Introduction:Diabetic wounds represent a growing clinical challenge worldwide, characterized by persistent immune dysregulation and excessive inflammation that lead to impaired healing and chronic progression. Methods:To address this, we developed a composite nanosystem, termed Ru@ACEI, composed of ruthenium-incorporated hollow mesoporous silica nanoparticles loaded with angiotensin-converting enzyme inhibitors (ACEIs). Results:The Ru@ACEI nanoparticles exhibit dual enzyme-mimetic activities (superoxide dismutase and catalase), effectively scavenging excess reactive oxygen species (ROS). This activity reduces cellular apoptosis and promotes endothelial cell proliferation. Following cellular uptake, Ru@ACEI catalyzes the decomposition of peroxides into water and oxygen, thereby suppressing the NLRP3/Caspase-3/Caspase-9 apoptosis pathway. The consequent improvement in endothelial cell survival helps reverse local hyperinflammation in diabetic wounds. Conclusion:Collectively, these findings demonstrate that the Ru@ACEI nanosystem accelerates diabetic wound healing by mitigating the inflammatory microenvironment and downregulating the expression of pro-inflammatory factors, offering a promising therapeutic strategy for managing chronic diabetic wounds.

Background Adverse left ventricular remodeling after myocardial infarction (MI) compromises cardiac function and increases heart failure risk. Until now, comprehension of the role transcription factor EB (TFEB) plays after MI is limited. Objectives The purpose of this study was to describe the effects of TFEB on fibroblasts differentiation and extracellular matrix expression after MI. Methods AAV9 (adeno-associated virus) mediated up- and down-regulated TFEB expressions were generated in C57BL/6 mice two weeks before the MI modeling. Echocardiography, Masson, Sirius red staining immunofluorescence, and wheat germ agglutinin staining were performed at 3 days, and 1, 2, and 4 weeks after MI modeling. Fibroblasts collected from SD neonatal rats were transfected by adenovirus and siRNA, and cell counting kit-8 (CCK8), immunofluorescence, wound healing and Transwell assay were conducted. Myocardial fibrosis-related proteins were identified by Western blot. PNU-74654 (100 ng/mL) was used for 12 hours to inhibit β-catenin-TCF/LEF1 complex. Results The up-regulation of TFEB resulted in reduced fibroblasts proliferation and its differentiation into myofibroblasts in vitro studies. A significant up-regulation of EF and down-regulation of myocyte area was shown in the AAV9-TFEB group. Meanwhile, decreased protein level of α-SMA and collagen I were observed in vitro study. TFEB didn’t affect the concentration of β-catenin. Inhibition of TFEB, which promoted cell migration, proliferation and collagen I expression, was counteracted by PNU-74654. Conclusions TFEB demonstrated potential in restraining fibrosis after MI by inhibiting the Wnt/β-catenin signaling pathway.

[Objective] Sudden cardiac death (SCD) caused by unexpected cardiovascular arrest remains a major public health threat globally. Cardiopulmonary resuscitation (CPR) is a basic but critical first aid skill to rescue patients with sudden cardiac arrest. This study aimed to ascertain whether the mind mapping technique, a note-taking and graphic thinking tool, could improve the learning of CPR among medical interns. [Methods] A total of 79 medical interns rotating in the emergency department in our center were selected as research participants. They were randomly divided into the control group (n=40) and the experimental group (n=39). The control group was trained with traditional PowerPoint (PPT) slide courseware combined with practical operations, while the experimental group was trained with mind mapping technique on the basis of traditional PPT courseware combined with practical operations. The theoretical test, operational assessment, and the survey regarding the satisfaction with the training were conducted between the two groups of interns after training. [Results] Although the interns in both groups mastered the CPR technique successfully with theoretical and operational assessment scores >90 (out of 100), the experimental group performed significantly better in both theoretical tests (score: 96.13±2.47 vs 93.71±4.48, p=0.0041) and operational assessment (score: 94.82±3.22 vs 91.32±3.46, p<0.0001). Moreover, all interns (100%) in the experimental group were satisfied with the CPR training experience, while only 75% of the interns in the control group were satisfied with the training. [Conclusions] Mind maps as a supplementary teaching tool could facilitate CPR learning for medical interns and improve their learning interest.

