Objectives: . Idiopathic sudden sensorineural hearing loss (ISSNHL) is a significant cause of hearing loss. Intratympanic steroid injection (ITSI) is commonly used as an initial or salvage treatment; however, the lack of a standardized treatment protocol has resulted in variability in clinical practice. In addition, no efficient prediction model currently exists to support personalized management. Therefore, this study aimed to develop tailored management strategies for ISSNHL using a machine-learning model. Methods: . This retrospective multicenter cohort study was conducted between January 2015 and December 2020, with data analysis performed between January 2021 and March 2024. Patients were selected based on the International Classification of Diseases, 10th Revision criteria for ISSNHL, along with relevant medication and procedure codes. Patients with pure-tone audiogram results not meeting ISSNHL criteria, better initial hearing in the affected ear, an identifiable etiology, no post-treatment audiogram, or delayed treatment (>6 weeks) were excluded. We included 770 patients diagnosed with ISSNHL who received ITSI. The primary outcome was the area under the receiver operating characteristic curve for prediction performance. Recovery status was determined using the last pure-tone audiogram. Modeling was conducted on the Quanta for Medical Care AI platform using five machine-learning algorithms and a nested cross-validation framework, in which feature selection and hyperparameter tuning were performed in the inner folds and model performance was evaluated in the outer folds. Results: . A random forest classifier outperformed the other models in predicting hearing outcomes, achieving an area under the receiver operating characteristic curve of 0.788. Time to ITSI was the most influential treatment-related factor, with ITSI administered within 10 days of hearing loss being associated with better outcomes. This model can be used to provide personalized prognostic estimates under different treatment protocols. Conclusion . The machine-learning-based prediction model facilitates personalized treatment strategies and timely treatment adjustments for ISSNHL, thereby optimizing the likelihood of complete recovery.

Objective:To investigate the mechanism of mitochondrial DNA (mtDNA)-reactive oxygen species (ROS)-dynamin-related protein 1 (Drp1) axis in regulating phenotypic transformation of vascular smooth muscle cells (VSMCs).Methods:(1) VSMCs were divided into a control group, a synthetic VSMCs group, and a Drp1 siRNA+synthetic VSMCs group; cells in the Drp1 siRNA+synthetic VSMCs group were transfected with 50 nmol/L Drp1 siRNA for 48 h; cells in the latter two groups were treated with 20 ng/mL platelet-derived growth factor (PDGF)-BB, while cells in the control group were treated with an equal volume of solvent. After another 24 h of culture, Drp1 expression in VSMCs, and mitochondrial Drp1 and mitofusin 2 (Mfn2) expressions were detected by Western blotting, and changes in mitochondrial morphology were detected by mitochondrial fluorescent staining. (2) VSMCs were divided into a control group, a synthetic VSMCs group, and a mitochondrial fission inhibitor 1 (Mdivi-1)+synthetic VSMCs group; cells in the Mdivi-1+synthetic VSMCs group were pretreated with 50 μmol/L Mdivi-1 for 2 h; and cells in the latter two groups were treated with 20 ng/mL PDGF-BB, while cells in the control group were treated with an equal volume of solvent. After 24 hours of continued culture, expressions of α-smooth muscle actin (α-SMA), smooth muscle protein 22-α (SM22-α), proliferating cell nuclear antigen (PCNA), and Cyclin D1 were detected by Western blotting; invasion and migration abilities of VSMCs were detected by Transwell assay and scratch wound healing assay, respectively. (3) VSMCs were divided into a control group, a synthetic VSMCs group, and a N-acetylcysteine (NAC)+synthetic VSMCs group; cells in the NAC+synthetic VSMCs group were pretreated with 5 mmol/L NAC for 1 h; cells in the latter two groups were treated with 20 ng/mL PDGF-BB, while cells in the control group were treated with an equal volume of solvent. After 24 h of continued culture, expressions of Drp1, phosphorylated (p)-Drp1, α-SMA, SM22-α, PCNA, and Cyclin D1 were detected by Western blotting; changes in