We tested the primary hypothesis that cardiac output (CO)-guided versus mean arterial pressure (MAP)-guided hemodynamic management reduces the fraction of patients with 90-day Glasgow Outcome scores ≤ 4 (on a 1–5 scale, 5 better) after supratentorial brain tumor resections in adults with cardiovascular disease. 202 adults were randomized to intraoperative hemodynamic management guided by either CO or MAP. In patients assigned to CO guidance, clinicians targeted CO > 4 L/min and > 90% of baseline values using a combination of fluids and vasoactive agents. In patients assigned to MAP guidance, clinicians targeted MAP within ± 20% of baseline and ≥ 65 mmHg. Patients randomized to CO guidance were given more crystalloid and vasoactive support, resulting in significantly higher intraoperative CO and MAP. The proportion of patients with unfavorable 90-day Glasgow Outcome Scores (≤ 4) was non-significantly lower in the CO group (34% vs. 45%, P = 0.112). However, CO-guided management significantly reduced the incidence of postoperative cerebral edema (3% vs. 11%), reduced new neurological events (27% vs. 44%), and shortened hospitalization (median 8 vs. 9 days). While encouraging, findings from our small should be considered exploratory and warrant confirmation in adequately powered trials.

Right ventricular failure (RVF) is the major cause of mortality in pulmonary arterial hypertension (PAH), and even mild inflammatory stress can precipitate rapid decompensation. Here we report that the long noncoding RNA TCONS_00052110 (TCONS) is upregulated in the right ventricle (RV) under inflammatory stress and may modulate stress-associated responses. In adult male Sprague-Dawley rats with monocrotaline-induced PAH, a low-dose lipopolysaccharide challenge precipitated acute RVF. Mechanistically, TCONS physically associates with polypyrimidine tract-binding protein 1 (PTBP1) and is associated with a prolonged PTBP1 protein half-life, consistent with reduced PTBP1 protein turnover. Elevated PTBP1 skews pyruvate kinase muscle (PKM) isoforms toward PKM2, favoring a PKM2-dominant metabolic state consistent with glycolysis-related remodeling. These changes are accompanied by mitochondrial injury and cytosolic cytochrome c release in vivo and in vitro. Using a cardiomyocyte-enriched AAV9-cTnT strategy, knockdown of TCONS was associated with normalization of the PKM2/PKM1 balance, attenuation of mitochondrial injury, preservation of RV functional indices after inflammatory challenge, and improved survival. Reanalysis of patient-derived datasets from PAH lung tissue and RV tissue spanning compensation-to-decompensation revealed enrichment of inflammatory and glycolysis-related pathways concordant with the TCONS-PTBP1 axis, supporting contextual relevance. These findings support a model of a post-transcriptional link between inflammatory stress, glycolysis-related remodeling, and mitochondrial injury in PAH-related RVF, warranting validation in human RV tissue.

Background/Objective Sleep fragmentation (SF) is a prevalent sleep disorder with an increased risk of cardiovascular diseases. Although epidemiological studies have shown a strong link between SF and adverse cardiac outcomes, specific central neural mechanisms through which SF exacerbates myocardial ischemia-reperfusion injury (MI/RI) are unclear. This study investigated the role of orexin receptor 1 (OX1R) in the hypothalamic paraventricular nucleus (PVN) in SF-induced aggravation of MI/RI and the underlying mechanism using a mouse model.Materials and methods C57BL/6 mice were subjected to chronic SF for 16 weeks before MI/RI modeling. Cardiac function was assessed by echocardiography. Sympathetic activity was evaluated based on the heart rate variability analysis. Molecular changes were evaluated by western blotting, qRT-PCR, and immunohistochemistry. The in vivo functional role of OX1R signaling was determined by administering OX1R-specific antagonist SB-334867 via stereotaxic injection into the PVN in the experimental groups of mice.Results SF mice exhibited significantly worse cardiac dysfunction and larger infarct areas following MI/RI compared to the controls. This was accompanied by enhanced sympathetic nerve activity and elevated catecholamine levels. Specifically, SF upregulated OX1R expression in the PVN and increased the levels of neuronal activation markers such as c-Fos. Pharmacological blockade of OX1R in the PVN significantly ameliorated SF-induced cardiac dysfunction, reduced the infarct size, and suppressed sympathetic hyperactivity post-MI/RI.Conclusions SF may aggravate MI/RI through PVN OX1R-associated sympathetic hyperactivation. Pharmacological inhibition of OX1R improved cardiac outcomes, supporting the involvement of the PVN OX1R-sympathetic pathway in sleep disruption related cardiac injury.

