Background and objective: Estimated pulse wave velocity (ePWV) is widely recognized as a practical surrogate marker for carotid-femoral pulse wave velocity (cfPWV) and has been validated as a prognostic indicator for a variety of diseases. Nevertheless, the association between ePWV and the risk of 30-day mortality in intensive care unit (ICU) patients diagnosed with atrial fibrillation (AF) remains insufficiently understood. This study aims to investigate the correlation between ePWV and 30-day mortality in critically ill patients with AF. Methods A retrospective analysis was conducted utilizing data from the MIMIC-IV database, focusing on ICU patients with AF. Participants were categorized into two groups based on an ePWV cutoff value determined through receiver operating characteristic (ROC) curve analysis. The relationship between ePWV levels and 30-day mortality was evaluated using Kaplan-Meier survival analysis, Cox proportional-hazards models, and restricted cubic spline (RCS) regression. Additionally, subgroup analyses were performed to assess the influence of ePWV on 30-day mortality across various patient subgroups. Results A cohort of 9,179 critically ill patients with AF was analyzed. The 30-day all-cause mortality rate was observed to be 15.47%. Upon adjusting for confounding variables, ePWV persisted as an independent risk factor for 30-day mortality ( P <0.001). RCS modeling revealed a non-linear association between ePWV and 30-day all-cause mortality (non-linear P <0.001). Conclusions The study identified ePWV as an independent predictor of 30-day mortality among critically ill patients with AF. Early identification of high-risk patients through ePWV assessment may enable timely interventions and enhance clinical outcomes. Clinical trial number Not applicable.

This study aims to analyze the distribution and drug resistance patterns of clinically isolated bacteria at the National Center for Cardiovascular Diseases (Fuwai Central China Cardiovascular Hospital) from 2018 to 2024, thereby guiding the precise selection of effective antimicrobial agents in clinical practice and providing data support for the development of individualized anti-infective treatment strategies. Clinical isolates from outpatients and inpatients were collected at the Fuwai Central China Cardiovascular Hospital, excluding duplicate strains. Statistical analysis was conducted using descriptive epidemiological methods with SPSS 22.0, Prism 10.0, and WHONET 5.6 software. Over seven years, 9,180 clinical isolates were identified, with a positive detection rate of 7.78

Background Acute kidney injury (AKI) is a common complication of cardiac surgery. Human umbilical cord mesenchymal stem cell (hUCMSC)-derived exosomes affect tissue damage and repair, and miR-21-5p reduces apoptosis and inflammation. However, miR-21-5p’s role in cardiac surgery remains unclear.Methods Kidney injury molecule (KIM-1), neutrophil gelatinase-associated lipid carrier protein (NGAL), serum creatinine, and blood urea nitrogen (BUN) levels were tested by enzyme-linked immunosorbent assay. hUCMSCs and exosomes were identified via Oil Red O staining kit, alkaline phosphatase staining kit, flow cytometry, transmission electron microscopy, Western blot, and immunofluorescence. Cell viability and apoptosis were detected by cell counting kit 8 and flow cytometry. Interleukin-1β, interleukin-6, and tumor necrosis factor-alpha levels were tested by ELISA kits. Relativity between miR-21-5p and TEA domain family member 1 (TEAD1) was verified by dual-luciferase reporter gene assay and western blot. TEAD1, BUN, and creatinine levels in vivo were tested via immunohistochemistry and automatic biochemistry analyzer.Results KIM-1, NGAL, serum creatinine, and BUN levels were increased and miR-21-5p expression was inhibited in AKI after cardiac surgery. In AKI after cardiac surgery, hUCMSCs-Exos inhibited apoptosis and pyroptosis and promoted viability via miR-21-5p regulation. hUCMSCs-Exos retarded AKI after cardiac surgery progression by facilitating miR-21-5p targeting of TEAD1. hUCMSCs-Exos promoted miR-21-5p and inhibited TEAD1 expression in vivo. miR-21-5p knockdown facilitated TEAD1 expression in vivo. Results were exactly the same in vivo and in vitro AKI models.Conclusions hUCMSCs-Exos protect against AKI by enhancing miR-21-5p/TEAD1 binding in vivo and in vitro.

