This study aimed to evaluate the efficacy of fluid responsiveness-guided strategies for preventing spinal anesthesia-induced hypotension (SAIH) in parturients undergoing cesarean delivery, comparing prophylactic fluid loading with norepinephrine infusion. In this fluid responsiveness-based stratified randomized controlled trial, eligible parturients were stratified into fluid responsive (FR(+)) and non-fluid responsive (FR(-)) cohorts according to carotid corrected flow time (FTc). Each stratum had a preset sample size of 236, and within each stratum, participants were randomly assigned to receive either prophylactic colloid infusion (Co) or norepinephrine infusion (NE), ultimately forming four subgroups: FR(+)/Co, FR(+)/NE, FR(-)/Co, and FR(-)/NE.Primary outcomes included the incidence of SAIH and maximum reduction in mean arterial pressure (MAP). Secondary outcomes encompassed neonatal umbilical cord blood gas analysis, Apgar scores, intraoperative hemodynamic changes, and postoperative recovery parameters. Among fluid-responsive parturients, prophylactic fluid loading (FR(+)/Co) and norepinephrine infusion (FR(+)/NE) demonstrated comparable efficacy in preventing SAIH (16.7

Background Herpes zoster-associated pain (ZAP) imposes a substantial burden with frequently suboptimal treatment outcomes. High-voltage long-duration pulsed radiofrequency (HL-PRF)) has emerged as a promising treatment. This study explored HL-PRF’s application in ZAP, identified efficacy-influencing factors, and established a clinical prediction model.​ Methods Retrospective analysis of 128 ZAP patients treated with HL-PRF (Department of Anesthesiology and Pain Medicine, First Affiliated Hospital of Wannan Medical College, Mar 2023–Dec 2024) was done. Independent predictors of treatment inefficacy were identified via univariate and multivariate logistic regression. A predictive model was developed utilizing a nomogram. Model performance was evaluated using area under the curve (AUC), calibration curves, Hosmer-Lemeshow test, and decision curve analysis (DCA). Results HL-PRF demonstrated 60% efficacy at 3-month follow-up. Univariate analysis identified significant associations ( P < 0.05) between HL-PRF efficacy and multiple factors, including age, disease duration, prolonged hormone use, early non-utilization of antiviral medications, use of antiepileptic drugs, tramadol use, coexisting connective tissue disorders, concurrent malignancy, coexisting cerebral infarction, acute-phase VAS score, and the CD4+/CD8 + T-cell ratio. Multivariate regression confirmed 7 risk factors for reduced efficacy (age, disease duration, connective tissue disease, malignant tumors, long-term hormone use, acute-phase VAS score, CD4+/CD8 + T-cell ratio; P < 0.05). The predictive model exhibited excellent discriminatory power(AUC = 0.988, 95%CI:0.976-1.000), good fit (Hosmer-Lemeshow P = 0.969), and high accuracy (93.0% overall accuracy, 90.7% sensitivity, 96.2% specificity).​ Conclusion HL-PRF is safe and effective for ZAP but affected by multiple factors. Older patients, prolonged disease duration, comorbidities (connective tissue disease/malignant tumors), long-term hormone use, acute-phase VAS > 7, and low CD4+/CD8 + ratio may have suboptimal outcomes. Future research should focus on individualized HL-PRF protocols.​

This study aimed to investigate the effects of dexamethasone on blood glucose in diabetic patients undergoing thoracoscopic surgery, providing a reference for its safe intraoperative use in this population. In this randomized, double-blind controlled trial, 60 diabetic patients with reasonably controlled blood glucose (HbA1c < 9