Background Right ventricular failure (RVF) is a major contributor to a poor prognosis in patients with pulmonary arterial hypertension (PAH); however, its underlying molecular mechanisms remain incompletely understood. We identified a significant upregulation of the cardiac fetal gene SND1 in the right ventricular myocardium of RVF rats. This upregulation may be a key component of cardiac fetal reprogramming and play a critical role in RVF progression. However, the precise molecular mechanisms by which SND1 contributes to RVF remain unelucidated. Methods Rat models of PAH were established by intraperitoneal injection of monocrotaline (MCT). The pulmonary artery pressure and right ventricular function of rats were assessed using transthoracic echocardiography combined with right heart catheterization. Weighted gene co-expression network analysis (WGCNA) of proteomic data identified a significant association between SND1 upregulation and RVF progression. Calcium transient and contractility measurements in single cardiomyocytes were performed to evaluate the effect of SND1 on sarcoplasmic reticulum (SR) function. Liquid chromatography with mass spectrometry/mass spectrometry analysis combined with co-immunoprecipitation (Co-IP) was used to identify sarcoplasmic/endoplasmic reticulum Ca2+-ATPase 2A (SERCA2a) as the protein interacting with SND1. The effect of SND1 on the progression of RVF was validated using cardiomyocyte-specific SND1 conditional knockout rats. Results Proteomic and molecular analyses revealed that the cardiac fetal gene SND1 is reactivated in RVF and may contribute to disease progression. In vitro, SND1 knockdown in neonatal rat ventricular myocytes (NRVMs) enhanced contractility, improved calcium transient amplitude and velocity, and increased cell survival under calcium overload. Mechanistically, SND1 interacts with SERCA2a and promotes its proteasomal degradation, impairing SR calcium reuptake. SND1 knockdown restored SERCA2a stability. In vivo, cardiomyocyte-specific SND1 knockout improved right ventricular function, reduced SERCA2a degradation and apoptosis, and increased survival in RVF rats. Conclusion Our study revealed that SND1 reactivation (a fetal gene) contributes to the progression of RVF by promoting SERCA2a degradation and impairing calcium handling. Targeted suppression of SND1 enhances cardiomyocyte contractility and survival, highlighting SND1 as a potential therapeutic target for improving right ventricular function in PAH. What Is New? What Are the Clinical Implications? ### Competing Interest Statement The authors have declared no competing interest. * ER : Endoplasmic reticulum ESPVR : End-systolic pressure-volume relationship FAC : Fractional area change FWS : Free wall strain GS : Global strain MM : Module membership NFAT : Nuclear factor of activated T-cells NRVMs : Neonatal rat ventricular myocytes PAH : Pulmonary arterial hypertension PV : Pressure-volume RV : Right ventricular RVA : Right ventricular end-systolic area RVF : Right ventricular failure SR : Sarcoplasmic reticulum TOP : Terminal oligo-pyrimidine TR : Tricuspid regurgitation WGCNA : Weighted gene co-expression network analysis H&E : Hematoxylin and Eosin TUNEL : Terminal deoxynucleotidyl transferase dUTP Nick-End Labeling

