Chemotherapy-induced neuropathic pain (CINP) involves chemotherapy toxicity to cortical tissues. DNA methylation, a key epigenetic mechanism for gene regulation, has been implicated in neuropathic pain pathogenesis. The anterior cingulate cortex (ACC) is critical for pain processing, yet its susceptibility to DNA methylation-mediated epigenetic regulation remains unexplored. In a mouse model of paclitaxel (PTX)-induced CINP, we found that PTX downregulated DNA methyltransferase 3a (DNMT3a) in the ACC and induced mechanical and thermal pain hypersensitivity. Overexpression of DNMT3a specifically in ACC pyramidal neurons alleviated these PTX-induced nociceptive behaviors, whereas knockdown of DNMT3a in the ACC alone was sufficient to produce pain hypersensitivity. Western blot analysis revealed that PTX selectively upregulated GluN2B, but not other NMDA (GluN1, GluN2A), AMPA (GluA1, GluA2), or GABAA receptor subunits. Mechanistically, pyramidal neuron-specific DNMT3a overexpression in the ACC silenced GluN2B expression in a DNA methylation-dependent manner, consequently suppressing GluN2B-mediated NMDA currents in ACC pyramidal neurons. Furthermore, intra-ACC application of the GluN2B antagonist Ifenprodil reversed pain hypersensitivity induced by either PTX or DNMT3a knockdown. Finally, our results establish DNMT3a-mediated epigenetic desilencing of GluN2B in the ACC as a key mechanism underlying PTX-induced neuropathic pain, identifying both as promising therapeutic targets for CINP.

Introduction: Total hip arthroplasty (THA) is an effective treatment for end-stage hip joint diseases but is frequently associated with postoperative hyperfibrinolysis, which elevates the risks of bleeding and thrombosis. Ginsenosides, the primary active components of Panax ginseng, exhibit a range of pharmacological activities, including anti-inflammatory and anti-apoptotic effects. However, their mechanism of action in counteracting postoperative hyperfibrinolysis after THA remains unclear. Methods Active ginsenoside components were first screened from databases such as TCMSP and BATMAN-TCM on the basis of ADME parameters. Key targets were identified through network pharmacology, followed by the construction of a protein–protein interaction (PPI) network and GO and KEGG enrichment analyses. Meanwhile, venous blood samples were collected from THA patients at 2 hours preoperatively and 24 hours postoperatively for untargeted metabolomics analysis using LC-MS/MS. Multivariate statistical analysis was applied to screen differential metabolites and perform pathway enrichment. Finally, the results of network pharmacology and metabolomics were integrated to construct a “component–target–metabolic pathway” association network. Results A total of 9 active ginsenoside components were obtained, yielding 351 component-related targets and 428 fibrinolysis-related targets, with an intersection of 65 key targets. PPI network analysis identified AKT1, PTGS2, and JUN as core targets. KEGG enrichment analysis revealed significant enrichment in the complement and coagulation cascades, platelet activation, and HIF-1 signaling pathways. Metabolomics identified 292 differential metabolites, mainly enriched in arachidonic acid metabolism, purine metabolism, and glycerophospholipid metabolism. Integrative analysis identified arachidonic acid metabolism and the cGMP-PKG, cAMP, and sphingolipid signaling pathways as common key pathways. Molecular docking of AKT1 with ginsenoside Rh7, JUN with ginsenoside Rg3, PIK3CA with ginsenoside Rh1, and PTGS2 with F2 all demonstrated favorable binding affinity, further supporting the reliability of the network pharmacology predictions. Conclusion This study is the first to systematically elucidate that ginsenosides modulate postoperative fibrinolysis following THA by regulating multiple targets (e.g., AKT1 and PTGS2) and multiple pathways (including arachidonic acid metabolism and the complement and coagulation cascades), thereby providing a new theoretical basis for their perioperative clinical application.

