ObjectiveThis study aimed to establish a monocrotaline （MCT）-induced pulmonary arterial hypertension （PAH） rat model to systematically evaluate the protective effect of Xiao Qinglongtang （XQLT） on right cardiac function in model rats and further elucidate the underlying regulatory mechanism. MethodsSixty male SD rats were randomly assigned to the normal group， model group， XQLT low-， medium-， and high-dose groups （XQLT-L/M/H）， and the beraprost sodium tablet group （BST）. Except for the normal group， rats in all other groups were given a single subcutaneous injection of MCT （60 mg·kg^-1） to induce PAH. Three weeks after injection， rats in the XQLT-L/M/H groups were administered XQLT intragastrically at 3.07， 6.14， 12.28 g·kg^-1·d^-1， respectively. Rats in the BST group received beraprost sodium at 12.6 μg·kg^-1·d^-1， and rats in the model group received an equal volume of saline. All treatments lasted for 3 weeks. Right ventricular systolic pressure （RVSP） was measured by right ventricular catheterization. Cardiac function was assessed by echocardiography. The right ventricle was weighed to calculate the right ventricular hypertrophy index （RVHI）. Hematoxylin-eosin （HE） staining， Masson staining， and transmission electron microscopy were used to observe myocardial morphology. Serum metabolomic changes were analyzed using ultra-performance liquid chromatography-tandem mass spectrometry （UPLC-MS/MS）. Data-independent acquisition （DIA） proteomics was used to detect differentially expressed （DE） proteins in the right ventricle， and Western blot was used to measure the expression of uncoupling protein 3 （UCP3）， phosphatidylinositol 3-kinase catalytic subunit p110α （PIK3CA）， L1 cell adhesion molecule （L1CAM）， and quinone oxidoreductase （CRYZ）. UPLC-MS/MS was used to analyze the chemical components of XQLT. ResultsCompared with the normal group， the model group showed significantly increased RVSP and RVHI （P<0.05）， along with pathological changes in myocardial morphology. Compared with the model group， all XQLT-treated groups exhibited reductions in RVSP and RVHI as well as significant improvements in cardiac function and myocardial morphology. Among the XQLT groups， XQLT-M showed the most pronounced effects （P<0.05）， comparable to the BST group. Serum metabolomics revealed 105 differential metabolites in the XQLT groups versus the model group ［variable importance in projection （VIP） >1， P<0.05］， including 58 upregulated and 47 downregulated metabolites. KEGG enrichment analysis indicated that XQLT intervention downregulated phenylalanine metabolism （P<0.01） and upregulated unsaturated fatty acid biosynthesis （P<0.05）. Proteomics analysis showed that 982 DE proteins were identified in the MCT groups versus the normal group， including 455 upregulated and 527 downregulated proteins （|fold change （FC）| >1.3， P<0.05）. Compared with the model group， 237 DE proteins were identified in the XQLT groups， including 124 upregulated and 113 downregulated proteins （|FC| >1.3， P<0.05）， with 57 overlapping DE proteins. KEGG enrichment suggested that XQLT mainly modulated pathways related to mineral absorption， ribosomal biogenesis， peroxisomes， glycolysis/gluconeogenesis， spliceosomes， and thyroid hormone signaling. Western blot analysis showed that， compared with the model group， XQLT increased the expression of UCP3， PIK3CA， and L1CAM， while decreasing the expression of CRYZ （P<0.05）. ConclusionXQLT exerts a protective effect on right heart function in MCT-induced PAH rats， and its mechanism is associated with maintaining myocardial homeostasis and alleviating right ventricular remodeling.

Liver injury has become an increasingly serious global health problem， and existing chemical drugs face the limitations in efficacy and adverse reactions， resulting in the urgent need to develop safe and effective drugs. Recent studies have highlighted the potential of flavonoids from natural medicinal plants in the prevention and treatment of liver injury. As a typical natural flavonoid， luteolin shows a good protective effect against liver injury due to various etiologies， but there is still a lack of systematic elaboration on its mechanism of action. This article summarizes related research advances in China and globally and reviews the mechanism of action of luteolin in inhibiting oxidative stress， exerting an anti-inflammatory effect， regulating cell death， alleviating hepatic fibrosis， modulating lipid metabolism disorders， and regulating the gut-liver axis， as well as the application prospect of luteolin in the treatment of liver injury， in order to provide a scientific reference for further research on this compound.

