514%, P<0.05), while no statistically significant trend was found in the Chinese population-standardized mortality (P>0.05). The Chinese population-standardized incidence of colorectal cancer showed upward trends in both males and females (AAPC=2.666% and 1.790%, both P<0.05). The Chinese population-standardized mortality showed an upward trend in males (AAPC=1.966%, P<0.05), but no statistically significant trend was found in females (P>0.05). The crude incidence of colorectal cancer in the groups aged 40-<50 years, 50-<60 years, 60-<70 years, 70-<80 years, and ≥80 years showed upward trends (AAPC=4.045%, 2.833%, 2.300%, 1.948%, and 1.775%, all P<0.05), and the crude mortality in the group aged ≥80 years showed an upward trend (AAPC=3.240%, P<0.05). The average age at onset of colorectal cancer increased at an annual average of 0.156 years (P<0.05), while the trend in the Chinese population-standardized average age at onset was not statistically significant (P>0.05). The average age at death and the Chinese population-standardized average age at death increased at an annual average of 0.325 and 0.153 years, respectively (both P<0.05). Conclusions From 2013 to 2022, both the crude incidence and mortality of colorectal cancer in Nantong City showed upward trends. Males and individuals aged ≥40 years faced a higher risk of both incidence and mortality. It is recommended to implement comprehensive prevention and control measures targeting these high-risk populations to reduce the burden of colorectal cancer.