BACKGROUND:Precise control of propofol anesthesia depth is critical for perioperative safety; however, the dynamic reorganization of large-scale cortical functional networks throughout propofol anesthesia and recovery remains incompletely understood. This study employs wide-field imaging to record neuronal activity and functional connectivity across the entire cortex to investigate these cortical network dynamics during propofol anesthesia and emergence. METHODS:By synchronously recording behavioral videos and electroencephalogram-electromyogram signals, we characterized the anesthesia depth in head-fixed mice. We performed retro-orbital sinus injections of AAV2/PHP.eB-hSyn-jGCaMP8s in 8-week-old C57BL/6J mice and recorded Ca2+ signals from the dorsal cortex under a wide-field microscope. Through functional connectivity analyses in different anesthesia stages, we elucidated the dynamic changes in functional connectivity between different cortical regions during propofol anesthesia. RESULTS:Wide-field Ca2+ imaging revealed a progressive, global suppression of cortical activity as propofol anesthesia deepened, followed by partial recovery upon emergence. During the burst-suppression stage, brief high-amplitude slow waves transiently synchronized activity across all recorded cortical regions, resulting in maximal functional connectivity. In contrast, the persistent desynchronization following emergence exhibited region-specific patterns, with a greater reduction in intra-area coherence observed in motor and somatosensory cortices (Wake_pre vs Recovery: secondary motor cortex (MOs)-primary motor cortex (MOp), somatosensory, barrel field cortex (SSb)-somatosensory, upper limb cortex (SSu), SSb-somatosensory, lower limb cortex (SSl), SSu-SSl; P < 0.05) compared with visual and retrosplenial cortices. After emergence, the inter-regional correlation coefficient declined and remained below pre-anesthesia baseline for at least 1.5 hours, despite recovery of local cortical Ca2+ activity (Wake_pre vs Recovery (mean ± SEM): 0.82 ± 0.02 vs 0.67 ± 0.03 for motor cortex (MO)-somatosensory cortex (SS), 0.61 ± 0.06 vs 0.46 ± 0.06 for MO-visual cortex (VIS), 0.69 ± 0.03 vs 0.54 ± 0.06 for MO-retrosplenial cortex (RSP), 0.72 ± 0.03 vs 0.50 ± 0.10 for SS-RSP; P < 0.05). CONCLUSIONS:These findings demonstrate a dissociation between recovery of local cortical activity and restoration of large-scale network coordination during emergence from propofol anesthesia. The persistence of impaired inter-regional synchrony after behavioral recovery suggests that normalization of cortical network integration lags behind the return of consciousness. This multimodal framework provides network-level insights into anesthesia-induced brain state transitions and has implications for improving perioperative monitoring and management.

Background: The oculocardiac reflex (OCR) is a common complication associated with ocular surgery. While cervical vagus nerve block (CVB) has demonstrated efficacy in reducing oculocardiac reflexe, the minimum effective preventing concentration of lidocaine in these procedures remains unvalidated. We investigated the median effective concentration (EC50) of lidocaine required to inhibit the left and right vagus nerves in ocular surgery. Methods: A prospective, randomized study was conducted on 60 patients undergoing hydroxyapatite orbital implantation at Daping Hospital, Army Medical University between October 2022 and November 2023. Patients were randomly allocated to receive either right or left cervical vagus nerve block. According to the up-down sequential allocation method, the initial concentration of lidocaine was 0.40% in all cases, while the concentration in the same group of two neighboring patients differed by 0.10%. The groups were classified as effective or ineffective based on whether the OCR occurred or not. We examined voice changes, nausea, and vomiting within 24 hours of the operation. Results: EC50 of lidocaine was 0.48% ± 0.39 (95% CI: 0.42%-0.62%) for right-sided blocks and 0.62% ± 0.40 (95% CI: 0.59%-0.76%) for left-sided blocks. The EC95 values were 0.72% (95% CI: 0.61%-1.49%) and 0.85% for right and left blocks, respectively. Patients with effective nerve blocks exhibited a higher incidence of postoperative hoarseness compared to those with ineffective blocks ( P =0.02). Conclusion: Ultrasound-guided cervical vagus nerve block using 0.48% lidocaine on the right side and 0.62% on the left side effectively suppresses OCR in 50% of patients undergoing hydroxyapatite orbital implantation surgery. These findings provide valuable guidance for anesthesiologists in managing OCR during ophthalmic procedures. Trial registration : ClinicalTrials.gov, NCT04950881 (registered on 20 June 2021). Written informed consent was obtained from all the patients.