Ischemic stroke remains a leading cause of global mortality and disability. While timely vascular recanalization is the most direct and clinically validated intervention for cerebral ischemia, reperfusion often induces secondary brain injury, with neuroinflammation playing a central role. Single-cell sequencing data from an ischemic stroke mouse model identify G protein-coupled receptor 35 (GPR35) as a potential regulator of post-ischemic inflammatory responses. GPR35 expression was markedly increased in both in vivo cerebral ischemia-reperfusion models and in vitro oxygen-glucose deprivation systems, predominantly localizing to microglia. Functional studies revealed that genetic knockdown of GPR35 in murine brain tissue significantly exacerbated cerebral infarction volume, neurological deficits, and neuroinflammation in animal models, whereas GPR35 overexpression produced therapeutic effects. Consistently, pharmacological activation of GPR35 using zaprinast attenuated ischemia-reperfusion injury and reduced proinflammatory cytokine production. Mechanistically, zaprinast-mediated GPR35 activation suppressed proinflammatory cytokine production via modulation of the Raf1/ERK1/2/MAPK signaling cascade. Notably, Raf1 knockdown attenuated the pathological exacerbation induced by GPR35 deficiency in peri-infarct regions. Co-immunoprecipitation analyses revealed a direct interaction between GPR35 and Raf1, with the CR2 domain, a critical region for Raf1 autoinhibition, identified as the primary binding interface. Collectively, these findings demonstrate that zaprinast confers cerebroprotective effects in cerebral ischemia-reperfusion injury by activating GPR35, ultimately attenuating infarct progression and neuroinflammation. This mechanistic insight positions GPR35 as a promising therapeutic target for mitigating reperfusion injury in ischemic stroke.

Background Neuropathic pain (NP) is frequently accompanied by anxiety and depression, and current treatments do not adequately address this comorbidity. The anterior cingulate cortex (ACC) plays a central role in sensory and emotional processing. However, the molecular pathways that connect these functions remain unclear. G protein-coupled receptor 35 (GPR35), an orphan receptor enriched in neurons, has been implicated in neuroinflammation and pain signaling. However, its specific involvement in NP and associated affective disturbances has not been fully elucidated.Methods Peripheral blood GPR35 expression was measured in human patients with NP and healthy controls. In mice, chronic constriction injury (CCI) was used to induce NP. Lentiviral knockdown or overexpression of GPR35 was performed in ACC cells. Behavioral assays were used to assess mechanical and thermal sensitivity, locomotor and anxiety metrics, cognitive performance, and depression-related behaviors. Molecular analyses included western blotting, RT-qPCR, immunofluorescence, RNA sequencing, and co-immunoprecipitation. Additional Nr4a1 knockdown and L-kynurenine (L-Kyna, a GPR35 agonist) administration were used to validate pathway involvement.Results Patients with NP had higher circulating GPR35 levels, which positively correlated with pain intensity. CCI induced a time-dependent increase in GPR35 expression in the ACC of mice, accompanied by hypersensitivity and emotional disturbances. GPR35 knockdown in the ACC worsens mechanical and thermal hypersensitivity, impairs cognition, increases depression-related behaviors, and amplifies microglial activation and pro-inflammatory cytokine production. GPR35 overexpression reversed these effects by reducing hypersensitivity, improving affective behaviors, and restoring the inflammatory balance. Transcriptomic and biochemical analyses identified Nr4a1 as a key downstream effector of GPR35, and Nr4a1 knockdown eliminated the protective effects of GPR35 overexpression. GPR35 primarily regulated the PI3K/AKT pathway. Treatment with L-Kyna reduced pain hypersensitivity, improved depression-related behaviors, and decreased neuroinflammation in CCI mice.Conclusions GPR35 is an essential regulator of NP and pain-related affective disturbances in the ACC. Its effects are mediated through the Nr4a1-dependent activation of the PI3K/AKT pathway and suppression of neuroinflammation. The pharmacological activation of GPR35 using L-Kyna provides analgesic and antidepressant benefits, highlighting GPR35 as a promising therapeutic target for NP and its emotional comorbidities.

