Objective: Inflammation and oxidative damage play critical roles in the pathogenesis of sepsis-induced cardiac dysfunction. Multiple EGF-like domains 9 (MEGF9) is essential for cell homeostasis; however, its role and mechanism in sepsis-induced cardiac injury and impairment remain unclear.Methods: Adenoviral and adeno-associated viral vectors were applied to overexpress or knock down the expression of MEGF9 in vivo and in vitro. To stimulate septic injury, cardiomyocytes and mice were treated lipopolysaccharide (LPS). To clarify the necessity of AMP-activated protein kinase (AMPK), global AMPK knockout mice were used.Results: We found that MEGF9 expressions were reduced in cardiomyocytes and mice by LPS stimulation. Compared with negative controls, plasma MEGF9 levels were also decreased in septic patients, and negatively correlated with LPS-induced cardiac dysfunction. In addition, MEGF9 overexpression attenuated, while MEGF9 knockdown aggravated LPS-induced inflammation and oxidative damage in vivo and in vitro, thereby regulating LPS-induced cardiac injury and impairment. Mechanistic studies revealed that MEGF9 overexpression alleviated LPS-induced cardiac dysfunction through activating AMPK pathway.Conclusion: We for the first time demonstrate that MEGF9 prevents LPS-related inflammation, oxidative damage and cardiac injury through activating AMPK pathway, and provide a proof-of-concept for the treatment of LPS-induced cardiac dysfunction by targeting MEGF9.

Objectives:This study explored the brain-targeting properties and mechanisms of 4-hydroxybenzaldehyde (4-HBd), the primary active component of Gastrodia elata, in mitigating ischemic stroke (IS)-induced injury by preserving blood-brain barrier (BBB) integrity, based on brain pharmacokinetic characteristics. Methods:The anti-IS effects of the G. elata extract were assessed using a rat middle cerebral artery occlusion/reperfusion (MCAO/R) model, leading to the identification of 4-HBd as the principal active ingredient. BBB protection was evaluated through neurological scoring, Evans Blue (EB) extravasation, cerebral infarct volume, and ultrastructural integrity. Oxidative stress markers, including superoxide dismutase (SOD), malondialdehyde (MDA), nitric oxide (NO), and inducible nitric oxide synthase (iNOS), were quantified in ischemic brain tissue via biochemical assays. The expression levels of tight junction (TJ) proteins claudin-5 and occludin, as well as matrix metalloproteinase MMP-2/9 and aquaporin-4 (AQP-4), were analyzed by Western blotting. Microdialysis, combined with liquid chromatography-tandem mass spectrometry (LC-MS/MS), was employed to determine the temporal distribution of 4-HBd in the brains of both normal and MCAO/R model rats. The ability of 4-HBd to scavenge intracellular reactive oxygen species (ROS) in brain endothelial cells (bEnd.3) was evaluated using a single-cell biochemical analyzer. Results:G. elata ethanol extract exhibited significant anti-IS effects. When compared with the model group, 4-HBd treatment markedly alleviated BBB disruption and neurological deficits, suppressed oxidative stress in ischemic brain tissue, reduced MDA and NO levels, and enhanced SOD activity. The expressions of claudin-5, occludin, MMP-2/9, and AQP-4 were significantly upregulated in the 4-HBd group relative to the model group. Additionally, 4-HBd selectively eliminated nuclear-derived ROS. Pharmacokinetic analysis demonstrated that 4-HBd preferentially accumulated in the striatum and cortex of both normal and MCAO/R model rats. Under ischemic conditions, 4-HBd exhibited accelerated cortical penetration, increased exposure, and prolonged retention. Conclusion:These findings indicate that 4-HBd exerts a pronounced brain-targeting effect and preserves BBB integrity via the RNS/ROS-MMP-TJ signaling pathway, highlighting its potential as a therapeutic agent for IS.