BACKGROUND:Regional anesthetic techniques are applied in cardiac surgery to improve postoperative pain and accelerate recovery. Pecto-intercostal fascial block (PIFB) combined with rectus sheath block (RSB) has been proved to provide ideal analgesia for cardiac surgery, but the effects of combing regional anesthetic techniques on postoperative recovery are uncertain. METHODS:This is a prospective and randomized controlled trial at Fuwai Hospital from 1 June 2024 to 3 July 2024. Eighty patients undergoing elective cardiac surgery via cardiopulmonary bypass were randomized at a 1:1 ratio to be allocated in the intervention group (PIFB combined with RSB) or control group (without regional blocks). The primary outcome was the global score of the 15-item quality of recovery (QoR-15) questionnaire at 24 h after surgery. Secondary outcomes included QoR-15 at 72 h, postoperative pain scores, time to extubation, length of stay, medical expenses in hospital and postoperative morbidities. RESULTS:The QoR-15 global score at 24 h after cardiac surgery was 122.35 ± 6.71 in the intervention group vs 115.30 ± 5.90 in the control group (P < .001). The proportion of patients experiencing better quality of recovery (Qor-15 ≥ 118) was higher in the intervention group (77.5% vs 55%, P = .033). Postoperative pain scores were 1.90 ± 0.18 in the intervention group compared to 2.95 ± 0.99 in the control group (P = .027) at 24 h. Time to extubation was earlier in the intervention group (274.40 ± 98.36 vs 741.28 ± 93.82 min, P < .001). There were no statistically differences in Qor-15 at 72 h and other recovery outcomes. CONCLUSION:The administration of PIFB combined with RSB could improve quality of recovery and relieve postoperative pain for patients following cardiac surgery. Key message What is already known on this topic Previous studies have demonstrated that ultrasound-guided nerve blocks effectively reduce postoperative pain in cardiac surgery patients. However, whether these techniques further enhance overall postoperative recovery remained unclear. What this study adds This trial revealed that ultrasound-guided nerve blocks improved postoperative QoR-15 scores, and combined regional techniques further improved recovery without compromising analgesia. How this study might affect research, practice, or policy The findings support applying combined nerve blocks into enhanced recovery protocols for cardiac surgery, offering evidence to optimize postoperative analgesia strategies.

BACKGROUND:Remimazolam besylate, despite being widely used in various clinical settings, lacks evidence in cardiac anesthesia. This trial compared its efficacy with propofol in elective cardiac surgery. METHODS:A total of 320 adult patients undergoing elective cardiac surgery via cardiopulmonary bypass between December 2024 and March 2025 were randomized 1:1 to either propofol (1 mg/kg for induction and 1-1.5 mg/kg/h for maintenance) or remimazolam besylate (0.3 mg/kg for induction and 1 mg/kg/h for maintenance) groups. The primary outcome was the sedation success rate (ie, bispectral index 40-60 throughout surgery with predefined dosages and without rescue sedatives), with an absolute difference of 3% as a noninferiority margin. Secondary outcomes included time from drug administration to bispectral index <60 (minute) and bispectral index variation within 15 minutes after drug withdrawal. Application of vasoactive drugs during induction, time to extubation (hour), length of stay in intensive care unit (hour), and hospital (day) were recorded. RESULTS:Of 320 enrolled patients, all patients completed the trial and 318 patients were analyzed eventually. The sedation success rate of the whole surgery was significantly higher in the remimazolam besylate group (159; 99.4%) than in the propofol group (130; 82.3%) (absolute difference 17.1%, 95% confidence interval 11.6%-23.9%; P < .001). No significant differences in time from drug administration to bispectral index <60 (P = .119), bispectral index variation after drug withdrawal (P = .658), time to extubation (P = .824), and length of stay in intensive care unit (P = .898) and hospital (P = .294) were observed. CONCLUSIONS:Remimazolam besylate is noninferior to propofol in terms of sedation efficacy during elective cardiac procedures.

Background: Mounting evidence indicates that opioid-sparing anesthesia (OSA) decreases opioid-related adverse events. Our goal was to determine whether OSA might improve initial recovery after cardiac surgery. Methods: Data from patients who underwent elective heart surgery between July 2023 and July 2024 were analyzed. Eligible patients were divided into an OSA group or a control group. Patients in the OSA group received 0.5 to 1 μg·kg −1 sufentanil and ultrasound-guided nerve block after anesthetic induction, whereas patients in the control group received traditional high-dose opioid management. Patients in both groups were managed with the same sedatives, muscle relaxants, and other drugs. The main outcome was the overall 15-item Quality of Recovery (QoR-15) survey score 24 hours after surgery. Results: A total of 1916 patients were scanned, and 1218 patients were included in the analysis: 392 in the OSA group and 826 in the control group. The QoR-15 global score measured 24 hours after surgery was 119.29 ± 3.25 in the OSA group and 113.87 ± 3.44 in the control group (P < 0.001). The OSA group had lower numeric rating scale scores 24 hours and 72 hours after surgery (P < 0.001) than the control group. The median (interquartile range) postoperative mechanical ventilation time was 1.0 (0–5) hours in the OSA group and 8.0 (6–14) hours in the control group (P < 0.001), and the duration of hospitalization was 11.5 (9–14) days and 12 (10–14) days, respectively (P = 0.012). Conclusion: OSA based on ultrasound-guided nerve blocks significantly improved QoR-15 scores after cardiac surgery and is expected to be a reasonable analgesic protocol to improve the prognosis of cardiac patients.