Sepsis is a life-threatening clinical syndrome caused by a severely dysregulated host response to infection. As a major global health challenge, it continues to exhibit high mortality. Copper, an essential trace element crucial for biological homeostasis, is central to a recently defined form of cell death: cuprotosis. This novel, copper-dependent mitochondrial cell death pathway is mechanistically distinct from classical apoptosis and pyroptosis. In sepsis, cuprotosis contributes significantly to immune dysfunction and organ failure by mediating the death of both immune cells (e.g. macrophages, lymphocytes) and parenchymal cells (e.g. cardiomyocytes, renal tubular cells). Therefore, modulating this regulatory mechanism in a cell type-specific manner may represent a novel potential therapeutic avenue for sepsis, although substantial clinical validation is still required. This review systematically outlines the core mechanisms of cuprotosis, elucidates its pathophysiological role in sepsis, and evaluates the potential and challenges of targeting cuprotosis for sepsis therapy.

BACKGROUND:Perioperative neurocognitive disorders (PNDs) are common complications in elderly surgical patients. Possible pathogenic mechanisms for the development of PNDs include loss of synaptic connections mediated by microglial activation, although the precise mechanisms are not fully understood. METHODS:Male and female C57BL/6J or male Cx3cr1-CreERT2 mice, aged 8-12 weeks, were subjected to aseptic tibial fracture surgery, and cognitive tests were carried out 3 days after surgery. Through a combination of bulk RNA sequencing, Western immunoblotting, immunofluorescence, and Golgi staining of the hippocampus, we investigated the role of complement C1q in activating microglia and phagocytosing synaptic connections in the pathogenesis of postoperative neurocognitive disorder. RESULTS:Postoperative mice displayed memory deficits in both the Y-maze (P<0.001) and the trace fear conditioning (TFC) paradigms (P=0.002); these memory deficits were associated with increased microglial activation, complement C1q upregulation, classical complement pathway transcriptomic upregulation, and synapse loss (all P<0.05). After surgery, there was a ∼2-fold increase in colocalisation of C1qa with Homer1 (excitatory) or gephyrin (inhibitory) synaptic proteins in microglia (P<0.001). Postoperative memory decline and synapse loss did not occur after treatment with microglial activity inhibitor minocycline, after exposure to C1q neutralising antibody JL-1, or after C1q depletion from CA1 microglia. Activation of NF-κB was correlated with elevated levels of complement C1q in models, and selective inhibition of NF-κB activation with pyrrolidinedithiocarbamate ammonium (PDTC) attenuated the surgery-induced elevation of C1q and improved cognitive function. CONCLUSIONS:The results demonstrate that hippocampal microglia prune both excitatory and inhibitory synapses in a C1q-dependent manner, contributing to postoperative synapse loss and cognitive dysfunction. Targeting C1q and NF-κB activation could be a promising therapeutic intervention to ameliorate perioperative neurocognitive disorders.

This study aims to evaluate the effects of two strategies for preventing hypotension after spinal anesthesia (prophylactic fluid loading and norepinephrine infusion) on intracranial pressure (ICP) in preeclamptic women by measuring the optic nerve sheath diameter (ONSD) using ultrasound. In this prospective, randomized, controlled trial, 60 healthy parturients and 60 preeclamptic parturients undergoing cesarean delivery under spinal anesthesia were enrolled. Normal parturients were randomly assigned to the infusion group (NA group, n = 30) and NE (norepinephrine) group (NB group, n = 30), while preeclamptic parturients were randomly assigned to the infusion group (PA group, n = 30) and NE group (PB group, n = 30). The primary outcome was bilateral ONSD values at baseline, pretreatment, 5 min after spinal anesthesia (Post-SA), and 5 min after fetal delivery (Post-birth). The secondary outcomes included maternal general characteristics, renal function indices, postoperative headache, fetal umbilical cord arterial blood gas indices, and Apgar scores. Pretreatment ONSD was significantly higher than baseline in both infusion groups, and baseline ONSD was higher in preeclamptic versus normal parturients (all P < 0.01). Among preeclamptic parturients, pretreatment ONSD was higher in the PA group than in the PB group (P < 0.01), with a similar difference (PA > PB) confirmed in normal parturients (P < 0.01). In addition, compared to the PA group, the PB group showed no significant differences in systolic blood pressure (SBP), diastolic blood pressure (DBP), or mean arterial pressure (MAP) at any time point in preeclamptic parturients (P > 0.05). Conversely, in normal parturients, post-birth SBP, DBP, and MAP were significantly higher in the NB than in the NA group (P < 0.01). Baseline hemodynamic values were higher in preeclamptic versus normal parturients (P < 0.01), and post-birth values decreased significantly from baseline in the PA and PB groups (P < 0.001). No significant intergroup differences were observed in maternal heart rate (HR), renal function indices, umbilical artery blood gas indices, Apgar scores, or the incidence of postpartum headache (all P > 0.05). For preeclamptic parturients, the risks induced by ICP increase should be noted. Compared to colloids, prophylactic infusion of NE was more effective and safer and did not increase ICP. This randomized controlled trial was registered on Chinese Clinical Trial Registry (ChiCTR2400092317; http://www.chictr.org.cn/) with the Clinical Trial Registry (1)