Atherosclerosis（AS）is a complex multifactorial disease that remains a major cause of high cardiovascular morbidity and mortality despite advances in lifestyle management and pharmacotherapy.MicroRNAs（miRNAs） are a group of small single-stranded noncoding RNAs that regulate a variety of physiological processes and molecular signaling pathways. More and more studies have confirmed that the expression profile of miRNAs plays an important role in the occurrence and development of AS. This article reviews the recent research on the mechanism of miRNAs regulating endothelial cells,vascular smooth muscle cells,inflammatory response and cholesterol homeostasis in AS,and further discusses the value of miRNAs as biomarkers in the diagnosis,efficacy monitoring,and prognosis of AS.

目的 探讨白细胞介素(IL)-1β、可溶性白细胞介素2受体(sIL-2R)、IL-6、IL-8、IL-10、肿瘤坏死因子α(TNF-α)水平与血脂正常的冠心病患者疾病严重程度和Gensini评分的相关性.方法 选取血脂正常的冠心病患者114例,根据临床类型分为稳定型心绞痛(SAP)组、不稳定型心绞痛(UAP)组、急性心肌梗死(AMI)组,以健康体检者74名作为正常对照组.检测所有研究对象IL-1β、sIL-2R、IL-6、IL-8、IL-10和TNF-α水平.分析促炎因子IL-1β、sIL-2R、IL-6、IL-8、TNF-α和抑炎因子IL-10与冠心病严重程度和Gensini评分的相关性.结果 AMI组、UAP组、SAP组IL-1β、sIL-2R、IL-6、IL-8、TNF-α水平依次降低(P<0.05),IL-10水平依次升高(P<0.05).SAP组与正常对照组之间各炎症因子差异均无统计学意义(P>0.05).Spearman相关分析结果显示,IL-1β、sIL-2R、IL-6、IL-8、TNF-α与Gensini评分呈正相关(r值分别为0.742、0.653、0.816、0.711、0.582,P<0.05),IL-10与Gensini评分呈负相关(r=-0.327,P<0.05).结论 血脂正常的冠心病患者IL-1β、sIL-2R、IL-6、IL-8、TNF-α水平显著升高,IL-10显著降低,且与冠心病的严重程度有关.

Objective:To establish the clinical laboratory genetic diagnosis procedures for Marfan syndrome (MFS) and carry out clinical laboratory genetic diagnosis for MFS families.Methods:The second generation high-throughput sequencing was used to sequence and analyze the FBN1 gene of two MFS families who visited to Fuwai Central China Cardiovascular Hospital (Heart Center of Henan People′s Hospital) from January to December 2020, and then Sanger sequencing was used to verify the second generation high-throughput sequencing results. At the same time, the sanger sequencing of mutation sites was performed on normal family members and 100 healthy people to identify the pathogenic mutations of FBN1 gene in the MFS families. The pregnant women of two families were guided for prenatal diagnosis in the second trimester of pregnancy.Results:The clinical laboratory diagnosis of MFS showed that two MFS patients had the pathogenic mutation of c.2560T>C heterozygous mutation and c.6772T>C heterozygous mutation in FBN1 gene, respectively. The mutation was not observed in 100 healthy people and normal members in two families. The prenatal diagnosis showed that there was a heterozygous mutation of FBN1 gene c.2560T>C in the first fetus of the MFS family, which was MFS. There was no mutation in the FBN1 gene in the second fetus of the MFS family, so it was recommended to continue the pregnancy. The results of postpartum follow-up were consistent with the results of clinical laboratory diagnosis.Conclusion:The clinical laboratory genetic diagnosis procedures for MFS have been established successfully, which provides an important reference for clarifying the clinical diagnosis of MFS.

