Objective To quantitatively assess the exposure-response association between exposure to heatwave and sudden death, estimate the attributable excess deaths, and identify potential vulnerable subgroups. Methods A time-stratified case-crossover study was conducted among residents who died from sudden death in Jiangsu Province, China between 2015 and 2021. Heatwave events in Jiangsu Province, defined using varying relative temperature thresholds and durations, were identified using temperature data from the China Meteorological Administration Land Data Assimilation System (CLDAS V2.0). Individual heatwave exposure was assessed based on each subject's residential address. The exposure-response association between heatwave and sudden death was evaluated using conditional logistic regression model combined with a Distributed Lag Nonlinear Model(DLNM). Heatwave-attributable excess deaths were estimated. Stratified analyses by sex and age were performed to assess potential effect modifications. Results Under all definitions, exposure to heatwave was significantly associated with an increased risk of sudden death, and the risk increased with the intensity of heatwave. Using the P95_3d definition (temperature exceeding the 95th percentile for ≥3 consecutive days), heatwave was significantlyassociated with a 56% increased risk of sudden death (95% CI: 31%, 86%). The population-attributable fraction of sudden death due to heatwave exposure was 1.45% (95% CI: 0.97%, 1.90%). Stratified analyses indicated no statistically significant differences in the association between heatwave exposure and sudden death across age or sex subgroups. Conclusion Heatwave exposure was associated with an increased risk of sudden death. Reducing heatwave exposure during summer may help lower the occurrence of sudden death.

ObjectiveGastrodia elata has evolved ecological types with shortened rhizome internodes and diversified flower and fruit coloration in response to different altitudes. Studying the genetic mechanisms of different ecotype germplasm is significant for guiding variety breeding in different cultivation areas. MethodsThe bHLH gene family was identified based on the whole-genome datasets of G. elata f. elata and G. elata f. glauca. Subsequently， the gene family members were subject to analysis， including gene structure， chromosomal localization， cis-acting elements， gene synteny， and phylogeny. Combined with transcriptome data and quantitative Real-time PCR， the expression patterns of bHLH genes in the stems of the different G. elata ecotype germplasm were analyzed. Finally， correlation analysis was conducted between gene expression patterns and color to obtain the key bHLH genes regulating the color formation of stem. ResultsA total of 63 bHLH genes were identified in both G elata f. elata and G. elata f. glauca， unevenly distributed across 17 chromosomes and clustered into 16 subfamilies， with significant expansion in some family members. Obvious inversions of bHLH genes on the same chromosome and interchromosomal translocations were detected in the two ecotype germplasm. Among these genes， 12 bHLH genes （such as bHLH62-3 and bHLH74） were associated with the bright yellow color of G elata f. elata stem， while 9 bHLH genes （such as PIL13， UNE12， and bHLH130） were correlated with the red color of G. elata f. glauca stem. Compared to G. elata f. glauca， the bHLH48 expression level was significantly higher in flowers and scale leaves of G elata f. elata， and the bHLH62-3 expression level was significantly higher in all organs of G elata f. elata. ConclusionsFunctional pathway divergence of the bHLH family members has occurred across different chromosomes in G elata f. elata and G. elata f. glauca. Through synergism or antagonism with other genes， 21 bHLH genes participate in the coloration metabolic pathway regulation of stems， flowers， and fruits. Specifically， bHLH62-3 is involved in regulating stem color differentiation in the anthocyanin biosynthesis pathway of G. elata， thus relevant to the color formation of stem. Additionally， GebHLH48 positively regulates flowering-related pathways to promote the early-flowering phenotype of G. elata f. elata. These findings have laid the foundation for analyzing the genetic regulatory mechanisms underlying the color formation of the G. elata stem.

