Objective To systematically evaluate the risk prediction models for postoperative delirium in adults with cardiac surgery. Methods The SinoMed, CNKI, Wanfang, VIP, PubMed, EMbase, Web of Science, and Cochrane Library databases were searched to collect studies on risk prediction models for postoperative delirium in cardiac surgery published up to January 29, 2025. Two researchers screened the literature according to inclusion and exclusion criteria, used the PROBAST bias tool to assess the quality of the literature, and conducted a meta-analysis of common predictors in the model using Stata 17.0 software. Results A total of 21 articles were included, establishing 45 models with 28733 patients. Age, cardiopulmonary bypass time, history of diabetes, history of cerebrovascular disease, and gender were the top five common predictors. The area under the curve (AUC) of the 45 models ranged from 0.544 to 0.98. Fourteen out of the 21 studies had good applicability, while the applicability of the remaining seven was unclear; 20 studies had a high risk of bias. Meta-analysis showed that the incidence of postoperative delirium in adults with cardiac surgery was 18.6% [95%CI (15.7%, 21.6%)], and age [OR=1.045 (1.036, 1.054), P<0.001], history of cerebrovascular disease [OR=1.758 (1.459, 2.057), P<0.001], gender [OR=1.732 (1.430, 2.034), P<0.001], mini-mental state examination score [OR=3.930 (1.859, 8.309), P<0.001], and length of ICU stay [OR=5.586 (4.289, 6.883), P<0.001] were independent influencing factors for postoperative delirium after cardiac surgery. Conclusion The risk prediction models for postoperative delirium after cardiac surgery have good predictive performance, but there is a high overall risk of bias. In the future, large-sample, multicenter, high-quality prospective clinical studies should be conducted to construct the optimal risk prediction model for postoperative delirium in adults with cardiac surgery, aiming to identify and prevent the occurrence of postoperative delirium as early as possible.

Sustained inflammatory responses are closely related to various severe diseases, and inhibiting the excessive activation of inflammasomes and pyroptosis has significant implications for clinical treatment. Natural products have garnered considerable concern for the treatment of inflammation. Huanglian-Wumei decoction (HLWMD) is a classic prescription used for treating inflammatory diseases, but the necessity of their combination and the exact underlying anti-inflammatory mechanism have not yet been elucidated. Inspired by the supramolecular self-assembly strategy and natural drug compatibility theory, we successfully obtained berberine (BBR)-chlorogenic acid (CGA) supramolecular (BCS), which is an herbal pair from HLWMD. Using a series of characterization methods, we confirmed the self-assembly mechanism of BCS. BBR and CGA were self-assembled and stacked into amphiphilic spherical supramolecules in a 2:1 molar ratio, driven by electrostatic interactions, hydrophobic interactions, and π-π stacking; the hydrophilic fragments of CGA were outside, and the hydrophobic fragments of BBR were inside. This stacking pattern significantly improved the anti-inflammatory performance of BCS compared with that of single free molecules. Compared with free molecules, BCS significantly attenuated the release of multiple inflammatory mediators and lipopolysaccharide (LPS)-induced pyroptosis. Its anti-inflammatory mechanism is closely related to the inhibition of intracellular nuclear factor-kappaB (NF-κB) p65 phosphorylation and the noncanonical pyroptosis signalling pathway mediated by caspase-11.

BACKGROUND:Sarcopenia is a comprehensive condition of aging induced decline in skeletal muscle mass and strength and represents a major health challenge for the elderly.Accumulating evidence suggests that mitochondrial dysfunction plays a key role in the pathogenesis of sarcopenia.OBJECTIVE:To summarize the mechanisms by which dysregulation of mitochondrial quality control leads to sarcopenia and to explore whether mitochondrial transplantation may be a potential target for the treatment of sarcopenia.METHODS:We searched PubMed and CNKI databases for relevant articles published from 2009 to 2023 using the keywords "sarcopenia,mitochondrial dysfunction,mitochondrial quality control,mitochondrial transplantation,limitations."RESULTS AND CONCLUSION:Given the key role of mitochondrial dysfunction in the pathogenesis of sarcopenia,mitochondrial transplantation may serve as a possible strategy for the treatment of sarcopenia by improving mitochondrial bioenergetics and modulating mitochondria related signaling pathways.Although some preclinical and clinical studies have confirmed the potential of mitochondrial transplantation for the treatment of various diseases,there are still some urgent questions regarding the specific details of mitochondrial transfer.