外泌体作为细胞间的通讯载体,可以与邻近细胞或远距离的细胞交换遗传物质和代谢信息,如脂质、核酸和蛋白质.脂质代谢受遗传、神经体液、激素、酶,以及肝脏等组织器官的调节,当以上因素出现异常时,可造成脂质代谢紊乱.外泌体会影响脂质代谢,同样脂质代谢也会影响外泌体的产生、分泌,以及和受体细胞间的相互作用.脂质可以在细胞信号的传递、膜结构的组成和功能中发挥作用,外泌体与脂质代谢相互作用的研究有望成为研究脂质代谢相关疾病诊断和治疗的热点.

LncRNAs are known to regulate a plethora of key events of cellular processes; however, little is known about the function of lncRNAs in autophagy. Here in the current study, we report lncRNA-IGFBP4 which has previously been known to regulate the proliferation and reprogramming of cancer cells, but its role in autophagy is not yet known. We found that serum starvation provokes autophagy-induced downregulation of lncRNA-IGFBP4 levels. Next, we determined that c-Myc can negatively regulate lncRNA-IGFBP4 in HeLa cells. Phenotypically, we found that upon depletion of lncRNA-IGFBP4, the HeLa cells undergo autophagy through ULK1/Beclin1 signaling. Furthermore, through TCGA data analysis, we found lncRNA-IGFB4 overexpressed in most cancers including cervical cancer. Based on these findings, we conclude that c-Myc maintains cellular homeostasis through negatively regulating lncRNA-IGFBP4 in cervical cancer cells.

The emergence of hypervirulent carbapenem-resistant Klebsiella pneumoniae (hv-CRKP) was regarded as an emerging threat in clinical settings. Here, we investigated the prevalence of CRKP strains among inpatients in a new hospital over 1 year since its inception with various techniques, and carried out a WGS-based phylogenetic study to dissect the genomic background of these isolates. The genomes of three representative bla(NDM-1)-positive strains and the plasmids of four bla(KPC-2)-positive strains were selected for Nanopore long-read sequencing to resolve the complicated MDR structures. Thirty-five CRKP strains were identified from 193 K. pneumoniae isolates, among which 30 strains (85.7%) harbored bla(KPC-2), whereas the remaining five strains (14.3%) were positive for bla(NDM-1). The antimicrobial resistance profiles of bla(NDM-1)-positive isolates were narrower than that of bla(KPC-2)-positive isolates. Five isolates including two bla(NDM-1)-positive isolates and three bla(KPC-2)-positive strains could successfully transfer the carbapenem resistance phenotype by conjugation. All CRKP strains were categorized into six known multilocus sequence types, with ST11 being the most prevalent type. Phylogenetic analysis demonstrated that the clonal spread of ST11 bla(KPC-2)-positive isolates and local polyclonal spread of bla(NDM-1)-positive isolates have existed in the hospital. The bla(NDM-1) gene was located on IncX3, IncFIB/IncHI1B, and IncHI5-like plasmids, of which IncFIB/IncHI1B plasmid has a novel structure. By contrast, all ST11 isolates shared the similar bla(KPC-2)-bearing plasmid backbone, and 11 of them possessed pLVPK-like plasmids. In addition, in silico virulome analysis, Galleria mellonella larvae infection assay, and siderophore secretion revealed the hypervirulence potential of most bla(KPC-2)-positive strains. Given that these isolates also had remarkable environmental adaptability, targeted measures should be implemented to prevent the grave consequences caused by hv-CRKP strains in nosocomial settings.

