Background. Endotoxin-associated acute kidney injury (AKI), a disease characterized by marked oxidative stress and inflammation disease, is a major cause of mortality in critically ill patients. Mitochondrial fission and pyroptosis often occur in AKI. However, the underlying biological pathways involved in endotoxin AKI remain poorly understood, especially those related to mitochondrial dynamics equilibrium disregulation and pyroptosis. Previous studies suggest that heme oxygenase- (HO-) 1 confers cytoprotection against AKI during endotoxic shock, and PTEN-induced putative kinase 1 (PINK1) takes part in mitochondrial dysfunction. Thus, in this study, we examine the roles of HO-1/PINK1 in maintaining the dynamic process of mitochondrial fusion/fission to inhibit pyroptosis and mitigate acute kidney injury in rats exposed to endotoxin. Methods. An endotoxin-associated AKI model induced by lipopolysaccharide (LPS) was used in our study. Wild-type (WT) rats and PINK1 knockout (PINK1KO) rats, respectively, were divided into four groups: the control, LPS, Znpp+LPS, and Hemin+LPS groups. Rats were sacrificed 6 h after intraperitoneal injecting LPS to assess renal function, oxidative stress, and inflammation by plasma. Mitochondrial dynamics, morphology, and pyroptosis were evaluated by histological examinations. Results. In the rats with LPS-induced endotoxemia, the expression of HO-1 and PINK1 were upregulated at both mRNA and protein levels. These rats also exhibited inflammatory response, oxidative stress, mitochondrial fission, pyroptosis, and decreased renal function. After upregulating HO-1 in normal rats, pyroptosis was inhibited; mitochondrial fission and inflammatory response to oxidative stress were decreased; and the renal function was improved. The effects were reversed by adding Znpp (a type of HO-1 inhibitor). Finally, after PINK1 knockout, there is no statistical difference in the LPS-treated group and Hemin or Znpp pretreated group. Conclusions. HO-1 inhibits inflammation response and oxidative stress and regulates mitochondria fusion/fission to inhibit pyroptosis, which can alleviate endotoxin-induced AKI by PINK1.

Some evidence indicates that some potential sleep-related markers are closely related to perioperative sleep disorder, which may provide a valuable reference for its prediction and diagnosis. This review summarizes the potential value of these sleep-related markers in the prediction of perioperative sleep disorder, such as orexin system, Homer1a protein, metabotropic glutamate receptor 5 (mGluR5) regulatory protein, melanin-concentrating hormone (MCH) system, amyloid β-protein (Aβ), Tau protein, synaptotagmin (SYT), and aims to provide new ideas for perfecting the prediction and diagnosis of perioperative sleep disorder.

Endotoxin-induced acute kidney injury (AKI) is commonly observed in clinical practice. Renal tubular epithelial cell (RTEC) pyroptosis is one of the main factors leading to the development of endotoxin-induced AKI. Mitochondrial dysfunction can lead to pyroptosis. However, the biological pathways involved in the potential lipopolysaccharide (LPS)-induced pyroptosis of RTECs, notably those associated with mitochondrial dysfunction, are poorly understood. Previous studies have demonstrated that heme oxygenase (HO)-1 confers cell protection via the induction of PTEN-induced putative kinase 1 (PINK1) expression through PTEN to regulate mitochondrial fusion/fission during endotoxin-induced AKI in vivo. Therefore, the present study investigated the role of HO-1/PINK1 in maintaining mitochondrial function and inhibiting the pyroptosis of RTECs exposed to LPS. Primary cultures of RTECs were obtained from wild-type (WT) and PINK1-knockout (PINK1KO) rats. An in vitro model of endotoxin-associated RTEC injury was established following treatment of the cells with LPS. The WT RTECs were divided into the control, LPS, Znpp + LPS and Hemin + LPS groups, and the PINK1KO RTECs were divided into the control, LPS and Hemin + LPS groups. RTECs were exposed to LPS for 6 h to assess cell viability, inflammation, pyroptosis and mitochondrial function. In the LPS-treated RTECs, the mRNA and protein expression levels of HO-1 and PINK1 were upregulated. Cell viability, adenosine triphosphate (ATP) levels and the mitochondrial oxygen consumption rate were decreased, whereas the inflammatory response, pyroptosis and mitochondrial reactive oxygen species (ROS) levels were increased. The cell inflammatory response and the induction of pyroptosis were inhibited, whereas the levels of mitochondrial ROS were decreased. In addition, the cell viability and ATP levels were increased in the WT RTECs following the upregulation of HO-1 expression. These effects were reversed by the downregulation of HO-1 expression. However, no statistically significant differences were noted between the LPS and the Hemin + LPS groups in the PINK1KO RTECs. Collectively, the findings of the present study indicate that HO-1 inhibits inflammation and regulates mitochondrial function by inhibiting the pyroptosis of LPS-exposed RTECs via PINK1.

