Objective To develop an enteral nutrition management system for critically ill patients and assess its application outcomes to standardize enteral nutrition management.Methods Based on relevant guidelines and indicator systems,a management system for enteral nutrition in critically ill patients was constructed,consisting of 4 modules:nutritional screening and assessment,nutritional implementation,nutritional monitoring,and statistical analysis.A convenience sampling method was used to select enteral nutrition patients and healthcare staff from the ICU of a tertiary hospital in Ningbo.Data from January to February 2024 served as an experimental group,while data from January to February 2023 constituted a control group.The 2 groups were compared regarding nutritional risk screening rate,feeding interruption rate,completion rate of the enteral nutrition plan,and incidence of complications.At the same time,the system's effectiveness was assessed by healthcare professionals using the clinical nursing information system effectiveness evaluation form.Results The study included 111 patients in the experimental group and 101 patients in the control group.The experimental group exhibited a significantly higher nutritional risk screening rate and enteral nutrition plan completion rate,as well as significantly lower feeding interruption rate and incidence of mechanical complications compared to the control group(P＜0.05).The system received a high effectiveness rating,with an average score of 104.73±9.34.Conclusion The application of the enteral nutrition management system effectively improves the nutritional risk screening rate and completion rate of enteral nutrition plans,while reducing both the feeding interruption rate and the incidence of mechanical complications.Healthcare staff highly rated the system.

Objectives:To investigate the effect of circular RNA (circRNA) hsa_circ_0019217 on the biological function of chorionic trophoblast cell line (HTR8/SVneo) and its mechanism in the occurrence of pre-eclampsia (PE).Methods:The circRNA expression database was used to analyze the differentially expressed circRNA in placental tissues of PE women. The expression levels of hsa_circ_0019217 and miR-526b-5p were detected by reverse transcription real-time fluorescent quantitative PCR (RT-qPCR), and the subcellular localization of hsa_circ_0019217 was detected by fluorescence in situ hybridization. The proliferation, migration and invasion of trophoblast cells were detected by cell counting kit-8 (CCK-8) assay and transwell assay. Western blot and enzyme-linked immunosorbent assay (ELISA) were used to verify the effects of hsa_circ_0019217, miR-526b-5p and decorin (DCN) on matrix metalloproteinase 2 (MMP2), tissue inhibitor of metalloproteinase 2 (TIMP2), placental growth factor (PlGF) and human chorionic gonadotropin (hCG) protein expression levels. Dual luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay were used to verify the interaction between hsa_circ_0019217, miR-526-5p and DCN.Results:(1) The analysis of circRNA expression database showed that the expression level of hsa_circ_0019217 was significantly increased in the placental tissues of PE women (fold change=67, P<0.05), and it was mainly located in the cytoplasm. (2) Knockdown of hsa_circ_0019217 promoted the proliferation, migration and invasion of HTR8/SVneo cells, increased the expression levels of MMP2 and PlGF, and decreased the expression levels of TIMP2 and hCG in HTR8/SVneo cells. (3) Hsa_circ_0019217 targeted adsorption of miR-526b-5p, and inhibition of miR-526b-5p reduced the proliferation, migration and invasion of HTR8/SVneo cells. The expression levels of MMP2 and PlGF in HTR8/SVneo cells were increased, and the expression levels of TIMP2 and hCG were decreased. Hsa_circ_0019217 knockdown and inhibiting miR-526b-5p could reverse the effect of hsa_circ_0019217 knockdown on promoting the proliferation, migration and invasion of HTR8/SVneo cells, and reversed the effect of hsa_circ_0019217 knockdown on the protein expression levels of MMP2, PlGF, TIMP2 and hCG. (4) miR-526b-5p targeted DCN in HTR8/SVneo cells, hsa_circ_0019217 knockdown reduced the expression level of DCN, and inhibiting miR-526b-5p increased the expression level of DCN. When hsa_circ_0019217 and miR-526b-5p were inhibited simultaneously, there was no significant change in the protein expression level of DCN. (5) Overexpression of miR-526b-5p promoted the proliferation, migration and invasion of HTR8/SVneo cells, while overexpression of DCN inhibited the proliferation, migration and invasion of HTR8/SVneo cells. Simultaneous overexpression of miR-526b-5p and DCN reversed the effects of miR-526b-5p overexpression on cell proliferation, migration and invasion. Overexpression of miR-526b-5p increased the expression levels of MMP2 and PlGF and decreased the expression levels of TIMP2 and hCG in HTR8/SVneo cells. Overexpression of DCN reduced the expression levels of MMP2 and PlGF and increased the expression levels of TIMP2 and hCG. Overexpression of miR-526b-5p and DCN reversed the effects of miR-526b-5p on the expression of these proteins. Conclusion:Hsa_circ_0019217 regulates the expression of DCN by adsorption of miR-526b-5p, thereby affecting the proliferation, migration and invasion of trophoblast cells and regulating the protein expression levels of MMP2, TIMP2, PlGF and hCG, which might be used as a target for early prevention of PE.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