Background:A nomogram model has been developed to forecast the incidence of emergence delirium (ED) in elderly patients undergoing laparoscopic surgery. Methods:A secondary analysis was performed on the eMODIPOD trial, which involved elective laparoscopic surgery patients at Xiangya Hospital between October 2017 and October 2019. To assess ED, the Richmond Agitation Sedation Scale (RASS) was combined with the Intensive Care Unit (CAM-ICU) scale, and patients were categorized as ED or non-ED based on the results. The two groups were compared in terms of perioperative information and test results. Logistic regression was utilized to investigate factors contributing to ED occurrence in elderly patients following laparoscopic surgery, and a nomogram was constructed to depict this. The diagnostic performance was evaluated through the utilization of the area under the receiver operating characteristic curve (AUROC) and a calibration plot. Simultaneously, to appraise the clinical value, decision curve analysis (DCA) was employed to assess the clinical value. Results:Of the 565 patients subject to laparoscopic surgery, 94 were subsequently diagnosed with emergence delirium (ED), yielding a positive rate of 16.6 %. The developed Nomogram model was an amalgamation of several variables, which included preoperative cognitive function, educational level, dezocine, penehyclidine, ASA grading, blood loss, fluid infusion, and Post Anesthesia Care Unit-numerical rating scale (PACU-NRS). The model's performance was commendable in terms of its discrimination power, as signified by an area under the curve of 0.713(95 % CI = 0.655-0.772). Furthermore, it exhibited adequate calibration, as affirmed by the Hosmer-Lemeshow test (χ2 = 2.243, p = 0.326). Internal validation of the model further emphasized its superior discrimination and calibration capabilities. The decision curve analysis pointed out that when the threshold probability exceeded 0.1, the Nomogram model delivered more substantial benefits compared to the treat-all and treat-none approaches. Conclusions:This scoring system represents the pioneering Nomogram model utilized for predicting emergence delirium (ED) in geriatric patients undergoing laparoscopic surgery. It exhibits robust efficacy in forecasting the risk of ED, thereby furnishing valuable insights for the prevention, management, and treatment of ED.

Sleep disorders increase the risk and mortality of heart disease, but the brain-heart interaction has not yet been fully elucidated. Cuproptosis is a copper-dependent type of cell death activated by the excessive accumulation of intracellular copper. Here, we showed that 16 weeks of sleep fragmentation (SF) resulted in elevated copper levels in the male mouse heart and exacerbated myocardial ischemia-reperfusion injury with increased myocardial cuproptosis and apoptosis. Mechanistically, we found that SF promotes sympathetic overactivity, increases the germination of myocardial sympathetic nerve terminals, and increases the level of norepinephrine in cardiac tissue, thereby inhibits VPS35 expression and leads to impaired ATP7A related copper transport and copper overload in cardiomyocytes. Copper overload further leads to exacerbated cuproptosis and apoptosis, and these effects can be rescued by excision of the sympathetic nerve or administration of copper chelating agent. Our study elucidates one of the molecular mechanisms by which sleep disorders aggravate myocardial injury and suggests possible targets for intervention.