Etomidate provides significant clinical benefits; however, its potential to suppress adrenal cortical function raises concerns. Adrenocorticosteroid secretion follows a distinct circadian rhythm, peaking in the morning and declining significantly in the evening. Nevertheless, the impact of these fluctuations on etomidate-induced adrenal suppression and postoperative outcomes remains unclear. In this study, we aim to investigate the differences in the inhibitory effects of etomidate on adrenal cortical function when administered in the morning versus the evening. 156 participants were randomized into the Morning Group (M group, receiving anesthesia between 8:00 and 9:00 AM) or the Evening Group (E group, receiving anesthesia between 4:00 and 5:00 PM). Anesthesia induction involved 0.3 mg kg -1 of etomidate, followed by maintenance with a 2:1 mixture of etomidate and propofol. Primary endpoints included serum cortisol, aldosterone, and adrenocorticotropic hormone concentrations preoperatively, immediately postoperatively, and at 8:00 AM on the first and third postoperative days. Secondary endpoints assessed postoperative recovery quality and related complications. Compared to the M group, the E group experienced a greater decrease in cortisol concentrations (34.0% [26.6% to 45.0%] vs. 27.2% [19.9% to 42.7%]; P = 0.0228) and aldosterone concentrations (44.8% [29.9% to 58.6%] vs. 26.2% [7.1% to 75.8%]; P < 0.0001) and a more pronounced increase in adrenocorticotropic hormone concentrations (39.0% [-3.8% to 121.1%] vs. 5.7% [-20.0% to 38.5%]; P = 0.0009). The correlation between the degree of etomidate inhibition and its total dose was higher in the E group (r = 0.4839 vs. r = 0.3666). Moreover, the proportions of patients maintaining normal aldosterone and adrenocorticotropic hormone levels immediately postoperatively were significantly lower in the E group ( P < 0.0001). However, there were no significant differences in postoperative recovery or complication rates between the two groups ( P > 0.05). Etomidate exerted stronger adrenal cortical suppression in the evening than in the morning, but postoperative recovery and complication rates were comparable in non-critically ill patients, supporting its safe clinical use. Trial registration Chinese Clinical Trial Registry identifier: ChiCTR2400082034, Date: 19/03/2024

Stroke is the second-leading global cause of death. The damage attributed to the immune storm triggered by ischemia–reperfusion injury (IRI) post-stroke is substantial. However, data on the transcriptomic dynamics of pyroptosis in IRI are limited. This study aimed to analyze the expression of key pyroptosis genes in stroke and their correlation with immune infiltration. Pyroptosis-related genes were identified from the obtained middle cerebral artery occlusion (MCAO) datasets. Differential expression and functional analyses of pyroptosis-related genes were performed, and differences in functional enrichment between high-risk and low-risk groups were determined. An MCAO diagnostic model was constructed and validated using selected pyroptosis-related genes with differential expression. High- and low-risk MCAO groups were constructed for expression and immune cell correlation analysis with pyroptosis-related hub genes. A regulatory network between pyroptosis-related hub genes and miRNA was also constructed, and protein domains were predicted. The expression of key pyroptosis genes was validated using an MCAO rat model. Twenty-five pyroptosis genes showed differential expression, including four hub genes, namely WISP2, MELK, SDF2L1, and AURKB. Characteristic genes were verified using real-time quantitative PCR analyses. The high- and low-risk groups showed significant expression differences for WISP2, MELK, and SDF2L1. In immune infiltration analysis, 12 immune cells showed differences in expression in MCAO samples. Further analysis demonstrated significant positive correlations between the pyroptosis-related hub gene SDF2L1 and immune cell-activated dendritic cells in the high-risk group and immune cell natural killer cells in the low-risk group. This study identified four pyroptosis-related hub genes, with elevated WISP2, MELK, and SDF2L1 expression closely associated with the high-risk group. The analysis of inflammatory cell types in immune infiltration can predict ischemic stroke risk levels and help to facilitate treatment.