High-density lipoprotein cholesterol (HDL-C) is widely recognized for its protective effects against cognitive decline. However, recent studies have presented conflicting results, with some suggesting no significant cognitive benefits or even an increased risk of dementia associated with high HDL-C levels. For those who suffer from depression, the cognitive benefits of HDL-C may be diminished or reversed. The purpose of this study is to investigate the associations between HDL-C, cognitive ability, and depressive symptoms in middle-aged and older Chinese adults. The datasets utilized were sourced from the China Health and Retirement Longitudinal Study (CHARLS) for the years 2011 and 2015, comprising 4,302 participants. Cross-lagged models were employed to explore the temporal sequence between cognitive performance and HDL-C levels, and to examine the interplay among depression, cognition, and HDL-C. Confounding factors such as sociodemographic characteristics, sleep conditions, and history of chronic diseases were controlled for. The analysis revealed unidirectional effects of baseline impaired cognition and greater severity of depression on increased HDL-C levels at follow-up (β = − 0.036 and β = 0.028, respectively, P < 0.05). However, higher baseline HDL-C levels did not significantly predict cognitive performance or depression 4 years later (β = − 0.008 and β = 0.023, respectively, P > 0.05). Depressive symptoms and cognition were found to have a significant bidirectional association (β = − 0.026 and β = − 0.053, respectively, P < 0.05). Cognitive impairment and depression are associated with higher HDL-C levels, whereas higher HDL-C levels do not appear to protect against cognitive decline or depressive symptoms. These findings underscore the importance of preserving cognitive and mental health, which may lower the likelihood of cardiovascular disease and dementia. Future studies should validate these findings and develop targeted interventions tailored to specific populations.

Introduction: Cardiac hypertrophy is an important contributor of heart failure, and the mechanisms remain unclear. Leucine zipper protein 1 (LUZP1) is essential for the development and function of cardiovascular system; however, its role in cardiac hypertrophy is elusive. Objectives: This study aims to investigate the molecular basis of LUZP1 in cardiac hypertrophy and to provide a rational therapeutic approach. Methods: Cardiac-specific Luzp1 knockout (cKO) and transgenic mice were established, and transverse aortic constriction (TAC) was used to induce pressure overload-induced cardiac hypertrophy. The possible molecular basis of LUZP1 in regulating cardiac hypertrophy was determined by transcriptome analysis. Neonatal rat cardiomyocytes were cultured to elucidate the role and mechanism of LUZP1 in vitro. Results: LUZP1 expression was progressively increased in hypertrophic hearts after TAC surgery. Gain- and loss-of-function methods revealed that cardiac-specific LUZP1 deficiency aggravated, while cardiac-specific LUZP1 overexpression attenuated pressure overload-elicited hypertrophic growth and cardiac dysfunction in vivo and in vitro. Mechanistically, the transcriptome data identified Stat3 pathway as a key downstream target of LUZP1 in regulating pathological cardiac hypertrophy. Cardiac-specific Stat3 deletion abolished the pro-hypertrophic role in LUZP1 cKO mice after TAC surgery. Further findings suggested that LUZP1 elevated the expression of Src homology region 2 domain-containing phosphatase 1 (SHP1) to inactivate Stat3 pathway, and SHP1 silence blocked the anti-hypertrophic effects of LUZP1 in vivo and in vitro. Conclusion: We demonstrate that LUZP1 attenuates pressure overload-induced cardiac hypertrophy through inhibiting Stat3 signaling, and targeting LUZP1 may develop novel approaches to treat pathological cardiac hypertrophy.