mitochondrial morphology were detected by mitochondrial fluorescent staining; intracellular ROS level was detected by 2', 7' -dichlorodihydrofluorescein diacetate (DCFH-DA) fluorescent probe; cell invasion and migration abilities were detected by Transwell assay and scratch wound healing assay, respectively. (4) VSMCs were divided into a control group, a synthetic VSMCs group, and a 5-Aza-2'-deoxycytidine (5-Aza-dC)+synthetic VSMCs group; cells in the 5-Aza-dC+synthetic VSMCs group were pretreated with 2 μmol/L 5-Aza-dC for 1 h; and then, cells in the latter two groups were treated with 20 ng/mL PDGF-BB, while cells in the control group were treated with an equal volume of solvent. After 24 h of continued culture, agarose gel electrophoresis was used to analyze the methylation degree in the mitochondrial D-loop region; intracellular ROS level was detected using DCFH-DA fluorescent probe; expressions of mitochondrial DNMT1, α-SMA, SM22-α, PCNA, and Cyclin D1 were detected by Western blotting; invasion and migration abilities were detected by Transwell assay and scratch wound healing assay, respectively.Results:(1) Compared with the control group and synthetic VSMCs group, the Drp1 siRNA+synthetic VSMCs group had significantly decreased Drp1 protein expression ( P<0.05). Compared with the control group, the synthetic VSMCs group had significantly increased Drp1 protein expression and decreased Mfn2 protein expression in the mitochondria ( P<0.05); compared with the synthetic VSMCs group, the Drp1 siRNA+synthetic VSMCs group had statistically decreased Drp1 protein expression and increased Mfn2 protein expression in the mitochondria ( P<0.05). Results of mitochondrial fluorescent staining showed that mitochondria in the control group were with filamentous structure, while mitochondrial fission in the synthetic VSMCs group was enhanced, and morphology of mitochondria in the Drp1 siRNA+synthetic VSMCs group tended to be continuous and complete. (2) Compared with the control group, the synthetic VSMCs group had statistically decreased α-SMA and SM22-α protein expressions and increased PCNA and Cyclin D1 protein expressions ( P<0.05). Compared with the synthetic VSMCs group, the Mdivi-1+synthetic VSMCs group had significantly increased α-SMA and SM22-α protein expressions and decreased PCNA and Cyclin D1 protein expressions ( P<0.05). Results of Transwell and scratch wound healing assays showed that compared with the control group, the synthetic VSMCs group had larger number of migrating cells and faster cell scratch healing; compared with the synthetic VSMCs group, the Mdivi-1+synthetic VSMCs group had smaller number of migrating cells and slower cell scratch healing. (3) Compared with the control group (1.10±0.02), the synthetic VSMCs group (1.53±0.02) had significantly increased p-Drp1 protein expression ( P<0.05). Compared with the synthetic VSMCs group, the NAC+synthetic VSMCs group (0.90±0.02) had statistically decreased p-Drp1 protein expression ( P<0.05). Results of mitochondrial fluorescent staining showed that mitochondria in cells of the control group were in a filamentous structure, while mitochondrial fission in cells of the synthetic VSMCs group was enhanced, and morphology of mitochondria in the NAC+synthetic VSMCs group tended to be continuous and complete. Results of DCFH-DA fluorescent probe showed that ROS level in the synthetic VSMCs group was higher than that in the control group, and ROS level in the NAC+synthetic VSMCs group was lower than that in the synthetic VSMCs group. Compared with the control group, the synthetic VSMCs group had significantly decreased α-SMA and SM22-α protein expressions and increased PCNA and Cyclin D1 protein expressions ( P<0.05). Compared with the synthetic VSMCs group, the NAC+synthetic VSMCs group had significantly increased α-SMA and SM22-α protein expressions and decreased PCNA and Cyclin D1 protein expressions ( P<0.05). Results of Transwell and scratch wound healing assays showed that compared with the control group, the synthetic VSMCs group had larger number of migrating cells and faster cell scratch healing; compared with the synthetic VSMCs group, the NAC+synthetic VSMCs group had smaller number of migrating cells and slower cell scratch healing. (4) Results of agarose gel electrophoresis showed