Predicting neurological outcomes after cardiac arrest remains a major issue. This study aimed to identify novel biomarkers capable of predicting neurological prognosis after cardiac arrest. Expression profiles of GSE29540 and GSE92696 were downloaded from the Gene Expression Omnibus (GEO) database to obtain differentially expressed genes (DEGs) between high and low brain performance category (CPC) scoring subgroups. Weighted gene co-expression network analysis (WGCNA) was used to screen key gene modules and crossover genes in these datasets. The protein-protein interaction (PPI) network of crossover genes was constructed from the STRING database. Based on the PPI network, the most important hub genes were identified by the cytoHubba plugin of Cytoscape software. Eight hub genes (RPL27, EEF1B2, PFDN5, RBX1, PSMD14, HINT1, SNRPD2, and RPL26) were finally screened and validated, which were downregulated in the group with poor neurological prognosis. In addition, GSEA identified critical pathways associated with these genes. Finally, a Pearson correlation analysis showed that the mRNA expression of hub genes EEF1B2, PSMD14, RPFDN5, RBX1, and SNRPD2 were significantly and positively correlated with NDS scores in rats. Our work could provide comprehensive insights into understanding pathogenesis and potential new biomarkers for predicting neurological outcomes after cardiac arrest.

Hypothermia preconditioning (HPC) improves cardiac function after cardiac arrest, yet the mechanism is unclear. We hypothesized that HPC-activated adenosine monophosphate-activated protein kinase (AMPK) activity may be involved. Adult male Wistar rats were randomly divided into normothermia Control, HPC (cooling to 32–34°C for 30 min), and HPC + Compound C (Compound C 10 mg/kg was injected intraperitoneally 30 min before HPC group). The rats underwent 7 min of untreated ventricular fibrillation (VF) followed by cardiopulmonary resuscitation (CPR). Cardiac function and hemodynamic parameters were evaluated at 4 h after return of spontaneous circulation (ROSC). Survival status was determined 72 h after ROSC. Mechanistically, we further examined the AMPK-Unc-51 Like Autophagy Activating Kinase 1 (ULK1)-mitophagy pathway and autophagic flux in vivo and in vitro. Six of twelve rats in the Control group, 10 of 12 rats in the HPC group, and 7 of 12 rats in HPC + Compound C group were successfully resuscitated. The 72-h survival rates were 1 of 12 Control, 6 of 12 HPC, and 2 of 12 HPC + Compound C rats, respectively ( P = 0.043). Rats in the HPC group demonstrated greater cardiac contractility and hemodynamic stability which were compromised by Compound C. Furthermore, HPC increased the protein levels of p-AMPKα and p-ULK1 and promoted the expression of mitochondrial autophagy-related genes. Compound C decreased the expression of mitochondrial autophagy-related genes and reduced autophagic flux. Consistent with the observations obtained in vivo, in vitro experiments in cultured neonatal rat cardiomyocytes (CMs) demonstrated that HPC attenuated simulated ischemia–reperfusion-induced CM death, accompanied by increased AMPK-ULK1-mitophagy pathway activity. These findings suggest that AMPK-ULK1-mitophagy pathway was activated by HPC and has a crucial role in cardioprotection during cardiac arrest. Manipulation of mitophagy by hypothermia may merit further investigation as a novel strategy to prevent cardiac ischemia–reperfusion injury.

Substantial morbidity and mortality are associated with postcardiac arrest brain injury (PCABI). MicroRNAs(miRNAs) are essential regulators of neuronal metabolism processes and have been shown to contribute to alleviated neurological injury after cardiac arrest. In this study, we identified miRNAs related to the prognosis of patients with neurological dysfunction after cardiopulmonary resuscitation based on data obtained from the Gene Expression Omnibus (GEO) database. Then, we explored the effects of miR-483-5p on mitochondrial biogenesis, mitochondrial-dependent apoptosis, and oxidative stress levels after ischemia‒reperfusion injury in vitro and in vivo. MiR-483-5p was downregulated in PC12 cells and hippocampal samples compared with that in normal group cells and hippocampi. Overexpression of miR-483-5p increased the viability of PC12 cells after ischemia‒reperfusion injury and reduced the proportion of dead cells. A western blot analysis showed that miR-483-5p increased the protein expression of PCG-1, NRF1, and TFAM and reduced the protein expression of Bax and cleaved caspase 3, inhibiting the release of cytochrome c from mitochondria and alleviating oxidative stress injury by inhibiting the production of ROS and reducing MDA activity. We confirmed that miR-483-5p targeted TNFSF8 to regulate the AMPK/JNK pathway, thereby playing a neuroprotective role after cardiopulmonary resuscitation. Hence, this study provides further insights into strategies for inhibiting neurological impairment after cardiopulmonary resuscitation and suggests a potential therapeutic target for PCABI.