Background:The dopamine D2/D3 antagonist amisulpride has demonstrated its superiority and efficacy in prophylaxis of postoperative nausea and vomiting (PONV). Given the branded intravenous amisulpride (Barhemsys®) has not been approved in China, there is unmet clinical need for amisulpride. Our primary objective was to ascertain the efficacy and safety of the generic intravenous amisulpride (QLG2069) in the prophylaxis of PONV. Methods:In this phase III, multicenter, randomized, double-blind, placebo-controlled study, 551 adult Chinese patients (with ≥2 Apfel risk factors for PONV) undergoing elective laparoscopic gynecological or abdominal surgery were randomly allocated in a 1:1 ratio to receive either generic intravenous amisulpride or placebo. The primary endpoint was the complete response (CR) rate, defined as the proportion of patients demonstrating neither emetic episodes (vomiting/retching) nor requiring rescue antiemetics throughout the 24-hour postoperative window. Results:Totally, 542 patients (amisulpride group: n=275; placebo group: n=267) were included in the full analysis set. Amisulpride demonstrated significantly higher CR rate compared to placebo (53.82% vs 40.07%; P=0.0011) within 24-h postoperative period. Patients treated with intravenous amisulpride exhibited significantly lower incidence of moderate-to-severe nausea (28.36% vs 37.08%; P=0.0266) and emesis (44.73% vs 57.30%; P=0.0030) compared to the incidence in the placebo group. The proportion of patients without nausea was numerically higher (45.09%) in the amisulpride group compared to that in the placebo group (37.45%), although the difference did not reach statistical significance (P=0.0685). No significant difference in the proportions of patients receiving rescue medication was noticed between the two groups (21.09% vs 28.09%; P=0.0569). The incidence of adverse events were comparable in two groups. Conclusion:The generic intravenous amisulpride was safe and effective in prophylaxis of PONV in Chinese patients with moderate-to-high risk of PONV to were undergoing laparoscopic gynecological or abdominal surgery.

Cycloastragenol, a triterpenoid saponin extracted from Astragalus membranaceus, exerts several pharmacological effects. However, its mechanism of action in acute lung injury treatment remains unclear. This study was conducted to test the hypothesis that cycloastragenol can inhibit lipopolysaccharide (LPS)-induced acute lung injury and investigate the underlying molecular mechanisms. This study systematically explored the effects and mechanism of action of cycloastragenol in LPS-induced acute lung injury treatment using network pharmacology, molecular docking, molecular dynamics simulation, and experimental validation. Gene Ontology and Kyoto Encyclopedia of Gene and Genomes enrichment analyses indicated that the effects of cycloastragenol are mediated by inflammation- and apoptosis-related genes. Both in vitro and in vivo experiments were conducted to assess the effectiveness of cycloastragenol in acute lung injury treatment. Lung function was evaluated using a pulmonary function test system with indicators, such as peak expiratory flow, minute ventilation, and lung resistance. The expression of inflammatory factors and apoptosis-related proteins was evaluated using Western blot analysis, quantitative real-time polymerase chain reaction, and immunofluorescence. Apoptosis in lung tissue and mouse primary peritoneal macrophages was assessed using terminal deoxynucleotidyl transferase dUTP nick-end labelling staining and flow cytometry, respectively. Cycloastragenol effectively alleviated pulmonary dysfunction and edema, mitigated histopathological damage, and suppressed the activation of both the NF-κB p65 and Akt signaling pathways induced by LPS, ultimately leading to reduced inflammation and apoptosis. The results suggest that cycloastragenol alleviates acute lung injury by exerting anti-inflammatory and anti-apoptotic effects. These findings suggest that cycloastragenol could be a potential therapeutic candidate for preventing and treating ALI.

