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超微病理

超微病理的相关文献在1990年到2022年内共计123篇,主要集中在基础医学、遗传学、水产、渔业 等领域,其中期刊论文111篇、会议论文12篇、专利文献269561篇;相关期刊79种,包括证据科学、厦门大学学报(自然科学版)、集美大学学报(自然科学版)等; 相关会议12种,包括中华医学会2015年器官移植年会、中华中医药学会第十次全国中医外治学术会议暨贵州省针灸学会2014年学术年会、第十三届华东六省一市肾脏病会议、上海市医学会肾脏病分会春季论坛、福建省医学会肾脏病分会学术年会等;超微病理的相关文献由381位作者贡献,包括孙异临、曲宝清、王国良等。

超微病理—发文量

期刊论文>

论文:111 占比:0.04%

会议论文>

论文:12 占比:0.00%

专利文献>

论文:269561 占比:99.95%

总计:269684篇

超微病理—发文趋势图

超微病理

-研究学者

  • 孙异临
  • 曲宝清
  • 王国良
  • 李德忠
  • 周晓军
  • 王素霞
  • 张翠萍
  • 章友康
  • 陆珍凤
  • 马捷
  • 期刊论文
  • 会议论文
  • 专利文献

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    • 张芳成; 程丹; 孙小玲; 肖艺; 官阳
    • 摘要: 目的:观察儿童遗传代谢性肝病的肝组织超微病理学改变特征,结合临床资料探讨电镜检查在诊断该类疾病中的作用。方法:收集2016年7月-2020年10月以肝大、肝功能不良等为主要临床表现,临床怀疑为遗传代谢性肝病的72例肝穿刺活检标本,电镜观察肝组织的超微结构改变。结果:遗传代谢性肝病患儿均有不同程度的肝大、肝酶升高等表现。肝穿刺活检电镜下显示不同程度的肝细胞损害及各自相应的特征性超微病理改变。电镜观察提示肝糖原累积症53例,其中肝糖原累积症Ⅰ型49例,Ⅱ型(Pompe病)2例,Ⅳ型2例,肝-豆状核变性13例,尼曼-匹克病5例,黏多糖累积症1例。结论:电镜观察肝组织超微病理学改变对于儿童遗传代谢性肝病的诊断有重要帮助,可明显提高诊断率。
    • 周瑶佳; 欧阳萍; 田思璐; 许佳雪; 李尹麒; 杨悦; 耿毅; 黄小丽; 陈德芳; 汪开毓
    • 摘要: 为探究疾病病因和流行特点,对患病鲫进行剖检、病理学观察、分子生物学检测及人工感染实验.结果 显示,患病鲫临床表现为离群独游、浮头、全身发黑及体表出血等.剖检发现鳃、肝脏、肾脏等器官出血、肿胀和坏死,鳔点状出血.组织病理观察显示,鳃呼吸上皮细胞肿胀、坏死及脱落;肾脏局灶性坏死;脾脏组织广泛变性坏死,造血系统崩解;肝脏发生空泡变性和坏死.透射电镜观察到脾脏和肾脏中存在4种大小不同的病毒颗粒,分别为DNA病毒内核、空衣壳、实心衣壳和有包膜的成熟病毒粒子.未成熟的病毒粒子存在于细胞核,成熟的病毒粒子存在于细胞质.电镜下可见鲤疱疹病毒Ⅱ型(CyHV-2)在细胞核内完成核酸复制和核衣壳装配,囊膜蛋白在出核后获得.细胞核萎缩、核染色质边缘化,线粒体肿胀、坏死、嵴断裂,细胞质空泡化.取患病鲫组织匀浆滤菌后接种到鲤上皮瘤细胞系(epithelioma papulosum cyprinid cell line,EPC)和胖头鲤肌肉细胞系(fathead minnow cell line,FHM),盲传3代后未见细胞病变.通过腹腔注射患病鲫组织匀浆进行人工感染实验,实验组鲫表现出与自然感染鲫相同的临床症状,对照组鲫正常,实验组累积死亡率为80%.用PCR方法检测CyHV-2的解旋酶基因片段,扩增出预期大小相符的目的 条带.利用邻近法对该病毒的解旋酶基因进行系统发育分析,结果显示与CyHV-2(YZ-01)的同源性为99%.以上实验结果证实了CyHV-2是导致这次疾病暴发的原因.
    • 王亚琼; 吴强; 周胜利; 吴金浪
    • 摘要: 目的:报道1例罕见的X连锁肌病伴过度自噬(X-linked myopathy with excessive autophagy,XMEA)的电镜超微病理观察.方法:分析患者的临床资料并对股四头肌进行病理活检电镜超微结构检测.结果:本例患者男性,5岁,因肌无力入院,智力正常,自行从蹲位转换为站位困难,下肢可见萎缩,肌力下降,血清肌酸激酶(CK)值明显升高,>3000 U·L-1,心电图正常,心脏传导无异常.股四头肌活检电镜超微结构观察到肌节中和肌膜下有大量聚集自噬体,内含大小不一致密颗粒和糖原颗粒等无定型物质.XMEA临床表现容易误诊为duchenne型肌营养不良和Becker型肌营养不良、包涵体肌病、重度肌无力综合症等肌病,电镜超微结构分析和DNA检测,可避免误诊.
    • 杨宗英; 曾柳根; 王玉兰; 姚毅; 侯玉洁; 雷小青; 许亮清; 熊春贤; 杨先乐