Background:The effect of 3D-printed bioresorbable vascular scaffolds (BRS) in coronary heart disease has not been clarified.Aims:We aimed to compare the safety and efficacy of 3D-printed BRS with that of metallic sirolimus-eluting stents (SES).Methods:Thirty-two BRS and 32 SES were implanted into 64 porcine coronary arteries. Quantitative coronary angiography (QCA) and optical coherence tomography (OCT) were performed at 14, 28, 97, and 189 days post-implantation. Scanning electron microscopy (SEM) and histopathological analyses were performed at each assessment.Results:All stents/scaffolds were successfully implanted. All animals survived for the duration of the study. QCA showed the two devices had a similar stent/scaffold-to-artery ratio and acute percent recoil. OCT showed the lumen area (LA) and scaffold/stent area (SA) of the BRS were significantly smaller than those of the SES at 14 and 28 days post-implantation (14-day LA: BRS vs SES 4.52±0.41 mm2 vs 5.69±1.11 mm2; p=0.03; 14-day SA: BRS vs SES 4.99±0.45 mm2 vs 6.11±1.06 mm2; p=0.03; 28-day LA: BRS vs SES 2.93±1.03 mm2 vs 4.82±0.74 mm2; p=0.003; 28-day SA: BRS vs SES 3.86±0.98 mm2 vs 5.75±0.71 mm2; p=0.03). Both the LA and SA of the BRS increased over time and were similar to those of the SES at the 97-day and 189-day assessments. SEM and histomorphological analyses showed no significant between-group differences in endothelialisation at each assessment.Conclusions:The novel 3D-printed BRS showed safety and efficacy similar to that of SES in a porcine model. The BRS also showed a long-term positive remodelling effect.

目的 探讨组蛋白H4在脂多糖诱导的小鼠急性呼吸窘迫综合征(ARDS)中对肺泡巨噬细胞(AM)极化的作用.方法 (1)将无特定病原体级C57BL/6雄性小鼠随机分为对照组和2、4、6、8 mg/kg脂多糖组,每组6只.采用一次性气管滴注法,后4组小鼠予相应剂量脂多糖染毒,对照组小鼠予等体积的0.9%氯化钠溶液.12 h后,采集各组小鼠动脉血进行血气分析,取肺组织观察肺水肿和病理组织学改变情况,采用酶联免疫吸附实验检测小鼠支气管肺泡灌洗液(BALF)中组蛋白H4水平,并采用贴壁法分离5组小鼠AM.(2)采用贴壁法分离正常小鼠AM,随机分为对照组、组蛋白H4损伤组、BALF损伤组和抗组蛋白H4中和抗体(anti-H4)干预组.组蛋白H4损伤组AM中加入终质量浓度为20 mg/L的组蛋白H4;BALF损伤组和anti-H4干预组AM中均加入经剂量为6 mg/kg体质量脂多糖染毒小鼠的BALF上清200 μL,后者同时加入终质量浓度为25 mg/L的anti-H4抗体;对照组AM中加入等体积的磷酸盐缓冲液溶液.刺激12 h后,收集AM.(3)采用实时定量聚合酶链式反应法检测AM中肿瘤坏死因子-α(Tnfa)、白细胞介素-1β(Il1b)、分化抗原206(Cd206)和精氨酸酶1(Arg1)的mRNA相对表达水平.结果 (1)与对照组比较,4个脂多糖组小鼠均出现呼吸急促,肺组织出现炎症反应和肺水肿,均呈剂量依赖性加重.随着脂多糖染毒剂量的增加,小鼠动脉血氧分压与吸入气中氧浓度分数比值下降(P<0.05),肺湿/干质量比值、BALF中组蛋白H4水平和AM的Tnfa、Il1b mRNA相对表达水平均增加(P值均<0.05).其中,6和8 mg/kg脂多糖组小鼠均出现ARDS.6和8 mg/kg脂多糖组小鼠BALF中组蛋白H4水平和AM的Tnfa、Il1b mRNA相对表达水平均高于其余3组(P值均<0.05).(2)与对照组比较,组蛋白H4损伤组、BALF损伤组AM中Tnfa和Il1b mRNA相对表达水平均升高(P值均<0.05),Cd206和Arg1 mRNA相对表达水平均下降(P值均<0.05).与BALF损伤组比较,anti-H4干预组AM中Tnfa和Il1b mRNA相对表达水平均下降(P值均<0.05),Arg1 mRNA相对表达水平升高(P<0.05).结论 脂多糖可诱导小鼠BALF中组蛋白H4水平出现剂量依赖性的升高;组蛋白H4通过激活AM向M1型极化,驱动ARDS的发生发展.拮抗组蛋白H4以干预AM向M1型极化可能是治疗ARDS的靶点.