OBJECTIVE:The aim of this study is to investigate the early prognostic efficacy of plasma soluble urokinase-type plasminogen activator receptor (suPAR), soluble tumor necrosis factor receptor 1 (sTNFR1), and soluble tumor necrosis factor receptor 2 (sTNFR2) in complicated acute kidney injury (AKI) in patients with coronavirus disease 2019 (COVID-19), and to analyze the relevant factors contributing to complicated AKI in these patients. METHODS:Patients with COVID-19 hospitalized at the Affiliated Baiyun Hospital of Guizhou Medical University from March 2022 to March 2024 were selected as study participants. A total of 589 patients met the inclusion and exclusion criteria, 68 patients complicated with AKI were classified as AKI group, and the remaining 521 cases were divided into proportion sampling method and randomly selected 200 samples, which were classified as non-AKI group. Additionally, 50 healthy controls were enrolled as the control group. Logistic regression analysis was conducted to identify the relevant factors associated with complicated AKI in patients with COVID-19. Receiver operating characteristic (ROC) curves were plotted to evaluate the prognostic efficacy of plasma suPAR, sTNFR1, and sTNFR2 indicators for complicated AKI in patients with COVID-19. RESULTS:Among the patients with COVID-19 in the AKI group, 43 were males (63.20 %), with a median age of 79.00 (interquartile range: 75.00, 83.00) years, while the non-AKI group comprised 83 males (41.50 %), with a median age of 73.00 (interquartile range: 60.00, 80.75) years. Comparison of the sex and age between the two groups indicated that males and elderly patients had increased risks of complicated AKI (P < 0.05). Plasma levels of suPAR, sTNFR1, and sTNFR2 in the AKI group were significantly higher than those in the non-AKI group (P < 0.05). Logistic regression analysis indicated that suPAR and sTNFR2 were independent factors influencing complicated AKI in patients with COVID-19 (P < 0.05). The ROC curve for a single indicator showed that suPAR had the highest prognostic efficacy for complicated AKI, with an area under the curve (AUC) of 0.813, a sensitivity of 79.4 %, and a specificity of 74.0 %. The combined use of suPAR and sTNFR2 for risk assessment yielded the highest AUC of 0.838, with a sensitivity of 66.2 % and a specificity of 87.5 %. The combined risk assessment using all three indicators (suPAR, sTNFR1, and sTNFR2) had an AUC of 0.837, with a sensitivity of 64.7 % and a specificity of 89.0 %. CONCLUSION:Elderly patients had increased risks of complicated AKI. Indicators such as suPAR, sTNFR1, and sTNFR2 can assist in assessing the risk in patients with COVID-19 complicated AKI, with suPAR demonstrating the highest prognostic efficacy as a single indicator. The combined detection of suPAR, sTNFR1, and sTNFR2 offers greater prognostic value than using any single indicator.

Abstract Background Delayed neurocognitive recovery (DNR) is a common complication in patients undergoing laparoscopic surgery, and there are currently no effective therapies. It is vital to provide a reliable basis for clinical prediction. This study tried to analyse the risk factors for DNR in patients undergoing laparoscopic colorectal surgery and to establish a risk prediction model. Methods A retrospective analysis of the clinical data and DNR status of patients undergoing laparoscopic colorectal surgery at Xiangya Hospital of Central South University from March 2018 to July 2020 was conducted. Logistic regression was performed to analyse the related risk factors for DNR post-operatively, and the predictive model of DNR post-operatively was constructed and validated internally. Patients who underwent laparoscopic colorectal surgery between January and July 2021 were also selected for external validation of the predictive model, to ultimately investigate the risk factors for DNR in patients undergoing laparoscopic colorectal surgery. Results The incidence of DNR in patients undergoing laparoscopic colorectal surgery was 15.2% (31/204). The maximum variability of cerebral oxygen, age, education, and pre-existing diabetes was related to the incidence of DNR (p < 0.05). The risk prediction model of DNR after laparoscopic colorectal surgery was established. The internal and external validation showed that the discrimination was good (the AUCs were 0.751 and 0.694, respectively). Conclusions The risk prediction model of DNR related to cerebral oxygen saturation monitoring shows good predictive performance and clinical value, providing a basis for postoperative DNR prevention.