The spread of plasmid-mediated carbapenem-resistant clinical isolates is a serious threat to global health. In this study, an emerging NDM-encoding IncHI5-like plasmid from Klebsiella pneumoniae of infant patient origin was characterized, and the plasmid was compared to the available IncHI5-like plasmids to better understand the genetic composition and evolution of this emerging plasmid. Clinical isolate C39 was identified as K. pneumoniae and belonged to the ST37 and KL15 serotype. Whole genome sequencing (WGS) and analysis revealed that it harbored two plasmids, one of which was a large IncHI5-like plasmid pC39-334kb encoding a wide variety of antimicrobial resistance genes clustered in a single multidrug resistance (MDR) region. The blaNDM-1 gene was located on a ΔISAba125-blaNDM-1-bleMBL-trpF-dsbC structure. Comparative genomic analysis showed that it shared a similar backbone with four IncHI5-like plasmids and the IncHI5 plasmid pNDM-1-EC12, and these six plasmids differed from typical IncHI5 plasmids. The replication genes of IncHI5-like plasmids shared 97.06% (repHI5B) and 97.99% (repFIB-like) nucleotide identity with those of IncHI5 plasmids. Given that pNDM-1-EC12 and all IncHI5-like plasmids are closely related genetically, the occurrence of IncHI5-like plasmid is likely associated with the mutation of the replication genes of pNDM-1-EC12-like IncHI5 plasmids. All available IncHI5-like plasmids harbored 262 core genes encoding replication and maintenance functions and carried distinct MDR regions. Furthermore, 80% of them (4/5) were found in K. pneumoniae from Chinese nosocomial settings. To conclude, this study expands our knowledge of the evolution history of IncHI5-like plasmids, and more attention should be paid to track the evolution pathway of them among clinical, animal, and environmental settings.

目的 探讨河南大学人民医院化脓性肝脓肿患者的临床特点、病原学分布、药敏试验结果 及治疗方法,为化脓性肝脓肿的早期诊断和有效治疗提供理论依据.方法 回顾性收集河南省人民医院2016年6月至2020年8月收治的198例化脓性肝脓肿患者的临床资料,根据细菌培养结果 将肺炎克雷伯菌化脓性肝脓肿(KP-PLA)设为KP-PLA组,大肠埃希菌化脓性肝脓肿(EC-PLA)设为EC-PLA组,分析比较两组患者的临床特点、实验室检查、治疗方法及并发症.结果 198例患者中细菌培养阳性99例,肺炎克雷伯菌培养阳性51例,大肠埃希菌培养阳性14例,共培养出细菌115株,KP-PLA组好发糖尿病(χ2=7.292,P=0.007),EC-PLA组常合并肿瘤(χ2=8.483,P=0.004)和肝胆系统手术史(χ2=6.945,P=0.008),脓肿更易复发(χ2=7.729,P=0.005)且常为多发(χ2=11.061,P=0.001),总胆红素水平相对比较高(t=-2.011,P=0.049),肺炎克雷伯菌对大部分抗菌药物均敏感,大肠埃希菌易出现多重耐药,共培养出超广谱β-内酰胺酶菌株14株,大肠埃希菌占78.6％,发现耐碳青霉烯类肠杆菌1株.本研究大多数患者采用抗菌药物联合超声或CT引导下穿刺引流方案治疗.结论 化脓性肝脓肿患者部分临床表现不典型,其主要致病菌为肺炎克雷伯菌,其次为大肠埃希菌.抗感染联合穿刺引流是化脓性肝脓肿的一线治疗方法,极大地改善了患者预后,应加强耐药检测,合理应用抗菌药物,避免多药耐药及高毒力菌株产生.