Vascular leakage in sepsis is critical factors in improving the prognosis of septic patients, with limited treatment options targeting underlying molecular mechanisms. Necroptosis is a form of cell death centered around the RIPK1/RIPK3/MLKL pathway, combining both programmed and inflammatory characteristics. However, its role and mechanism in sepsis-induced vascular leakage remain unclear. In vivo and in vitro, CLP and LPS were used to simulate sepsis model. It was found that the expression levels of RIPK1/RIPK3/p-MLKL in septic VECs were significantly increased, and necroptosis inhibitors significantly improved septic vascular leakage. Transcriptomic and Western blot results suggested that TNFRSF21 plays a key role in necroptosis. shTNFRSF21 inhibited the formation of necrosome (RIPK3/p-MLKL) in septic VECs, improved vascular leakage in septic rats, and prolonged their survival time. The compound Phen-DC3 of inhibiting TNFRSF21 and the anesthetic remimazolam, both downregulated TNFRSF21, thereby improving septic vascular leakage. Our results suggest that TNFRSF21-regulated necroptosis plays an important role in septic vascular leakage, and targeting TNFRSF21 inhibition may be a potential therapeutic strategy for septic vascular leakage. KEY MESSAGES: Necroptosis plays a crucial role in sepsis-induced vascular leakage. TNFRSF21 promotes necrosome formation by upregulating RIPK3/p-MLKL, leading to endothelial cell death and disruption of the vascular barrier. The TNFRSF21 inhibitor Phen-DC3 was identified as a compound that improves sepsis-induced vascular leakage, providing a potential new therapeutic strategy for sepsis treatment. The anesthetic remimazolam inhibits TNFRSF21, improving sepsis-induced vascular leakage, offering experimental evidence for the repurposing of existing drugs like remimazolam in the treatment of sepsis.

Postoperative atrial fibrillation (POAF) in trauma patients is closely related to poor prognosis. This study aims to identify the risk factors of POAF and establish a predictive model. We extracted data from the MIMIC-IV 2.2 database on ICU trauma patients who underwent surgery. The patients were randomly divided into a training set and a validation set at a ratio of 7:3. We used least absolute shrinkage and selection operator (LASSO) regression combined with multivariable logistic regression to select predictive factors. Receiver operating characteristic (ROC) curves, calibration curves, and decision curves were used to evaluate the developed nomogram model. Among 5170 included patients, POAF incidence was 9.15

Objectives To evaluate health outcomes and identify risk factors for reinfection and persistent symptoms among COVID-19 survivors 4 years after hospital discharge.Design Longitudinal cohort study.Setting Two hospitals in Wuhan, China.Participants 1076 COVID-19 survivors discharged from hospital.Outcome measures Self-reported symptom questionnaire, Chronic Obstructive Pulmonary Disease Assessment Test, Hospital Anxiety and Depression Scale and Checklist Individual Strength (CIS) fatigue subscale. Long covid was defined according to WHO criteria.Results Median age was 58 years and 50.2% were male. Reinfection during December 2022–April 2023 occurred in 36.1%; 21 developed pneumonia and 14 required hospitalisation. At least 12 months after reinfection, 12.1% reported sequelae compared with 46.9% after the initial infection. At 4 years, 16.7% reported long covid symptoms, commonly fatigue, chest tightness, cough and dyspnoea. In multivariable analysis, risk factors for abnormal fatigue (CIS ≥27) included age (OR 1.020, 95% CI 1.007 to 1.034; p=0.003), reinfection (OR 2.393, 95% CI 1.708 to 3.352; p<0.001), severe disease (OR 1.553, 95% CI 1.088 to 2.218; p=0.015) and tumour (OR 3.420, 95% CI 1.177 to 9.936; p=0.024).Conclusions At 4 years post discharge, symptom burden was lower than at earlier follow-up time points for most survivors. Reinfection and older age were associated with persistent symptoms.