Objective There is a large population of patients classified as complex higher-risk and indicated patients (CHIPs) in China with a poor prognosis. The treatment of these patients is complex and challenging, especially when acute cardiac events occur, such as acute coronary syndrome (ACS) or heart failure. Pharmacotherapy and some mechanical circulatory support (MCS) therapeutic devices can provide stable hemodynamic support for CHIPs-percutaneous coronary intervention (PCI). LDL-C is an important pathogenic factor in atherosclerosis, and the target of blood lipid control. Recent studies have revealed that lipoprotein(a) [Lp(a)], which is formed when a covalent bond between apolipoprotein(a) and apolipoprotein B-100 is made, produces an LDL-like particle. This particle is an independent risk factor for the development of atherosclerosis, and is closely correlated to stent thrombosis and restenosis. Furthermore, this requires active intervention. PCSK9 inhibitors have been used in lipid-lowering treatment, and preventing atherosclerosis. The present study explores the efficacy of PCSK9 inhibitors in CHIPs-ACS, and the association between the change in Lp(a) and survival after 2 years of follow-up. Methods The present real-world, prospective control study enrolled 321 CHIPs-ACS who underwent emergency PCI from August 2019 to November 2020, and these patients were followed up for 2 years. These patients were divided into two groups: PCSK9 group ( n =161) given the combined PCSK9 inhibitor (140 mg of evolocumab every 2 weeks) and statins-based therapy, and SOC group ( n =160) treated with statin-based lipid-lowering therapy alone. Then, the change in lipid index was measured, and the cardiovascular (CV) event recurrence rate was evaluated after one month and 2 years. Afterwards, the contribution of serum lipid parameters, especially the Lp(a) alteration, in patients with earlier initiation of the PCSK9 inhibitor to the CV outcome was analyzed. Results The LDL-C level was significantly reduced in both groups: 52.3% in the PCSK9 group and 32.3% ( P <0.001) in the SOC group. It is noteworthy that the Lp(a) level decreased by 13.2% in the PCSK9 group, but increased by 30.3% in the SOC group ( P <0.001). Furthermore, the number of CV events was not significantly different between the PCSK9 and SOC groups after the 2-year follow-up period. In the PCSK9 group, the Lp(a) reduction was associated with the baseline Lp(a) levels of the patients ( r 2 =−0.315, P <0.001). Moreover, the decrease in Lp(a) contributed to the decline in CV events in patients who received ACS CHIPs-PCI, and the decrease in Lp(a) level was independent of the LDL-C level reduction. Conclusion The early initiation of PCSK9 inhibitors can significantly reduce the LDL-C and Lp(a) levels in ACS CHIPs-PCI. However, further studies are needed to confirm whether PCSK9 inhibitors can reduce the incidence of CV disease in CHIPs.

我国的职业病防治面临着十分严峻的挑战,良好的职业健康教育是职业病防治的前提和基础.理想的职业健康教育模式应该既实现对劳动者的全面覆盖,又实现对劳动者的个性化教育,目前传统的职业健康教育无法满足这些需求.相比于传统教学模式,慕课教学有三个主要特点,即大规模、开放和在线,可以覆盖需要培训的所有人群.慕课的独特优势是以学习者为中心构建课程,有助于解决职业健康教育中劳动者的个性化教学问题.可见,慕课教学在职业健康教育中有着巨大的应用潜力.