Background Homer1, an immediate early gene, is related to sleep deprivation (SD), and its protein products are involved in synaptic plasticity affecting the cognitive process. This study aimed to identify the SD-associated key Homer1 gene in the brain and explore the value of Homer1 proteins acting on synaptic plasticity in SD. Methods GSE9441 was extracted from Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) between SD and Control samples were achieved by R software and were analyzed by the Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, and gene set enrichment analysis (GSEA). Protein–protein interactions (PPI) network was built by the GeneMANIA databases. In animal experiments, male C57BL/6 J mice (aged 12–13 weeks) were sleep deprived for 6 h, followed by independent behavioral tests and in vitro assays. Morris water maze (MWM) was used to evaluate learning and memory function. The expression of hippocampal Homer1 proteins was detected by Western blot analysis and its distribution in CA1 by immunohistochemistry and immunofluorescence staining. Synaptic plasticity was assessed by Golgi staining and long-term potentiation (LTP) testing in the hippocampal CA1 region. Results Homer1 was the hub gene most associated with SD, and its protein products specifically acted on the regulation of synaptic plasticity in bioinformatics. SD mice exhibited spatial memory impairment accompanied by increased Homer1a expression in hippocampal tissue and CA1 region. SD did not induce Homer1b/c overexpression of mice in the hippocampus. SD impaired the hippocampal synaptic plasticity of mice by reducing the density of dendritic spines and inhibiting LTP in the hippocampal CA1 region, which may involve the overexpression of Homer1a in the hippocampus. Conclusion Homer1 gene is a core brain molecule associated with acute SD, and its protein product Homer1a is involved in the changes in cognitive brain function following short-term SD, especially the impact on hippocampal synaptic plasticity.

近年来,全身麻醉药物对发育大脑的影响成为关注的焦点.全身麻醉药物可造成动物胎儿及幼崽随着生长发育出现短期及长期认知功能障碍,而临床中回顾性研究结果与动物实验结果尚不一致.因此,全身麻醉药物对发育大脑有无影响尚无统一定论.小胶质细胞作为中枢神经系统免疫细胞在发育的不同阶段表现不同形态,执行不同的功能,在神经元损伤修复、神经炎症、神经网络构建等方面发挥重要作用.本文将常用全身麻醉药物包括吸入麻醉药、静脉麻醉药、阿片类药物等对发育大脑小胶质细胞的影响机制做一综述.

目的 探讨右美托咪定预处理对老年术后认知功能障碍(POCD)大鼠工作记忆损伤的影响.方法 选择健康雄性SD大鼠18只,18月龄,体质量500～550 g,采用随机数表法分为3组(n=6):对照组(C组)、手术组(S组)和右美托咪定预处理组(DP组).各组实验鼠用Morris水迷宫进行5 d工作记忆训练后,S组和DP组行脾切除制作POCD模型.DP组于术前30 min腹腔注射右美托咪定12μg/kg,术后第7日进行工作记忆测试.以心尖取血法采集血样,ELISA法检测血浆IL-1β、IL-6和TNF-a浓度,采用Western blot检测海马区BDNF蛋白含量.结果 在训练期,实验鼠第二组逃避潜伏期较第一组缩短;在测试期,与C组相比较,S组和DP组逃避潜伏期延长,达标前测试次数增加,海马区BDNF含量降低,血浆IL-1β、IL-6和TNF-α浓度增加;与S组比较,DP组逃避潜伏期缩短,达标前测试次数减少,海马区BDNF含量增加,血浆IL-1β、IL-6和TNF-a浓度降低(P＜0.05).结论 右美托咪定可通过降低炎症反应、增加海马区BDNF表达而改善老年POCD大鼠工作记忆损伤.

