C1q tumor necrosis factor–related protein 15 (CTRP15), a newly identified myokine, is closely implicated in cardiovascular disease. However, the role of CTRP15 in atherosclerosis is still unclear. This study aims to determine the role of CTRP15 in atherosclerosis and explore the underlying mechanisms. Our findings revealed that lentivirus-mediated CTRP15 overexpression significantly decreased atherosclerotic plaque lesions and increased reverse cholesterol transport (RCT) efficiency and circulating HDL-C levels in apolipoprotein E-deficient (apoE−/−) mice. Consistently, in vitro, overexpression of CTRP15 also inhibited intracellular lipid accumulation and promoted cholesterol efflux from macrophages. Mechanistically, CTRP15 decreased the expression of miR-101-3p by upregulating T-cadherin, thereby facilitating ABCA1 expression and cholesterol efflux. In summary, these data indicate that CTRP15 inhibits the development of atherosclerosis by enhancing RCT efficiency and increasing plasma HDL-C levels via the T-cadherin/miR-101-3p/ABCA1 pathway. Targeting CTRP15 may serve as a novel and promising therapeutic strategy for atherosclerotic cardiovascular diseases.

Municipal wastewater treatment plants (WWTPs) are recognized as the significant source of fungal aerosols, which pose a significant threat to human health globally. Herein, the occurrences characterization, community structure, and health risk assessment of airborne fungi were investigated from a semiunderground WWTP. The concentrations of culturable fungi emitted into the air from the WWTP ranged from 30.6 to 1431.1 colony forming units (CFU)/m3, with primary and biochemical treatments constituting the principal sources of emission (P < 0.05). Diversity analysis revealed seasonal and facility-dependent fluctuations in culturable fungal communities. Approximately 13.5% of the total airborne fungal genera detected in the WWTP were culturable. Some airborne fungi in the WWTP with relatively low abundance but high cultivability, such as Cladosporium, Trichoderma, Neurospora, Filobasidium, and Hannaella, tended to be overlooked because of their limited presence in airborne environments. We also developed a health risk assessment method for fungi, utilizing seven indicators to characterize the risk posed by fungal pathogens from multiple perspectives, providing a comprehensive evaluation of potential health impacts. The simulated risk values of the air outlet and biochemical treatment exceeded those of other treatment facilities, with median risks of 2.2 × 102 and 1.4 × 102, respectively. Consequently, management strategies should prioritize enhanced controls for fungal aerosols to mitigate the risk of disease transmission.

BACKGROUND AND OBJECTIVE:Alpha-ketoglutarate (AKG), is a major intermediate metabolite of the tricarboxylic acid cycle, and is closely associated with cardiometabolic disease prognosis. Previous studies indicated that AKG is related to myocardial energy expenditure levels and reflects adverse short-term outcomes in heart failure (HF) patients. In this prospective cohort study, we examined the long-term prognostic value of AKG levels in acute HF (AHF) patients. METHODS:Plasma AKG levels were assessed in patients hospitalized with AHF. Hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause mortality were calculated via multiple Cox regression. All-cause mortality was compared between patients with NT-proBNP < 1000 pg/ml and those with NT-proBNP ≥ 1000 pg/ml via subgroup analysis. RESULTS:Patients with AKG ≥ 9.83 μg/ml had higher heart rates and NT-proBNP and lower left ventricular ejection fraction (LVEF) and systolic blood pressure (SBP). After multiple adjustment, higher AKG was associated with an increased all-cause mortality risk (HR = 1.078, p < 0.001). Compared with AKG < 9.83 μg/ml, AKG ≥ 9.83 μg/ml nearly doubled (HR = 1.929, p < 0.001) and quadrupled (HR = 4.160, p < 0.001) the all-cause mortality risk in patients with NT-proBNP ≥ 1000 pg/ml and those with NT-proBNP < 1000 pg/ml, respectively. CONCLUSIONS AND RELEVANCE:Plasma AKG was independently associated with greater all-cause mortality risk in patients with AHF. Higher AKG levels retained prognostic value for patients with relatively low NT-proBNP.