BACKGROUNDS:Trauma patients who undergo surgery are at high risk for acute pulmonary embolism (PE). We aimed to investigate the connection between the preoperative serum calcium level of trauma patients and their risk of postoperative PE. METHODS:We included 5598 trauma patients from four centers (2017-2023). Patients were categorized as Hypocalcemia (< 2.2 mmol/L) and Non-hypocalcemia (≥ 2.2 mmol/L). Propensity score matching (PSM) was used to match Hypocalcemia group and Non-hypocalcemia group 1:1. We applied logistic regression to determine the correlation between preoperative hypocalcemia and the risk of postoperative PE. We plotted the receiver operating characteristic (ROC) curve to assess the predictive value of preoperative serum calcium levels for postoperative PE. RESULTS:The overall incidence of PE in trauma patients was 2.1% (120/5598). Before and after PSM, PE in the Hypocalcemia group was significantly higher than that in the Non-hypocalcemia group [2.9% vs. 1.6%, p = 0.001] and [2.9% vs. 1.9%, p = 0.039]. Post-PSM logistic regression revealed that trauma patients with preoperative hypocalcemia had a 1.54-fold increased risk of postoperative PE formation (95% CI 1.04-2.30, p = 0.032). Within the observed range of this cohort, for every 1 mmol/L increase in preoperative serum calcium, the risk of postoperative PE formation was reduced by 62% (OR 0.38, 95% CI 0.22-0.73; p = 0.001). ROC results showed that the area under the curve (AUC) of preoperative serum calcium in predicting the occurrence of PE was 0.59 (95% CI 0.54-0.64), p = 0.001. CONCLUSION:Preoperative hypocalcemia is significantly associated with an increased risk of postoperative PE formation in trauma patients. TRIAL REGISTRATION:ChiCTR2300078097.

BackgroundSepsis is a life-threatening organ dysfunction caused by a dysregulated host response to infection. The vascular endothelial cells (VECs) play a pivotal role in the progression of sepsis-induced vascular leakage. While therapeutic strategies targeting pathogen elimination and inflammation exist, direct interventions on the endothelial barrier are limited. The mechanisms of endothelial damage related to mitochondrial dysfunction during sepsis require further elucidation.MethodsThe study utilized a cecal ligation and puncture (CLP) rat model of sepsis and lipopolysaccharide (LPS)-stimulated VECs to investigate vascular leakage mechanisms. These models were utilized to investigate the changes in vascular permeability, mitochondrial function and protein crotonylation in VECs, aiming to identify potential therapeutic targets for sepsis.ResultsIn septic rats, significant lung injury and increased vascular leakage were observed, linked to mitochondrial dysfunction and decreased survival rates. A marked downregulation of Platelet Activating Factor Acetylhydrolase 2 (PAFAH2) in VECs was identified post-sepsis, causing an upregulation of Enoyl-CoA Hydratase, Short Chain 1 (ECHS1), which inhibited crotonylation and compromised mitochondrial function, leading to increased apoptosis of VECs. Restoration experiments showed that modulating PAFAH2 and ECHS1 levels could mitigate these adverse effects. PAFAH2 overexpression alleviated sepsis-induced vascular leakage by downregulating ECHS1 and enhancing crotonylation.ConclusionsThe study identifies the PAFAH2-ECHS1 pathway as a critical axis in sepsis-induced vascular leakage, influencing mitochondrial function and crotonylation, which leads to endothelial apoptosis. These insights could guide the development of new therapies targeting the endothelial barrier for treating sepsis.

