Objective To explore the changes in ability to cope with ethical conflicts in palliative care in neonatal intensive care units(NI CU)before and after ethical sensitivity theory training.Methods A descriptive phenomenological research method was employed.Using purposive sampling,we recruited 16 NICU nurses from a tertiary general comprehensive hospital in the city.After ethical sensitivity theory training between January and March 2025,the nurses participated in a semi-structured interview.Data were analyzed using Colaizzi's seven-step analysis method.Results All participants completed the interview.The data were abstracted to three main themes encompassing eight sub-themes:experiences of ethical conflict dilemmas before ethical sensitivity theory training(conflicts between treatment decision-making and family expectations,trust crises triggered by family cognitive biases),the changes of strategy to cope with ethical conflicts after ethical sensitivity theory training(individualized coping strategies,teamwork and communication,introduction and support of external resources),and the role of ethical sensitivity theory training in enhancing coping ability(improving the ability to identify ethical issues,optimizing the decision-making process,and promoting effective communication).Conclusion Palliative care nurses in the NICU face various ethical conflicts,and ethical sensitivity training can enhance their ability to manage these conflicts.

To construct a recombinant fowl adenovirus 4(FAdV-4)expressing the Cap protein of goose astrovirus genotype 2(GoAstV-2),the expression cassette of Cap gene was inserted into the natural 1 966 bp deletion region of the FAdV-4 genome in the infectious clone p15A-cm-FAdV4-HNJZ.The resulted recombinant plasmid p15A-cm-FAdV4-HNJZ-Cap/GoAstV-2 was linearized with restriction enzyme and transfected into chicken hepatoma cell line(LMH)to rescue the recombinant FAdV-4 expressing the Cap protein of GoAstV-2,rF Ad V4-Cap/GoAstV-2.After 15 passages in LMH cells,the recombinant rFAdV4-Cap/GoAstV-2 was identified by PCR using primers flanking the insertion site of the Cap gene expression cassette and using viral genome DNA extracted from rFAdV4-Cap/GoAstV-2 infected LMH cells as template.LMH cells were in-fected with 15th passage rFAdV4-Cap/GoAstV-2 and indirect immunofluorescence was performed with a polyclonal antibody against Cap protein as the primary antibody.Western blot was carried out with lysates of rFAdV4-Cap/GoAstV-2 infected LMH cells.The in vitro replication dynamic of the 15th passage of the rFAdV4-Cap/GoAstV-2 was also investigated in LMH cells.The results demonstrated that the Cap gene of GoAstV-2 was presented in the genome of the recombinant vi-rus rF AdV4-Cap/Go Ast V-2,and could be expressed stably.The prepared recombinant virus in this study will lay a foundation for developing inactivated bivalent vaccine candidate against co-in-fection of FAdV-4 and GoAstV-2 in goose.

Objective To observe the correlations between left atrial myocardial strain and left ventricular function in children with Duchenne muscular dystrophy(DMD).Methods Fifty-one DMD children(DMD group)and 42 healthy one(control group)were prospectively enrolled.The parameters of routine ultrasound and three-dimensional speckle-tracking echocardiography(3D-STE)were compared between groups,and the correlations between left atrial strain parameters and left ventricular function parameters were analyzed.Results The mitral annular lateral wall velocity(e'),left ventricular ejection fraction(LVEF),left atrial ejection fraction(LAEF),left atrioventricular coupling index(LACI),left ventricular global longitudinal strain(LVGLS),left atrial strain during reservoir phase(LASr)and left atrial strain during conduit phase(LAScd)were all lower,while mitral early diastolic peak flow velocity/e'(E/e'),left atrial stiffness index(LASI)and left atrial filling index(LAFI)were higher in DMD group than those in control group(all P＜0.05).In DMD group,LAEF,LASr and LAScd were moderately positively correlated with LVGLS(r=0.409,0.437,0.440,all P＜0.05),LAFI and LASI were weakly negatively correlated with LVGLS(r=-0.207,-0.223,both P＜0.05),while LASr was moderately positively correlated with e'(r=0.419,P＜0.05).Conclusion The left atrial myocardial strain was correlated with left ventricular systolic and diastolic function in DMD children.

To enhance hospital operational management capability,the sample hospital initiated a financial talent development program aligned with current development needs and policy directions.This program established a talent development framework encompassing hierarchical training,employment mechanisms,and digital empowerment,forming a three-tier financial talent echelon comprising senior,intermediate,and junior professionals.It effectively facilitated the transformation of financial functions toward"strategic support,business service,risk prevention and control,and value creation".It analyzes the hospital's practical experience in financial talent development,aiming to offer insights for financial workforce development in public hospitals.These efforts synergize with the modernization of governance systems and capabilities in health economics,driving high-quality development in public healthcare institutions.