    • 摘要: 采用透射电镜技术和生化分析等方法,对患"水瘪子"病病蟹的超微病理和病理生理进行研究.超微结构观察表明,病蟹肝胰腺、鳃、肌肉等组织细胞发生了不同程度的病变,主要表现为肝细胞变性、坏死,脂滴锐减,微绒毛肿胀、断裂,细胞内线粒体肿胀,内嵴紊乱、减少甚至消失形成空泡,内质网扩张或断裂为片层状结构;鳃上皮细胞角质膜变薄,细胞核异染色质化,角质层面伸出的指状突起破裂消失,上皮细胞顶膜形成的微绒毛杂乱、断裂甚至消失,角质膜下空腔增大,线粒体畸变,数量减少,内嵴减少,形成空泡,溶酶体数量增多,并与空泡和空泡化的线粒体形成自噬体,严重病变的鳃上皮细胞中出现细菌颗粒,未见包涵体等病毒样颗粒;肌肉的病变主要是肌纤维松弛、断裂,肌质网溶解消失或者形成小泡,线粒体数量减少、体积变小,细胞核固缩且边缘化.病理生理分析结果显示,病蟹血淋巴中血糖含量和谷草转氨酶活力显著高于健康蟹,碱性磷酸酶和谷丙转氨酶活力极显著高于健康蟹,甘油三酯的含量极显著低于健康蟹;病蟹肝胰腺中肝糖原含量极显著低于健康蟹,碱性磷酸酶和酸性磷酸酶活力显著低于健康蟹.
    • 严爽; 火子榕; 尹晓玲; 张治华
    • 摘要: 目的 探讨囊/实性前庭神经鞘膜瘤超微病理及生物学特性的差异.方法 收集15例囊性前庭神经鞘膜瘤(cystic vestibular schwannoma,CVS)肿瘤组织作为实验组,15例实性前庭神经鞘膜瘤(solid vestibular schwanno-ma,SVS)作为对照组,通过光镜及透射电子显微镜观察并分析肿瘤组织超微结构,用特异性LC3单克隆抗体进行免疫组化标记,观察自噬在其中的表达量.结果 电镜下CVS瘤体及囊壁均可见典型自噬体,在SVS瘤体则未见;免疫组织化学检测显示,自噬标记蛋白LC3在SVS瘤体、CVS瘤体及囊壁中阳性率分别为13.3%,60.0%,和73.3%, SVS瘤体中,LC3表达量显著低于CVS瘤体(P=8×10-4)及CVS囊壁(P=1.2×10-5).结论 自噬水平的调控与改变在前庭神经鞘膜瘤囊性变中可能发挥重要作用.%Objective Experiments were conducted to demonstrate differences of ultrastructural pathological changes and biological characteristics between cystic and solid vestibular schwannoma. Methods Cystic vestibular schwannoma (CVS) specimens collected from 15 patients (study group), as well as specimens of solid vestibular schwannoma(SVS)(control group,n=15)were studied by light microscopy and transmission electron microscopy.The specimens were stained with LC3 monoclonal antibodies to demonstrate expression of autophagy. Results Under the electron microscope,typical autophagosomes were seen in CVS,but not in SVS.The rates of positive LC3 immunohis-tochemistry staining was 13.3%,60.0% and 73.3% in SVS tumor body,CVS tumor body and CVS cyst wall,respective-ly.In SVS,the expression of LC3 was significantly lower than in CVS.Conclusions The regulation of autophagy may play an important role in the cystic degeneration of vestibular schwannoma.
    • 严爽; 火子榕; 尹晓玲; 张治华
    • 摘要: 目的 探讨囊/实性前庭神经鞘膜瘤超微病理及生物学特性的差异.方法 收集15例囊性前庭神经鞘膜瘤(cystic vestibular schwannoma,CVS)肿瘤组织作为实验组,15例实性前庭神经鞘膜瘤(solid vestibular schwanno-ma,SVS)作为对照组,通过光镜及透射电子显微镜观察并分析肿瘤组织超微结构,用特异性LC3单克隆抗体进行免疫组化标记,观察自噬在其中的表达量.结果 电镜下CVS瘤体及囊壁均可见典型自噬体,在SVS瘤体则未见;免疫组织化学检测显示,自噬标记蛋白LC3在SVS瘤体、CVS瘤体及囊壁中阳性率分别为13.3%,60.0%,和73.3%,SVS瘤体中,LC3表达量显著低于CVS瘤体(P=8×10-4)及CVS囊壁(P=1.2×10-5).结论 自噬水平的调控与改变在前庭神经鞘膜瘤囊性变中可能发挥重要作用.
    • 高超; 刘阳; 王宇飞; 张雪松; 徐维盛; 杨月欣