that compared with the control group, the synthetic VSMCs group had significantly increased methylation rate in the mitochondrial D-loop region ( P<0.05); compared with the synthetic VSMCs group, the 5-Aza-dC+synthetic VSMCs group had statistically decreased methylation rate in the mitochondrial D-loop region ( P<0.05). Compared with the control group, the synthetic VSMCs group had statistically increased mitochondrial DNMT1 protein expression (1.03±0.03 vs. 0.55±0.03, P<0.05); and compared with the synthetic VSMCs group, the the 5-Aza-dC+synthetic VSMCs group (0.62±0.03) had significantly decreased mitochondrial DNMT1 protein expression ( P<0.05). Results of DCFH-DA fluorescent probe showed that ROS level in the synthetic VSMCs group was higher than that in the control group; ROS level in the 5-Aza-dC+synthetic VSMCs group was lower than that in the synthetic VSMCs group. Compared with the control group, the synthetic VSMCs group had significantly decreased α-SMA and SM22-α protein expressions and increased PCNA and Cyclin D1 protein expressions ( P<0.05). Compared with the synthetic VSMCs group, the 5-Aza-dC+synthetic VSMCs group had significantly increased α-SMA and SM22-α protein expressions and decreased PCNA and Cyclin D1 protein expressions ( P<0.05). Results of Transwell and scratch wound healing assays showed that compared with the control group, the synthetic VSMCs group had larger number of migrating cells and faster scratch healing. Compared with the synthetic VSMCs group, the 5-Aza-dC+synthetic VSMCs group had smaller number of migrating cells and slower scratch healing. Conclusion:The mtDNA-ROS-Drp1 axis may regulate the phenotypic transformation of VSMCs by modulating mitochondrial epigenetic modifications.

Objectives:To evaluate the predictive value of Tabular Prior-data Fitted Network(TabPFN) for short-term outcome in patients with spontaneous intracerebral hemorrhage (sICH), and compared with the Extreme Gradient Boosting (XGboost) model and traditional logistic regression (LR) model. Methods:Patients with sICH admitted to the Department of Neurology, Hefei Second People's Hospital from January 2018 to March 2024 were included retrospectively. The demographic and baseline data were collected. At 3 months after onset, the modified Rankin Scale score was used to determine the outcome, 0-2 was defined as good outcome and >2 was defined as poor outcome. All enrolled patients were randomly divided into a training set and a testing set at a ratio of 7:3. Feature selection was performed using recursive feature elimination (RFE) method, and then the selected feature variables were included into TabPFN, XGboost, and LR models for training and testing. The area under the curve (AUC) of receiver operating characteristic (ROC) curve was used to evaluate the predictive ability of the models. Shapley additive explanations (SHAP) method was used for model interpretation.Results:A total of 547 patients with sICH were enrolled, including 367 males (67.1%), with a median age of 65 (interquartile range, 54-76) years. Two hundred twenty-six patients (41.3%) had poor outcome. Age, baseline blood pressure (systolic blood pressure, diastolic blood pressure), baseline laboratory tests (white blood cell count, red blood cell count, platelet count, neutrophil count, hemoglobin, fasting blood glucose, creatinine, uric acid, urea nitrogen, alanine aminotransferase, aspartate aminotransferase), hematoma rupture into the ventricle, island sign, baseline hematoma volume, and baseline National Institutes of Health Stroke Scale (NIHSS) score were selected as characteristic variables using RFE method. ROC curve analysis showed that the ROC AUC for TabPFN, Xgboost, and LR models predicting poor short-term outcome in the testing set were 0.918 (95% confidence interval [ CI] 0.870-0.966], 0.883 (95% CI 0.826-0.940), and 0.905 (95% CI 0.854-0.957), respectively. SHAP analysis showed that the top four important variables in the TabPFN model were baseline NIHSS score, baseline hematoma volume, baseline aspartate aminotransferase, and age. Conclusions:The TabPFN model is superior to the LR model and the XGBoost model in predicting poor outcome in patients with sICH. In the TabPFN model, baseline NIHSS score, baseline hematoma volume, aspartate aminotransferase, and age are