Objective To establish atopic dermatitis(AD)-like models in BALB/c mice using three chemical inducers,calcipotriol(MC903),2,4-dinitrochlorobenzene(DNCB),and oxazolone(OXA),and to explore the occurrence of ferroptosis in the different models.Methods Healthy 7-week-old female BALB/c mice were divided randomly into eight groups(n=8 mice per group)based on the induction site(ear/dorsal skin)and inducer:ear/dorsal control groups,MC903 ear/dorsal model groups,DNCB ear/dorsal model groups,and OXA ear/dorsal model groups.Models were established by topical application of the respective agents at specified concentrations.Mice in the MC903 ear/dorsal groups underwent continuous induction for 14 d.Mice in the DNCB and OXA ear/dorsal groups were sensitized for 3 consecutive days,4 days after the sensitization was completedand then challenged 12 times on day 8 and every other day for up to day 30.Skin lesions were observed and skin thickness was measured.Plasma levels of reactive oxygen species(ROS),interleukin(IL)-4,interferon(IFN)-γ,and malondialdehyde(MDA)were detected,the skin was examined by histopathological staining and ultrastructural observation,and expression levels of ferroptosis-related proteins(glutathione peroxidase 4(GPX4),ferritin heavy chain 1(FTH1),long-chain-fatty-acid-CoA ligase 4(ACSL4),transferrin receptor 1(TfR1))were detected by Western Blot.Results Compared with each control mice,all model mice exhibited obvious redness,swelling,scratching,desquamation,and rough thickening of the skin,and skin thickness was significantly increased(P＜0.01).ROS,IFN-γ,IL-4,and MDA levels were elevated to varying extents(P＜0.05)and histopathological features,including epidermal hyperplasia,keratinocyte degeneration,dermal vascular congestion,and immune cell infiltration,were detected in model mice.Transmission electron microscopy also revealed mitochondrial membrane rupture,increased density,and cristae reduction.Expression levels of ferroptosis markers were dysregulated,including significantly decreased GPX4/FTH1(P＜0.05)and increased ACSL4/TfR1 expression(P＜0.05).Conclusions All three chemicals successfully induced AD-like phenotypes in BALB/c mice through site-specific applications.Ferroptosis is involved in the pathological process of AD,but heterogeneity exists among inducers and modeling sites.

Objective To investigate how dietary supplementation with tetrahydrocurcumin(THC)improves kidney injury in type 2 dia-betic mellitus(T2DM)and its mechanism of action using transcriptome sequencing(RNA-seq).Methods C57BL/6J mice were randomly assigned to the control,T2DM,and T2DM+THC groups.After a high-fat meal and streptozotocin injection,the body weights and fasting blood glucose levels of each mouse with T2DM were measured.Hematoxylin and eosin staining,Oil red O staining,and RNA-seq were performed to examine kidney pathology,lipid deposition,and differentially expressed genes,respectively,in the mice.Results Mice in T2DM group exhibited significantly higher fasting blood glucose levels(P＜0.001),renal tubule degeneration,glomeruli enlargement,disordered epithelial cells,and increased kidney lipid deposition after 12 weeks compared with those of the control group.THC adminis-tration alleviated all these conditions(P＜0.001).RNA-seq analysis revealed significant gene expression variations among the control,T2DM,and T2DM+THC groups.THC may protect against T2DM-induced kidney injury and lipid deposition by regulating the cell cycle(apoptosis),P53 signaling pathway,and PPARγ signaling path way,as indicated by Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway enrichment analyses.In mice with T2DM,THC intervention may upregulate the expression of Cd36,Lpl,PPARγ,and Plin4 genes in renal tissues,while downregulating Ccnb1,Ccnb2,Cdk1,Bub1,and Cdc25c gene expressions.The proteins encoded by the four upregulated genes interact,as do those encoded by the five downregulated genes.Conclusion THC administration improves fasting blood glucose levels,reduces renal damage,and decreases fat deposition in mice with T2DM.The processes may involve decreasing apoptosis,blocking the P53 signaling pathway,and activating the PPARγ signaling pathway.