Cell senescence-associated endothelia dysfunction is a vital point in the pathological progression of atherosclerosis (AS). G-protein coupled receptor 4 (GPR4) is a proton-sensing receptor involved in developing endothelial dysfunction. In this study, we investigated the protective role of NE 52-QQ57, a GPR4 inhibitor in endothelial cell senescence induced using an oxidized low-density lipoprotein (ox-LDL). We also unravel the underlying molecular mechanism of NE 52-QQ57 as a therapeutic agent. Endothelial cell senescence model was established using human aortic endothelial cells (HAECs) stimulated with ox-LDL. The expression levels of GPR4, p53, p16, and sirtuin1 (SIRT1) were evaluated using real-time PCR and western blot assays. ROS production was determined using dihydroethidium (DHE) staining. Further, interleukin-6 (IL-6) and monocyte chemotactic protein 1 (MCP-1) secretion and expression were determined using ELISA and real-time PCR analysis, respectively. Finally, β-galactosidase (SA-β-Gal) staining associated with cell senescence, telomerase activity, and cell cycle assay were used to determine the state of cell senescence. Firstly, GPR4 was found to be upregulated in the ox-LDL-stimulated HAECs. We also identified elevated ROS, IL-6, and MCP-1 levels induced by ox-LDL and significantly abrogated by NE 52-QQ57 treatment. Second, a reversal in SA-β-Gal activity, telomerase activity, and G0/G1 proportion, with an upregulation in p53 and p16 expressions was observed on NE 52-QQ57 treatment in the ox-LDL induced model. Lastly, the decreased expression level of SIRT1 was extremely elevated by NE 52-QQ57. Notably, the inhibitory effect of NE 52-QQ57 against ox-LDL-induced cell senescence was abolished by the SIRT1 inhibitor EX-527. The GPR4 antagonist NE 52-QQ57 might prevent cellular senescence by promoting the expression of SIRT1.

Incretin receptor agonists (IRAs), primarily composed of glucagon-like peptide-1 receptor agonists (GLP-1RAs) and glucose-dependent insulinotropic polypeptide receptor agonists (GIPRAs), work by mimicking the actions of the endogenous incretin hormones in the body. GLP-1RAs have been approved for use as monotherapy and in combination with GIPRAs for the management of type 2 diabetes mellitus (T2DM). In addition to their role in glucose regulation, IRAs have demonstrated various benefits such as cardiovascular protection, obesity management, and regulation of bone turnover. Some studies have suggested that IRAs not only aid in glycemic control but also exhibit anti-atherosclerotic effects. These agents have been shown to modulate lipid abnormalities, reduce blood pressure, and preserve the structural and functional integrity of the endothelium. Furthermore, IRAs have the ability to mitigate inflammation by inhibiting macrophage activation and promoting M2 polarization. Research has also indicated that IRAs can decrease macrophage foam cell formation and prevent vascular smooth muscle cell (VSMC) phenotype switching, which are pivotal in atheromatous plaque formation and stability. This review offers a comprehensive overview of the protective effects of IRAs in atherosclerotic disease, with a focus on their impact on atherogenesis.

Airborne pathogens constitute a growing threat to global public health. Wastewater treatment plants (WWTPs) are important sources of airborne bacteria, which pose great health risks to the employee and nearby residents. In this study, the distribution, transmission and health risk of the airborne culturable and inhalable bacteria carried by PM2.5 in a semiunderground WWTP were evaluated. The concentrations of culturable bacteria in the air were 21.2-1431.1 CFU/m3, with the main contributions of primary and biological treatments. The relative abundances of culturable and total inhalable bacterial taxa were positively correlated (p < 0.05). However, certain bacteria, including Bacillus, Acinetobacter and Enterococcus, exhibited high reproductive capacity despite their low concentration in the air, suggesting that they can survive and regrow in suitable environments. Transmission modeling revealed that the concentrations of airborne bacteria exponentially decreased with distance from 18.67 to 24.12 copies /m3 at the source to 0.06-0.14 copies /m3 at 1000 m downwind. The risks of 8-h exposure in this WWTP except the outlet exceeded the reference value recommended by WHO, which were primarily dependent on P. aeruginosa, Salmonella, and E. coli. Management practices should consider improved controls for bioaerosols in order to reduce the risk of disease transmission.