the most important predictors of poor outcome in patients with sICH.Objectives To evaluate the predictive value of Tabular Prior-data Fitted Network(TabPFN) for short-term outcome in patients with spontaneous intracerebral hemorrhage (sICH), and compared with the Extreme Gradient Boosting (XGboost) model and traditional logistic regression (LR) model. Methods Patients with sICH admitted to the Department of Neurology, Hefei Second People's Hospital from January 2018 to March 2024 were included retrospectively. The demographic and baseline data were collected. At 3 months after onset, the modified Rankin Scale score was used to determine the outcome, 0-2 was defined as good outcome and >2 was defined as poor outcome. All enrolled patients were randomly divided into a training set and a testing set at a ratio of 7:3. Feature selection was performed using recursive feature elimination (RFE) method, and then the selected feature variables were included into TabPFN, XGboost, and LR models for training and testing. The area under the curve (AUC) of receiver operating characteristic (ROC) curve was used to evaluate the predictive ability of the models. Shapley additive explanations (SHAP) method was used for model interpretation. Results A total of 547 patients with sICH were enrolled, including 367 males (67.1%), with a median age of 65 (interquartile range, 54-76) years. Two hundred twenty-six patients (41.3%) had poor outcome. Age, baseline blood pressure (systolic blood pressure, diastolic blood pressure), baseline laboratory tests (white blood cell count, red blood cell count, platelet count, neutrophil count, hemoglobin, fasting blood glucose, creatinine, uric acid, urea nitrogen, alanine aminotransferase, aspartate aminotransferase), hematoma rupture into the ventricle, island sign, baseline hematoma volume, and baseline National Institutes of Health Stroke Scale (NIHSS) score were selected as characteristic variables using RFE method. ROC curve analysis showed that the ROC AUC for TabPFN, Xgboost, and LR models predicting poor short-term outcome in the testing set were 0.918 (95% confidence interval [ CI] 0.870-0.966], 0.883 (95% CI 0.826-0.940), and 0.905 (95% CI 0.854-0.957), respectively. SHAP analysis showed that the top four important variables in the TabPFN model were baseline NIHSS score, baseline hematoma volume, baseline aspartate aminotransferase, and age. Conclusions The TabPFN model is superior to the LR model and the XGBoost model in predicting poor outcome in patients with sICH. In the TabPFN model, baseline NIHSS score, baseline hematoma volume, aspartate aminotransferase, and age are the most important predictors of poor outcome in patients with sICH.

Objective: Whether elevation in plasma levels of amyloid and tau protein biomarkers are better indicators of cognitive decline than higher baseline levels in patients with amnestic mild cognitive impairment (aMCI) and Alzheimer’s disease (AD) remains understudied. Methods: We included 67 participants with twice testing for AD-related plasma biomarkers via immunomagnetic reduction (IMR) assays (amyloid beta [Aβ]1-40, Aβ1-42, total tau [t-Tau], phosphorylated tau [p-Tau] 181, and alpha-synuclein [α-Syn]) and the Mini-Mental State Examination (MMSE) over a 1-year interval. We examined the correlation between biomarker levels (baseline vs. longitudinal change) and annual changes in the MMSE scores. Receiver operating characteristic curve analysis was conducted to compare the biomarkers. Results: After adjustment, faster cognitive decline was correlated with lower baseline levels of t-Tau (β=0.332, p=0.030) and p-Tau 181 (β=0.369, p=0.015) and rapid elevation of t-Tau (β=-0.330, p=0.030) and p-Tau 181 levels (β=-0.431, p=0.004). However, the levels (baseline and longitudinal changes) of Aβ1-40, Aβ1-42, and α-Syn were not correlated with cognitive decline. aMCI converters had lower baseline levels of p-Tau 181 (p=0.002) but larger annual changes (p=0.001) than aMCI non-converters. The change in p-Tau 181 levels showed better discriminatory capacity than the change in t-Tau levels in terms of identifying AD conversion in patients with aMCI, with an area under curve of 86.7% versus 72.2%. Conclusion We found changes in p-Tau 181 levels may be a suitable biomarker for identifying AD conversion.