BACKGROUND Fiberoptic bronchoscopy-guided intubation (FOI) is a reliable method for managing difficult airways, typically requiring a 2-operator technique using jaw thrust. This study introduces a novel 3D-printed transoral guiding device (TGD) enabling single-operator FOI without jaw thrust. The aim was to assess the feasibility and effectiveness of TGD compared to a modified oropharyngeal airway (MOA) with assistant-applied jaw thrust. MATERIAL AND METHODS A total of 218 patients undergoing elective orotracheal intubation were randomized into 2 groups: TGD and MOA. After anesthesia induction, Group TGD underwent FOI using the TGD without jaw thrust, while Group MOA used the MOA combined with jaw thrust. Outcome measures included time to successful intubation, first-attempt success rate, number of attempts or device adjustments, and airway visibility (epiglottis and bronchoscope view). RESULTS Successful FOI was achieved in all patients in the TGD group versus 95.4% in the MOA group (P=0.024). The TGD group had significantly shorter times to visualize the vocal cords and tracheal carina (both P<0.001) and to complete intubation (P<0.001). First-attempt success was higher in the TGD group (99.1%) than in the MOA group (67.0%; P<0.001). Fewer attempts and device adjustments were needed in the TGD group. CONCLUSIONS The 3D-printed transoral guiding device (TGD) facilitates faster, more effective single-operator FOI without jaw thrust, offering a promising alternative to traditional 2-operator techniques.

Despite equalizing blood pressure(BP), ephedrine and phenylephrine exhibit distinct impacts on rSO2. However, whether this heterogeneity in rSO2 affects the occurrence of POD remains understudied. This study aimed to explore the effects of maintaining BP with ephedrine versus phenylephrine on the incidence of POD in elderly patients undergoing knee arthroplasty under general anesthesia. A total of 120 patients aged 60-90 years undergoing knee arthroplasty were included in this study.The patients were randomly divided into two groups: the ephedrine group and the phenylephrine group. After anesthesia induction, continuous infusion of the respective medication was initiated to maintain intraoperative mean arterial pressure within the normal range (baseline mean arterial pressure ± 20%).The primary outcome measures included the incidence of POD within 1-3 days after the surgery. The incidence of POD on the first day after surgery was lower in the ephedrine group compared to the phenylephrine group (33% vs 7%, P < 0.001 ). However, there was no significant difference in the incidence of POD between the two groups on the second and third postoperative days. During surgery, the ephedrine group exhibited significantly increased CO and rSO2 compared to the phenylephrine group (P < 0.05). Clinical Trials Registry: ChiCTR2200064849, principal investigator: Changjian Zheng.

Postoperative pain management is one of the most challenging treatments after orthopaedic surgery, and improved medical treatment options are urgently needed. This study aimed to evaluate the efficacy and safety of 4-hydroxy-2-methyl-N-(5-methyl-2-thiazolyl)-2H-1, 2-benzothiazin-3-carboxamide 1,1-dioxide (QP001) for moderate to severe pain following orthopaedic surgery. This randomized clinical trial enlisted patients experiencing moderate to severe pain following orthopaedic surgery in 20 hospitals in China. We allocated randomly 132 participants to receive 30 mg QP001 and 66 participants to receive 0.9