Objective:To summarize and analyze the risk of pregnancy recurrence of women with Duchenne muscular dystrophy (DMD) birth history in families with new DMD gene mutations, clarify the laws of DMD gene mutations and discuss the mode of genetic counseling in such families.Methods:Collected DMD families from January 2013 to December 2017 in Henan Provincial People′s Hospital. Firstly, the 79 exons of DMD gene were analyzed by multiplex ligation-dependent probe amplification (MLPA) in DMD patients and their mothers. The families that DMD patients with DMD gene mutations but no mutations in their mothers were selected for this study, and then MLPA combined with STR-gene linkage analysis were used to perform prenatal diagnosis for females in these DMD gene new mutation families.Results:A total of 64 families with new DMD gene mutations were included in this study. All mutations were DMD gene exon deletion mutations. A total of 65 fetuses were conducted prenatal diagnosis, included 26 SRY negative, 39 SRY positive; 63 fetuses′ DMD gene normal and 2 fetues′ DMD gene with exon deletion mutations. The results of postpartum follow-up and prenatal diagnosis were consistent.Conclusions:Exon mutations in newly mutated DMD families were mainly manifested as exon deletion, mainly presented in the 45-55 exon region. For families with new DMD mutations, even if there is no DMD gene mutation in women which had reproductive history of DMD, prenatal diagnosis for DMD during pregnancy was still recommended.

心脏淀粉样变是一类由于前体蛋白发生异常β折叠形成的淀粉样纤维不断浸润损伤心肌细胞,最终导致以心肌舒张功能受损为主要临床表现的心脏疾病.该病临床表现复杂,诊断困难,治疗方法局限,预后差.近年,随着新检测技术的不断发展,心脏淀粉样变的诊断率明显提高.为提高对心脏淀粉样变的认识,推进该病的规范化诊治,本文就心脏淀粉样变的发病机制和实验室检查的研究进展作一综述.

Congenital dysfibrinogenemia (CD) is a rare hereditary fibrinogen disorder characterized by normal fibrinogen antigen levels associated with lower functional activities. The aim of this study is to analyze the phenotype and genotype of a family of CD. Routine coagulation screening tests were performed on the proband, her parents, and her grandparents. Then, the purified genomic DNA extracted from peripheral blood was amplified by PCR, and Sanger sequencing was performed to further confirm the mutation. The prothrombin time and activated partial thromboplastin time of the proband were normal, thrombin time prolonged, and the activity of fibrinogen (Fg:Ac) decreased significantly, but fibrinogen antigen (Fg:Ag) level was normal. The coagulation function indices of the proband's father and grandfather were similar to her, and the indices of her mother and grandmother were normal. Sequencing results showed that the proband had a heterozygous missense mutation in FGA gene c.92G > A, which caused the mutation of amino acid 31 from glycine to glutamic acid (p.Gly31Glu). Her father had the same heterozygous mutation. In conclusion, the proband suffered from CD. The change of Gly31Glu in A chain due to the c.92G > A heterozygous missense mutation in the FGA gene is the cause of CD in the family. To the best of our knowledge, the mutation site is new and first reported so far.

心肌梗死是严重威胁人类健康的心血管疾病之一,它是由于冠状动脉急性、持续性的缺血缺氧所引起的心肌坏死.外泌体是由多囊泡体与细胞膜融合形成的直径30～200 nm的膜性小囊泡.具有细胞间通信功能,能刺激免疫应答,参与抗原呈递、免疫反应、细胞增殖等多种生理过程的调控.外泌体是微小核糖核酸(miRNA)的富集体,miRNA在外泌体双层脂质膜的保护下更能稳定表达,外泌体miRNA参与心血管疾病的病理生理过程,并在心肌梗死患者的诊断、预后、治疗中具有重要价值.本文就外泌体miRNA在心肌梗死诊断和干细胞治疗中的意义作一综述.

Multiple myeloma (MM) is an immunoglobulin-producing tumor of plasma cells, which occurs commonly in the elderly. The incidence of myocardial amyloidosis with MM is extremely low and early clinical manifestations are nonspecific. The diversity of clinical manifestations and first episode symptoms often cause misdiagnosis in young patients with myocardial amyloidosis following MM. In this study, we analyzed the clinical data of a young woman with MM and impaired cardiac function combined with echocardiography, electrocardiography (ECG), laboratory data, cell Congo Red staining, and other manifestations to diagnose amyloidosis. Considering the rapid progression, short survival, and poor prognosis in most patients, a clear, definitive, and timely diagnosis is essential for the treatment of patients with MM complicated with myocardial amyloidosis.