    • 摘要: [Objective] To investigate the protective role of curcumin in intense swimming-triggered dysfunction focused on hepatic mitochondria.[Method] Adult male BALB/C mice were randomly divided into four groups including rested controls,intense exercise,intense exercise + curcumin (100 mg/kg body weight) and rested plus curcumin (100 mg/kg body weight) pretreatment.Curcumin was administrated for 4 weeks and intense exercise program (swimming for 90 min/d) was performed concurrently at the fourth week.Immediately upon final swimming,the mice were sacrificed.Serum alanine aminotransferase (ALT),aspartate transaminase (AST),and hepatic ultrastructural malformation were examined.Hepatic mitochondrial membrane potential (MMP) and respiratory control ratio (RCR) were measured.[Result] Compared to swimming group,curcumin intervention decreased intense swinmming-triggered the leakage of ALT (P < 0.05) and AST (P < 0.05) and hepatic ultrastructural malformation.Curcumin pretreatment evidently alleviated mitochondrial dysfunction by inhibiting the decline of membrane potential (P < 0.05) and respiratory control ratio (P < 0.05) in hepatic mitochondria of intense swimming mice.[Conclusion] Curcumin exhibited protective role in intense exercise-induced hepatic mitochondrial ultrastructural damage and dysfunction,highlighting a promising strategy for sports anti-fatigue by naturally occurring phytochemicals.%目的:探讨姜黄素对大强度游泳运动小鼠肝脏线粒体功能紊乱的拮抗作用.方法:成年雄性BALB/C小鼠随机分为安静对照组、运动对照组、运动+姜黄素组[100 mg/(kg·d)]和安静+姜黄素组[100 mg/(kg·d)].干预期为4w,干预期最后1w同时进行游泳运动训练,每天训练90 min,每天采用上述方式游泳运动7d,动物末次运动完成后处死.观察肝脏超微病理形态改变,测定血清谷丙转氨酶、谷草转氨酶水平,以及肝脏线粒体膜电位、呼吸控制率等线粒体功能学指标.结果:与安静对照组相比,姜黄素干预明显抑制了大强度运动导致的小鼠血清谷丙转氨酶(P<0.05)和谷草转氨酶(P<0.05)水平的上升,减轻了运动导致的肝细胞线粒体超微病理结构异常.姜黄素干预显著抑制了运动导致的小鼠肝脏线粒体膜电位(P<0.05)和呼吸控制率水平(P<0.05)的下降.结论:姜黄素对大强度运动小鼠肝细胞线粒体超微结构损伤和功能紊乱具有良好的拮抗作用,为天然植物化学物应用于抗运动疲劳提供新的前景方向.
    • 高超; 刘阳; 赵佳; 张雪松; 王宇飞; 杨月欣
    • 摘要: 目的:探讨姜黄素对急性游泳训练小鼠骨骼肌损伤的保护作用.方法:成年雄性BALB/C小鼠随机分为安静对照组、运动对照组、运动+姜黄素组[100 mg/ (kg·d)]和安静+姜黄素组[100 mg/ (kg·d)].干预期为4w,干预期最后1w同时进行游泳运动训练,每天训练90min,采用以上运动方式连续运动7d,末次运动完成后即刻处死小鼠.测定血清肌酸激酶(CK)含量及骨骼肌超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、活性氧(ROS)和丙二醛(MDA)水平,并观察骨骼肌普通及超微病理学改变.结果:与运动对照组相比,姜黄素干预明显抑制了游泳运动导致的小鼠血清CK水平的上升(P<0.01),减轻了运动导致的骨骼肌普通及超微病理结构异常.姜黄素干预显著抑制了运动导致的小鼠骨骼肌GSH水平的下降(P<0.05),同时拮抗了ROS和MDA含量水平的上升(P<0.01).结论:姜黄素对小鼠急性游泳训练导致的骨骼肌损伤具有明显的抗氧化保护作用.%[Objective] To investigate protective effect of curcumin against intense swimming training-induced skeletal muscle damage.