Objective:To analyze the clinical characteristics and related factors of cognition disorders in elderly hypertensive patients.Methods:It was a cross-sectional study. A total of 612 hypertensive patients with the age of (69.06±6.58) years (median 68.00 years) admitted in the Department of Cardiology, General Hospital of Chinese People′s Liberation Army from October 2022 to April 2024 were enrolled. The demographic and clinical data were collected, the cognition status was assessed with Mini-Mental State Examination (MMSE) at admission. The related factors of cognition disorders were analyzed with univariate and multivariate logistic regression.Results:The results showed that female hypertensive patients and those with older age, lower education, higher fasting blood glucose (FBG) and diabetes mellitus, higher low-density lipoprotein cholesterol (LDL-C) level, higher systolic blood pressure (SBP) and more cardiovascular comorbidities were likely to have cognition disorders (all P<0.05). Multivariate logistic regression analysis showed that smoking history, elevated SBP, elevated heart rate, elevated FBG, and elevated LDL-C were independent risk factors for cognition disorders in elderly hypertensive patients,while higher education level was an independent protective factor (all P<0.05). Conclusion:Smoking, increased SBP, increased heart rate, increased FBG, increased LDL-C and lower education level are independently associated with cognition disorders in elderly hypertensive patients.

Objective:To screen risk factors for ICU-acquired weakness in patients with mechanical ventilation and construct a predictive model, so as to provide a basis for the health management of patients with mechanical ventilation.Methods:Convenience sampling was used to select 312 ICU patients with mechanical ventilation admitted to the Tenth People's Hospital of Tongji University from October 2019 to August 2020 for the study. Patients were divided into training set ( n=220) and test set ( n=92) in a 7∶3 ratio. Based on machine learning algorithms, decision random forest (DRF), extremely-randomized trees (XRT) and generalized linear model (GLM) were used to construct three ICU-acquired weakness risk prediction models for patients with mechanical ventilation, respectively. The performance of the prediction model was evaluated using the area under the receiver operating characteristic curve ( AUC), the area under the precision-recall curve ( AUPRC), and the root mean square error ( RMSE) . Results:There were 7 predictors of risk of ICU-acquired weakness in patients with mechanical ventilation, including age, gender, braking, duration of mechanical ventilation, blood glucose, lactic acid, and parenteral nutrition. Test set and training set validation showed that AUC and AUPRC of GLM prediction model were greater than those of DRF, XRT prediction model. Test set validation indicated that the RMSE, logarithmic loss of GLM prediction model was less than those of DRF, XRT prediction model. Conclusions:Machine learning algorithm based GLM prediction model has good prediction performance. Healthcare professionals can construct evidence-based decisions for interventions in areas such as braking, duration of mechanical ventilation, and blood glucose management.