The purpose of this cross-sectional survey study is to quantitatively examine the differences in patient trust towards physicians between four different clinical departments in a Chinese hospital. Using a validated modified Chinese version of the Wake Forest Physician Trust Scale, we measured patient trust in each department, and also collected data on patient demographics. A total of 436 patients or family members were surveyed in the departments of emergency medicine, pediatrics, cardiology, and orthopedic surgery. Significant differences were found between the departments, especially between pediatrics (trust score 43.23, range 11-50) and emergency medicine and cardiology (trust scores 45.29 and 45.79, respectively with range of 11-50). The average total score across all four departments was 44.72. There are indications that specifically comparing departments, such as patient demographics or department structure, could be helpful in tailoring patient care to improve physician-patient relationships.

Background and Objective: The role of percutaneous coronary intervention (PCI) after return of spontaneous circulation (ROSC) in patients with acute myocardial infarction (AMI) complicated by cardiac arrest (CA) is controversial. This study aimed to evaluate the effects of PCI on the in-hospital mortality after ROSC in patients with AMI complicated by CA. Methods: The clinical data of 66 consecutive patients with ROSC after CA caused by AMI from January 2006 to December 2015 at the First Affiliated Hospital of Sun Yat-sen University were collected. Among these patients, 21 underwent urgent PCI. We analyzed the clinical characteristics of the patients during hospitalization. Results: The patients who underwent PCI had a higher rate of ST-segment elevation, and their initial recorded heart rhythms were more likely to have a shockable rhythm. Further, they had a high PCI success rate of 100%. The in-hospital mortality in the patients who did not undergo PCI was significantly higher than that in the patients who underwent PCI (68.9% vs 9.5%, P<0.05). Multivariate logistic regression analysis showed that cardiogenic shock (odds ratio [OR], 3.537; 95% CI, 1.047-11.945; P=0.042) and Glasgow Coma Scale score of <= 8 after ROSC (OR, 14.992; 95% CI, 2.815-79.843; P=0.002) were the independent risk factors for in-hospital mortality among the patients. Meanwhile, PCI was a protective factor against in-hospital mortality (OR, 0.063; 95% CI, 0.012-0.318; P=0.001). After propensity matching analysis, the results still showed that PCI (OR, 0.226; 95% CI, 0.028-1.814; P=0.0162) was a protective factor for in-hospital death. Conclusion: The patients with ROSC after CA caused by AMI who underwent PCI had a lower in-hospital mortality than those who did not undergo PCI.

目的:观察外源性导入转录因子EB(TFEB)对缺血性脑卒中小鼠神经功能损伤的影响.方法:(1)15只10周龄雄性C57BL/6小鼠用于建立永久性大脑中动脉阻塞(pMCAO)模型,随机分为假手术组、梗阻2 h组、梗阻4 h组、梗阻8 h组和梗阻24 h组,每组3只,Western blot法检测pMCAO后皮层神经元TFEB、溶酶体相关膜蛋白1(LAMP-1)、微管相关蛋白1轻链3B(LC3B)和cleaved caspase-3蛋白的表达;(2)45只8周龄雄性C57BL/6小鼠分为假手术组、TFEB过表达组、过表达对照组、TFEB敲减组和敲减对照组,每组9只.除假手术组外,其余4组小鼠均经侧脑室注射9型腺相关病毒(AAV9),分别为AAV9-TFEB、AAV9-NC、AAV9-shTFEB和AAV9-shNC,注射2周后建立pMCAO模型,24 h后采用Longa评分法评估小鼠神经功能,磁共振法检测并计算脑梗死体积,TUNEL染色检测皮层神经元细胞凋亡情况,尼氏染色观察皮层神经元细胞形态及数量,Western blot法检测皮层神经元TFEB、LAMP-1、LC3B、cleaved caspase-3蛋白的表达.结果:与假手术组相比,pMCAO后2～24 h,皮层神经元TFEB、LAMP-1及LC3B-II蛋白表达水平均显著下降,而cleaved caspase-3表达升高(P<0.05).侧脑室注射AAV9-TFEB可改善pMACO后小鼠Longa评分,而注射AAV9-shTFEB则恶化Longa评分(P<0.05).磁共振结果显示侧脑室注射AAV9-TFEB可减少脑梗死体积,而注射AAV9-shTFEB则增加脑梗死体积(P<0.05).尼氏染色显示AAV9-TFEB组小鼠皮层神经元细胞数量显著多于AAV9-NC组,AAV9-shTFEB组小鼠皮层神经元细胞数量则显著少于AAV9-shNC组(P<0.05).Western blot结果显示过表达TFEB可增加皮层脑组织LAMP-1和LC3B-II表达,降低cleaved caspase-3表达(P<0.05);敲减TFEB则降低皮层脑组织LAMP-1和LC3B-II表达,增加cleaved caspase-3表达(P<0.05).结论:利用AAV9外源性导入TFEB可通过激活自噬及溶酶体功能而减少pMCAO后皮层神经元细胞凋亡,改善小鼠神经功能.