Sepsis is a systemic inflammatory syndrome that can cause coagulation abnormalities, leading to damage in multiple organs. Vascular endothelial cells (VECs) are crucial in the development of sepsis-induced coagulopathy (SIC). The role of Parthenolide (PTL) in regulating SIC by protecting VECs remains unclear. The study utilized septic rats and lipopolysaccharide (LPS)-stimulated VECs to simulate a SIC model and observe the therapeutic effects of PTL. Additionally, nanotechnology was employed to produce Nano-PTL (N-PTL), to observe whether it has advantages over PTL in treating SIC. PTL has been shown to mitigate lung injury in septic rats, significantly reduce tumor necrosis factor-α (TNF-α) levels, and increase survival rates. PTL treatment also enhances coagulation function, augments vascular endothelial cell (VEC) function, reduces mitochondrial fragmentation, and increases both mitochondrial oxygen consumption rate (OCR) and mitochondrial membrane potential (MMP), while inhibiting reactive oxygen species (ROS) production. By increasing BRD4/BCL-xL levels, PTL can prevent mitochondrial-mediated apoptosis in VECs, improve VEC function, and consequently ameliorate SIC. Additionally, nanotechnology-synthesized N-PTL further enhances the protective effects on VECs and coagulation function. This study clarifies the therapeutic effects and mechanisms of PTL on SIC, offering new strategies and directions for the treatment of sepsis.

Background:Sepsis is a major clinical challenge, with in-hospital mortality of 25%-40% in intensive care unit patients. The gastrointestinal tract is recognized as both the "initiating organ" of multiple organ dysfunction syndrome and the "central organ" in orchestrating the host stress response during critical illness. ACSL4, a regulator of lipid metabolism and ferroptosis, is a potential target for sepsis-induced intestinal injury, but its inhibitor parishin has not been evaluated in this context. Methods:Key genes implicated in sepsis pathogenesis were identified through bioinformatic analysis of publicly available datasets from the GEO. Network pharmacology approaches were used to screen for small-molecule compounds with high binding affinity to the identified hub genes. Molecular docking, followed by in vivo and in vitro validation, was employed to evaluate the therapeutic efficacy and mechanistic impact of the top candidate compound in a murine sepsis model. Results:Weighted Gene Co-expression Network Analysis identified five genes most significantly associated with sepsis diagnosis. Protein-protein interaction network analysis revealed 157 hub genes, among which ACSL4 was the sole gene shared across diagnostic and functional modules. Molecular docking analysis indicated that Parishin exhibited the strongest binding affinity to ACSL4 (docking score: -17.701). In septic animal models, ACSL4 expression was markedly upregulated in both plasma monocytes and intestinal tissues (P < 0.05), accompanied by increased levels of inflammatory cytokines, lipid peroxidation (LPO), MDA, and Fe2+ (P < 0.05). Expression of ferroptosis-associated proteins was also evidently elevated (P < 0.05). Treatment with Parishin notably attenuated these pathological changes, reduced ferroptosis-related markers, and improved 72-hour survival rates in septic mice (P < 0.05). Conclusion:Parishin ameliorates sepsis-induced intestinal injury by downregulating ACSL4 expression, thereby inhibiting Smad3 phosphorylation and suppressing ferroptosis. These findings suggest that ACSL4 is a promising therapeutic target for mitigating intestinal damage in sepsis.