Liver injury has become an increasingly serious global health problem， and existing chemical drugs face the limitations in efficacy and adverse reactions， resulting in the urgent need to develop safe and effective drugs. Recent studies have highlighted the potential of flavonoids from natural medicinal plants in the prevention and treatment of liver injury. As a typical natural flavonoid， luteolin shows a good protective effect against liver injury due to various etiologies， but there is still a lack of systematic elaboration on its mechanism of action. This article summarizes related research advances in China and globally and reviews the mechanism of action of luteolin in inhibiting oxidative stress， exerting an anti-inflammatory effect， regulating cell death， alleviating hepatic fibrosis， modulating lipid metabolism disorders， and regulating the gut-liver axis， as well as the application prospect of luteolin in the treatment of liver injury， in order to provide a scientific reference for further research on this compound.

Short stature(SS) and disorder of sex development(DSD) are two types of conditions characterized by high clinical heterogeneity and complex etiology. There is interplay and mutual influence between the pathways regulated by growth hormone and sex hormones in skeletal and gonadal development. Causing co-occurrence of SS and DSD, as seen in conditions such as Turner syndrome, mixed gonadal dysgenesis, Noonan syndrome, and Prader-Willi syndrome. Patients with these disorders are often accompanied by distinctive facial features, endocrine and metabolic disturbances, cardiovascular disease, and other systemic complications. Genetic factors involved include chromosomal numerical and structural abnormalities; mutations in genes such as SHOX, CHD7, SOX8, and PTPN11, dysregulation of the RAS/mitogen activated protein kinase signaling pathway, and defects in imprinted genes. This article aims to systematically review the relevant research progress, in order to provide a reference for the clinical diagnosis and treatment strategies of patients with coexisting SS and DSD.

Background Prehospital emergency medical personnel (PEMP) are exposed to long-term high-pressure work, which can exacerbate psychological distress and impair job satisfaction and sleep quality. However, in-depth research on the interactions among these factors is lacking. Objective To assess the status of psychological distress, job satisfaction, and sleep quality of PEMP in Guangzhou and to explore the mediating role of sleep quality in the relationship between psychological distress and job satisfaction. Methods From February to May 2025, 1085 PEMP from "120" emergency network hospitals in Guangzhou were selected using convenience sampling. Data were collected via the General Information Questionnaire, Kessler Psychological Distress Scale, Minnesota Satisfaction Questionnaire, and Pittsburgh Sleep Quality Index. Statistical analyses were performed using SPSS 25.0, and The mediation model of sleep quality in linking psychological distress and job satisfaction was constructed using AMOS 28.0. The bias-corrected Bootstrap method was employed to assessed the significance of the mediating effect. Results A total of 1063 valid responses were received (97.97% valid response rate). The mean scores were: psychological distress (27.99±10.75), job satisfaction (69.45±15.84), and sleep quality (9.82±4.47). Significant differences in the three scores were found across gender, age, monthly night shift frequency, and hospital grade (P<0.05). Higher job satisfaction was linked to lower psychological distress and better sleep quality and its dimensions, while psychological distress directly correlated with poorer sleep quality (P<0.01). Sleep quality partially mediated the relationship between psychological distress and job satisfaction, with a mediating effect of −0.195, accounting for 43.62% of the total effect. Conclusion The participants report moderate psychological distress, moderate-to-high job satisfaction, and poor sleep quality. Psychological distress directly affects job satisfaction and indirectly through its impact on sleep quality. Interventions aimed at improving sleep health and mental health are essential to improve personnel well-being and work efficiency.