Objective To investigate the neuroprotective mechanism of sevoflurane in rats resuscitated from cardiac arrest (CA).Methods A ventricular fibrillation-induced CA model was established.Forty Wistar rats were randomly divided into the sham group,sevoflurane group and control group.Apoptosis-related proteins were measured by Western blot at 24 h after restoration of spontaneous circulation (ROSC).The status of mitochondrial permeability transition pore (MPTP) were measured using a spectrophotometer,and the mitochondrial membrane potential (MMP) were measured with JC-1 fluorescent probe.At 72 h after ROSC,the apoptotic index of neurons in hippocampal CA1 region was counted by TUNEL staining.Results The protein expression of Bax,Bak,cleaved-caspase 9,cleavedcaspase 3 and cytosolic cytochrome c were lower in the sevoflurane group (all P＜0.05),the protein expression of Bcl-2 was higher in the sevoflurane group compared with the control group (P＜0.05).The sevoflurane group had a less opening status of MPTP and a higher MMP compared with the control group (all P＜0.05).The sevoflurane group had less apoptotic neurons compared with the control group (P＜0.05).Conclusion By up-regulating the expression of Bcl-2,down-regulating Bax and Bak,sevoflurane could reduce the apoptosis of neurons and decrease the opening of MPTP,eventually reduce cerebral injuries.

Objective To investigate the characteristics of myocardial injury and its underlying mechanism in rats resuscitated from cardiac arrest. Methods Forty-two male Wistar rats were randomly(random number) assigned into the post-resuscitation (PR) 4 h, PR 24 h, PR 48 h, and sham groups. Ventricular fibrillation was induced by transcutaneous electrical epicardium stimulation and untreated for 6 min, followed by cardiopulmonary resuscitation (CPR). Myocardial function, glucose metabolism, myocardial ultrastructure, the status of mitochondrial permeability transition pore (MPTP) and mitochondrial membrane potential (MMP) were evaluated at different time points. Results Myocardial dysfunction was found at 4 h after restoration of spontaneous circulation (ROSC). The ejection fraction and cardiac output were decreased (all P<0.01), the diastole left ventricular posterior wall became thicker (P<0.01), and the end-diastolic volume was reduced (P<0.05). However, cardiac function was recovered almost completely at 48 h after ROSC. The PR 4 h group had a higher SUVmax, a more obvious decreased absorbance, and a lower MMP than the sham group (all P<0.01), but no statistically significant differences were noted between the PR 48 h group and the sham group (P>0.05). At 4 h and 24 h after ROSC, the mitochondria was swollen and the mitochondrial crista was sparse, but the myocardial ultrastructure was complete. Conclusions Post resuscitation myocardial dysfunction occurs after ROSC and the myocardial dysfunction is completely reversible at 48 h after ROSC, which may be related to the reversibility of myocardial injury and the gradual recovery of mitochondrial structure and function.

