Background migration of USPIO/MLs is a major drawback for in situ labeling of endogenous neural progenitor cells

MR‐labeling of endogenous neural progenitor cells (NPCs) to follow up cellular migration with in vivo magnetic resonance imaging (MRI) is a very promising tool in the rapidly growing field of cellular imaging. To date, most of the in situ labeling work has been performed using micron‐sized iron oxide particles. In this work magnetoliposomes (MLs), i.e. ultrasmall superparamagnetic iron oxide cores (USPIOs), each individually coated by a phospholipid bilayer, were used as the MR contrast agent. One of the main advantages of MLs is that the phospholipid bilayer allows easy modification of the surface, which creates the opportunity to construct a wide range of MLs optimized for specific biomedical applications. We have investigated the ability of MLs to label endogenous NPCs after direct injection into the adult mouse brain. Whereas MRI revealed contrast relocation towards the olfactory bulb, our data strongly imply that this relocation is independent of the migration of endogenous NPCs but represents background migration of MLs along a white matter tract. Our findings suggest that the small size of USPIOs/MLs intrinsically limits their potential for in situ labeling of NPCs. Copyright © 2010 John Wiley & Sons, Ltd.     

幽门螺杆菌根除前后胃癌组织中MUC5AC表达的变化

目的调查幽门螺杆菌（Hp）根除前后的胃癌组织中MUC5AC表达的变化。方法采用Western Blot 和 PCR RT-PCR方法检测根除Hp前后的胃癌组织中MUC5AC蛋白及mRNA的相对含量。以Hp阴性的胃癌组织作为对照组。结果胃癌组织中MUC5AC蛋白及mRNA的表达在根除Hp后较根除前明显增高（P〈0.05）,但仍然明显低于对照组。Hp阳性胃癌组织中MUC5AC的表达明显低于Hp阴性胃癌组织的表达;转移淋巴结数目大于5的Hp阳性胃癌组织中的MUC5AC相对含量明显低于Hp阴性胃癌组织。结论胃癌组织中Hp感染与MUC5AC的降低相关,但是它可能不是胃癌组织中MUC5AC减少的唯一因素,MUC5AC的减少可能只是Hp引起胃癌的一个中间环节,但可能是胃癌发生和进展的一个重要因素。     

An approach towards molecular imaging of activated platelets allows imaging of symptomatic human carotid plaques in a new model of a tissue flow chamber

The development of magnetic resonance imaging (MRI) contrast agents targeting epitopes in atherosclerosis is of general interest. In particular, early detection of activated platelets as key players in plaque rupture could provide improved triage of patients. However, so far the efficiency of contrast agents targeting human pathologies can only be examined in animal experiments, which do not necessarily reflect human in vivo conditions. We therefore describe application of a contrast agent targeting activated human platelets in an MRI tissue flow chamber, allowing detection and characterization of contrast agent binding. Microparticles of iron oxide (MPIO) were conjugated to an antibody targeting ligand‐induced binding sites (LIBS) on the activated platelet glycoprotein IIb/IIIa‐receptor or to control antibody, resulting in LIBS–MPIO or control–MPIO contrast agent. Human endarterectomy specimens from patients with acute stroke or transient ischemic attack were imaged ex vivo before and after contrast agent perfusion using a 9.4 T MRI system. Specimens were measured under static (n = 18) or flow conditions (n = 18) in a specially designed flow chamber setup, simulating physiological conditions in a stenosed vessel. A significant MPIO‐induced negative contrast was achieved in MRI by LIBS–MPIO in specimens under static and flow conditions (LIBS–MPIO vs control–MPIO: p < 0.01), and the location of LIBS–MPIO binding corresponded well between histology and MRI (p < 0.05). The number of MPIOs per platelet area on endarterectomy specimens in histology was significantly higher with LIBS–MPIO (p < 0.001). Furthermore, the intensity of contrast agent binding and signal change showed the potential to reflect the severity of clinical symptoms. LIBS–MPIO allows the detection of activated platelets on the surface of symptomatic atherosclerotic human plaques using molecular MRI. Furthermore, the MRI tissue flow chamber setup described could help to evaluate binding properties of contrast agents, and might therefore be an interesting tool for contrast agent development from animal experiments towards clinical application. Copyright © 2012 John Wiley & Sons, Ltd.     