OBJECTIVES:Inflammation in the central nervous system plays a crucial role in the occurrence and development of sepsis-associated encephalopathy. This study aims to explore the effects of maresin 1 (MaR1), an anti-inflammatory and pro-resolving lipid mediator, on sepsis-induced neuroinflammation and cognitive impairment. METHODS:Mice were randomly assigned to 4 groups: A sham group (sham operation+vehicle), a cecal ligation and puncture (CLP) group (CLP operation+vehicle), a MaR1-LD group (CLP operation+1 ng MaR1), and a MaR1-HD group (CLP operation+10 ng MaR1). MaR1 or vehicle was intraperitoneally administered starting 1 h before CLP operation, then every other day for 7 days. Survival rates were monitored, and serum inflammatory cytokines [tumor necrosis factor alpha (TNF-α), interleukin (IL)-1β, and IL-6] were measured 24 h after operation using enzyme-linked immunosorbent assay (ELISA). Cognitive function was assessed 7 days after operation using the Morris water maze (MWM) test and novel object recognition (NOR) task. The mRNA expression of TNF-α, IL-1β, IL-6, inducible nitric oxide synthase (iNOS), IL-4, IL-10, and arginase 1 (Arg1) in cortical and hippocampal tissues was determined by real-time reverse transcription PCR (RT-PCR). Western blotting was used to determine the protein expression of iNOS, Arg1, signal transducer and activator of transcription 6 (STAT6), peroxisome proliferator-activated receptor gamma (PPARγ), and phosphorylated STAT6 (p-STAT6) in hippocampal tissue. Microglia activation was visualized via immunofluorescence. Mice were also treated with the PPARγ antagonist GW9662 to confirm the involvement of this pathway in MaR1's effects. RESULTS:CLP increased serum levels of TNF-α, IL-1β, and IL-6, and reduced body weight and survival rates (all P<0.05). Both 1 ng and 10 ng doses of MaR1 significantly reduced serum TNF-α, IL-1β, and IL-6 levels, improved body weight, and increased survival rates (all P<0.05). No significant difference in efficacy was observed between the 2 doses (all P>0.05). MWM test and NOR task indicated that CLP impaired spatial learning, which MaR1 mitigated. However, GW9662 partially reversed MaR1's protective effects. Real-time RT-PCR results demonstrated that, compared to the sham group, mRNA expression of TNF-α, IL-1β, and iNOS significantly increased in hippocampal tissues following CLP (all P<0.05), while IL-4, IL-10, and Arg1 showed a slight decrease, though the differences were not statistically significant (all P>0.05). Compared to the CLP group, both 1 ng and 10 ng MaR1 decreased TNF-α, IL-1β, and iNOS mRNA expression in hippocampal tissues and increased IL-4, IL-10, and Arg1 mRNA expression (all P<0.05). Immunofluorescence results indicated a significant increase in Iba1-positive microglia in the hippocampus after CLP compared to the sham group (P<0.05). Administration of 1 ng and 10 ng MaR1 reduced the percentage area of Iba1-positive cells in the hippocampus compared to the CLP group (both P<0.05). Western blotting results showed that, compared to the CLP group, both 1 ng and 10 ng MaR1 down-regulated the iNOS expression, while up-regulated the expression of Arg1, PPARγ, and p-STAT6 (all P<0.05). However, the inclusion of GW9662 counteracted the MaR1-induced upregulation of Arg1 and PPARγ compared to the MaR1-LD group (all P<0.05). CONCLUSIONS:MaR1 inhibits the classical activation of hippocampal microglia, promotes alternative activation, reduces sepsis-induced neuroinflammation, and improves cognitive decline.

PURPOSE:Metabolic reprogramming is currently considered a hallmark of tumor and immune development. It is obviously of interest to identify metabolic enzymes that are associated with clinical prognosis in head and neck squamous cell carcinomas (HNSCC).METHODS:Candidate genes were screened to construct folate metabolism scores by Cox regression analysis. Functional enrichment between high- and low-folate metabolism groups was explored by GO, KEGG, GSVA, and ssGSEA. EPIC, MCPcounter, and xCell were utilized to explore immune cell infiltration between high- and low-folate metabolism groups. Relevant metabolic scores were calculated and visually analyzed by the "IOBR" software package.RESULTS:To investigate the mechanism behind metabolic reprogramming of HNSCC, 2886 human genes associated with 86 metabolic pathways were selected. Folate metabolism is significantly enriched in HNSCC, and that the six-gene (MTHFD1L, MTHFD2, SHMT2, ATIC, MTFMT, and MTHFS) folate score accurately predicts and differentiates folate metabolism levels. Reprogramming of folate metabolism affects CD8T cell infiltration and induces immune escape through the MIF signaling pathway. Further research found that SHMT2, an enzyme involved in folate metabolism, inhibits CD8T cell infiltration and induces immune escape by regulating the MIF/CD44 signaling axis, which in turn promotes HNSCC progression.CONCLUSIONS:Our study identified a novel and robust folate metabolic signature. A folate metabolic signature comprising six genes was effective in assessing the prognosis and reflecting the immune status of HNSCC patients. The target molecule of folate metabolic reprogramming, SHMT2, probably plays a very important role in HNSCC development and immune escape.