Lipotoxicity has been shown to induce the loss of functional β-cell mass and lead to type 2 diabetes, but the mechanism remains unknown. In this study, we aim to explore the role of secretagogin (SCGN) in lipotoxicity-induced β-cell injury. Our results indicate that ox-LDL treatment leads to autophagic cell death, as evidenced by decreased cell viability, aggravated cell apoptosis, and the accumulation of the p62 protein in MIN6 cells. LysoTracker Red staining, TEM and mRFP-GFP-LC3 assays demonstrate that autophagic flux is blocked in ox-LDL-treated MIN6 cells. Intriguingly, SCGN is significantly decreased in MIN6 cells under lipotoxic conditions. Additionally, siRNA-guided SCGN knockdown blocks autophagic flux triggered by rapamycin, while SCGN restoration alleviates autophagic flux retardation and mitigates cell apoptosis. The physical interaction between SCGN and SNAP29 is validated by bioinformatics analysis, coimmunoprecipitation assay and SCGN knockdown test. Downregulation of SCGN expression reduces the interaction of these two proteins. Taken together, our results indicate that ox-LDL treatment induces apoptotic β-cell death by blocking autophagic flux dependent on SCGN downregulation. SCGN administration prevents lipotoxic β-cell injury and may be a potential therapeutic strategy to promote β-cell expansion in type 2 diabetes.

目的:探讨微课在PBL翻转教学模式中对急诊医学科临床实习教学的成果分析.方法:选取2021年1月-2022年12月进入急诊医学科轮转的实习学生80名作为研究对象,每人轮转4周,利用随机表法将其分成对照组和观察组,各40例,对照组为传统模式带教法带教,观察组采用微课在PBL翻转教学模式进行带教,比较两组临床实习学生出科考核成绩(40％临床技能+60％临床理论)、临床综合处理能力评分、教学满意度等.结果:带教前,两组医学实习生考核成绩比较,差异无统计学意义(P＞0.05),带教15d时候、带教结束时,观察组医

Purpose: To study the effect of isoglycyrrhizin on LPS-mediated acute respiratory distress syndrome (ARDS) in a mouse model, as well as the associated mechanism of action.Methods: Ninety (90) wild-type C57BL/6 male mice were randomly assigned to 3 groups, viz, control, ARDS and isoglycyrrhizin groups. Pathological lesions in mice lungs were determined using H&E staining. The mRNA and protein expressions of inducible nitric oxide synthase (iNOS), heme oxygenase (HO-1), cyclooxygenase-2 (COX-2), AMP- dependent protein kinase (AMPK), serine/threonine proteinkinase (Akt), glycogen synthase kinase 3 (GSK3), nucleotide-binding domain-like receptor protein 3 (NLRP3), and Nrf2 were assayed using quantitative reverse transcription polymerase chain reaction (RT-PCR) and immunoblotting, respectively.Results: The levels of mRNA and protein expressions of INO) and COX-2 were significantly upregulated in ARDS, when compared to control, but were markedly down-regulated by isoglycyrrhizin (p < 0.05). Similarly, exposure of ARDS mice to isoglycyrrhizin led to upregulations of mRNA and proteinlevels of Nrf2, NQO1, HO-1, GCLM, GCLC, p-GSK3, GSK3, p-AMPK, AMPK, p-Akt and AKT (p < 0.05). Moreover, isoglycyrrhizin significantly downregulated p-IκB and Nucl-p65 with respect to protein and mRNA levels, but upregulated IκBα expression. Histopathological examination revealed that pretreatment of ARDS mice with isoglycyrrhizin significantly reduced the number of infiltrating inflammatory cells, edema and ARDS score (p < 0.05).Conclusion: Isoglycyrrhizin protects mouse lungs against ARDS via regulation of AMPK/Nrf2/ARE pathway. Thus, this compound has potential for use in the treatment of ARDS.

The cyclophilin A-CD147 interaction has been reported to be one of the most potential therapeutic targets for the treatment of acute pulmonary embolism. The signalling of extracellular signal-regulated kinase 1/2 (ERK1/2) was also reported in the pathogenesis of cardiac injury. Since SP-8356 is regarded as a novel Inhibitor of CD147-Cyclophilin, the study aimed to evaluate potential therapeutic effects of SP-8356 for pulmonary embolism-associated cardiac injury. Western blot and immunohistochemistry were carried out to analyse the expression of MMP-9, ERK1/2, phosphorylated ERK1/2 (p-ERK1/2), P65, p-P65, and CyA protein in PE cell and rat models under distinct conditions. Flow cytometry and TUNEL were carried out to examine the apoptosis of primary rat myocardiocytes and PE rat models under distinct conditions. CyA treatment on primary rat myocardiocytes remarkably raised the expression of MMP-9, p-ERK1/2 and p-P65 protein expression; SP8536 treatment effectively restored the CyA-induced up-regulation of MMP-9, p-ERK1/2 and p-P65 protein expression in primary rat myocardiocytes. Besides, flow cytometry analysis showed that SP8536 remarkably suppressed the CyA-induced elevation of cell apoptosis rate of primary rat myocardiocytes. Moreover, SP8536 notably diminished the abnormal elevation of right ventricular systolic pressure (RVSP), Troponin I and Myeloperoxidase activity in PE rat models. Furthermore, SP-8536 significantly restored the up-regulation of MMP-9, p-ERK1/2, p-P65, CyA protein and the cellular apoptosis in the PE rat model. Our study validated that SP-8356 could suppress cell apoptosis and inflammatory response via down-regulating the highly expressed MMP-9, p-ERK1/2, and p-P65 and MMP-9 in PE-associated cardiac injury in a dose-dependent manner.