A novel foam fluid negative contrast medium for clear visualization of the colon wall in CT imaging

Computed tomography (CT) imaging is a valuable tool for the diagnosis of colorectal diseases. However, the colonic wall depiction in 2D CT images is usually poor because of the low contrast between the colonic wall and the luminal content. In order to improve the visualization of the colonic wall and any abnormality on its surface, we report in this paper the development of an oil‐free foam fluid negative contrast medium for improved CT imaging of the colon. The foam fluid negative contrast medium was prepared by dispersing and stabilizing microbubbles in a polymeric solution. The stabilities of both the individual bubbles and the foam fluid system were optimized by incorporating bovine serum albumin and gluconolactone as the stabilization agent. The medium had a mean X‐ray density of ?120 Hounsfield units (close to that of the extraluminal tissues), and enabled clear 2D visualization of the colonic wall in both ex vivo and in vivo imaging studies. The measured colonic wall thicknesses at different segments in a beagle dog based on the 2D CT images obtained with the negative contrast medium accurately reflected the anatomical values, as compared with the values based on air‐contrasted images. In vivo study of a simulated polyps pig model demonstrated sensitive detection of 11 out of 12 polyps with the smallest one 2 mm in diameter. We believe this new and safe foam fluid negative medium would enable the implementation of CT imaging as a convenient and useful tool for diagnosis of colon cancer, especially in the elderly population. Copyright © 2011 John Wiley & Sons, Ltd.     

Antibody‐mediated cell labeling of peripheral T cells with micron‐sized iron oxide particles (MPIOs) allows single cell detection by MRI

Labeling cells with iron oxide is a useful tool for MRI based cellular imaging. Here it is demonstrated that peripheral rat T cells can be labeled in whole blood, in vitro, with streptavidin‐coated micron‐sized iron oxide particles (MPIOs), achieving iron concentrations as high as 60 pg iron per cell. This is 30 times the amount of labeling reported with ultrasmall particles of iron oxide (USPIOs). Labeling was mediated by use of a biotinylated anti‐CD5 antibody, which is specific for peripheral T cells. Such labeling allowed the in vitro detection of single lymphocytes by MRI, using conditions well suited for in vivo animal work. Electron microscopic analysis demonstrated that MPIOs remained largely extracellular after labeling, with some evidence of intracellular uptake. Cell viability and early and late cytokine release studies showed no significant differences between labeled and unlabeled cells. Therefore, the use of MPIOs for achieving high iron concentrations for cellular MRI is potentially an effective new modality for non‐invasive imaging of lymphocytes. Published in 2007 by John Wiley & Sons, Ltd.     

Preparation and characterization of peptide modified ultrasmall superparamagnetic iron oxides used as tumor targeting MRI contrast agent

As desirable contrast agents for magnetic resonance imaging (MRI), ultrasmall superparamagnetic iron oxides (USPIOs) are required to exhibit both low cytotoxicity and specific targetability besides superparamagnetism to achieve better imaging contrast at lower dose, and cladding with biocompatible polymers and modification with targeting ligands are considered to be the most effective strategies. In this study, novel dextran wrapped and peptide WSGPGVWGASVK (peptide-WSG) grafted USPIOs were meticulously prepared and systematically characterized. Firstly, dextran (Dex) cladded USPIOs (USPIOs@Dex) were synthesized with a well-designed co-precipitation procedure in which the biocompatible dextran played dual roles of grain inhibitor and cladding agent. After that, sodium citrate was applied to carboxylize the hydroxyls of the dextran molecules via an esterification reaction, and then tumor targeting peptide-WSG was grafted to the carboxyl groups by the EDC method. The XRD, TEM, and FTIR results showed that inverse spinel structure Fe₃O₄ crystallites were nucleated and grown in aqueous solution, and the catenulate dextran molecules gradually bound on their surface, meanwhile the growth of grains was inhibited. The size of original crystallite grains was about 7 nm, but the mean size of USPIOs@Dex aggregates was 165.20 nm. After surface modification by sodium citrate and peptide-WSG with ultrasonic agitation, the size of the USPIOs@Dex-WSG aggregates was smaller (66.06 nm) because the hydrophilicity was improved, so USPIOs@Dex-WSG could evade being eliminated by RES more easily, and prolong residence time in blood circulation. The VSM and T₂-weighted MRI results showed that USPIOs@Dex-WSG were superparamagnetic with a saturation magnetization of 44.65 emu g⁻¹, and with high transverse relaxivity as the R₂ relaxivity coefficient value was 229.70 mM⁻¹ s⁻¹. The results of MTT assays and the Prussian blue staining in vitro revealed that USPIOs@Dex-WSG exhibited nontoxicity for normal cells such as L929 and HUVECs, and were specifically targeted to the SKOV-3 cells. Thus, the novel dextran wrapped and WSG-peptide grafted USPIOs have potential to be applied as tumor active targeting contrast agents for MRI.