Background: Enhanced recovery after surgery (ERAS) protocol strategies can shorten the hospital stays and ICU stays of patients undergoing cardiac valve surgery. The aim of this study was to explore the long-term quality of life (QOL) and survival of patients undergoing the ERAS protocol.Methods: A randomized clinical trial was conducted between July 2015 and November 2016. A QOL assessment was applied in both groups after 3 years, and assessment scores were compared. QOL was measured by the Short-Form 36 health survey (SF-36). The mortality rate and the incidence of adverse events were analyzed statistically.Results: The questionnaire return rate after 3 years was 73.66%. There were no significant differences noted between the two groups with regard to preoperative risk factors on admission or the questionnaire return rate. No intergroup difference was observed in SF-36 scores at 3 years after discharge (p > 0.05). The incidence of cardiovascular-related adverse events was lower in the ERAS group than in the control group 3 years after the surgery (p < 0.01).Conclusion: Our results showed that there was no significant difference in survival or quality of life between the two groups three years after surgery. Except the incidence of cardiovascular-related adverse events, ERACS procedures have no effect on long-term outcomes.

In China, dezocine is commonly employed as a partial agonist of mu/kappa opioid receptors during anesthesia induction for surgical patients, yet evidence supporting its causal association with emergence delirium is limited. The objective of this investigation was to evaluate the impact of intravenous dezocine administered during anesthesia induction on emergence delirium. The retrospective studied existing data containing medical records of patients undergoing an elective laparoscopy procedure and the study was conducted with ethics-board approval. The primary outcome was the incidence of emergence delirium. Secondary outcomes included the VAS in the PACU and 24 h after surgery, the RASS score in the PACU, postoperative MMSE, hospital stay, and ICU stay. A total of 681 patients were analyzed, after being propensity score-matched, the dezocine and non-dezocine group each had 245 patients. Emergence delirium occurred in 26/245 (10.6%) of patients who received dezocine and 41/245 (16.7%) of patients did not receive dezocine. Patients on whom dezocine was used were associated with a significantly lower incidence of emergence delirium (absolute risk difference, -6.1%, 95% CI, -12% to -0.2%; relative risk [RR], 0.63; 95% CI, 0.18-0.74). All secondary outcome measures and adverse outcomes were not significantly different. The use of dezocine during anesthesia induction was associated with a decreased incidence of emergence delirium after elective laparoscopic surgeries.

Background Right ventricle failure (RVF) is a progressive heart disease that has yet to be fully understood at the molecular level. Elevated M-type pyruvate kinase 2 (PKM2) tetramerization alleviates heart failure, but detailed molecular mechanisms remain unclear. Objective We observed changes in PKM2 tetramerization levels during the progression of right heart failure and in vitro cardiomyocyte hypertrophy and explored the causal relationship between altered PKM2 tetramerization and the imbalance of redox homeostasis in cardiomyocytes, as well as its underlying mechanisms. Ultimately, our goal was to propose rational intervention strategies for the treatment of RVF. Method We established RVF in Sprague Dawley (SD) rats by intraperitoneal injection of monocrotaline (MCT). The pulmonary artery pressure and right heart function of rats were assessed using transthoracic echocardiography combined with right heart catheterization. TEPP-46 was used both in vivo and in vitro to promote PKM2 tetramerization. Results We observed that oxidative stress and mitochondrial disorganization were associated with increased apoptosis in the right ventricular tissue of RVF rats. Quantitative proteomics revealed that PKM2 was upregulated during RVF and negatively correlated with the cardiac function. Facilitating PKM2 tetramerization promoted mitochondrial network formation and alleviated oxidative stress and apoptosis during cardiomyocyte hypertrophy. Moreover, enhancing PKM2 tetramer formation improved cardiac mitochondrial morphology, mitigated oxidative stress and alleviated heart failure. Conclusion Disruption of PKM2 tetramerization contributed to RVF by inducing mitochondrial fragmentation, accumulating ROS, and finally promoted the progression of cardiomyocyte apoptosis. Facilitating PKM2 tetramerization holds potential as a promising therapeutic approach for RVF.

We analyze the effects of local government debt on the proliferation of zombie firms. With aggregated prefecture-level debt data and firm-level data from 2006 to 2013, the empirical evidence demonstrates that the local government debt significantly exacerbates the "zombification" of local firms, mainly through the credit-favoritism to state-owned enterprises and capital misallocation. Our analysis also shows that the magnitude of zombification effects is influenced by debt liquidity and the primary functions of local government financing vehicles.