This study investigated the effects of hypothermia induced before cardiac arrest or after return of spontaneous circulation (ROSC) on cardiac function and myocardial mitochondrial injury after ROSC in a rat cardiac arrest model. Sixty healthy, male Wistar rats were randomly divided into the Normothermia group, pre-arrest hypothermia (Pre-HT) group, and post-resuscitation hypothermia (Post-HT) group. The rats underwent 8 min of untreated ventricular fibrillation followed by cardiopulmonary resuscitation. Twelve rats in each group were used to evaluate the left ventricular ejection fraction before ventricular fibrillation and 4 h after ROSC. Survival was determined at 24 h after ROSC. The remaining eight rats in each group were used to detect for heart malondialdehyde, reduced glutathione, adenosine triphosphate levels and mitochondrial histology. Oxygen consumption rate and mitochondrial membrane potential were evaluated 4 h after ROSC; 10 of 12 rats in Pre-HT group, 5 of 12 in Post-HT group, and 6 of 12 in normothermia group were successfully resuscitated. The survival rate of each group was 66.7%, 33.3%, and 25%, respectively. Rats in the Pre-HT group showed less alteration of the mitochondrial ultrastructure and oxidative stress injury, better maintenance of adenine nucleotides, and more preservation of the mitochondrial membrane potential and respiratory function when compared with rats in the Post-HT and normothermia groups. Transient hypothermia is an effective preconditioning stimulus to induce ischemic tolerance in a cardiac arrest model and worthy of further evaluation for potential clinical use. Impact statement In this paper, we investigated the effects of hypothermia induced before ischemia or after ROSC on cardiac function, oxidative stress damage, and myocardial mitochondrial ischemia–reperfusion injury after cardiac arrest in a rat model with VF. We demonstrated that pre-arrest hypothermia conferred greater cardio-protective benefits than delayed post-resuscitation hypothermia, reduced the number of defibrillations required and dosages of epinephrine during CPR, decreased oxidative stress, ameliorated mitochondrial dysfunction, and subsequently improved survival rate.

Neural stem cells (NSCs) transplantation is one of the most promising strategies for the treatment of CA-induced brain damage. The transplanted NSCs could differentiate into new neuron and replace the damaged one. However, the poor survival of NSCs in severe hypoxic condition is the limiting step to make the best use of this kind of therapy. In the present study, we investigated whether the overexpression of miR-26a improves the survival of NSCs in hypoxic environment in vitro and in vivo. In vitro hypoxia injury model is established in NSCs by CoCl2 treatment, and in vivo cardiac arrest (CA) model is established in Sprague-Dawley (SD) rats. Quantitative real-time polymerase chain reaction is used to detect the mRNA level and Western blot is used to examine the protein level of indicated genes. TUNEL staining and flow cytometry are applied to evaluate apoptosis. Dual-luciferase reporter assay is utilized to analyze the target gene of miR-26a. The expression of miR-26a is reduced in both in vitro and in vivo hypoxic model. MiR-26a directly targets 3'-UTR of glycogen synthase kinase 3β (GSK-3β), resulting in increased β-catenin expression and decreased apoptosis of NSCs. Overexpression of miR-26a in transplanted NSCs improves the survival of NSCs and neurological function in CA rats. MiR-26a prevents NSCs from apoptosis by activating β-catenin signaling pathway in CA-induced brain damage model. Modulating miR-26a expression could be a potential strategy to attenuate brain damage induced by CA.

Mild hypothermia treatment (MHT) improves the neurological function of cardiac arrest (CA) patients, but the exact mechanisms of recovery remain unclear. Herein, we generated a CA and cardiopulmonary resuscitation (CPR) mouse model to elucidate such function. Naïve mice were randomly divided into two groups, a normothemia (NT) group, in which animals had normal body temperature, and a MHT group, in which animals had a body temperature of 33 °C (range: 32–34 °C), after the return of spontaneous circulation (ROSC), followed by CA/CPR. MHT significantly improved the survival rate of CA/CPR mice compared with NT. Mechanistically, MHT increased the expression of Silent Information Regulator 1 (Sirt1) and decreased P53 phosphorylation (p-P53) in the cortex of CA/CPR mice, which coincided with the elevated autophagic flux. However, Sirt1 deletion compromised the neuroprotection offered by MHT, indicating that Sirt1 plays an important role. Consistent with the observations obtained from in vivo work, our in vitro study utilizing cultured neurons subjected to oxygen/glucose deprivation and reperfusion (OGD/R) also indicated that Sirt1 knockdown increased OGD/R-induced neuron necrosis and apoptosis, which was accompanied by decreased autophagic flux and increased p-P53. However, the depletion of P53 did not suppress neuron death, suggesting that P53 was not critically involved in MHT-induced neuroprotection. In contrast, the application of autophagic inhibitor 3-methyladenine attenuated MHT-improved neuron survival after OGD/R, further demonstrating that increased autophagic flux significantly contributes to MHT-linked neuroprotection of CA/CRP mice. Our findings indicate that MHT improves neurological outcome of mice after CA/CPR through Sirt1-mediated activation of autophagic flux.