ObjectiveGastrodia elata has evolved ecological types with shortened rhizome internodes and diversified flower and fruit coloration in response to different altitudes. Studying the genetic mechanisms of different ecotype germplasm is significant for guiding variety breeding in different cultivation areas. MethodsThe bHLH gene family was identified based on the whole-genome datasets of G. elata f. elata and G. elata f. glauca. Subsequently， the gene family members were subject to analysis， including gene structure， chromosomal localization， cis-acting elements， gene synteny， and phylogeny. Combined with transcriptome data and quantitative Real-time PCR， the expression patterns of bHLH genes in the stems of the different G. elata ecotype germplasm were analyzed. Finally， correlation analysis was conducted between gene expression patterns and color to obtain the key bHLH genes regulating the color formation of stem. ResultsA total of 63 bHLH genes were identified in both G elata f. elata and G. elata f. glauca， unevenly distributed across 17 chromosomes and clustered into 16 subfamilies， with significant expansion in some family members. Obvious inversions of bHLH genes on the same chromosome and interchromosomal translocations were detected in the two ecotype germplasm. Among these genes， 12 bHLH genes （such as bHLH62-3 and bHLH74） were associated with the bright yellow color of G elata f. elata stem， while 9 bHLH genes （such as PIL13， UNE12， and bHLH130） were correlated with the red color of G. elata f. glauca stem. Compared to G. elata f. glauca， the bHLH48 expression level was significantly higher in flowers and scale leaves of G elata f. elata， and the bHLH62-3 expression level was significantly higher in all organs of G elata f. elata. ConclusionsFunctional pathway divergence of the bHLH family members has occurred across different chromosomes in G elata f. elata and G. elata f. glauca. Through synergism or antagonism with other genes， 21 bHLH genes participate in the coloration metabolic pathway regulation of stems， flowers， and fruits. Specifically， bHLH62-3 is involved in regulating stem color differentiation in the anthocyanin biosynthesis pathway of G. elata， thus relevant to the color formation of stem. Additionally， GebHLH48 positively regulates flowering-related pathways to promote the early-flowering phenotype of G. elata f. elata. These findings have laid the foundation for analyzing the genetic regulatory mechanisms underlying the color formation of the G. elata stem.

ObjectiveThe biosynthesis of heterophyllin B （HB）， a cyclopeptide from Pseudostellaria heterophylla， is regulated by various abiotic stresses. Elucidating the transcriptional regulatory mechanism underlying HB biosynthesis is of great guiding significance for the directional improvement of P. heterophylla varieties and the enhancement of HB content. MethodsBased on transcriptome data from different tissues of P. heterophylla， transcription factors （TFs） specifically upregulated and highly expressed in the phloem of tuberous roots were screened through a combination of Mfuzz time-series clustering， transcription factor family prediction， and correlation analysis. Quantitative real-time polymerase chain reaction （Real-time PCR） was employed to analyze expression patterns of candidate TFs under abscisic acid （ABA） induction， and the dual-luciferase reporter assay was applied to verify their regulatory effects on HB precursor genes. ResultsContent determination showed that HB accumulated at the highest in the phloem of P. heterophylla tuberous roots （34 μg·g^-1 fresh weight）. Transcriptome analysis identified 15 868 up-regulated differentially expressed genes （DEGs）， among which 4 375 were specifically up-regulated in the phloem. From these， 25 TFs highly expressed in the phloem were screened. Correlation analysis revealed that the expression level of WRKY70 was significantly positively correlated with HB content， the expression of precursor genes prePhHB， and PhPOP1. Additionally， WRKY70 expression was significantly upregulated under ABA induction. Dual-luciferase reporter assay confirmed that WRKY70 specifically activated the transcriptional activity of the prePhHB promoter （Pro-prePhHB）. ConclusionHB is mainly accumulated in the phloem of P. heterophylla tuberous roots. WRKY70 positively regulates HB biosynthesis by directly activating the promoter activity of prePhHB. This study clarifies the key role of WRKY70 in the regulation of HB biosynthesis and provides an important theoretical basis for the in-depth analysis of the molecular regulatory mechanism underlying HB biosynthesis.

Cholangiocarcinoma (CCA) is a malignancy characterized by tumor cells originating in the liver or bile ducts, exhibiting features of cholangiocyte differentiation. It poses a significant clinical challenge due to the limited diagnostic and therapeutic options available. Robust animal models are essential for advancing our understanding of CCA pathogenesis and developing effective treatments. This review provides a comprehensive overview of CCA mouse models, highlighting various approaches, including chemical induction, genetically engineered models, and tumor xenografts. Each model is discussed in terms of its establishment techniques, pathological characteristics, and research significance, with a focus on intrahepatic CCA. Chemical induction models, such as diethylnitrosamine- and azoxymethane-induced models, offer insights into tumorigenesis processes, whereas genetically modified models involving alterations in key genes such as Kirsten rat sarcoma viral oncogene homolog, tumor protein 53, and isocitrate dehydrogenase serve as important tools for studying the molecular mechanisms underlying CCA. Xenograft models, including patient-derived xenografts, bridge the gap between experimental research and clinical applications, allowing for precise therapeutic evaluations. By comparing these models, this review underscores their respective advantages and limitations, paving the way for future studies aiming to optimize and innovate CCA modeling strategies.