Background Prehospital emergency medical personnel (PEMP) are exposed to long-term high-pressure work, which can exacerbate psychological distress and impair job satisfaction and sleep quality. However, in-depth research on the interactions among these factors is lacking. Objective To assess the status of psychological distress, job satisfaction, and sleep quality of PEMP in Guangzhou and to explore the mediating role of sleep quality in the relationship between psychological distress and job satisfaction. Methods From February to May 2025, 1085 PEMP from "120" emergency network hospitals in Guangzhou were selected using convenience sampling. Data were collected via the General Information Questionnaire, Kessler Psychological Distress Scale, Minnesota Satisfaction Questionnaire, and Pittsburgh Sleep Quality Index. Statistical analyses were performed using SPSS 25.0, and The mediation model of sleep quality in linking psychological distress and job satisfaction was constructed using AMOS 28.0. The bias-corrected Bootstrap method was employed to assessed the significance of the mediating effect. Results A total of 1063 valid responses were received (97.97% valid response rate). The mean scores were: psychological distress (27.99±10.75), job satisfaction (69.45±15.84), and sleep quality (9.82±4.47). Significant differences in the three scores were found across gender, age, monthly night shift frequency, and hospital grade (P<0.05). Higher job satisfaction was linked to lower psychological distress and better sleep quality and its dimensions, while psychological distress directly correlated with poorer sleep quality (P<0.01). Sleep quality partially mediated the relationship between psychological distress and job satisfaction, with a mediating effect of −0.195, accounting for 43.62% of the total effect. Conclusion The participants report moderate psychological distress, moderate-to-high job satisfaction, and poor sleep quality. Psychological distress directly affects job satisfaction and indirectly through its impact on sleep quality. Interventions aimed at improving sleep health and mental health are essential to improve personnel well-being and work efficiency.

Methods: Cervical radiographs were analyzed. EOP hyperplasia was classified into three subtypes with standardized length measurements. Variables encompassed demographics, ONL-related indices, and sagittal parameters. Subtype comparisons and multivariate regression analyses (with EOP length as dependent variable) were conducted. Results: Analysis of 187 CSM patients (64.2% male) identified gender-specific patterns: males exhibited greater EOP length (9.4±6.8 mm vs. 4.6±3.4 mm, p<0.001). Type III EOP demonstrated male predominance (82.4% vs. type I 31.8%, type II 51.4%; p<0.001), with associated longer hyperplasia length (11.6±6.6 mm vs. type II 5.1±1.9 mm, p<0.001). Type III EOP was associated with higher ONL prevalence (type III 64.8% vs. type I 45.5%, type II 41.9%; p=0.010) and longer ONL osteophyte length (type III 18.8±9.8 mm vs. type I 14.2±8.1 mm, type II 14.2±9.4 mm; p=0.046). Multivariate regression confirmed male sex (β=–3.82, p=0.009), ONL osteophyte length (β=0.16, p=0.017), T1 slope (β=0.27, p=0.041), and spino-cranial angle (β=–0.19, p=0.009) as factors independently associated with EOP length (adjusted R²=0.382). Conclusions Severe EOP hyperplasia exhibits a male-predominant distribution pattern and demonstrates significant radiological associations with ONL and cervical sagittal imbalance in CSM patients. These findings advocate for EOP evaluation in clinical evaluations to identify high-risk biomechanical profiles.

Objectives: . This study aimed to investigate the regulatory functions of gamma-aminobutyric acid (GABA)ergic neural circuits from the inferior colliculus (IC) to the medial geniculate body (MGB) in salicylate-induced tinnitus. Methods: . Mice were treated with salicylate to induce tinnitus, and tinnitus-like behaviors were evaluated via gap prepulse inhibition of acoustic startle. Using combined viral tracing methodologies, we identified and mapped the pathways and connections from the IC to the MGB. Furthermore, we employed Gq-coupled human M3 designer receptors exclusively activated by designer drugs (DREADDs) and Gi-coupled human M4 DREADDs to achieve targeted excitation or suppression of GABAergic neurons in the IC and MGB. Following the administration of clozapine N-oxide, which binds to these receptors, we modulated these neural circuits to assess their impact on tinnitus severity in a mouse model. Results: . Our findings demonstrated that mice exposed to salicylate exhibited tinnitus-like behaviors. GABAergic neurons projecting retrogradely from the MGB to the IC were primarily concentrated in the external nucleus of the IC. After clozapine N-oxide administration, chemogenetic activation of IC-MGB GABAergic neurons aggravated salicylate-induced tinnitus. Additionally, activation of GABAergic neurons between the IC and MGB induced the perception of tinnitus even without salicylate. However, chemogenetic inhibition of the IC-MGB GABAergic circuit did not reverse salicylate-induced tinnitus. Conclusion . These findings suggest that activation of the IC-MGB GABAergic neural circuit may contribute to tinnitus generation through a mechanism distinct from that of salicylate-induced tinnitus. This study provides novel insights into the mechanisms underlying tinnitus.