Through a comprehensive review of the records and use of Chinese medicine in medieval Western Asia, this article believes that the foreign exchange of Chinese medicine is a two-way process.The western Asian doctors’ cognition of traditional Chinese medicine and their unique writing method have reflected the local cultural characteristics, enriched the treasure reserve of Islamic medical knowledge, and also promote the development of medicine.The interest of West Asian scholars in traditional Chinese medicine is not only closely related to medical practice, trade interests and academic exchanges, but also related to cultural imagination, which reflects their exotic feelings towards China as a faraway place.

This study mainly attempts to develop Mg-based alloy materials with excellent corrosion resistance by means of multi-principal alloying. The alloy elements are determined based on the multi-principal alloy elements and the performance requirements of the components of biomaterials. Mg30Zn30Sn30Sr5Bi5 alloy was successfully prepared by vacuum magnetic levitation melting. Through the electrochemical corrosion test with m-SBF solution (pH7.4) as the electrolyte, the corrosion rate of alloy Mg30Zn30Sn30Sr5Bi5 alloy decreased to 20% of pure Mg. It could also be seen from the polarization curve that when the self-corrosion current density is low, the alloy shows superior corrosion resistance. Nevertheless, with the increase in self-corrosion current density, although the anodic corrosion performance of the alloy is obviously better than that of pure Mg, the cathode shows the opposite situation. The Nyquist diagram shows that the self-corrosion potential of the alloy is much higher than that of pure Mg. In general, under the condition of low self-corrosion current density, the alloy materials display excellent corrosion resistance. It is proved that the multi-principal alloying method is of positive significance for improving the corrosion resistance of Mg alloys.

马坚(1906-1978),字子实,云南省个旧市沙甸村人,肄业于上海伊斯兰学校.1931年11月9日,马坚由中国回教学会选派,随第一届留埃学生团,从昆明启程,12月20日,抵达开罗,开始留学生涯①.马坚先后就读开罗爱资哈尔大学和阿拉伯语专科大学,专攻阿拉伯文伊斯兰教经籍和哲学②.1932年,马坚被聘为《月华》海外通讯员③.马坚在埃及留学期间,表现突出,成为青年学者的代表,与纳子嘉(纳忠)、海维谅被誉为"回教三杰".马坚留学期间,参与了多项活动,不仅自己留下了一些日记(《留埃日记选》《留埃见闻录》)④,也出现在《中国回教近东访问团日记》、陶行知(《海外的故事》)、庞士谦(《埃及九年》《一九三九年留埃学生朝觐团日记》)、马松亭(《二次旅埃日记》)等人的日记、报告甚至新闻媒体的报导之中.

Lipid metabolism disorders are recognized to be one of the most frequent complications of renal transplantation, while dyslipidemia and chronic kidney disease (CKD) are strong risk factors for arteriosclerotic cardiovascular disease (ASCVD). Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) are novel lipid-lowering drugs, the safety and efficacy of which are yet to be confirmed in transplanted patients. There have been several small-sample studies using PCSK9i in patients after heart transplantation, while fewer cases use PCSK9i after kidney transplantation. We report a case of a renal transplant recipient complicated with hepatitis B treated with PCSK9i, which achieved a remarkable lipid-lowering efficacy, and no significant adverse effects were found during the follow-up.

Background: Stent implantation has been increasingly applied for the treatment of obstructive coronary artery disease, which, albeit effective, often harasses patients by in-stent restenosis (ISR). Purpose: The present study was to explore the role of compound Chinese medicine Cardiotonic Pills (R) (CP) in attenuating ISR-evoked myocardial injury and fibrosis. Study Design: Chinese miniature pigs were used to establish ISR model by implanting obsolete degradable stents into coronary arteries. Quantitative coronary angiography (QCA) was performed to confirm the success of the model. Methods: CP was given at 0.2 g/kg daily for 30 days after ISR. On day 30 and 60 after stent implantation, the myocardial infarct and myocardial blood flow (MBF) were assessed. Myocardial histology was evaluated by hematoxylin-eosin and Masson's trichrome staining. The content of ATP, MPO, and the activity of mitochondria) respiratory chain complex IV were determined by ELISA. Western blot was performed to assess the expression of ATP5D and related signaling proteins, and the mediators of myocardial fibrosis. Results: Treatment with CP diminished myocardial infarct size, retained myocardium structure, attenuated myocardial fibrosis, and restored MBF. CP ameliorated energy metabolism disorder, attenuated TGF beta 1 up-regulation and reversed its downstream gene expression, such as Smad6 and Smad7, and inhibited the increased expression of MCP-1, PR S19, MMP-2 and MMP-9. Conclusion: CP effectively protects myocardial structure and function from ISR challenge, possibly by regulating energy metabolism via inactivation of RhoA/ROCK signaling pathway and inhibition of monocyte chemotaxis and TGF beta 1/Smads signaling pathway.