As desirable contrast agents for magnetic resonance imaging (MRI), ultrasmall superparamagnetic iron oxides (USPIOs) modified with targeting ligands are considered to be the most effective strategies to achieve better imaging contrast at lower dose.     

Airway mucins promote immunopathology in virus-exacerbated chronic obstructive pulmonary disease

The respiratory tract surface is protected from inhaled pathogens by a secreted layer of mucus rich in mucin glycoproteins. Abnormal mucus accumulation is a cardinal feature of chronic respiratory diseases, but the relationship between mucus and pathogens during exacerbations is poorly understood. We identified elevations in airway mucin 5AC (MUC5AC) and MUC5B concentrations during spontaneous and experimentally induced chronic obstructive pulmonary disease (COPD) exacerbations. MUC5AC was more sensitive to changes in expression during exacerbation and was therefore more predictably associated with viral load, inflammation, symptom severity, decrements in lung function, and secondary bacterial infections. MUC5AC was functionally related to inflammation, as Muc5ac-deficient (Muc5ac^–/–) mice had attenuated RV-induced (RV-induced) airway inflammation, and exogenous MUC5AC glycoprotein administration augmented inflammatory responses and increased the release of extracellular adenosine triphosphate (ATP) in mice and human airway epithelial cell cultures. Hydrolysis of ATP suppressed MUC5AC augmentation of RV-induced inflammation in mice. Therapeutic suppression of mucin production using an EGFR antagonist ameliorated immunopathology in a mouse COPD exacerbation model. The coordinated virus induction of MUC5AC and MUC5B expression suggests that non-Th2 mechanisms trigger mucin hypersecretion during exacerbations. Our data identified a proinflammatory role for MUC5AC during viral infection and suggest that MUC5AC inhibition may ameliorate COPD exacerbations.     

Development of a functional human bronchial model of mucin secretion

In an attempt to study the functional aspects of respiratory mucin secretion and the effects of mediators of inflammation on the release of M1/MUC5AC mucins in airways diseases, an ex vivo human bronchial model of mucin secretion was developed. Anti-M1 mucin monoclonal antibodies raised against the peptidic core of ovarian cyst M1 mucins were used. PAS and Alcian blue stainings of sections of bronchial rings revealed the presence of mucins in epithelial goblet cells as well as in glandular mucous cells. Immunohistochemical labelling of these sections with anti-M1 monoclonal antibodies revealed a preferential localization of M1/MUC5AC mucins in epithelial goblet cells. Functional studies were performed on this bronchial model using various secretagogues (methacholine, leukotrienes D4 and anti-human immunoglobulin E antibodies). No statistical difference of M1/MUC5AC mucin secretion was observed after a one-hour stimulation of bronchial rings with these agents. The development of an ex vivo functional human bronchial model of mucin secretion and the use of specific anti-M1 antibodies are essential tools in studying the regulation of the M1/MUC5AC mucin release from human airways.     

北京大学首钢医院社区大肠癌筛查调查分析

目的总结本院社区大肠癌筛查及结肠镜检查结果,探讨进一步提高癌前病变和早期大肠癌检出率、减少大肠癌发病率的方法。方法2016年3月至2018年9月对本院所属四个社区卫生服务中心消化科就诊患者进行问卷调查及粪便潜血试验,针对高危人群进行结肠镜检查,对结肠镜检查结果进行分析。结果参与筛查及完成结肠镜检查的女性患者均多于男性;息肉总检出率为35.6%,男性检出率(42.6%)高于女性(31.7%)(P<0.05);腺瘤总检出率为29.3%,男性检出率(35.5%)高于女性(25.8%)(P<0.05)。结论对无明显症状的社区居民进行大肠癌筛查,尤其是男性居民,可提早发现并处理癌前病变和早期大肠癌,有效降低大肠癌的发病率。     

Exocyst复合物关键亚基Sec3蛋白在气道黏液高分泌中的作用研究

目的 探讨Exocyst复合物关键亚基Sec3蛋白在气道黏液高分泌形成过程中的作用.方法 将60只大鼠随机分成3组:正常对照组,烟雾暴露组、烟雾暴露+人中性粒细胞弹性蛋白酶(HNE)组.烟雾暴露组大鼠采用烟雾暴露法建立慢性支气管炎症病理性改变,HNE攻击形成气道黏液高分泌大鼠模型.取肺组织支气管上皮,观察气道上皮杯状细...     