Purpose To investigate the value of non-invasive preoperative prediction of programmed death ligand 1 expression status in extrahepatic cholangiocarcinoma using MRI radiomics combined with clinical features through nomograms.Materials and Methods A retrospective collection was made of 87 cases of extrahepatic cholangiocarcinoma diagnosed through surgical pathology in the Affiliated Hospital of Southwest Medical University from January 2011 to December 2021.These were randomly divided into training and testing sets at a 7∶3 ratio.Using 3D-Slicer software,regions of interest were manually delineated layer-by-layer on MRI images,and radiomic features were extracted.Data normalization,feature dimensionality reduction and selection were then performed.A Gaussian naive Bayes classifier was used to construct the radiomics model,and radiomics scores were obtained.Multivariate Logistic regression was used to screen clinical features,and individual clinical and combined models were constructed.The predictive performances of the three models were evaluated using the area under the receiver operating characteristic curve(AUC),and the goodness of fit and clinical net benefit of the combined model nomogram were assessed through calibration and decision curves.Results Nine radiomic features and three clinical features were finally selected.The clinical features included alanine transaminase(P=0.020),aspartate transaminase(P=0.025)and total bilirubin(P=0.026).The predictive performance of the combined model(training set AUC 0.813,testing set AUC 0.818)was superior to that of the individual clinical model(training set AUC 0.711,testing set AUC 0.705)and the radiomics model(training set AUC 0.769,testing set AUC 0.767).Calibration and decision curves indicated good fit and better clinical net benefit for the combined model nomogram.Conclusion Based on preoperative multi-sequence MRI images and the radiomics score,along with alanine transaminase,aspartate transaminase and total bilirubin as clinical features,the constructed combined model nomogram effectively predicts the programmed death ligand 1 expression status in extrahepatic cholangiocarcinoma.This provides guidance for the precise and personalized immunotherapy for patients.

Objective To explore the changes in ability to cope with ethical conflicts in palliative care in neonatal intensive care units(NI CU)before and after ethical sensitivity theory training.Methods A descriptive phenomenological research method was employed.Using purposive sampling,we recruited 16 NICU nurses from a tertiary general comprehensive hospital in the city.After ethical sensitivity theory training between January and March 2025,the nurses participated in a semi-structured interview.Data were analyzed using Colaizzi's seven-step analysis method.Results All participants completed the interview.The data were abstracted to three main themes encompassing eight sub-themes:experiences of ethical conflict dilemmas before ethical sensitivity theory training(conflicts between treatment decision-making and family expectations,trust crises triggered by family cognitive biases),the changes of strategy to cope with ethical conflicts after ethical sensitivity theory training(individualized coping strategies,teamwork and communication,introduction and support of external resources),and the role of ethical sensitivity theory training in enhancing coping ability(improving the ability to identify ethical issues,optimizing the decision-making process,and promoting effective communication).Conclusion Palliative care nurses in the NICU face various ethical conflicts,and ethical sensitivity training can enhance their ability to manage these conflicts.

Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.

Background and Objectives: SH3 and multiple ankyrin repeat domains 3 (Shank3) proteins play crucial roles as neuronal postsynaptic scaffolds. Alongside neuropsychiatric symptoms, individuals with SHANK3 mutations often exhibit symptoms related to dysfunctions in other organs, including the heart. However, detailed insights into the cardiac functions of Shank3 remain limited. This study aimed to characterize the cardiac phenotypes of Shank3-overexpressing transgenic mice and explore the underlying mechanisms. Methods: Cardiac histological analysis, electrocardiogram and echocardiogram recordings were conducted on Shank3-overexpressing transgenic mice. Electrophysiological properties, including action potentials and L-type Ca2+ channel (LTCC) currents, were measured in isolated cardiomyocytes. Ca2+ homeostasis was assessed by analyzing cytosolic Ca2+transients and sarcoplasmic reticulum Ca2+ contents. Depolarization-induced cell shortening was examined in cardiomyocytes. Immunoprecipitation followed by mass spectrometrybased identification was employed to identify proteins in the cardiac Shank3 interactome.Western blot and immunocytochemical analyses were conducted to identify changes in protein expression in Shank3-overexpressing transgenic cardiomyocytes. Results: The hearts of Shank3-overexpressing transgenic mice displayed reduced weight and increased fibrosis. In vivo, sudden cardiac death, arrhythmia, and contractility impairments were identified. Shank3-overexpressing transgenic cardiomyocytes showed prolonged action potential duration and increased LTCC current density. Cytosolic Ca2+ transients were increased with prolonged decay time, while sarcoplasmic reticulum Ca2+ contents remained normal. Cell shortening was augmented in Shank3-overexpressing transgenic cardiomyocytes. The cardiac Shank3 interactome comprised 78 proteins with various functions. Troponin I levels were down-regulated in Shank3-overexpressing transgenic cardiomyocytes. Conclusions This study revealed cardiac dysfunction in Shank3-overexpressing transgenic mice, potentially attributed to changes in Ca2+ homeostasis and contraction, with a notable reduction in troponin I.