Systemic factors confound blood tests for the diagnosis of Alzheimer's disease (AD). The Delta Method study explored whether blood biomarkers from the vein proximal to the brain perform better in detecting cerebral Alzheimer's pathologies using PET or cerebrospinal fluid (CSF) biomarkers as reference standards in two independent cohorts (n = 463). Blood was collected from the internal jugular vein (IJV) and median cubital vein (MCV), and AD biomarkers were measured with Lumipulse G and Simoa methods. The results showed that the levels of Aβ42, Aβ40, p-tau217, p-tau181, GFAP, and NfL were higher in the IJV than in MCV and were highly correlated between the two sites. IJV-Aβ42/40 had stronger correlations with Aβ PET Centiloids and tau PET meta-temporal SUVR than MCV-Aβ42/40. In detecting cerebral Aβ positivity, IJV-Aβ42/40 demonstrated a significantly higher accuracy (79.9%-92.9% vs. 72.4%-88.8%) and a lower percentage of uncertain individuals (17.8%-54.5% vs. 31.3%-70.1%) than MCV-Aβ42/40. Moreover, the diagnostic accuracy of Lumipulse G IJV-Aβ42/40 (88.2%-92.9%) was statistically equivalent to that of MCV-p-tau217 (90.2%-94.3%), although the intermediate percentage of IJV-Aβ42/40 was higher (17.8%-34.0% vs. 0.7%-17.5%). These findings were verified in the validation cohort. This study demonstrated the superior performance of IJV-Aβ42/40 to MCV-Aβ42/40 in detecting cerebral Alzheimer's pathologies, offering a novel perspective to reduce the impacts of systemic factors and comorbidities on blood tests.

The present study aims to elucidate the role of the Sigma‑1 receptor in the pathogenesis of neuropathic pain and evaluate its potential therapeutic implications. To systematically assess the effects of the Sigma‑1 receptor, neuropathic pain was induced in rats using the chronic constriction injury (CCI) model. Subjects were subsequently divided into three groups: Sham, CCI, and CCI+BD1047 (where BD1047 is a Sigma‑1 receptor antagonist). Following intrathecal administration of the respective agents, thermal withdrawal latency (TWL) and mechanical withdrawal threshold (MWT) were measured. Additionally, Western blotting was utilized to examine Sigma‑1 receptor, phosphorylated protein kinase Cα (p‑PKCα), and P2X3 receptor expression in the dorsal root ganglia (DRG). Immunofluorescence techniques were employed to examine p‑PKCα and P2X3 receptor expression. The results indicate a direct correlation between Sigma‑1 receptor activity and pain perception, evidenced by changes in TWL and MWT. In the CCI group, both TWL and MWT were significantly reduced compared to the Sham group. Furthermore, protein levels of the Sigma‑1 receptor, p‑PKCα, and P2X3 receptor in the DRG were elevated, and immunofluorescence expression of p‑PKCα and the P2X3 receptor also increased. Conversely, in the CCI+BD1047 group, TWL and MWT were significantly enhanced. Additionally, protein levels of the Sigma‑1 receptor, p‑PKCα, and P2X3 receptor in the DRG decreased, along with reduced immunofluorescence expression of p‑PKCα and P2X3 receptor. The findings indicate that neuropathic pain is intricately associated with the Sigma‑1 receptor, p‑PKCα, and P2X3 receptor in the dorsal root ganglia. Notably, the Sigma‑1 receptor regulates the expression of p‑PKCα and P2X3 receptor, presenting a novel therapeutic target for neuropathic pain management.