Objective:To evaluate the effect of electroacupuncture on the heme oxygenase-1 (HO-1)/PTEN-induced putative kinase 1 (PINK1)/Parkin signaling pathway during acute kidney injury in endotoxemic rats.Methods:Twenty-four SPF healthy male Sprague-Dawley rats, aged 6-8 weeks, weighing 180-220 g, were divided into 4 groups ( n=6 each) by a random number table method: control group(group C), endotoxemia group(group E), acupoint electroacupuncture+ endotoxemia group(group EE), and non-acupoint electroacupuncture+ endotoxemia group(group NE). The endotoxemia model was developed by intraperitoneal injection of lipopolysaccharide 10 mg/kg. The equal volume of normal salinewas injected in group C. LPS 10 mg/kg was intraperitoneally injected in group E. In group EE, 30-min electroacupuncture was performed at bilateral Zusanli and Shenshu acupoints using disperse-dense waves with a frequency of 2/15 Hz to induce slight muscle tremor once a day starting from 5 days before developing the model, and the needle was retained until 6 h after injection. Electroacupuncture was performed at the points 0.5 cm lateral to the acupoints of Zusanli and Shenshu in group NE. The rats were anesthetized at 6 h after lipopolysaccharide injection, and blood samples from the femoral vein were obtained for determination of the serum creatinine (Cr) and urea nitrogen (BUN) concentrations(with a biochemical analyzer) and concentrations of neutrophil gelatinase-associated lipid transport protein (NGAL), interleukin-6 (IL-6), tumor necrosis factor (TNF-α) and kidney injury molecule-1(KIM-1) in serum (by enzyme-linked immunosorbent assay). Then the rats were sacrificed and kidney tissues were taken for determination of histological score of kidneys (HSK, using HE staining) and expression of HO-1, PINK1, Parkin, mitochondrial fusion protein 2(Mfn2), optic atrophy protein 1(OPA1) and mitochondrial dynamic-related protein 1 (Drp1) (by Western blot). Results:Compared with group C, serum concentrations of Cr, BUN, KIM-1, NGAL, IL-6 and TNF-α and HSK score of renal tissues were significantly increased, the expression of HO-1, PINK1, Parkin and Drp1 was up-regulated, and the expression of Mfn2 and OPA1 was down-regulated in E, EE and NE groups ( P<0.05). Compared with group E, serum concentrations of Cr, BUN, KIM-1, NGAL, IL-6 and TNF-α and HSK score of renal tissues were significantly decreased, and the expression of HO-1, PINK1, Parkin, Mfn2 and OPA1 was up-regulated, and Drp1 expression was down-regulated in group EE( P<0.05), and no significant change was found in the parameters mentioned above in group NE ( P>0.05). Conclusions:The mechanism by which electroacupuncture alleviates acute kidney injury is associated with activation of HO-1/PINK1/Parkin signaling pathway in endotoxemic rats.

BACKGROUND:Aging and preoperative sleep disorders are the main risk factors affecting postoperative cognitive outcomes. However, the pathogenesis of delayed neurocognitive recovery after surgery remains ambiguous, and there is still a lack of potential biomarkers for delayed neurocognitive recovery in older adult patients with preoperative sleep disorders. Our study aimed to explore the relationship between melanin-concentrating hormone (MCH) and delayed neurocognitive recovery early after surgery in older adult patients with preoperative sleep disorders. METHODS:In this monocentric prospective observational study, 156 older adult patients (aged 65 years or older) with preoperative sleep disorders undergoing elective total hip arthroplasty (THA) or total knee arthroplasty (TKA) were included at an academic medical center in Inner Mongolia, China, from October 2021 to November 2022, and all patients underwent spinal anesthesia. The Pittsburgh Sleep Quality Index (PSQI) was applied to assess the preoperative sleep quality of all patients, and preoperative sleep disorders were defined as a score of PSQI >5. We measured the levels of cerebrospinal fluid (CSF) MCH and plasma MCH of all patients. The primary outcome was delayed neurocognitive recovery early after surgery. All patients received cognitive function assessment through the Montreal Cognitive Assessment (MoCA) 1 day before and 7 days after surgery (postoperative day 7 [POD7]). Delayed neurocognitive recovery was defined as a score of POD7 MoCA <26. The potential confounders included variables with P < .2 in the univariate logistic analysis, as well as the important risk factors of delayed neurocognitive recovery reported in the literature. Multivariable logistic regression model based on the Enter method assessed the association of MCH and delayed neurocognitive recovery in older adult patients with preoperative sleep disorders. RESULTS:Fifty-nine (37.8%) older adult patients with preoperative sleep disorders experienced delayed neurocognitive recovery at POD7. Increase in CSF MCH levels (odds ratio [OR] for an increase of 1 pg/mL = 1.16, 95% confidence interval [CI], 1.09-1.23, P < .001) and decrease in plasma MCH levels (OR for an increase of 1 pg/mL = 0.92, 95% CI, 0.86-0.98, P = .003) were associated with delayed neurocognitive recovery, after adjusting for age, sex, education, baseline MoCA scores, American Society of Anesthesiologists (ASA) grade, and coronary heart disease (CHD). CONCLUSIONS:In older adult patients with preoperative sleep disorders, MCH is associated with the occurrence of delayed neurocognitive recovery after surgery. Preoperative testing of CSF MCH or plasma MCH may increase the likelihood of identifying the high-risk population for delayed neurocognitive recovery in older adult patients with preoperative sleep disorders.