We analyzed the epidemiological features and spatial distribution characteristics of human brucellosis in Jining city from 2014 to 2023,to provide a reference for further development of targeted prevention and control strategies and measures.Descrip-tive epidemiological methods were used to analyze the epidemiological characteristics of brucellosis cases in Jining from 2014 to 2023.The spatial regional correlation of brucellosis incidence in Jining and the clustering patterns of local areas were studied through spatial autocorrelation analysis with townships as the basic unit.A total of 3 520 cases of brucellosis were reported in Jining from 2014 to 2023,and the average annual incidence rate was 4.23/100 000,thus indicating a fluctuating trend overall.Reported cases peaked from March to August,and a sex ratio of 2.71 males to 1 female was observed.The 40-59 year age group had the most reported cases(50.39％).The incidence of brucellosis in Jining showed an imbalanced spatial distribution.Brucellosis incidence showed a spatially clustered distribution(Moran's I>0,P<0.05).Hotspots were distributed primarily in Sishui,Qufu,and Zoucheng.A total of one class Ⅰ clustering area and one class Ⅱ clustering area were detected in the spatial and temporal scans,and were located in Sishui,Qufu,and Liangshan county.After pathogenic AMOS-PCR typing analysis,64 Brucella isolates collected from Jinan City from 2022 to 2024 were all of the sheep strain,and sheep biovar 3 was predominant(70.31％).In 2014-2023,although Jining City experienced a high incidence of brucellosis,a downward trend was observed.Brucellosis showed a spatial clustering pattern concentrated in the northeastern region.Therefore,awareness and education must be strengthened among brucellosis practitioners in cluster areas,to en-hance case surveillance,improve the level of protection,and achieve early detection and treatment.

Objective:To explore the potential mechanism of action of Xian Fang Huo Ming Yin modified formula(XFHMY)in the treatment of medication-related osteonecrosis of the jaw(MRONJ)through bioinformatics analysis and in vitro and in vivo experiments.Methods:Firstly,the efficacy of XFHMY was evaluated by establishing a mice model of MRONJ induced by zoledronic acid(ZOL);Subsequently,the potential molecular mechanism of XFHMY in the treatment of MRONJ was predicted by using network pharmacology;Lastly,the network pharmacology prediction results were collectively validated through MC3T3-E1 cell proliferation and differentiation experiments,Western blot analysis,and immunohistochemical staining of mouse maxillary bone tissue.Results:Animal experiments showed that,compared to the model group,the XFHMY group exhibited significantly improved wound healing in the tooth extraction socket(P＜0.001),a significant reduction in bone volume fraction and empty lacunae rate in the maxilla(P＜0.0001,P＜0.001),and a significant increase in trabecular separation and osteoclast number(P＜0.01,P＜0.05).Network pharmacology analysis identified 59 common targets,with both GO and KEGG analyses indicating the Wnt/β-catenin signaling pathway as a crucial mechanism for XFHMY in treating MRONJ.Ten key active components,including quercetin,luteolin,and fisetin,were screened,and these compounds demonstrated strong binding affinity with CTNNB1,a core target of this pathway.In vitro experiments revealed that XFHMY(0.25,0.5,1,2,4 mg/mL)promoted MC3T3-E1 cell proliferation(P＜0.0001)and activated the Wnt/β-catenin pathway by upregulating β-catenin and Runx2 protein expression,thereby reversing ZOL-induced inhibition of MC3T3-E1 cell proliferation and differentiation while enhancing both processes.Immunohistochemical analysis of mouse maxillae showed that,compared to the model group,the XFHMY group had significantly increased β-catenin and Runx2 protein expression(P＜0.05,P＜0.01),consistent with the in vitro findings.Conclusion:XFHMY promotes the proliferation and differentiation of osteoblasts through activating the Wnt/β-catenin signaling pathway,which in turn attenuates MRONJ.The novel pharmacological mechanism proposed in this study provides a theoretical basis for the clinical application of XFHMY.