[Method] Adult male BALB/C mice were randomly divided into 4 groups including rested controls,intense exercise,exercise + curcumin(100 mg/kg BW) and rested plus curcumin (100 mg/kg BW) supplementation.Curcumin was administrated for 4 weeks and exercise program (swimming for 90 min/d) was performed concurrently at the fourth week.Immediately upon final exercise,the mice were sacrificed.Serum creatine kinase and skeletal muscle ultrastructural malformation were examined.SOD,GSH,ROS,and MDA of skeletal muscle were analyzed.[Result] Compared to exercise group,curcumin treatment declined intense swinmming-triggered the leakage of creatine kinase (P < 0.01) and skeletal muscle uhrastructural malformation.Curcumin pretreatment evidently alleviated oxidative stress by inhibiting glutathione depletion (P < 0.05),ROS over-generation (P < 0.01),and lipid peroxidation in skeletal muscle of intense exercise mice (P <0.01).[Conclusion] Curcumin exhibited antioxidative protective role in intense exercise-induced injuries of skeletal muscle.
    • 胡新月; 胡成平; 罗丽莎; 唐薇; 冯俊涛
    • 摘要: 目的:报道1例原发性纤毛运动障碍(primary ciliary dyskinesia,PCD)患者的临床和病理资料,总结其临床特征和诊治要点.方法:对1例可疑原发性纤毛运动障碍患者进行病史采集、体格检查、胸部X线和CT、肺功能检查、支气管镜检查及支气管黏膜活检、电镜超微病理观察、染色体检查等相关检查,确诊为原发性纤毛运动障碍.结合该例患者诊治过程进行文献分析,明确原发性纤毛运动障碍的诊治要点及注意事项.结果:该例患者具有咳嗽、喘息等呼吸道症状,胸部X线及CT提示肺部感染及脏器全反位;肺功能提示基本正常且支气管激发试验为阴性;支气管镜检查示支气管反位及支气管炎症,取黏膜活检提示支气管黏膜慢性炎症改变;超微病理发现气道上皮细胞呈现形态扁平化、纤毛极性消失、细胞内纤毛,纤毛动力臂结构未见异常;染色体检查:46,XX,400-550条带阶段未见染色体异常;确诊为原发性纤毛运动障碍.结论:原发性纤毛运动障碍临床少见且复杂多样,容易漏诊和误诊.临床症状、胸部影像学、纤毛超微结构观察以及基因检测等相关检查联合应用有助于原发性纤毛运动障碍的临床诊断和治疗.对于呼吸道感染迁延不愈并发内脏反位者,无论有无鼻窦炎和支气管扩张,均应考虑原发性纤毛运动障碍存在可能,应当及时进行呼吸道黏膜超微病理学检查,以便尽早进行诊断和干预,减少和延缓并发症的发生.%Objective:To report the clinical and pathological data of one case of primary ciliary dyskinesia (PCD),analyze and summarize the clinical characteristics and key points for the diagnosis and treatment of PCD.Methods:History collection,physical examination,chest X-ray and CT,pulmonary function tests,bronchoscopy and bronchial mucosal biopsy,ultrastructural observation of electron microscopy,chromosome inspection were performed to diagnose one suspected PCD patient.The key points and announcements for diagnosing PCD were more clearly via analyzing the process of diagnosis and treatment of patient and related literature.Results:Firstly,The