ObjectiveTo investigate the potential therapeutic effects of Dengzhan Shengmai capsules （DZSM） on myocardial fibrosis after myocardial infarction and decipher the underlying molecular mechanisms by virtue of network robustness algorithm. MethodsA rat model of myocardial infarction was established by ligating the left anterior descending coronary artery. Successfully modeled Sprague-Dawley rats were randomly allocated into a model group， an enalapril group（3.15 mg·kg^-1）， and high- and low-dose DZSM groups（226.8，113.4 mg·kg^-1）. In addition， a sham group was set up. After four consecutive weeks of intervention， the cardiac function was assessed via echocardiography， and myocardial collagen deposition was observed through Sirius red staining. The key regulatory pathways of DZSM were analyzed by the network robustness algorithm. Enzyme-linked immunosorbent assay （ELISA） and immunofluorescence assay were employed to validate the mechanisms. ResultsCompared with the sham group， the model group exhibited decreased left ventricular ejection fraction （LVEF%） and fractional shortening （FS%） （P<0.01） and increased myocardial collagen volume fraction （CVF%） （P<0.01）. Compared with the model group， high-dose DZSM and enalapril improved LVEF% and FS% （P<0.01）. Both high- and low-dose DZSM reduced the CVF% （P<0.05， P<0.05，）. Network analysis indicated that DZSM exerted its effects by regulating neutrophil infiltration and related inflammatory pathways. Experimental validation showed that DZSM significantly reduced the protein levels of nuclear factor （NF）-κB， Janus kinase 2 （JAK2）， and signal transduction activator and transducer 3 （STAT3） in the cardiac tissue， as well as the levels of chemokine （C-X-C motif） ligand 1 （CXCL1）， interleukin （IL）-1β， neutrophil elastase-DNA complex （NE-DNA）， and myeloperoxidase-DNA complex （MPO-DNA） in the plasma. ConclusionDZSM may ameliorate myocardial fibrosis by inhibiting neutrophil infiltration and extracellular trap formation and regulating the NF-κB/JAK2/STAT3 signaling pathway.

Objective: To explore the relationship between parenting styles and depressive symptoms in adolescents with nightmare disorder, so as to provide a scientific basis for formulating effective family intervention measures and psychological counseling. Methods: From January 2023 to August 2024, 90 adolescents diagnosed with nightmare disorder and admitted to Hangzhou Seventh Peoples Hospital, along with 176 healthy controls from the urban areas of Hangzhou, were recruited as participants in the study. All participants were assessed using the Nightmare Experience Questionnaire (NEQ), Family Relationship Questionnaire (FRQ), and Plutchik-van Praag Selfreport Depression Scale (PVP). The ttest and Chisquare test were conducted to compare two groups. Pearson correlation and stepwise multiple linear regression were employed to explore the correlations between PVP and NEQ or FRQ. The Process model was used to testing the mediating effects among NEQ/FRQ/PVP. Results: The nightmare disorder group had higher scores in nightmare frequency, the four factors of NEQ (physical effect, negative emotion, meaning interpretation, horrible stimulation), and PVP than the healthy control group (24.86±18.89, 10.12±3.67, 19.01±3.51, 17.02±3.31, 15.14±3.26, 14.02±4.38; 2.34±1.04, 6.49±2.18, 17.63±4.76, 13.91±4.24, 12.40±4.49, 9.39±3.28)(t=15.79, 10.11, 2.43, 6.09, 5.14, 27.46, P<0.05). The nightmare disorder group reported significantly lower scores in FRQ general attachment and maternal encouragement than the healthy control group (7.22±2.81, 16.39±3.28) (t=-5.53, -4.95). In contrast, they exhibited significantly higher scores in maternal abuse, maternal dominance, paternal freedom release, and paternal dominance than the healthy control group (8.23±1.80, 13.11±3.73, 18.36±3.37, 12.04±3.29; 6.07±1.85, 8.48±3.80, 15.15±2.51, 9.47±3.03) (t=6.70, 8.96, 5.90, 7.04, P<0.01). The results of Pearson correlation analysis showed that, in the nightmare disorder group, the PVP score was positively correlated with negative emotion, nightmare frequency, maternal abuse, and maternal dominance score (r=0.14, 0.63, 0.26, 0.51, P<0.05). The results of multiple linear regression analysis showed that when using FRQ score to predict NEQ score, the adjusted R2 in the nightmare disorder group was 0.01-0.59. Mother abuse could prediced physical effect (β=0.33); maternal dominance significantly predicted negative emotion, horrible stimulation, and nightmare frequency (β=0.29, 0.30, 0.79); paternal freedom release could predict negative emotion (β=0.26), paternal dominance predicted both negative emotion and nightmare frequency (β=0.22, 0.45) (P<0.05). Mediation analysis further revealed that, in the nightmare disorder group, PVP scores served as a mediating variable between FRQ and NEQ. Conclusion Abusive, controlling, and neglectful family upbringing styles as well as depression maybe are key factors that may contribute to the development of nightmare disorder among adolescents.