Objective: Whether elevation in plasma levels of amyloid and tau protein biomarkers are better indicators of cognitive decline than higher baseline levels in patients with amnestic mild cognitive impairment (aMCI) and Alzheimer’s disease (AD) remains understudied. Methods: We included 67 participants with twice testing for AD-related plasma biomarkers via immunomagnetic reduction (IMR) assays (amyloid beta [Aβ]1-40, Aβ1-42, total tau [t-Tau], phosphorylated tau [p-Tau] 181, and alpha-synuclein [α-Syn]) and the Mini-Mental State Examination (MMSE) over a 1-year interval. We examined the correlation between biomarker levels (baseline vs. longitudinal change) and annual changes in the MMSE scores. Receiver operating characteristic curve analysis was conducted to compare the biomarkers. Results: After adjustment, faster cognitive decline was correlated with lower baseline levels of t-Tau (β=0.332, p=0.030) and p-Tau 181 (β=0.369, p=0.015) and rapid elevation of t-Tau (β=-0.330, p=0.030) and p-Tau 181 levels (β=-0.431, p=0.004). However, the levels (baseline and longitudinal changes) of Aβ1-40, Aβ1-42, and α-Syn were not correlated with cognitive decline. aMCI converters had lower baseline levels of p-Tau 181 (p=0.002) but larger annual changes (p=0.001) than aMCI non-converters. The change in p-Tau 181 levels showed better discriminatory capacity than the change in t-Tau levels in terms of identifying AD conversion in patients with aMCI, with an area under curve of 86.7% versus 72.2%. Conclusion We found changes in p-Tau 181 levels may be a suitable biomarker for identifying AD conversion.

Objective: Whether elevation in plasma levels of amyloid and tau protein biomarkers are better indicators of cognitive decline than higher baseline levels in patients with amnestic mild cognitive impairment (aMCI) and Alzheimer’s disease (AD) remains understudied. Methods: We included 67 participants with twice testing for AD-related plasma biomarkers via immunomagnetic reduction (IMR) assays (amyloid beta [Aβ]1-40, Aβ1-42, total tau [t-Tau], phosphorylated tau [p-Tau] 181, and alpha-synuclein [α-Syn]) and the Mini-Mental State Examination (MMSE) over a 1-year interval. We examined the correlation between biomarker levels (baseline vs. longitudinal change) and annual changes in the MMSE scores. Receiver operating characteristic curve analysis was conducted to compare the biomarkers. Results: After adjustment, faster cognitive decline was correlated with lower baseline levels of t-Tau (β=0.332, p=0.030) and p-Tau 181 (β=0.369, p=0.015) and rapid elevation of t-Tau (β=-0.330, p=0.030) and p-Tau 181 levels (β=-0.431, p=0.004). However, the levels (baseline and longitudinal changes) of Aβ1-40, Aβ1-42, and α-Syn were not correlated with cognitive decline. aMCI converters had lower baseline levels of p-Tau 181 (p=0.002) but larger annual changes (p=0.001) than aMCI non-converters. The change in p-Tau 181 levels showed better discriminatory capacity than the change in t-Tau levels in terms of identifying AD conversion in patients with aMCI, with an area under curve of 86.7% versus 72.2%. Conclusion We found changes in p-Tau 181 levels may be a suitable biomarker for identifying AD conversion.