Ischemic/hypoxic injury significantly damages vascular function, detrimentally impacting patient outcomes. Changes in mitochondrial structure and function are closely associated with ischemia/hypoxia-induced vascular dysfunction. The mechanism of this process remains elusive. Using rat models of ischemia and hypoxic vascular smooth muscle cells (VSMCs), we combined transmission electron microscopy, super-resolution microscopy, and metabolic analysis to analyze the structure and function change of mitochondrial cristae. Multi-omics approaches revealed arginase 1 (Arg1) upregulation in ischemic VSMCs, confirmed by in vivo and in vitro knockout models showing Arg1’s protective effects on mitochondrial cristae, mitochondrial and vascular function, and limited the release of mtDNA. Mechanistically, Arg1 interacting with Mic10 led to mitochondrial cristae remodeling, together with hypoxia-induced VDAC1 lactylation resulting in the opening of MPTP and release of mtDNA of VSMCs. The released mtDNA led to PANoptosis of VSMCs via activation of the cGAS-STING pathway. ChIP-qPCR results demonstrated that lactate-mediated Arg1 up-regulation was due to H3K18la upregulation. VSMCs targeted nano-material PLGA-PEI-siRNA@PM-α-SMA (NP-siArg1) significantly improved vascular dysfunction. This study uncovers a new mechanism of vascular dysfunction following ischemic/hypoxic injury: a damaging positive feedback loop mediated by lactate-regulated Arg1 expression between the nucleus and mitochondria, leading to mitochondria cristae disorder and mtDNA release, culminating in VSMCs PANoptosis. Targeting VSMCs Arg1 inhibition offers a potential therapeutic strategy to alleviate ischemia/hypoxia-induced vascular impairments.

Glioblastoma (GBM), Isocitrate Dehydrogenase-wildtype (IDH-WT) represents the most prevalent and clinically aggressive subtype of adult diffuse gliomas, typically associated with poor prognosis. Temozolomide (TMZ) remains the first-line chemotherapeutic agent for GBM; however, the emergence of TMZ resistance represents a major therapeutic obstacle in clinical practice. This study identifies placenta-specific 8 (PLAC8) as a novel mediator of TMZ resistance in IDH-WT GBM. Elevated PLAC8 expression was strongly correlated with poorer survival rates, higher tumor grades in glioma, establishing it as an independent prognostic factor. Notably, consistent upregulation of PLAC8 was observed in both TMZ-resistant GBM cells and TMZ-treated patients, suggesting its potential as a biomarker for TMZ resistance. Mechanistic studies revealed that PLAC8 regulates TMZ sensitivity in GBM cells through the AKT-mTOR signaling pathway. Additionally, integrated bioinformatics and clinical analyses demonstrated that PLAC8 expression positively correlates with immune cell infiltration while promoting an immunosuppressive tumor microenvironment and modulating immunotherapy-related biomarkers, suggesting its potential as a predictive biomarker for immunotherapy response. In conclusion, PLAC8 represents a promising biomarker and therapeutic target for overcoming TMZ resistance and guiding immunotherapy in GBM. This study provides valuable insights for the development of personalized treatment strategies aimed at improving patient outcomes.

Postoperative cognitive dysfunction (POCD) negatively impacts patients’ post-surgery recovery, and, in severe cases, raises the risk of mortality. Nonetheless, the underlying mechanism of POCD remains incompletely elucidated, and there is a notable dearth of effective treatment strategies. A randomized allocation was conducted among a total of 90 patients who underwent arthroplasty surgery, with 45 patients assigned to the dexmedetomidine group and 45 patients assigned to the control group. The Dexmedetomidine (DEX) group received an intravenous infusion of 1 µg/kg dexmedetomidine for 10 min, followed by a maintenance dose of 0.4 µg/kg/h for 30 min before surgery completion; the control (CON) group received 0.9