ObjectiveTo establish and validate a new prediction model for the risk of death in patients with acute-on-chronic liver failure （ACLF） based on sarcopenia and other clinical indicators， and to improve the accuracy of prognostic assessment for ACLF patients. MethodsA total of 380 patients with ACLF who were admitted to Beijing YouAn Hospital， Capital Medical University， from January 2019 to January 2022 were enrolled， and they were divided into training group with 228 patients and testing group with 152 patients in a ratio of 6∶4 using the stratified random sampling method. For the training group， CT images were used to measure the cross-sectional area of the skeletal muscle at the third lumbar vertebra （L3）， and L3 skeletal muscle index （L3-SMI） was calculated. Sarcopenia was diagnosed based on the previously established L3-SMI reference values for healthy adults in northern China. Univariate and multivariable Cox regression analyses were used to establish a sarcopenia-ACLF model which integrated sarcopenia and clinical risk factors， and a nomogram was developed for presentation. The area under the ROC curve （AUC） was used to assess the predictive performance of the model， the calibration curve was used to assess the degree of calibration， and a decision curve analysis was used to investigate the clinical application value of the model. The independent-samples t test or the Mann-Whitney U test was used for comparison of continuous data between two groups， and the chi-square test was used for comparison of categorical data between two groups. The Kaplan-Meier method was used to plot survival curves， and the Log-rank test was used for comparison between groups. The DeLong test was used for comparison of AUC between different models. ResultsThe multivariate Cox regression analysis showed that sarcopenia （hazard ratio ［HR］=1.962， 95% confidence interval ［CI］： 1.185‍ ‍—‍ ‍3.250， P=0.009）， total bilirubin （HR=1.003， 95%CI： 1.002‍ ‍—‍ ‍1.005， P<0.001）， international normalized ratio （HR=1.997， 95%CI： 1.674‍ ‍—‍ ‍2.382， P<0.001）， and lactic acid （HR=1.382， 95%CI： 1.170‍ ‍—‍ ‍1.632， P<0.001） were included in the sarcopenia-ACLF model. In the training cohort， the sarcopenia-ACLF model had a larger AUC than MELD-Na score in predicting 90-day mortality in patients with ACLF （0.80 vs 0.73， Z=1.97， P=0.049）. In the test cohort， the sarcopenia-ACLF model had a significantly larger AUC than MELD score （0.79 vs 0.69， Z=2.70， P=0.007） and MELD-Na score （0.79 vs 0.68， Z=2.92， P=0.004）. The calibration curve showed that the model had good calibration ability， with a relatively good consistency between the predicted risk of mortality and the observed results. The DCA results showed that within a reasonable range of threshold probabilities， the sarcopenia-ACLF model showed a greater net benefit than MELD and MELD-Na scores in both the training cohort and the test cohort. ConclusionThe sarcopenia-ACLF model developed in this study provides a more accurate tool for predicting the risk of 90-day mortality in ACLF patients， which provides support for clinical decision-making and helps to optimize treatment strategies.

Objective: Neuronal apoptosis is considered to be a critical process in spinal cord injury (SCI). Despite growing evidence of the antiapoptotic, anti-inflammatory, and modulation of ischemic injury tolerance effects of extracellular ubiquitin (eUb), existing studies have paid less attention to the impact of eUb in neurological injury disorders, particularly in SCI. This study aimed to investigate whether eUb can play a protective role in neurons, both in vitro and in vivo, and explores the underlying mechanisms. Methods: By utilizing an oxygen glucose deprivation cellular model and a SCI rat model, we firstly investigated the therapeutic effects of eUb on SCI and further explored its effects on neuronal autophagy and mitochondria-dependent apoptosis-related indicators, as well as the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mechanical target of rapamycin (mTOR) signaling pathway. Results: In the SCI models both in vivo and in vitro, early intervention with eUb enhanced neuronal autophagy and inhibited mitochondrial apoptotic pathways, significantly mitigating SCI. Further studies had shown that this protective effect of eUb was mediated through its receptor, CXC chemokine receptor type 4 (CXCR4). Additionally, eUb-enhanced autophagy and antiapoptotic effects were possibly associated with inhibiting the PI3K/Akt/mTOR pathway. Conclusion In summary, the study demonstrates that early eUb intervention can enhance autophagy and inhibit mitochondrial apoptotic pathways via CXCR4, protecting neurons and promoting SCI repair.