Systemic analysis of the differential gene expression profile in a colonic adenoma-normal SSH library

BACKGROUND: The discovery of differentially expressed genes of colonic adenoma minus normal mucosa enables the understanding of early molecular events in colorectal carcinogenesis. In our previous study, we have developed an adenoma minus normal mucosa suppression subtractive hybridization (SSH) library and identified 109 differentially expressed clones. METHODS: An in-house EST pipeline and the Gene Ontology web-based tool () were used to analyze these clones. Realtime quantitative RT-PCR (Q-PCR) was applied to detect the expression of 14-3-3 zeta, REG4 and 6 ribosomal protein genes (RPS2, RPS12, RPS27A, RPL5, RPL7a and RPL10a) in 14 adenomas (8 with concurrent cancers) and 44 colorectal adenocarcinomas with paired normal mucosa. RESULTS: Sixty-two candidate genes were obtained from this library. Bioinformatics analysis indicated that both ribosomal protein genes and immune-related genes were enriched. REG4 was significantly upregulated in colorectal adenomas (medium fold: 1.676, p<0.05, Wilcoxon test) and 14-3-3 zeta in cancers (medium fold: 1.202, p<0.01, Wilcoxon test), as compared with those of paired normal mucosa. However, all ribosomal protein genes were not significantly overexpressed in colorectal adenomas or cancers. CONCLUSIONS: A differential gene expression profile in A-N SSH library may be helpful in understanding the molecular mechanism of colorectal cancer initiation and progression. REG4 and 14-3-3 zeta may be potential biomarkers for early colorectal cancer detection.     

Immunomodulatory Effect of Linezolid on Methicillin-Resistant Staphylococcus aureus Supernatant-Induced MUC5AC Overexpression in Human Airway Epithelial Cells

Linezolid is the first member of the oxazolidinones and is active against drug-resistant Gram-positive pathogens, such as methicillin-resistant Staphylococcus aureus (MRSA). Additionally, linezolid shows an immunomodulatory effect, such as inhibition of inflammatory cytokine production. In this study, we examined the effect of linezolid on MRSA-induced MUC5AC overexpression in airway epithelial cells. In this study, an MRSA supernatant was used to avoid the direct effect of linezolid on MRSA. MUC5AC protein production was significantly increased with a 40-fold dilution of MRSA supernatant. At the mRNA level, MUC5AC gene expression was significantly increased 6 and 9 h after stimulation. In an inhibition study, linezolid significantly reduced MRSA-induced MUC5AC protein and mRNA overexpression at concentrations of 5 and 20 μg/ml, which were the same as the trough and peak concentrations in human epithelial lining fluid. In an analysis of cell signaling, among the mitogen-activated protein kinase inhibitors, only the extracellular signal-regulated protein kinase 1/2 (ERK1/2) inhibitor reduced the MUC5AC protein production to the same level as that of the control; on Western blot analysis, only ERK1/2 was phosphorylated by the MRSA supernatant. In addition, the ERK1/2 phosphorylation was inhibited by linezolid. MUC5AC and MUC5B are the major barrier that traps inhaled microbial organisms, particulates, and foreign irritants. However, in patients with chronic respiratory diseases, pathogen-induced MUC5AC overexpression causes many problems, and control of the overexpression is important. Thus, this study revealed that linezolid showed a direct immunomodulatory effect in airway epithelial cells.     

Imaging monocytes with iron oxide nanoparticles targeted towards the monocyte integrin MAC‐1 (CD11b/CD18) does not result in improved atherosclerotic plaque detection by in vivo MRI