Abstract Objective: This study is dedicated to uncovering the relationship between critical thinking (CT) and learning styles and the level of each learning mode, as a way of proposing a predictive model of CT that relies on the learning mode. Methods: In this study, 187 students from Xiangya School of Medicine, Central South University were surveyed between 24 February and 7 March 2022. The questionnaire consisted of three parts: demographic characteristics, the Chinese version of the California Critical Thinking Skills Questionnaire (CTDI-CV) and the Kolb Learning Style Inventory (LSI). Results: The CTDI-CV total score was positive (293.02±25.66), with the highest scores for inquisitiveness (45.09±6.19) and analyticity (43.70±5.20) and the lowest for self-confidence (39.21±6.22) and systematicity (39.41±5.26) in the seven subscales. On learning styles, there are most Assimilaters (52.9%; 293.89±25.11) and least Convergers (5.9%; 301.66±20.99), with having better CT than Divergers (20.9%; 286.08±27.58) and Accommodaters (20.3%; 279.91±26.26). The differences in CT-related indicators across learning modes were statistically significant (P<0.05), with CE and RO negatively affecting CT(r<0) and AC positively(r>0). Linear regression models for CT scores based on learning modes were constructed. Conclusion: As a result of our findings, CT and learning modes, the basis of learning styles, were quantified and their relationship was described. These results inform medical education reform, particularly with respect to teaching and assessment systems around improving CT.

A myocardial infarction (MI) is the leading cause of morbidity and mortality, seriously threatens human health, and becomes a major health burden of our society. It is urgent to pursue effective therapeutic strategies for the regeneration and restore myocardial function after MI. This review discusses the role of hydrogel in cardiac repair and regeneration for MI. Hydrogel-based cardiac patches and injectable hydrogels are the most commonly used applications in cardiac regeneration medicine. With injectable hydrogels, bioactive compounds and cells can be delivered in situ, promoting in situ repair and regeneration, while hydrogel-based cardiac patches reduce myocardial wall stress, which passively inhibits ventricular expansion. Hydrogel-based cardiac patches work as mechanically supportive biomaterials. In cardiac regeneration medicine, clinical trials and commercial products are limited. Biomaterials, biochemistry, and biological actives, such as intelligent hydrogels and hydrogel-based exosome patches, which may serve as an effective treatment for MI in the future, are still under development. Further investigation of clinical feasibility is warranted. We can anticipate hydrogels having immense translational potential for cardiac regeneration in the near future.

Background Online education has become increasingly popular, but research on the effectiveness of different teaching models in developing cognitive skills is limited. This study investigated the relationship between different teaching models (online and offline) and the development of cognitive skills in clinical medicine students. Methods Survey data were collected from 2018 entry students who participated in online teaching and 2019 entry students in offline teaching at Xiangya School of Medicine, Central South University. National Quality Open Courses (NQROC) were provided to both groups of students. The study examined the total score of physiology final exam, score of each type of question, and NQROC learning engagement in different score segments under the two teaching models. Non-parametric statistical methods were utilized to analyze the total score of physiology final exam, score of each type of question, and the NQROC learning engagement. Spearman’s rank correlation was utilized to analyze the relationship between the score of physiology final exam and the students’ NQROC learning engagement. Results The study found no statistically significant difference in the total score, short-answer questions (SAQs) score, and case study questions (CSQs) score between online and offline teaching models. However, the multiple-choice questions (MCQs) score was higher in the online teaching model ( Z =-4.249, P < 0.001), suggesting that online teaching may be an effective way to improve lower-order cognitive skills among students. In contrast, low-achieving students had higher total scores ( Z =-3.223, P = 0.001) and scores in both MCQs ( Z =-6.263, P < 0.001) and CSQs ( Z =-6.877, P < 0.001) in the online teaching model. High-achieving students in the online teaching model had higher total scores ( Z =-3.001, P = 0.003) and MCQs scores ( Z =-5.706, P < 0.001) but lower scores in CSQs ( Z =-2.775, P = 0.006). Furthermore, students’ NQROC learning engagement was greater in the online teaching model. Conclusions The results of this study suggested that online teaching was not statistically significantly different from offline in cognitive domains and was more desirable than offline in strengthening lower-order cognitive skills. However, it was important to note that offline teaching may be more effective in reinforcing higher-order cognitive skills among high-achieving students. In conclusion, this study provided important insights into the effectiveness of different teaching models in developing cognitive skills among medical students and highlighted the potential benefits of online teaching in enhancing students’ lower-order cognitive skills.