Normal sleep and sleep-wake cycle are critical for cognitive functions such as learning and memory, while sleep deprivation (SD) impairs learning and memory through a variety of mechanisms, in which memory consolidation function of rapid eye movement (REM) sleep and synaptic plasticity play a critical role. In recent years, studies have shown that melanin-concentrating hormone (MCH) system plays an essential role in learning and memory impairment induced by sleep deprivation. This review summarizes the changes of MCH system function in sleep deprivation, its effect on REM sleep and synaptic plasticity, and how it affects learning and memory function, so as to provide new ideas for further exploring the mechanism of learning and memory impairment of sleep deprivation.

Background: This multicenter prospective, randomized controlled clinical trial compared the clinical performance of supraglottic airway device (SAD) BlockBuster (TM) and laryngeal mask airway (LMA) Supreme for airway maintenance in anesthetized, paralyzed adult patients. Methods: A total of 651 adult patients scheduled for elective surgery in 13 hospitals were randomly allocated into BlockBuster group (n = 351) or Supreme group (n = 300). The primary outcome was oropharyngeal leak pressure (OLP). Duration and ease of insertion, fiberscopic view of positioning, airway manipulations, and complications were also assessed. Results: The OLP was significantly higher in BlockBuster group compared with Supreme group (29.9 +/- 4.2 cmH(2)O vs 27.4 +/- 4.3 cmH(2)O, p < 0.001). Success rate of insertion at the first attempt (90.2% vs 85.1%, p = 0.027), rate of optimal fiberscopic view (p = 0.002) and satisfactory positioning of SAD (p < 0.001) were significantly increased in BlockBuster group. Conclusions: Both SAD BlockBuster (TM) and LMA Supreme are safe, effective, and easy-to-use devices for airway maintenance in anesthetized, paralyzed adult patients, but the SAD BlockBuster (TM) is superior to LMA Supreme in terms of OLP, success rate at the first attempt, and fiber-optic view of positioning.

脓毒症急性肾损伤临床常见,发病率和病死率高.线粒体功能障碍引起的肾小管细胞死亡是其发病机制之一.线粒体质量控制失调是导致线粒体功能障碍的主要原因.线粒体质量控制包括线粒体生物合成、线粒体融合/分裂和线粒体自噬.线粒体质量控制在脓毒症急性肾损伤中发挥着至关重要的作用,目前很多研究将线粒体质量控制作为脓毒症急性肾损伤的靶向治疗策略.因此,本文就线粒体质量控制在脓毒症急性肾损伤的相关研究进展进行综述,为临床防治脓毒症急性肾损伤提供参考和理论依据.

目的 研究右美托咪定复合七氟醚行麻醉维持应用于儿童腺样体肥大切除手术的效果.方法 选取2018年6月～2020年5月收治的腺样体肥大患儿98例,均行腺样体切除术,其中49例采用七氟醚麻醉维持为对照组,49例采用右美托咪定复合七氟醚麻醉维持为复合组.比较两组麻醉前(T0)、气管插管时(T1)、术后即刻(T2)血流动力学指标[平均动脉压(MAP)、心率(HR)]、术后6 h躁动率、疼痛程度[面部表情量表法(FPS评分)]及补救镇痛药舒芬太尼用量.结果 T1、T2时复合组MAP、HR小于对照组(P<0.05);复合组躁动率6.12％小于对照组20.41％(P<0.05);复合组FPS评分低于对照组(P<0.05);复合组补救镇痛药舒芬太尼用量小于对照组(P<0.05).结论 右美托咪定复合七氟醚行麻醉维持应用于儿童腺样体肥大切除手术能维持术中血流动力学稳定,减少术后躁动情况发生,减轻疼痛程度,降低补救镇痛药舒芬太尼用量.