Acute lung injury (ALI) is an urgent disease lacking effective therapies, resulting in relatively high morbidity and mortality. The pathological mechanism of ALI is reported to be related to excessive inflammation and activated oxidative stress. The present study aims to investigate the protective effects of the DPP-4 inhibitor Trelagliptin against lipopolysaccharide (LPS)-induced ALI and the underlying mechanism. LPS was used to induce ALI mice models. The pathological condition of ALI mice was evaluated using MPO activity assay, lung wet to dry weight ratio detection, and HE staining on the lung tissues. Lung function was assessed using a spirometer. The oxidative stress level in the lung tissues was checked by MDA measurement and GPx detection using commercial kits. The leukocyte and neutrophil numbers were determined using a hemocytometer and the total concentration of protein in the BALF was detected using a bicinchoninic acid method. The expression levels of TNF-α, IL-6, and CXCL2 in the lung tissues were evaluated using qRT-PCR and ELISA. Western blot analysis was used to determine the expression levels of TLR4 and p-NF-κB p65. LPS-induced elevated MPO activity, pulmonary wet to dry weight ratio, airway resistance (RAW), the total number of leukocytes and neutrophils, production of inflammatory factors, decreased pulmonary dynamic compliance (Cdyn), and peak expiratory flow (PEF), and an aggravated histopathological state (such as disordered alveolar structure, significant pulmonary interstitial edema, and large numbers of red blood cells and inflammatory cells in the alveolar cavity) were significantly reversed by the administration of Trelagliptin. The TLR4/NF-κB signaling pathway was activated and oxidative stress was induced by stimulation with LPS; however, both effects were suppressed by the administration of Trelagliptin. Trelagliptin might alleviate LPS-induced inflammation and oxidative stress in acute lung injury mice.

Several studies show that even a level of urine albumin/creatinine ratio (UACR) within the normal range (below 30 mg/g) increases the risk of cardiovascular diseases. We speculate that mildly increased UACR is related to left ventricular hypertrophy (LVH) in patients with type 2 diabetes mellitus (T2DM). In this retrospective study, 317 patients with diabetes with normal UACR, of whom 62 had LVH, were included. The associations between UACR and laboratory indicators, as well as LVH, were examined using multivariate linear regression and logistic regression, respectively. The diagnostic efficiency and the optimal cutoff point of UACR for LVH were evaluated using the area under the receiver operating characteristic curve (AUC) and Youden index. Our results showed that patients with LVH had significantly higher UACR than those without LVH (P<0.001). The prevalence of LVH presented an upward trend with the elevation of UACR. UACR was independently and positively associated with hemoglobin A1c (P<0.001). UACR can differentiate LVH (AUC = 0.682, 95% CI (0.602–0.760),P<0.001). The optimal cutoff point determined with the Youden index was UACR = 10.2 mg/g. When categorized by this cutoff point, the odds ratio (OR) for LVH in patients in the higher UACR group (10.2–30 mg/g) was 3.104 (95% CI: 1.557–6.188,P=0.001) compared with patients in the lower UACR group (<10.2 mg/g). When UACR was analyzed as a continuous variable, every double of increased UACR, the OR for LVH was 1.511 (95% CI: 1.047–2.180,P=0.028). Overall, UACR below 30 mg/g is associated with LVH in patients with T2DM. The optimal cutoff value of UACR for identifying LVH in diabetes is 10 mg/g.