目的:观察封闭式吸痰对急诊观察区内机械通气患者呼吸机相关性肺炎(VAP)发生率的影响.方法:回顾性分析中山大学附属第一医院急诊观察区2017年1月1日-2018年12月30日急诊观察区内机械通气患者的临床资料,依据住院时间患者所用吸痰管的不同,分为开放式吸痰组和封闭式吸痰组.结果:急诊观察区共收治机械通气患者244例,其中开放式吸痰组152例、封闭式吸痰组92例,发生VAP 81例(33.2％).封闭式吸痰组的VAP发生率明显低于开放组(39.5％vs 22.8％,P<0.001).开放式吸痰组鲍曼不动和大肠埃希菌感染的比率显著高于封闭式吸痰组,且耐药菌较多.结论:封闭式吸痰可减少急诊观察区内机械通气患者VAP的发生率和降低耐药菌感染的机会.

AIM: To investigate whether neural stem cell-derived exosomes promote the viability and inhibit the apoptosis of neurons under cobalt chloride(CoCl2)-induced hypoxia in vitro.METHODS:The exosomes were isolated based on ultracentrifugation.The exosomal markers,ALG-2-interacting protein X(Alix)and tumor susceptibility gene 101 (TSG101)were identified by Western blot.The shape of exosomes was observed under transmission electron microscope (TEM).The size distributions of exosomes were analyzed by nanoparticle analysis(qNano).The neurons were exposed in CoCl2at different doses(200~600 μmol/L)for 24 h.The exosomes were co-cultured with the neurons pre-treated with CoCl2.The viability and apoptosis of the neurons were measured by CCK-8 assay and TUNEL method.RESULTS: The exosomes released from the neural stem cells expressed exosomal markers Alix and TSG 101.They also displayed a cup-shaped appearance observed under TEM and their sizes were(95.0 ±23.5)nm(n=370).The neuronal viability was sig-nificantly inhibited by CoCl 2in a dose-dependent manner(P<0.05).After treatment with exosomes,the viability of the neuron pre-treated with CoCl2was increased and the apoptotic rate was decreased(P<0.05).CONCLUSION: Neural stem cell-derived exosomes promote the viability and inhibit the apoptosis of rat neurons uneder hypoxia.

心脏骤停(cardiac arrest,CA)和心肺复苏(CPR)长期以来都是急诊医学中的研究热点.由于CA发生突然,难以进行临床对照试验,因而动物实验不可或缺,建立一种能够最大限度模拟临床的动物CA模型成为亟待解决的问题.目前常用于CA和CPR研究的实验动物大致分为小动物,如大鼠等;中等动物,如家兔等;大动物,如猪、犬等.而就CA诱发方式而言,有电击法、窒息法、钳夹大血管法等.本文就国内外对CPR动物模型的基本要求、种类、制作方法及其特点等予以综述.

Objective To determine the relationship between brain injury and cerebral glucose metabolism in rat model of cardiac arrest. Methods Asphyxia-induced cardiac arrest model was established. Forty-two male Wistar rats were randomly assigned to sham or experimental groups. Rats in the CA4,CA6 and CA8 group were treated with cardiopulmonary resuscitation(CPR) 4 min, 6 min and 8 min after cardiac arrest, respectively. The maximum standardized uptake value (SUVmax) of glucose was detected by PET, and neural defi cit score (NDS) were evaluated at 24 h and 72 h after ROSC. The numbers of injured neurons and apoptotic cells and the protein level of hexokinase I (HXK I) were measured at 72 h after ROSC. Results SUVmax, NDS and the level of HXK I were all decreased after ROSC, and interestingly, this declination of these markers was correlated with the prolongation of the duration of CA, the longer duration of CA the more declination of these biomarkers. Accordingly, the number of injured neurons and apoptotic cells increased were correlated with duration of CA, and thus CA8 group had greater numbers of those cells than CA6 group and CA4 group (P<0.05),and CA6 group had greater numbers of those cells than CA4 group(P<0.05). In addition, the SUVmaxwas positively correlated with NDS(P<0.05), and negatively correlated with the numbers of injured neurons and apoptotic index(P<0.05). Conclusions The degree of brain injury is associated with cerebral glucose metabolism, and PET may become a novel method to assess the severity of brain damage after CA.