OBJECTIVE: To explore the potential effects and mechanisms of Liang-Ge-San (LGS) for the treatment of acute respiratory distress syndrome (ARDS) through network pharmacology analysis and to verify LGS activity through biological experiments. METHODS: The key ingredients of LGS and related targets were obtained from the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform. ARDS-related targets were selected from GeneCards and DisGeNET databases. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed using the Metascape Database. Molecular docking analysis was used to confirm the binding affinity of the core compounds with key therapeutic targets. Finally, the effects of LGS on key signaling pathways and biological processes were determined by in vitro and in vivo experiments. RESULTS: A total of LGS-related targets and 496 ARDS-related targets were obtained from the databases. Network pharmacological analysis suggested that LGS could treat ARDS based on the following information: LGS ingredients luteolin, wogonin, and baicalein may be potential candidate agents. Mitogen-activated protein kinase 14 (MAPK14), recombinant V-Rel reticuloendotheliosis viral oncogene homolog A (RELA), and tumor necrosis factor alpha (TNF-α) may be potential therapeutic targets. Reactive oxygen species metabolic process and the apoptotic signaling pathway were the main biological processes. The p38MAPK/NF-κ B signaling pathway might be the key signaling pathway activated by LGS against ARDS. Moreover, molecular docking demonstrated that luteolin, wogonin, and baicalein had a good binding affinity with MAPK14, RELA, and TNF α. In vitro experiments, LGS inhibited the expression and entry of p38 and p65 into the nucleation in human bronchial epithelial cells (HBE) cells induced by LPS, inhibited the inflammatory response and oxidative stress response, and inhibited HBE cell apoptosis (P<0.05 or P<0.01). In vivo experiments, LGS improved lung injury caused by ligation and puncture, reduced inflammatory responses, and inhibited the activation of p38MAPK and p65 (P<0.05 or P<0.01). CONCLUSION LGS could reduce reactive oxygen species and inflammatory cytokine production by inhibiting p38MAPK/NF-κ B signaling pathway, thus reducing apoptosis and attenuating ARDS.
Drugs, Chinese Herbal/pharmacology* ; Respiratory Distress Syndrome/enzymology* ; p38 Mitogen-Activated Protein Kinases/metabolism* ; NF-kappa B/metabolism* ; Animals ; Signal Transduction/drug effects* ; Molecular Docking Simulation ; Humans ; Male ; Network Pharmacology ; Apoptosis/drug effects* ; Mice

OBJECTIVE: To identify the underlying mechanism by which quercetin (Que) alleviates sepsis-related acute respiratory distress syndrome (ARDS). METHODS: In vivo, C57BL/6 mice were assigned to sham, cecal ligation and puncture (CLP), and CLP+Que (50 mg/kg) groups (n=15 per group) by using a random number table. The sepsisrelated ARDS mouse model was established using the CLP method. In vitro, the murine alveolar macrophages (MH-S) cells were classified into control, lipopolysaccharide (LPS), LPS+Que (10 μmol/L), and LPS+Que+acetylcysteine (NAC, 5 mmol/L) groups. The effect of Que on oxidative stress, inflammation, and apoptosis in mice lungs and MH-S cells was determined, and the mechanism with reactive oxygen species (ROS)/p38 mitogen-activated protein kinase (MAPK) pathway was also explored both in vivo and in vitro. RESULTS: Que alleviated lung injury in mice, as reflected by a reversal of pulmonary histopathologic changes as well as a reduction in lung wet/dry weight ratio and neutrophil infiltration (P<0.05 or P<0.01). Additionally, Que improved the survival rate and relieved gas exchange impairment in mice (P<0.01). Que treatment also remarkedly reduced malondialdehyde formation, superoxide dismutase and catalase depletion, and cell apoptosis both in vivo and in vitro (P<0.05 or P<0.01). Moreover, Que treatment diminished the release of inflammatory factors interleukin (IL)-1β, tumor necrosis factor-α, and IL-6 both in vivo and in vitro (P<0.05 or P<0.01). Mechanistic investigation clarifified that Que administration led to a decline in the phosphorylation of p38 MAPK in addition to the suppression of ROS expression (P<0.01). Furthermore, in LPS-induced MH-S cells, ROS inhibitor NAC further inhibited ROS/p38 MAPK pathway, as well as oxidative stress, inflammation, and cell apoptosis on the basis of Que treatment (P<0.05 or P<0.01). CONCLUSION Que was found to exert anti-oxidative, anti-inflammatory, and anti-apoptotic effects by suppressing the ROS/p38 MAPK pathway, thereby conferring protection for mice against sepsis-related ARDS.
Animals ; Sepsis/drug therapy* ; Quercetin/therapeutic use* ; Respiratory Distress Syndrome/enzymology* ; p38 Mitogen-Activated Protein Kinases/metabolism* ; Mice, Inbred C57BL ; Reactive Oxygen Species/metabolism* ; Apoptosis/drug effects* ; Male ; Oxidative Stress/drug effects* ; MAP Kinase Signaling System/drug effects* ; Lung/drug effects* ; Mice ; Lipopolysaccharides ; Macrophages, Alveolar/pathology* ; Inflammation/pathology* ; Protective Agents/therapeutic use*