Sepsis is a complication of infection caused by disease or trauma. Increasing evidence have shown that long noncoding RNAs (lncRNAs) are involved in the regulation of sepsis. However, the mechanism of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in the regulation of sepsis progression remains to be elucidated. Lipopolysaccharide (LPS) was used to induce a sepsis cell model. The expression levels of NEAT1 and microRNA (miR)-590-3p were determined by reverse transcription-quantitative PCR. Cell viability and apoptosis were detected using Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. Western blot analysis was performed to evaluate the levels of apoptosis- and NF-κB signaling pathway-related proteins. The concentration of inflammatory cytokines was determined using ELISA. In addition, dual-luciferase reporter assay, RNA immunoprecipitation and biotin-labeled RNA pull-down assay were performed to verify the interaction between NEAT1 and miR-590-3p. The results showed that NEAT1 was highly expressed in patients with sepsis and LPS-induced H9c2 cells. Knockdown of NEAT1 decreased LPS-induced cell apoptosis and inflammation response in H9c2 cells. Meanwhile, miR-590-3p showed decreased expression in sepsis, and its overexpression could relieve LPS-induced H9c2 cell damage. Further experiments revealed that NEAT1 could sponge miR-590-3p. Knockdown of miR-590-3p reversed the inhibitory effect of NEAT1 knockdown on LPS-induced H9c2 cell damage. Additionally, the NEAT1/miR-590-3p axis could regulate the activity of the NF-κB signaling pathway. To conclude, lncRNA NEAT1 accelerated apoptosis and inflammation in LPS-stimulated H9c2 cells via sponging miR-590-3p. These findings may provide a new strategy for the treatment of sepsis.

针对污水处理厂污水处理构筑物藻类生长与黏附现象严重的问题,采用共混方法制备季铵盐(QAC)/环氧树脂复合涂层,并探究QAC投加量对复合涂层的性质和抑藻性能的影响.结果 表明:QAC与环氧树脂涂料成功复合,改性涂层表面的季铵基团(R4N+)数量随QAC投加量增大而增加;QAC改性对涂层的疏水性、耐水性不产生明显影响.但与环氧树脂涂层相比,随QAC浓度的增加,复合涂层表面的Zeta电位向正电性偏移,粗糙度略微减小;以小球藻(Chlorella vulgaris)作为模型藻类进行的涂层抑藻性能研究表明,QAC/环氧树脂复合涂层表面黏附的小球藻数目明显少于环氧树脂涂层,且QAC投加量越多,涂层抗藻污染性能越好.

目的 研究2019冠状病毒病(COVID-19)轻症患者的临床特点和核酸转阴时间.方法 回顾性纳入2020年2月12日至2月29日武汉黄陂方舱医院的2019新型冠状病毒(2019-nCoV)核酸阳性的患者,分为轻型和普通型,随访至2020年3月10日,分析患者的临床特点和核酸检测结果.结果 本研究共纳入75例患者,平均年龄41.2±11.5岁,男性占52.0％.患者中有发热表现者44.0％,CT影像阳性者54.7％.首次核酸检出阳性率69.3％,核酸转阴天数中位数为9.0天(6.0～14.0天).随访至2020年3月10日,无患者转为重型或死亡.轻型(34例)和普通型(41例)患者的年龄、白细胞计数差异无显著性.与普通型组比较,轻型组女性占61.8％,显著高于男性(P＜0.05);两组患者核酸转阴天数差异无显著性[8.5天(7.0～13.8天)比9.0天(5.0～14.0天),P=0.973].亚组分析发现轻型患者中,女性的核酸转阴时间少于男性(P=0.020),服用连花清瘟胶囊亚组核酸转阴时间缩短(P=0.026).结论 相同治疗下轻型和普通型患者核酸转阴时间差异无显著性,轻型患者中女性和服用连花清瘟亚组核酸转阴时间缩短;根据临床表现和影像学诊断COVID-19可能漏诊部分轻症患者,急需准确及时的核酸检测或其它病原学、血清学检测方法.

目的 探讨姜黄素通过FGF21对巨噬细胞源性的泡沫细胞胆固醇流出的影响.方法 通过体外共培养THP-1、Hepa1-6细胞,并使用ox-LDL诱导THP-1产生泡沫细胞后,将实验分为对照组、泡沫细胞组、姜黄素A、B、C5组进行,显微镜下观察油红O染色后细胞形态;测定细胞内游离胆固醇、总胆固醇、胆固醇酯的变化;Western Blot和RT-qPCR检测ABCA1的蛋白与mRNA表达情况;ELISA测定姜黄素处理后Hepa1-6细胞中FGF21表达的变化.结果 姜黄素治疗后泡沫细胞的形成、游离胆固醇、总胆固醇以及胆固醇酯与未使用姜黄素治疗相比明显减少,ELISA结果表明了姜黄素可以促进细胞FGF21的表达,而加入不同浓度的FGF21单独处理细胞后,明显的看到了ABCA1的表达上调,同时结果显示姜黄素上调ABCA1的表达,与其浓度呈正相关.结论 姜黄素可以通过FGF21促进泡沫细胞胆固醇流出,防止动脉粥样硬化的发生.