Imaging of macrophages with superparamagnetic iron oxide particles (SPIO) has been performed to improve detection of atherosclerotic plaque inflammation in human and mouse studies by molecular magnetic resonance imaging (MRI). Since affinity of the monocyte/macrophage integrin MAC‐1 (CD11b/CD18) is upregulated in inflammation, we generated a contrast agent targeting CD11b (CD11b‐SPIOs) for improved macrophage detection in plaques. CD11b‐SPIOs and non‐targeted SPIOs (control‐SPIOs) were incubated in vitro with human monocytes/macrophages. As quantified by SPIO‐induced MRI signal extinction, intracellular iron‐content was significantly higher in monoytes/macrophages incubated with CD11b‐SPIO than with control‐SPIO in vitro (p < 0.05), suggesting an improved uptake of CD11b‐SPIOs into monocytes. Therefore, the aortic arch (AA) and vessel branches of ApoE^?/?‐knockout mice on a Western‐type diet were imaged before and 48 h after contrast agent injection of either CD11b‐SPIOs or control‐SPIOs, using a 9.4 T animal MRI system. The SPIO‐induced change in the MRI signal was quantified, as well as the macrophage‐content by anti‐CD68 immunhistochemistry and the iron‐content by Prussian‐blue staining. However, SPIO‐induced signal extinction in in vivo‐MRI was similar in CD11b‐SPIO and control‐SPIO‐injected animals, with a non‐significant trend towards an improved uptake of CD11b‐SPIOs in the subclavian artery and subsections of the AA. These data correlated well with the results obtained by histology. Although in vitro MRI‐data indicated an increased uptake of targeted CD11b‐SPIOs in monocytes/macrophages, in vivo mouse data do not allow improved atherosclerotic plaque detection compared WITH non‐targeted SPIOs. Therefore, CD11b‐targeted MRI contrast labelling of monocytes/macrophages does not seem to be a successful strategy in stable atherosclerotic plaques such as found in the ApoE^?/?‐knockout‐model. However, the impressive correlation between MRI and histology data encourages further development of inflammation‐ and plaque‐specific contrast agents for vulnerable plaque imaging. Copyright © 2010 John Wiley & Sons, Ltd.     

Survivin表达对良、恶性胃溃疡鉴别的临床意义

目的:研究生存素(Survivin)在良、恶性胃溃疡中的表达及其相关性与临床意义。方法:选择良性胃溃疡、有癌前期病变的胃溃疡和溃疡型胃癌病理标本,采用免疫组化S-P染色法检测病理组织中survivin的表达,用AB-PAS法检测区分伴有肠化胃溃疡的结肠化生及小肠化生。结果:Survivin在溃疡型胃癌中的阳性表达明显高于良性胃溃疡(P<0.01),在有癌前病变胃溃疡中的表达明显高于无癌前病变的胃溃疡(P<0.01),伴有结肠化生中的表达高于小肠化生(P<0.05),伴有肠化的胃溃疡中的表达高于有不典型增生胃溃疡中的表达(P<0.05),在溃疡型胃癌中的表达与有癌前病变胃溃疡中的表达无明显统计学意义(P>0.1)。结论:对于有癌前期病变的胃溃疡患者,检测胃黏膜survivin表达水平,并动态随访survivin表达水平的变化,可能对胃溃疡的演变和良、恶性胃溃疡的鉴别有一定的临床价值。     

Adenovirus-Mediated MUC1 gene transduction into human blood-derived dendritic cells

MUC1 protein is widely expressed on various human cancer cells and has a specific highly glycosylated core structure with multiple tandem repeats, which may include an immunogenic peptide sequence. The potency of MUC1 protein to induce human histocompatibility leukocyte antigen-class I-restricted cytotoxic T-lymphocyte (CTL) induction remains to be fully clarified in human beings. In the current study, we made MUC1-expressing human dendritic cells (DCs) using recombinant adenovirus vector. Adenovirus vector plasmid containing human MUC1 cDNA, pAdHM4-MUC1 was constructed using in vitro ligation with a shuttle vector, pHMCMV5. Adenovirus vector expressing MUC1 was generated by the transfection of PacI-digested recombinant vector plasmid into 293 cells. Human blood DCs were obtained from 7-day culture of monocytes with recombinant human (rh) granulocyte-macrophage (GM) colony-stimulating factor (CSF) and (rh)interleukin (IL)-4. Then, 1 x 10(6) DCs were incubated with viral supernatant at a multiplicity of infection of 200 for 24 h in the presence of rhGM-CSF and rhIL-4. Flow cytometric analysis showed that 30% to 40% of the transduced DCs expressed MUC I protein; by contrast, nontransduced or transduced DCs with mock virus expressed only small amounts of MUC1 protein. Adenovirus-mediated MUC1 gene transduction into DCs had no significant effect on DC surface marker expressions or functions such as mixed leukocyte reaction. Furthermore, MUCI-specific CD8+ CTLs could be induced from healthy donor blood lymphocytes using MUC1-expressing DCs as stimulators. These results suggested that MUC1 gene-transduced DCs are a functional and potent tool for triggering a CTL response against MUC1 cancer cells.     