Abstract4‐hydroxy 2‐methyl‐N‐(5‐methyl‐2‐thiazolyl)‐2H‐1, 2‐benzothiazin‐3‐carboxamide 1,1‐dioxide (QP001), a novel long‐lasting meloxicam formulation, may provide adequate postoperative pain relief with a good safety profile. This study aimed to evaluate the efficacy and safety of QP001 for moderate‐to‐severe pain following abdominal surgery. This multicenter, randomized, double‐blind, placebo‐controlled phase III trial recruited patients undergoing abdominal surgery at 23 centers between October 30, 2022, and July 10, 2023. Patients were randomized to a QP001 or placebo group in a 2:1 ratio. Postoperative pain intensity was evaluated using the Numerical Rating Scale. The primary efficacy outcome was the area under curve (AUC) of pain intensity‐time 0–24 h after awakening from anesthesia (AUC0–24). Adverse events and drug reactions were recorded to evaluate safety. A total of 258 patients underwent randomization, and 255 patients received at least one trial drug, including 170 in the QP001 group and 85 in the placebo group. Among these patients, 250 completed the study. The AUC0–24 was significantly lower in the QP001 group than in the placebo group (50.5 vs. 85.19, difference of 34.69 [40.7%], p < 0.0001). This was accompanied by a decrease in morphine use and an increase in patient satisfaction. Moreover, the overall adverse events or adverse drug reaction rates were similar between the QP001 and placebo groups. Among patients undergoing abdominal surgery, postoperative pain was significantly lower in the QP001 group than in the placebo group. QP001 has a great analgesic effect of up to 24 h and satisfactory safety in patients with moderate‐to‐severe abdominal pain.

Emergence agitation (EA) is more commonly observed after thoracic surgeries and can lead to serious complications. This study aimed to evaluate the effectiveness of serratus anterior plane block (SAPB) combined with oxycodone for transitional analgesia in preventing EA after video-assisted thoracoscopic surgery (VATS). A total of 121 adult patients scheduled for VATS under one-lung ventilation anesthesia were enrolled and randomly divided into three groups: preoperative SAPB without opioids for transitional analgesia near the end of the surgery (SAPB + SAL group, n = 39); preoperative SAPB with sufentanil at 0.1 mu g/kg for transitional analgesia (SAPB + SF group, n = 42); and preoperative SAPB with oxycodone at 0.1 mg/kg for transitional analgesia (SAPB + OCD group, n = 40). In primary outcomes, the incidences of EA in the SAPB + SAL, SAPB + SF, and SAPB + OCD groups were 38.5%, 28.6%, and 7.5% respectively. There was a statistically significant difference in EA incidence between the SAPB + OCD and SAPB + SF groups (P = 0.0136). In secondary outcomes, compared to the SAPB + SF group, the SAPB + OCD group experienced shorter tracheal extubation time [15(9, 25) min vs. 21.5(14.5, 32.5) min; P = 0.0473] and PACU stay [67.5(55.0, 85.0) min vs. 87.5(70.0, 110.0) min; P = 0.0026]; lower NRS scores at 15 min and 2 h post-extubation (P < 0.01), and higher Quality of Recovery-15 (QoR-15) scores post-surgery [113(98, 123) vs. 102(88, 112); P = 0.0122]. Our results suggest SAPB combined with oxycodone for transitional analgesia, compared with sufentanil, is more effective in preventing EA after VATS and conductive to rapid recovery postoperatively. Trial registration: Chinese Clinical Trial Registry, identifier: ChiCTR2300077473, Date: 09/11/2023.