目的 对重症监护病房(ICU)呼吸机相关肺炎病原菌分布及耐药性进行分析.方法 对2017年1月-2019年12月来源于ICU且确诊为呼吸机相关肺炎(VAP)的195例患者的544株病原菌及抗菌药物耐药性进行分析.结果 分离的病原菌中革兰氏阴性菌和革兰氏阳性菌分别占了85.6％和14.4％.其中鲍曼不动杆菌占30.1％,铜绿假单胞菌占12.3％,肺炎克雷伯菌占11.8％,大肠埃希氏菌占10.8％,洋葱伯克霍尔德菌占7.4％,金黄色葡萄球菌占6％.鲍曼不动杆菌和铜绿假单胞菌对抗生素的耐药率很高.2017-2019年肺炎克雷伯菌对亚胺培南的耐药率分别为5.1％,8.3％和24.3％,耐药率显著性升高.结论 革兰氏阴性杆菌是呼吸机相关肺炎最常见的病原菌且耐药率较高.肺炎克雷伯对碳青霉烯类抗生素的耐药率有显著上升.因此,必须合理谨慎的使用碳青霉烯类抗生素以较少耐碳青霉烯肠杆菌克隆株的流行.

Objective To carry out genetic testing and prenatal diagnosis for 90 families affected with spinal muscular atrophy (SMA),and discuss the necessity for carrier screening.Methods All families were subjected to multiplex ligation-dependent probe amplification (MLPA) analysis.Combined MLPA and allele-specific PCR (AS-PCR) was used for prenatal diagnosis of the pregnant women.Results Among the 90 couples,84 (93％) had a negative family history,85 (94％) had given birth to an affected child before.Eighty-five husbands and 88 wives carried heterozygous deletion of exon 7 of the SMN1 gene.Two wives had homozygous deletion of exon 7 of the SMN1 gene and were affected.Prenatal diagnosis showed that 19 fetuses were SMA patients,48 fetuses were carriers,and 23 fetuses were normal.Of note,eighteen affected fetuses were conceived by couples without a family history,which accounted for 20％ of all pregnancies and 95％ of all affected fetuses.Conclusion To screen SMA carriers using MLPA and carry out prenatal diagnosis using combined MLPA and AS-PCR can ensure accurate diagnosis,which has a significant value for the prevention of SMA affected births.

原发性干燥综合征是一种多系统受累的慢性进展性自身免疫病,以外分泌腺受累为主.本病临床起病隐匿,临床表现缺乏特异性,因此,临床漏诊和误诊率较高.本例患者为中年女性,以"D-二聚体升高查因"入院,伴有腰腿痛、胸闷、乏力、咳嗽等不典型临床症状,临床医生结合患者症状及D-二聚体顽固性升高表现,经一系列实验室辅助检查及泪膜影像、唾液腺核素显像检查后,最终确诊"原发性干燥综合征"并给予免疫抑制剂治疗后,患者好转出院.

目的 探讨微小RNA-27a-3p在肝癌细胞增殖与凋亡中的表达.方法 回顾性分析2015年3月至2016年6月期间于我院接受治疗的69例肝癌患者的临床资料,随访3年后,分析是否发生复发患者肝癌细胞内微小RNA-27a-3p的表达情况.结果 经3年随访发现,复发患者有23例,未复发患者有46例;经检测,复发组患者微小RNA-27a-3p表达水平为(0.26±0.13),显著低于未复发组的(0.62±035),差异有统计学意义(P＜0.05);微小RNA-27a-3p表达水平用于预测肝癌患者术后复发风险评估的ROC曲线下面积:AUC=0.948,在微小RNA-27a-3p表达水平临界值为0.375时,可以获得最为理想的敏感度及特异度,分别为:0.913、0.717.结论 微小RNA-27a-3p在肝癌未复发组患者体内表达水平较高,临床可通过提高肝癌患者微小RNA-27a-3p水平,降低肝癌复发率.