patient had cough and wheezing.Lung infection and viscera trans were detected by chest X-ray and CT.Secondly,lung function was normal and bronchial provocation test was negative.Bronchial trans and bronchial inflammation was observed by bronchoscopy while bronchial mucosal chronic inflammation change was found by bronchial mucosal biopsy.Moreover,we can see epithelial cells formed fat,cilium polarity was disappeared,cilium was inside cells,but the arm structure of cilium power was no exception through the ultrastructural observation of electron microscopy.Checking of Chromosome,46,XX,400-550 band stage,was suggested regularly.According to the detection results described above,the patient could be diagnosed with PCD.Conclusions:PCD,a rare and complicated kind of disease,is easily misdiagnosed.The combined applications of clinical symptoms,chest radiographic,cilium ultrastructural observation of electron microscopy and genetic test were contributed to diagnosis and treatment of PCD.To avoid missing diagnosis,the detection of ultrastructural pathology in airway tract is very necessary for the patients who suffered form recurrent infections combined with situs inversus.
    • 陈晨; 孙异临; 张在强; 李少武; 张岩; 王芹芹; 张翠萍; 皇埔秉轩
    • 摘要: 目的:探讨线粒体脑肌病的超微病理特点和发病机制.线粒体脑肌病MELAS (mitochondrial encephal myopathy with lactic acidosis and strokelike episodes)是一种以卒中样发作同时伴有血乳酸增高为主要临床表现的线粒体病,病因为遗传性基因缺陷所致.方法:对19例线粒体脑肌病患者肌肉活检标本的超微病理变化及核磁共振特点进行分析.结果:研究提示核磁共振检查MELAS病患者大脑颞、顶、枕皮层可见不按血管解剖学分布的梗死样病灶;电子显微镜检查见病变肌细胞内线粒体形态异常,出现矩阵样结晶包涵体结构.结论:MELAS的诊断需结合临床、病理、电镜、影像、血清学和基因检查,其中肌肉活检的电子显微镜检查可作为金标准.%In this paper,ultrastructural pathological change and MRI feature of muscle biopsy specimens of mitochondrial myopathy in 19 cases were analyzed.MRI examination indicated that there were infarct-like lesions in cerebral temporal,top and occipital cortex,the vascular distribution was not according to anatomy.Electron microscopy showed abnormal mitochondrial morphology changes in muscle cells and matrix like crystalline inclusions structure.MELAS diagnosis should be combined with clinic,pathology,electron microscopy,imaging,serology and genetic examination,of which the electron microscopic diagnosis of the muscle biopsy is the most important.
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