Objectives:To investigate the effect of circular RNA (circRNA) hsa_circ_0019217 on the biological function of chorionic trophoblast cell line (HTR8/SVneo) and its mechanism in the occurrence of pre-eclampsia (PE).Methods:The circRNA expression database was used to analyze the differentially expressed circRNA in placental tissues of PE women. The expression levels of hsa_circ_0019217 and miR-526b-5p were detected by reverse transcription real-time fluorescent quantitative PCR (RT-qPCR), and the subcellular localization of hsa_circ_0019217 was detected by fluorescence in situ hybridization. The proliferation, migration and invasion of trophoblast cells were detected by cell counting kit-8 (CCK-8) assay and transwell assay. Western blot and enzyme-linked immunosorbent assay (ELISA) were used to verify the effects of hsa_circ_0019217, miR-526b-5p and decorin (DCN) on matrix metalloproteinase 2 (MMP2), tissue inhibitor of metalloproteinase 2 (TIMP2), placental growth factor (PlGF) and human chorionic gonadotropin (hCG) protein expression levels. Dual luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay were used to verify the interaction between hsa_circ_0019217, miR-526-5p and DCN.Results:(1) The analysis of circRNA expression database showed that the expression level of hsa_circ_0019217 was significantly increased in the placental tissues of PE women (fold change=67, P<0.05), and it was mainly located in the cytoplasm. (2) Knockdown of hsa_circ_0019217 promoted the proliferation, migration and invasion of HTR8/SVneo cells, increased the expression levels of MMP2 and PlGF, and decreased the expression levels of TIMP2 and hCG in HTR8/SVneo cells. (3) Hsa_circ_0019217 targeted adsorption of miR-526b-5p, and inhibition of miR-526b-5p reduced the proliferation, migration and invasion of HTR8/SVneo cells. The expression levels of MMP2 and PlGF in HTR8/SVneo cells were increased, and the expression levels of TIMP2 and hCG were decreased. Hsa_circ_0019217 knockdown and inhibiting miR-526b-5p could reverse the effect of hsa_circ_0019217 knockdown on promoting the proliferation, migration and invasion of HTR8/SVneo cells, and reversed the effect of hsa_circ_0019217 knockdown on the protein expression levels of MMP2, PlGF, TIMP2 and hCG. (4) miR-526b-5p targeted DCN in HTR8/SVneo cells, hsa_circ_0019217 knockdown reduced the expression level of DCN, and inhibiting miR-526b-5p increased the expression level of DCN. When hsa_circ_0019217 and miR-526b-5p were inhibited simultaneously, there was no significant change in the protein expression level of DCN. (5) Overexpression of miR-526b-5p promoted the proliferation, migration and invasion of HTR8/SVneo cells, while overexpression of DCN inhibited the proliferation, migration and invasion of HTR8/SVneo cells. Simultaneous overexpression of miR-526b-5p and DCN reversed the effects of miR-526b-5p overexpression on cell proliferation, migration and invasion. Overexpression of miR-526b-5p increased the expression levels of MMP2 and PlGF and decreased the expression levels of TIMP2 and hCG in HTR8/SVneo cells. Overexpression of DCN reduced the expression levels of MMP2 and PlGF and increased the expression levels of TIMP2 and hCG. Overexpression of miR-526b-5p and DCN reversed the effects of miR-526b-5p on the expression of these proteins. Conclusion:Hsa_circ_0019217 regulates the expression of DCN by adsorption of miR-526b-5p, thereby affecting the proliferation, migration and invasion of trophoblast cells and regulating the protein expression levels of MMP2, TIMP2, PlGF and hCG, which might be used as a target for early prevention of PE.

Objective To develop an enteral nutrition management system for critically ill patients and assess its application outcomes to standardize enteral nutrition management.Methods Based on relevant guidelines and indicator systems,a management system for enteral nutrition in critically ill patients was constructed,consisting of 4 modules:nutritional screening and assessment,nutritional implementation,nutritional monitoring,and statistical analysis.A convenience sampling method was used to select enteral nutrition patients and healthcare staff from the ICU of a tertiary hospital in Ningbo.Data from January to February 2024 served as an experimental group,while data from January to February 2023 constituted a control group.The 2 groups were compared regarding nutritional risk screening rate,feeding interruption rate,completion rate of the enteral nutrition plan,and incidence of complications.At the same time,the system's effectiveness was assessed by healthcare professionals using the clinical nursing information system effectiveness evaluation form.Results The study included 111 patients in the experimental group and 101 patients in the control group.The experimental group exhibited a significantly higher nutritional risk screening rate and enteral nutrition plan completion rate,as well as significantly lower feeding interruption rate and incidence of mechanical complications compared to the control group(P＜0.05).The system received a high effectiveness rating,with an average score of 104.73±9.34.Conclusion The application of the enteral nutrition management system effectively improves the nutritional risk screening rate and completion rate of enteral nutrition plans,while reducing both the feeding interruption rate and the incidence of mechanical complications.Healthcare staff highly rated the system.