Background: Multimodal postoperative analgesia with intravenous ibuprofen can reduce the consumption of opioids and reduce the postoperative pain intensity. Recommended dose in the USA and Europe is 800 mg every 6 hours for the management of moderate to severe postoperative pain. The purpose of this study was to investigate whether 800 mg is needed in the Chinese population. Methods: This is a multicenter, randomized, controlled multi-center trial. Adult patients (18-65 years of age) scheduled for abdominal or orthopedic surgery under general anesthesia with endotracheal intubation were eligible. Subjects were randomized at a ratio of 1:1:1 to receive ibuprofen at 400 or 800 mg or saline every 6 hours for 48 hours after the operation. All subjects received morphine access through patient-controlled intravenous analgesia (PCIA) device, which was set as background infusion rate 0.5 mg/h, bolus 1 mg, 5-minute lock interval and 20-mg 4-hour limit. The primary endpoint was morphine consumption within the first 24 hours after surgery. Results: A total of 396 patients were enrolled (180 men, 216 women; 46±12.4 years of age; 106 patients receiving abdominal surgery, and 290 patients receiving orthopedic surgery). The number of patients was 131 in the placebo group, 132 in the 400-mg group, and 133 in the 800-mg group. The 3 groups did not differ in age, sex, BMI and the type of surgery. Median 24-hour morphine consumption was 39.1 mg (IQR: 29.7, 61.7) mg in the placebo control, 29.8 mg (IQR: 24.3, 43.7) mg in the 400-mg group, and 28.0 mg (IQR: 24.1, 35.9) in the 800-mg group (P<0.001 for comparisons between placebo versus 400 and 800 mg ibuprofen). There was no significant difference between the two ibuprofen groups (P=0.125). Analgesia-related adverse events did not differ among the 3 groups. Conclusions: Intravenous ibuprofen at either 400 or 800 mg every 6 hours could reduce postoperative morphine consumption, with apparently equal efficacy in Chinese population.

Objective:To evaluate the effect of electroacupuncture (EA) on pyroptosis in renal tubular epithelial cells of rats with acute kidney injury (AKI) induced by endotoxin.Methods:Twenty-four healthy clean-grade Sprague-Dawley rats of either gender, aged 6-8 weeks, weighing 160-182 g, were divided into 4 groups ( n=6 each) using a random number table method: control group (group C), group AKI, EA plus AKI group (group EA), sham EA at non-acupoint plus AKI group (group SEA). The model of endotoxemia was established by intraperitoneally injecting 10 mg/kg lipopolysaccharide.Bilateral 30 min EA stimulation of Zusanli and Shenyu (according to atlas of animal acupoint) was performed starting from 5 days before establishing the model (once a day) and at 30 min before lipopolysaccharide administration on the day of establishing the model, with disperse-dense waves, frequency of 15 Hz, and the needle was kept until 6 h after injection of LPS in group EA.EA was performed at the points 0.5 cm lateral to the acupoints of Zusanli and Shenyu in group SEA.At 6 h after LPS injection, blood was taken from the heart, and the concentrations of serum blood urea nitrogen (BUN) and creatinine (Cr) were detected by an automatic biochemical analyzer, and the serum concentrations of neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) by enzyme-linked immunosorbent assay.The rats were then sacrificed, and the left renal cortex was obtained for determination of pyroptosis rate of renal tubular epithelial cells (by TUNEL). The right renal cortex was obtained to detect the expression of caspase-1 and IL-1β by Western blot, and the expression of caspase-1 mRNA and IL-1β mRNA was detected by real-time polymerase chain reaction. Results:Compared with group C, the concentrations of BUN, Cr, NGAL, KIM-1, TNF-α, and IL-6 were significantly increased, the pyroptosis rate of renal tubular epithelial cells was increased, the expression of caspase-1 and IL-1β protein and mRNA in the renal cortex was up-regulated in group AKI ( P<0.05). Compared with group AKI, the concentrations of BUN, Cr, NGAL, KIM-1, TNF-α, and IL-6 were significantly decreased, the pyroptosis rate of renal tubular epithelial cells was decreased, the expression of caspase-1 and IL-1β protein and mRNA in the renal cortex was down-regulated in group SEA ( P>0.05). Conclusion:The mechanism by which EA reduces AKI may be related to inhibiting pyroptosis in renal tubular epithelial cells of rats.