目的 探索构建医院行政部门绩效考核指标,为医院科学准确考核行政部门绩效提供测量工具.方法 在文献回顾及德尔菲专家咨询法的基础上建立层次结构模型,运用层次分析法,对各级指标分别进行两两比较,建立一系列判别矩阵,以计算指标权重.结果 构建了4个一级指标,10个二级指标,28个三级指标的指标体系层次结构,一级指标中权重最高的是"业绩维度",权重为0.410;二级指标中权重最高的指标是"工作完成情况",权重为0.264;三级指标中权重最高的指标是"承担重点工作",权重为0.084.结论 本研究探索构建了医院行政部门绩效考核指标体系,为优化医院行政部门绩效考核的理论与实践提出了参考依据.

目的 分析患者对医院品牌评价的影响因素,探讨医院品牌管理对策.方法 采用便利抽样方法选取北京市某三甲综合医院617名患者作为调查对象开展问卷调查,采用结构方程模型、重要性矩阵分析等方法进行分析.结果 对医院品牌总体评价影响程度最大的指标是品牌忠诚度(重复就医意向、满意度、愿意支付的价格成本溢价),影响程度最小的指标是品牌知名度(熟悉度).品质认知度(技术质量、服务质量)是优势因素,品牌忠诚度(满意度、愿意支付的价格成本溢价、愿意支付的时间成本溢价、重复就医意向)、品质认知度(环境质量、流程便利性)是需要改进的主要劣势因素.结论 提升品牌忠诚度是提升医院品牌评价的关键因素.医院应以巩固高医疗技术水平和高知名度优势为基础,将提升患者体验作为品牌管理策略的重要落脚点.

We applied a new idea that the potential effect can change the ion adsorption structure on the cell surface to explore the mechanism of digoxin poisoning and the regulation of ion channels. The effects of digoxin on the electrophoretic mobility and behaviors (non-contraction or contraction or autorhythmicity) of cardiomyocytes were observed by single-cell electrophoresis technique (imitate the opening method of in vivo channel) and the method of decomposing surface potential components on the cells. As well as affect the association with electrical activity. The results suggested that the increase of cardiomyocytes transmembrane potential and the Na + –K + exchange on the cell surface of the action potential phase 4 caused by the poisoning dose of digoxin, leading to the oscillation of adsorbed ions on the cell surface and the incomplete channel structure, which were the mechanism of cardiac ectopic beats. The results revealed that the opening of ion channels is regulated by the surface electric double layer of the cell membrane.