Inactivating cholecystokinin-2 receptor inhibits progastrin-dependent colonic crypt fission,proliferation, and colorectal cancer in mice

Hyperproliferation of the colonic epithelium, leading to expansion of colonic crypt progenitors, is a recognized risk factor for colorectal cancer. Overexpression of progastrin, a nonamidated and incompletely processed product of the gastrin gene, has been shown to induce colonic hyperproliferation and promote colorectal cancer in mice, but the mechanism of pathogenesis has not been defined. Cholecystokinin-2 receptor (CCK2R) is the primary receptor for cholecystokinin (CCK) and amidated gastrin. Here, we show that Cck2r was expressed in murine colonic crypts and upregulated in the transgenic mice that overexpress human progastrin. Murine deletion of Cck2r abrogated progastrin-dependent increases in colonic proliferation, mucosal thickness, and β-catenin and CD44 expression in the colon tumor. In addition, either deletion or antagonism of Cck2r resulted in the inhibition of progastrin-dependent increases in progenitors expressing doublecortin and CaM kinase–like-1 (DCAMKL1), stem cells expressing leucine rich repeat–containing G protein–coupled receptor 5 (LgR5), and colonic crypt fission. Furthermore, in the azoxymethane mouse model of colorectal carcinogenesis, Cck2r deletion in human progastrin–overexpressing mice resulted in markedly decreased aberrant crypt foci formation and substantially reduced tumor size and multiplicity. Taken together, these observations indicate that progastrin induces proliferative effects, primarily in colonic progenitor cells, through a CCK2R-dependent pathway. Moreover, our data suggest that CCK2R may be a potential target in the treatment or prevention of colorectal cancer.     

HIF-1α与MUC5AC、MUC5B mRNA在慢性鼻-鼻窦炎中的表达水平与其相关性

目的探讨缺氧诱导因子1α(HIF-1α)与MUC5AC、MUC5B mRNA在慢性鼻-鼻窦炎(CRS)中的表达水平及其相关性。方法选取2014年5月至2015年5月于辽宁中药大学附属医院进行治疗的80例伴鼻息肉CRS患者、80例不伴鼻息肉CRS患者以及80例无CRS健康者(对照组)。收集并处理3组鼻窦黏膜,采用半定量反转录聚合酶链反应法(RT-PCR)检测HIF-1α与MUC5AC、MUC5B mRNA的表达,并分析其相关性。结果在伴或不伴鼻息肉CRS患者中,HIF-1α、MUC5AC、MUC5BmRNA的相对表达量分别为:1.35±0.85、1.35±0.91,0.80±0.55、0.79±0.49,1.18±1.01、1.21±1.02,而在对照组中,它们的相对表达量分别为:0.42±0.33,0.43±0.36,0.47±0.43,CRS组与对照组比较,差异具有统计学意义(P0.05)。伴或不伴鼻息肉CRS患者HIF-1α与MUC5AC、MUC5BmRNA均呈正相关(r=0.476、P=0.023;r=0.476、P=0.026;r=0.478、P=0.035;r=0.508、P=0.021)。受试者工作特征曲线分析结果显示曲线下面积=0.956 4。结论 HIF-1α与MUC5AC、MUC5BmRNA在CRS中的表达水平明显升高,且HIF-1α与MUC5AC、MUC5BmRNA存在密切联系。     

379例结肠憩室病的临床特点及内镜表现

目的通过回顾电子结肠镜检出结肠憩室患者的资料,分析结肠憩室发病特点及其与伴发疾病的相关性。方法回顾性分析2014年6月-2019年5月该院13 638例行电子结肠镜检查的内镜资料,采用SPSS 19.0统计软件分析结肠憩室患者检出情况及内镜下组织表现,以及其与伴发疾病的相关性。结果共发现结肠憩室379例,检出率为2.78%,呈逐年升高趋势,由1.79%增长至3.35%,第5年较第1年检出率明显提高(P 0.05)。结肠憩室发病与结肠息肉、结肠癌、结肠脂肪瘤、结肠黏膜黑变病和肠道手术史呈正相关(P 0.05),与缺血性结肠炎无明显相关性(P 0.05)。结论 5年间电子结肠镜下结肠憩室检出率明显升高,结肠憩室检出率与结肠息肉、结肠癌、结肠脂肪瘤、结肠黑变病及肠道手术史均有相关性。