BACKGROUND:Neurocognitive disorders (NCDs) and sleep disturbance are highly prevalent in the perioperative period and intensive care unit (ICU). There has been a lack of individualized evaluation tools designed for the high-risk NCDs in critically ill patients with sleep disturbance.OBJECTIVES:The aim of this study was to develop and validate prediction models for NCDs among adult patients with sleep disturbance.METHODS:The R software was used to analyze the dataset of adult patients admitted to the ICU with sleep disturbance, who were diagnosed following the codes of the International Classification of Diseases, 9th Revision (ICD-9) and 10th Revision (ICD-10) using the MIMIC-IV database. We used logistic regression and LASSO analyses to identify important risk factors associated with NCDs and develop nomograms for NCDs predictions. We measured the performances of the nomograms using the bootstrap resampling procedure, sensitivity, specificity of the receiver operating characteristic (ROC), area under the ROC curves (AUC), and decision curve analysis (DCA).RESULTS:The prediction models shared the 10 risk factors (age, gender, midazolam, morphine, glucose, diabetes diseases, potassium, international normalized ratio, partial thromboplastin time, and respiratory rate). Cardiovascular diseases were included in the logistic regression, the sensitivity was 74.1%, and specificity was 64.6%. When platelet and Glasgow Coma Score (GCS) were included and cardiovascular diseases were removed in the LASSO prediction model, the sensitivity was 86.1% and specificity was 82.8%. Discriminative abilities of the logistic prediction and LASSO prediction models for NCDs in the validation set were evaluated as the AUC scores, which were 0.730 (95% CI 0.716-0.743) and 0.920 (95% CI 0.912-0.927). Net benefits of the prediction models were observed at threshold probabilities of 0.567 and 0.914.CONCLUSIONS:The LASSO prediction model showed better performance than the logistic prediction model and should be preferred for nomogram-assisted decisions on clinical risk management of NCDs among adult patients with sleep disturbance in the ICU.

目的 比较超声引导下两种不同浓度罗哌卡因用于腹股沟韧带上髂筋膜间隙阻滞(S-FICB)的起效时间.方法 限期行股骨近端髓内针内固定术的股骨转子间骨折患者60例,男28例,女32例,年龄65～85岁,ASAⅠ ～ Ⅲ级,所有患者在行椎管内麻醉摆放体位前20 min,均在超声引导下行S-FICB,根据给药浓度不同,随机分为两组,每组30例,A组注射0.25％ 罗哌卡因30 ml,B组注射0.4％ 罗哌卡因30 ml.记录阻滞操作时间、股神经及股外侧皮神经阻滞起效时间及阻滞效果.记录阻滞前(T1)和阻滞后5 min(T2)、10 min(T3)、15 min(T4)及侧卧位即刻(T5)的VAS疼痛评分、MAP和HR.结果 两组阻滞操作时间、股神经阻滞效果差异无统计学意义.B组股神经及股外侧皮神经阻滞起效时间明显短于A组(P<0.05),与T1时比较,T2～T5时两组VAS疼痛评分明显降低(P<0.05).T2-4时B组VAS评分明显低于A组(P<0.05),T1和T5时两组VAS疼痛评分差异无统计学意义.与T1时比较,T2～T5时两组患者M AP明显降低(P<0.05),HR变化及两组患者各时点M AP和HR差异无统计学意义.结论 采用0.25％ 罗哌卡因30 ml和0.4％ 罗哌卡因30 ml用于超声引导下S-FICB对股骨转子间骨折患者术前摆放侧卧位时均有良好镇痛效果,后者起效更快.