Objective:To explore the predictive value of a scoring model based on MRI images for diagnosing invasive placenta accreta and associated adverse clinical outcomes.Methods:This retrospective cohort study involved 260 patients delivered at Peking University Third Hospital from January 2015 to December 2018, who were suspected to be placenta accreta with two or more ultrasound image findings and underwent MRI examination. Placenta accreta was finally diagnosed and classified based on the intraoperative clinical findings or pathological examination. Adverse clinical outcomes were defined as intraoperative bleeding ≥1 500 ml and/or having hysterectomy. Quantitative and qualitative interpretation of five MRI signs were performed, including intraplacental low-intensity band on T2 weighted imaging, abnormal intraplacental vascularization, vascularization of uterovesical interface, uterine bulging and cervical involvement. Chi-square and t test were used for univariate analysis of the five MRI signs and the receiver operating characteristics (ROC) curve of each MRI sign for predicting invasive placenta accreta and adverse clinical outcomes were drawn. The predictive value was assigned as 1 when ≥ the cutoffs that matched to the maximum Yoden index values, and was assigned as 0 when below the cutoffs. A scoring model based on the five MRI signs was established, ROC curves of the model for predicting invasive placenta accreta and adverse clinical outcomes were drawn and the area under the curve (AUC), sensitivity, specificity and Youden index were calculated. Results:(1) Univariate analysis showed that all five MRI signs were significantly associated with invasive placenta accreta and adverse clinical outcomes. Except for cervical involvement, the other four signs had an AUC value of greater than 0.5 in predicting invasive placenta accreta and adverse clinical outcomes. (2) The predictive cut-off values of abnormal intraplacental vascularization image and intraplacental dark band area on T2 weighted imaging were 2.0 cm 2 and 0.6 cm 2, respectively, and were all 1.0 for the other three signs. The AUC value of MRI signs-based scoring model for predicting invasive placenta accreta was 0.863. When the score was ≥ 2 points, the diagnostic sensitivity was 0.836 and the specificity was 0.726. The scoring model predicted adverse clinical outcomes with an AUC of 0.841. When the score was ≥3 points, the predictive sensitivity was 0.707 and the specificity was 0.818. Conclusions:The scoring model based on MRI signs is of good value for the diagnosis of invasive placenta accreta and the prediction of adverse clinical outcomes.

Background: Numerous studies have shown that high-dose statin pretreatment may reduce the risk of periprocedural myocardial infarction (PMI) and short-term major adverse cardiac events (MACE) in western people undergoing percutaneous coronary intervention (PCI). However, the effects in East Asian patients are still controversial. The objective was to evaluate the effects of short-term high-dose statin (all types) pretreatment compared with the control (low-dose or no statin) on the reduction of the rate of MACE and PMI in East Asian patients. Methods: PubMed/Medline, EMBASE, and the Cochrane Central Register of Controlled Trials were systematically searched for randomized controlled trials (RCTs) in East Asian patients up to December 2019, in which short-term high-dose statin pretreatment was compared with control for patients undergoing PCI. The primary outcome measure was the incidence of MACE at 30 days. The secondary outcome measure was the incidence of PMI. The meta-analysis was performed with the fixed-effect model or random-effects model according to the heterogeneity. The meta-analysis was performed using RevMan 5.3 software (Cochrane Collaboration). Results: Fifteen RCTs that enrolled 4313 East Asian patients were identified. High-dose statin pretreatment was associated with a 54% relative reduction in 30-day MACE (OR, 0.46; 95% CI, 0.31-0.67; P < .001) and a 50% relative reduction in PMI (OR, 0.50; 95% CI, 0.34-0.76; P = .001). Conclusions: High-dose statin pretreatment can significantly reduce 30-day MACE and PMI for East Asian patients undergoing PCI.

在变态反应门诊中,经常发现不少晕厥患者误以为自己是过敏性休克,坚持要求到变态反应科仔细排查过敏性疾病;而另一些过敏性休克患者则把发病情形描述为晕厥或晕倒,从而被导诊到心内科、神经科或内分泌科诊治.混淆晕厥和过敏性休克两者的界限,误选误用,不仅延误了到医院的及早诊治,也影响了院前急救的正确实施.

血管性水肿是由皮肤或黏膜局部血管通透性增加,随后液体渗出到皮肤或黏膜间质而形成.现有研究显示,血管性水肿是由血管内皮细胞通透性的可逆性异常改变引起,血管每次发生阵发性的异常通透性改变后,其完整性可完全恢复;而血管本身并不存在持续性的炎症反应、退行性变、缺血性损伤等病理改变[ 1?2].