BackgroundAlthough red cell distribution width (RDW) has been linked to venous thromboembolism, its predictive value for postoperative pulmonary embolism (PE) in surgical trauma patients remains ambiguous. This study aimed to investigate the correlation between preoperative RDW and postoperative PE risk.MethodsWe incorporated 46506 surgical trauma patients from three medical institutions and the MIMIC-IV 2.2 database. We constructed receiver operating characteristic curves (ROC) utilizing preoperative (at admission) RDW and postoperative PE and classified patients into two groups. Firstly, univariate logistic regression was conducted to identify factors correlated with postoperative PE, and the variance inflation factor was computed to evaluate multicollinearity. Multivariate logistic regression analysis was subsequently conducted to identify the independent risk factors for PE. Propensity score matching (PSM) was conducted using a caliper value of 0.1, balancing 26 covariates between the two groups, including demographic features, vital signs, injury severity scores, comorbidities, and laboratory parameters. A total of 10235 pairs were successfully matched.ResultsThe postoperative PE incidence was 0.56%. RDW showed significant predictive value for PE with an area under the curve (AUC) of 0.723 (0.696-0.750). Before PSM, RDW ≥14.4% was associated with increased PE risk (OR 4.70, 95% CI 3.63-6.09, P < 0.001). Multivariate analysis confirmed a 1.90-fold risk increase (95% CI 1.42-2.55, P < 0.001). After PSM, RDW ≥14.4% remained significantly associated with higher PE risk (OR 1.67, 95% CI 1.22-2.29, P = 0.002).ConclusionElevated preoperative RDW is an independent risk factor for postoperative PE in trauma patients, with ≥14.4% indicating significantly increased risk.

Observe the effects of dexmedetomidine(Dex) and sevoflurane(Sev) on the optic nerve sheath diameter(ONSD) in patients undergoing microvascular decompression (MVD). Find the most appropriate anesthetic maintenance medication scheme to reduce intracranial pressure (ICP)fluctuation and reduce the incidence of adverse reactions such as postoperative nausea and vomiting(PONV). In this retrospective cohort study, 90 patients undergoing elective MVD surgery were allocated into Groups P, D, and S. Maintenance of anaesthesia: Group P propofol(Propo) 4-12mg/(kg.h) + remifentanil 0.1–0.2ug/(kg.min); Group D Dex 0.4ug/(kg. h) + Propo 4-12mg/(kg.h) + remifentanil 0.1–0.2ug/(kg.min); Group S 1–2 www.chictr.org.cn (07/02/2024,ChiCTR MR-50–24-010856). Questions: Do Dex and Sev have effect on ONSD and PONV in MVD? Findings: Dex has a lower effect on ONSD of MVD during the perioperative phase than Sev, and it can, to a certain extent, reduce the fluctuation of ICP. Dex reduces the incidence of PONV within 24 h after MVD and acts as a protective factor against PONV. Meaning: The usage of 0.4ug/(kg.h) Dex was a protective factor for PONV in MVD.

Trauma-induced coagulopathy (TIC) has a high incidence in patients with severe trauma. Patients who develop TIC usually have a poor prognosis, characterised by increased organ dysfunction, susceptibility to sepsis, and high mortality. Nonetheless, there are still few studies specifically focusing on postoperative TIC in severely traumatic patients. Therefore, the aim of this study was to construct a machine learning model for early identification of people at high risk of postoperative TIC. This retrospective analysis included data of severe trauma patients undergoing surgical treatment from January 2013 to February 2023 across four hospitals in China. Data of one hospital (n = 1204) was used for the development dataset, while other three hospitals contributed to the external validation dataset (n = 863). The study employed various machine learning algorithms, including random forests, logistic regression, gradient boosting decision trees, support vector machines, backpropagation artificial neural networks, extreme gradient boosting, and naïve Bayes. Model performance was estimated on the basis of accuracy, sensitivity, specificity, and area under the curve. In the internal cross-validation dataset, Shapley’s additive interpretation was applied to the model with the largest area under the receiver operating characteristic curve. TIC occurred in 25.4% (306/1204) and 2.9% (25/863) of patients in the developing and external validation set, respectively. Among the models evaluated, the Random Forest model demonstrated the highest performance, achieving an area under the curve of 0.82 for the test cohort and 0.73 for the external validation cohort. The findings suggest that machine learning models can effectively identify severely traumatized patients at a higher risk of postoperative trauma-induced coagulopathy. Utilizing machine learning may enhance clinical decision-making and improve management strategies for postoperative coagulation issues.