Abstract The aim of this study was to evaluate the association of non-hepatic hyperammonemia (NHH) with the prognosis of critically ill patients with NHH. According to the serum ammonia level, the patients with NHH (n = 498) were retrieved by us. The risk factors of the mortality with NHH patients were investigated by conducting univariate and multivariate logistic regression analyses. A nomogram to predict the risk of hospital mortality was constructed. Receiver operating characteristic curve (ROC) analysis was conducted to compare nomogram (ammonia into a prognostic model, P1) with the simplified acute physiology II (SAPSII) and quick sequential organ failure assessment (qSOFA). Five independent factors for the mortality in patients with NHH were identified, including age, platelets, bun, hemoglobin, and ammonia. Models P1 using ammonia showed good prediction power. The AUROC of P1 (AUROC, 0.755 [95% CI, 0.713–0.796]) was higher than that of qSOFA (AUROC, 0.500 [95% CI, 0.449–0.551]), and SAPS II (AUROC, 0.703[95% CI, 0.658–0.748]). Ammonia was an independent prognostic predictor of mortality for NHH patients. We developed a nomogram that can predict hospital mortality with patients. Nomogram had superior discriminative power to qSOFA and SAPS II, indicating that the nomogram may have clinical utility.

Neuropathic pain is a kind of intractable pain syndrome, and its pathogenesis has always been a hot and difficult point in pain medical research. Recent studies have shown that microglia polarization and the consequent pro-inflammatory reaction play a crucial role in the neuropathic pain. Microglia can be polarized to "classical activation" M1 or "alternatively activated" M2 during neuroinflammation and exert neurotoxic or neuroprotective effects in the nervous system. This article focuses on the relationship between microglia polarization and neuropathic pain, and explores how to use the neuroprotective and anti-inflammatory properties of microglia to develop new targeted drugs and searches out a new way for the treatment of the neuropathic pain.

Background Sleep disorders, the serious challenges faced by the intensive care unit (ICU) patients are important issues that need urgent attention. Despite some efforts to reduce sleep disorders with common risk-factor controlling, unidentified risk factors remain. Objectives This study aimed to develop and validate a risk prediction model for sleep disorders in ICU adults. Methods Data were retrieved from the MIMIC-III database. Matching analysis was used to match the patients with and without sleep disorders. A nomogram was developed based on the logistic regression, which was used to identify risk factors for sleep disorders. The calibration and discrimination of the nomogram were evaluated with the 1000 bootstrap resampling and receiver operating characteristic curve (ROC). Besides, the decision curve analysis (DCA) was applied to evaluate the clinical utility of the prediction model. Results 2,082 patients were included in the analysis, 80% of whom (n = 1,666) and the remaining 20% (n = 416) were divided into the training and validation sets. After the multivariate analysis, hemoglobin, diastolic blood pressure, respiratory rate, cardiovascular disease, and delirium were the independent risk predictors for sleep disorders. The nomogram showed high sensitivity and specificity of 75.6% and 72.9% in the ROC. The threshold probability of the net benefit was between 55% and 90% in the DCA. Conclusion The model showed high performance in predicting sleep disorders in ICU adults, the good clinical utility of which may be a useful tool for providing clinical decision support to improve sleep quality in the ICU.

BACKGROUND:Pain management after the total joint arthroplasty is still challenging, but worthy of attention, because good pain management can improve the outcomes of patient. It is still controversial whether fascia iliaca compartment block (FICB) can effectively decrease the opioid consumption and pain after total hip replacement (THR) owing to the number of published investigations is small. The purpose of this present study is to assess the efficacy and safety of FICB for postoperative analgesia after THR. METHODS:This is a single center, placebo-controlled randomized trial which is performed in accordance with the SPIRIT Checklist for randomized studies. It was authorized via the Chifeng Municipal Hospital institutional review committee (H2020-19-8). 100 patients undergoing THR will be included in this study. Patients are randomly divided into 2 groups: FICB group or Non-FICB group, FICB with 5mgmL of epinephrine and 40 mL of ropivacaine 0.2%. Primary outcomes are pain score at different time point. Visual analog scale is used to assess the pain (10: the maximum possible pain and 0: absent pain). The secondary outcomes are the postoperative complications, length of hospital stay and total consumption of opioid. All the needed analyses are implemented through utilizing SPSS for Windows Version 15.0. RESULTS:Figure 1 will show the primary and secondary outcomes. CONCLUSION:This trial can provide an evidence for the use of FICB for analgesia after THR.