Objective: Whether elevation in plasma levels of amyloid and tau protein biomarkers are better indicators of cognitive decline than higher baseline levels in patients with amnestic mild cognitive impairment (aMCI) and Alzheimer’s disease (AD) remains understudied. Methods: We included 67 participants with twice testing for AD-related plasma biomarkers via immunomagnetic reduction (IMR) assays (amyloid beta [Aβ]1-40, Aβ1-42, total tau [t-Tau], phosphorylated tau [p-Tau] 181, and alpha-synuclein [α-Syn]) and the Mini-Mental State Examination (MMSE) over a 1-year interval. We examined the correlation between biomarker levels (baseline vs. longitudinal change) and annual changes in the MMSE scores. Receiver operating characteristic curve analysis was conducted to compare the biomarkers. Results: After adjustment, faster cognitive decline was correlated with lower baseline levels of t-Tau (β=0.332, p=0.030) and p-Tau 181 (β=0.369, p=0.015) and rapid elevation of t-Tau (β=-0.330, p=0.030) and p-Tau 181 levels (β=-0.431, p=0.004). However, the levels (baseline and longitudinal changes) of Aβ1-40, Aβ1-42, and α-Syn were not correlated with cognitive decline. aMCI converters had lower baseline levels of p-Tau 181 (p=0.002) but larger annual changes (p=0.001) than aMCI non-converters. The change in p-Tau 181 levels showed better discriminatory capacity than the change in t-Tau levels in terms of identifying AD conversion in patients with aMCI, with an area under curve of 86.7% versus 72.2%. Conclusion We found changes in p-Tau 181 levels may be a suitable biomarker for identifying AD conversion.

Traumatic brain injury (TBI) is intricately linked to the most severe clinical manifestations of brain damage. It encompasses dynamic pathological mechanisms, including hemodynamic disorders, excitotoxic injury, oxidative stress, mitochondrial dysfunction, inflammation, and neuronal death. This review provides a comprehensive analysis and summary of biomaterial-based tissue engineering scaffolds and nano-drug delivery systems. As an example of functionalized biomaterials, nano-drug delivery systems alter the pharmacokinetic properties of drugs. They provide multiple targeting strategies relying on factors such as morphology and scale, magnetic fields, pH, photosensitivity, and enzymes to facilitate the transport of therapeutics across the blood-brain barrier and to promote selective accumulation at the injury site. Furthermore, therapeutic agents can be incorporated into bioscaffolds to interact with the biochemical and biophysical environment of the brain. Bioscaffolds can mimic the extracellular matrix environment, regulate cellular interactions, and increase the effectiveness of local treatments following surgical interventions. Additionally, stem cell-based and exosome-dominated extracellular vesicle carriers exhibit high bioreactivity and low immunogenicity and can be used to design therapeutic agents with high bioactivity. This review also examines the utilization of endogenous bioactive materials in the treatment of TBI.

The structure of intestinal tissue is complex. In vitro simulation of intestinal structure and function is important for studying intestinal development and diseases. Recently, organoids have been successfully constructed and they have come to play an important role in biomedical research. Organoids are miniaturized three-dimensional (3D) organs, derived from stem cells, which mimic the structure, cell types, and physiological functions of an organ, making them robust models for biomedical research. Intestinal organoids are 3D micro-organs derived from intestinal stem cells or pluripotent stem cells that can successfully simulate the complex structure and function of the intestine, thereby providing a valuable platform for intestinal development and disease research. In this article, we review the latest progress in the construction and application of intestinal organoids.