In the context of medical insurance payment reform,the sample hospital has implemented performance management optimization to effectively address the challenges posed by diagnosis-intervention packet(DIP)payment.Reform measures focused on disease quality,rational diagnosis and treatment,operational management,medical technological value,and policy orientation,and they have significantly optimized service ability and performance evaluation indexes of the hospital.Main achievements included a reduction in the cost consumption index and an increase in the clinical performance index,with the overall DIP payment rate increasing from 88.86%to 103.23%and a marked improvement in operational management.The quality control and operational efficiency of the hospital have been effectively enhanced by choosing proper DIP payment evaluation indexes and improving performance management,and provided strong support for the high-quality development of the hospital.

Naval hospitals,the backbone of naval health service system,are the key to build a world-class naval health service system.On the basis of the requirements of military transformation and high-quality development of public hospitals,this paper summarized five aspects of high-quality development of naval hospitals,including directions and regulations,support and contribution of combats,efficiency,sustainable development momentum,and the expansion of service functions.It is very important to strengthen the top-level design and policy support for naval hospitals,to improve the level of governance and innovation,and to find the right target for the naval hospital construction in naval health service system reform.

Objective To establish a stable,reliable,and clinically relevant porcine model of endotoxin-induced acute respiratory distress syndrome(ARDS).Methods Ten 8-month-old male Bama minipigs were deeply sedated,followed by invasive mechanical ventilation and electrocardiographic monitoring.Lipopolysaccharide(LPS)was intravenously pumped at 600 μg/(kg·h)for 3 hours,then maintained at 15 μg/(kg·h)thereafter.Dynamic monitoring was performed at five time points after LPS injection(LPS 0,1,3,5,and 8 h),including arterial blood gas analysis and chest computed tomography(CT)scans.Pathological examination of lung tissues obtained via bronchoscopic biopsy(HE staining and transmission electron microscopy)was conducted.These indicators were comprehensively used to evaluate the success of the animal model.Results At 5 hours after LPS administration,8 minipigs developed symptoms such as skin cyanosis,elevated body temperature,and respiratory distress.The oxygenation index decreased to<300 mmHg.Chest CT scans showed diffuse pulmonary infiltrates.Histopathology revealed alveolar edema and hyaline membrane formation.Transmission electron microscopy demonstrated disruption of pulmonary blood-air barrier,depletion of lamellar bodies in type Ⅱ pneumocytes,inflammatory cell infiltration,and exudation of plasma proteins and fibrin.Compared with LPS 0 h,at LPS 8 h,the oxygenation index and arterial blood pH were significantly decreased(P<0.001),while blood lactic acid and serum potassium were significantly increased(P<0.05);serum calcium and base excess were significantly decreased(P<0.05),and the lung injury score based on HE-stained lung sections was significantly increased(P<0.01).Conclusion The porcine ARDS model established by continuous LPS injection can dynamically simulate the pathophysiological characteristics and typical pathological manifestations of clinical septic ARDS,making it an effective tool to study the pathogenesis,prevention,and treatment strategies of septic ARDS.