Abstract Background: Stroke is the second-leading global cause of death. The immune storm triggered by ischemia-reperfusion injury after stroke is a crucial damaging factor. This study analyzed the expression of key pyroptosis genes in stroke and their correlation with immune infiltration. Methods: Middle Cerebral Artery Occlusion datasets were obtained and pyroptosis-related genes were identified. Differential expression and functional analyses of pyroptosis-related genes were performed. Differences in functional enrichment between high-risk and low-risk groups were determined. After selecting pyroptosis-related genes with differential expression, a MCAO diagnostic model was constructed and validated. High and low-risk MCAO groups were constructed for expression and immune cell correlation analysis with pyroptosis-related hub genes. A regulatory network between pyroptosis-related hub genes and miRNA was built, and protein domains were predicted. The expression of key pyroptosis genes was validated in the MCAO rat model. Results: Twenty-five pyroptosis genes showed differential expression, including four hub genes (WISP2, MELK, SDF2L1, and AURKB). The high- and low-risk groups showed significant expression differences for WISP2, MELK and SDF2L1. In immune infiltration analysis, 12 immune cells exhibited expression differences in MCAO samples. Further analysis demonstrated significant positive correlations between the pyroptosis-related hub gene SDF2L1 and immune cell-activated dendritic cells in the high-risk group and immune cell natural killer cells in the low-risk group. Conclusion: This study identified four pyroptosis-related hub genes, with elevated WISP2, MELK, and SDF2L1 expression closely associated with the high-risk group. Analysis of inflammatory cell types in immune infiltration provides a theoretical basis for predicting ischemic stroke risk levels and treatment.

In addition to stabilizing blood pressure (BP), ephedrine and phenylephrine have distinct effects on regional cerebral oxygen saturation (rSO2). However, whether its effect on rSO2 affects the occurrence of postoperative delirium (POD) remains unclear. Therefore, the aim of this study is to compare the effects of ephedrine and phenylephrine for BP maintenance on the incidence of POD in olderly adults who underwent knee arthroplasty under general anesthesia. One hundred twenty patients who were between 60 and 90 years old and underwent knee arthroplasty were included in this study. The patients were randomly divided into two groups: the ephedrine group and the phenylephrine group. After anesthesia induction, ephedrine and phenylephrine were continuously infused to maintain the intraoperative mean arterial pressure within the normal range (baseline mean arterial pressure ± 20%). The primary outcome measures included the incidence of POD within 1-3 days after surgery. The incidence of POD on the first day after surgery was lower in the ephedrine group than in the phenylephrine group (33% vs. 7%, P < 0.001). However, there was no significant difference in the incidence of POD between the two groups on the second and third postoperative days. Compared with the phenylephrine group, the ephedrine group experienced significantly greater cardiac output (CO) and rSO2 (P < 0.05).Clinical Trials Registry: ChiCTR2200064849, principal investigator: Changjian Zheng.

To explore the relationship between the timing of non-emergency surgery in mild or asymptomatic SARS-CoV-2 (severe acute respiratory syndrome coronavirus 2) infected individuals and the quality of postoperative recovery from the time of confirmed infection to the day of surgery. We retrospectively reviewed the medical records of 300 cases of mild or asymptomatic SARS-CoV-2 infected patients undergoing elective general anaesthesia surgery at Yijishan Hospital between January 9, 2023, and February 17, 2023. Based on the time from confirmed SARS-CoV-2 infection to the day of surgery, patients were divided into four groups: ≤2 weeks (Group A), 2–4 weeks (Group B), 4–6 weeks (Group C), and 6–8 weeks (Group D). The primary outcome measures included the Quality of Recovery-15 (QoR-15) scale scores at 3 days, 3 months, and 6 months postoperatively. Secondary outcome measures included postoperative mortality, ICU admission, pulmonary complications, postoperative length of hospital stay, extubation time, and time to leave the PACU. Concerning the primary outcome measures, the QoR-15 scores at 3 days postoperatively in Group A were significantly lower compared to the other three groups (P < 0.05), while there were no statistically significant differences among the other three groups (P > 0.05). The QoR-15 scores at 3 and 6 months postoperatively showed no statistically significant differences among the four groups (P > 0.05). In terms of secondary outcome measures, Group A had a significantly prolonged hospital stay compared to the other three groups (P < 0.05), while other outcome measures showed no statistically significant differences (P > 0.05). The timing of surgery in mild or asymptomatic SARS-CoV-2 infected patients does not affect long-term recovery quality but does impact short-term recovery quality, especially for elective general anaesthesia surgeries within 2 weeks of confirmed infection. Therefore, it is recommended to wait for a surgical timing of at least greater than 2 weeks to improve short-term recovery quality and enhance patient prognosis.