应用机器学习的分类决策树方法对脓毒症患者的预后进行分析,建立评估脓毒症预后的简易模型.收集并分析急诊科收治的167名脓毒症患者的临床资料,根据入院30天的生存状态将患者分为生存组和死亡组.结果显示,心率和收缩压两个自变量组成的精简模型能够对72.5％的病例正确分类,心率大于118次/分是脓毒症30天死亡重要的分类指标.本研究说明,心率和收缩压结合分类决策树方法可以对脓毒症患者的预后进行高效的分类.

Background Changes in baseline resting heart rate (RHR) appear to predict new-onset hypertension (NOH). However, RHR is a dynamic anthropometric parameter; thus, the association between changes in RHR and NOH requires further investigation. Methods We studied 10 403 participants who were initially normotensive and who had at least one routine health examination at baseline and 1 year later during 2011–2016. We compared the RHR between the baseline and 1-year follow-up. We defined hypertension as SBP ≥140 mmHg or DBP ≥90 mmHg. Participants were divided into three groups: RHR decreased, RHR unchanged [from 0 to 10 beats per minute (bpm)], and RHR increased ≥10 bpm. Cox regression analysis was performed to calculate relative risk with 95% confidence intervals (CIs) for the association between NOH and RHR change. Results During a mean follow-up period of 2.42 years, 1173 (11.28%) participants developed hypertension. After adjusting for age, sex, SBP, DBP, RHR and other confounders obtained at baseline, and compared with participants with unchanged RHR, participants with decreased RHR had a 17% decreased risk of NOH (adjusted hazard ratio: 0.83, 95% CI 0.73–0.95), whereas subjects with RHR that increased ≥10 bpm had a 23% increased risk of NOH (adjusted hazard ratio: 1.23, 95% CI 1.04–1.46). Conclusion A 1-year increase in RHR for initially normotensive subjects is an independent risk factor for subsequent hypertension.

目的 观察纳洛酮用于脑复苏的临床疗效.方法 选择2018年01月～2019年08月在我进行治疗的80例心脏骤停患者作为研究对象.按照随机数表法将其分为两组,各40例.其中对照组均实施常规心肺脑复苏方式进行抢救.实验组在对照组的基础上加用纳洛酮治疗.观察并记录两组患者治疗后急性生理和慢性健康状态(APACHEⅡ)评分、格拉斯哥昏迷指数评分(GSC评分)、自主呼吸恢复、自主循环恢复情况以及治疗效果;取患者心肺复苏成功后1天外周静脉血,检测其血乳酸、β-内啡肽(β-EP)指标.结果 实验组患者β-EP、血乳酸、GSC、A-PACHEⅡ评分均低于对照组;且实验组患者治疗后自主呼吸恢复及自主循环恢复时间均低于对照组,且自主呼吸恢复及自主循环恢复比例要高于对照组,差异具有统计学意义(P<0.05).结论 纳洛酮能够明显提高脑复苏的成功率,、疗效确切,效果显著,值得临床推广使用.

目的: 探讨学生标准化病人(Students Standardized Patient,SSP)在急诊心肺复苏术教学中的效果.方法: 选2014级全科医学班学生48人为研究对象,随机分为学生标准化病人教学的实验组与传统教学的对照组每组24名,分别采用SSP教学及传统教学模式进行心肺复苏授课,通过实践操作考核 、案例分析考核及发放调查问卷来评价不同教学方法授课效果.结果: 实验组的心肺复苏实践操作成绩(P<0.05)及案例分析的成绩明显高于对照组(P<0.01),差异有统计学意义.调查问卷结果,实验组学生的学习积极性 、对教师的满意度 、对知识的掌握程度及自信心均高于对照组(P<0.01).结论: SSP的教学模式能提高学生对临床病例的分析及处理能力,增强学生对抢救的自信心,得到学生的认可及好评.