Organoids/cytology* ; Intestines/physiology* ; Humans ; Animals ; Pluripotent Stem Cells

Objective To observe the effects of 3 different nutritional support modes of nasogastric tube nutrition,nasoenteric tube nutrition and nasoenteric tube combined with nasogastric tube nutrition on the biliary-related indices of critically ill patients.Methods The observational research method was conducted,the patients admitted to the department of intensive care unit(ICU)of Qingdao Hospital,University of Health and Rehabilitation Sciences(Qingdao Municipal Hospital)from June 2023 to May 2024 serving as the subjects of the study.The subjects were divided into three groups,namely the nasogastric tube group(indwelling nasogastric tube for enteral nutrition),the nasoenteric tube group(indwelling nasoenteric tube for enteral nutrition),and the mixed nutrition group(indwelling nasoenteric tube combined with naso-gastric tube for enteral nutrition)according to the different modes of enteral nutrition given.The clinical data of the patients was collected,including gender,age,previous underlying diseases,nutritional risk screening 2002(NRS2002)score,acute physiology and chronic health evaluationⅡ(APACHEⅡ),gallbladder volume,data on laboratory-related indices,and prognosis during hospitalisation.Compare the differences between the observed indicators and their change values before and after the initiation of enteral nutrition within each group;analyse the correlation between gallbladder volume and other observed indicators using Spearman's correlation analysis;screen the influencing factors of gallbladder volume using univariate regression analysis;screen the influencing factors of ICU patients'survival during hospitalisation using multifactorial Logistic regression analysis,and plot the receiver operator characteristic curve(ROC curve)of the subjects to analyse the predictive value of each influencing factor on patients'prognosis.Results A total of 141 patients who met the inclusion criteria were included in the study,comprising 54 cases in the nasogastric tube group,38 cases in the nasoenteric tube group,and 49 cases in the mixed nutrition group.Of the patients who survived during ICU hospitalization,105 survived,while 36 died,mortality was 25.53%.① No statistically significant differences were observed in the comparison of gender,age,previous underlying disease,NRS2002 score,and APACHEⅡscore among the enrolled groups.② A comparative analysis was conducted on the biliary-related indexes of the nasogastric tube and nasoenteric tube groups before and after the initiation of enteral nutrition.The results revealed no statistically significant differences between the two groups.On the 7th day of enteral nutrition initiation,the gallbladder volume of the nasoenteric tube group was found to be significantly larger than the gallbladder volume on the 1st day(cm3:28.00±6.36 vs.25.20±4.75,P<0.05).In the mixed nutrition group,the gallbladder volume on the initiation of enteral nutrition on day 7 was significantly smaller than that on the 1st day of initiating enteral nutrition(cm3:25.03±4.69 vs.28.68±5.96,P<0.05).③A comparative analysis was conducted among the three groups,revealing significant variations in the values of alanine aminotransferase(ALT),aspartate aminotransferase(AST),total bilirubin(TBil),indirect bilirubin(IBil),alkaline phosphatase(ALP),γ-glutamyltranspeptidase(γ-GT),and gallbladder volume across the groups.From 1-7 days following the initiation of enteral nutrition,the bile-related indexes in the nasoenteric tube group exhibited an increasing trend,while the bile-related indexes in the mixed nutrition group demonstrated a decreasing trend.④ Spearman correlation analysis showed that gallbladder volume was significantly and positively correlated with AST,ALT,ALP,and γ-GT(r values of 0.398,0.299,0.242,and 0.262,respectively,all P<0.01).⑤ Multivariate Logistic regression analysis demonstrated that the initiation of enteral nutrition for 7 days was associated with a significant advantage,as indicated by an odds ratio(OR)of 1.031,with a 95%confidence interval(95%CI)of 1.004-1.058,and a P value was 0.024.Furthermore,the initiation of enteral nutrition for 7 d AST(OR=1.031,95%CI was 1.004-1.058,P=0.024),TBil(OR=1.187,95%CI was 1.039-1.355,P=0.011),and IBil(OR=0.707,95%CI was 0.542-0.921,P=0.010),and γ-GT(OR=0.985,95%CI was 0.972-0.999,P=0.034)were all factors affecting the survival of ICU patients during hospitalisation.Conclusions In the context of patients receiving intensive care,the prolonged utilisation of nasoenteric feeding tubes for a duration exceeding seven days has been observed to potentially induce an augmentation in gallbladder volume and an elevation in biliary-related indices,including ALT,AST,ALP,and γ-GT.The concomitant administration of nasogastric feeding,grounded in the foundation of simple nasoenteric tube nutrition,has been demonstrated to result in a reduction of these biliary-related indices to a certain extent.