Objective: To compare the changes in the concentration of relevant growth factors released from platelet-rich plasma (PRP) stored at -80℃ by cryopreservation and at 4℃ by refrigerated lyophilization over 2 years, aiming to provide a theoretical basis for prolonging PRP storage duration. Methods: PRP (n=15) was separated using a blood cell separator and stored under -80℃ cryopreservation (F-PRP group) and 4℃ refrigerated freeze-drying conditions (FD-PRP group). The contents of growth factors (PDGF-AA, PDGF-BB, EGF, TGF-β1, and VEGF) in both groups were measured by ELISA at 1, 3, 6, 9, 12 and 24 months. Results: PDGF-AA and VEGF maintained good stability in both groups for up to 24 months. PDGF-BB and TGF-β1 showed high stability in the first 12 months but their stability decreased gradually from 12th to 24th months. EGF demonstrated good stability in the first 6 months, and its stability gradually decreased from the 9th to 24th months. Comparing the F-PRP and FD-PRP groups, the concentrations of the five growth factors in the FD-PRP group were either not statistically different or higher than those in the F-PRP group at all time points. Specifically, the concentrations of EGF were significantly higher in the FD-PRP group at all time points. Conclusion: Both -80℃ freezing and 4℃ freeze-drying enable long-term preservation of PRP. Freeze-drying imposes less stringent storage requirements and facilitates growth factor compared to frozen storage.

BACKGROUND:Sarcopenia is a comprehensive condition of aging induced decline in skeletal muscle mass and strength and represents a major health challenge for the elderly.Accumulating evidence suggests that mitochondrial dysfunction plays a key role in the pathogenesis of sarcopenia.OBJECTIVE:To summarize the mechanisms by which dysregulation of mitochondrial quality control leads to sarcopenia and to explore whether mitochondrial transplantation may be a potential target for the treatment of sarcopenia.METHODS:We searched PubMed and CNKI databases for relevant articles published from 2009 to 2023 using the keywords "sarcopenia,mitochondrial dysfunction,mitochondrial quality control,mitochondrial transplantation,limitations."RESULTS AND CONCLUSION:Given the key role of mitochondrial dysfunction in the pathogenesis of sarcopenia,mitochondrial transplantation may serve as a possible strategy for the treatment of sarcopenia by improving mitochondrial bioenergetics and modulating mitochondria related signaling pathways.Although some preclinical and clinical studies have confirmed the potential of mitochondrial transplantation for the treatment of various diseases,there are still some urgent questions regarding the specific details of mitochondrial transfer.

Objective:To screen risk factors for ICU-acquired weakness in patients with mechanical ventilation and construct a predictive model, so as to provide a basis for the health management of patients with mechanical ventilation.Methods:Convenience sampling was used to select 312 ICU patients with mechanical ventilation admitted to the Tenth People's Hospital of Tongji University from October 2019 to August 2020 for the study. Patients were divided into training set ( n=220) and test set ( n=92) in a 7∶3 ratio. Based on machine learning algorithms, decision random forest (DRF), extremely-randomized trees (XRT) and generalized linear model (GLM) were used to construct three ICU-acquired weakness risk prediction models for patients with mechanical ventilation, respectively. The performance of the prediction model was evaluated using the area under the receiver operating characteristic curve ( AUC), the area under the precision-recall curve ( AUPRC), and the root mean square error ( RMSE) . Results:There were 7 predictors of risk of ICU-acquired weakness in patients with mechanical ventilation, including age, gender, braking, duration of mechanical ventilation, blood glucose, lactic acid, and parenteral nutrition. Test set and training set validation showed that AUC and AUPRC of GLM prediction model were greater than those of DRF, XRT prediction model. Test set validation indicated that the RMSE, logarithmic loss of GLM prediction model was less than those of DRF, XRT prediction model. Conclusions:Machine learning algorithm based GLM prediction model has good prediction performance. Healthcare professionals can construct evidence-based decisions for interventions in areas such as braking, duration of mechanical ventilation, and blood glucose management.