高温致金黄地鼠神经管畸形中细胞凋亡的组织学观察

为研究细胞凋亡与高温致神经管畸形的关系，采用核固红－结晶紫染色方法和电镜技术，观察高温后胚胎发育变化。结果显示，高温后８ｈ胚胎发育迟滞，神经管延迟闭合或不闭合，胚胎各段尤期是头部的神经上皮和周围间充质的细胞凋亡比对照组增多，其超微结构改变为染色质浓缩，边聚，核膜皱缩，微绒毛消失并出现异常的包质突起；１６ｈ后细胞凋亡明显增多，胞质内出现了大量空泡，凋亡小体增多；     

肠病型肠道T细胞淋巴瘤临床病理分析

目的通过分析小肠肠病型肠道T细胞淋巴瘤(enter-opathytype Tcell lymphoma,ETCL)患者的临床表现、病理改变,提高临床医师和病理医师对ETCL的认识,以期改善患者的生存率。方法回顾分析2005年2月～2009年7月收治的2例ETCL患者的临床和组织病理学表现;采用免疫组化方法标记CD45RO、CD3、CK、CD20、CD45、CD79α、Pax-5、CD56。结果 2例ETCL患者均有肠病史,确诊后2例均存活但一般情况差。病变均发生于小肠,1例为回肠多发性溃疡性病变,1例为空肠肠穿孔。肿瘤细胞为多形性T细胞,组织学形态为多形性淋巴细胞弥散分布,以血管中心性浸润,淋巴上皮病变,大片或多灶性坏死为特征。2例患者肿瘤组织CD45RO、CD3、CD45、CD56均为阳性。结论 ETCL临床症状多无特异性,病程发展迅猛,预后差,病损肠管表现为多发性溃疡,以穿孔为首发症状者应多取材,避免漏诊。结合免疫组织化学,早期诊治提高患者生存率。     

肠平滑肌细胞在肠道炎性疾病中作用的研究进展

肠平滑肌细胞(ISMC)作为胃肠道主要成员之一,在肠管蠕动、结肠运输、肠道内环境稳态等方面发挥重要作用,其结构及功能改变参与肠道炎性疾病发病过程。肠道炎性疾病常伴肠功能亢进、肠腔狭窄等症状。明确ISMC在肠道炎性疾病中的作用将为其临床治疗提供新思路。     

基于AFM形态学观察的细胞铺展机理的假想

本研究提出了细胞铺展机理的三个可能模型：“橡皮泥”模型、“钢筋混泥土”模型和“自我膨胀”模型。应用原子力显微镜观察了处于不同铺展程度、具有不同形态的人骨髓间充质干细胞的整体和局部外部形貌，并根据观察结果，初步推断“钢筋混泥土”模型可能就是细胞铺展的机理。尽管证据还不够充分，需要进一步的研究，却为今后的研究提供了可能的模型和研究手段。细胞铺展机理的解决必将进一步促进细胞生物学和生物医学工程等学科的发展。     

人羊膜定向诱导胚胎干细胞分化为表皮样细胞机理的初步探讨

目的:初步探讨人羊膜诱导小鼠胚胎干细胞向表皮样细胞定向分化的机理。方法: 小鼠胚胎干细胞与人羊膜在双层6孔培养板中共培养4-5 d,对照组未加羊膜,观察其形态学分化。分别用β₁整合素、角蛋白19/15和套膜蛋白免疫组化检测胚胎干细胞向表皮样细胞的分化。结果: 共培养4-5 d后,小鼠胚胎干细胞分化为表皮细胞样的单层细胞,细胞排列紧密,呈多边形,免疫组织化学染色显示,大部分细胞呈现β₁整合素阳性,少数细胞呈角蛋白19和角蛋白15阳性,未见套膜蛋白阳性细胞,对照组大部分细胞死亡,存活细胞形态各异,未见β₁整合素、角蛋白19/15和套膜蛋白免疫组化染色阳性细胞。结论: 人羊膜分泌的可溶性物质可能对小鼠胚胎干细胞向表皮样细胞分化起重要作用。     

油酸钠对大鼠肠粘膜促胰液素细胞的影响

本研究通过免疫组化方法，观察油酸钠对大鼠小肠粘膜促胰液素细胞的影响。结果表明，十二指肠灌流０．１２ｍｍｏｌ／ｈ后，十二指肠粘膜促胰液素细胞数明显增加，细胞内促胰液素阳性免疫反应物质增加。而对照组和灌流生理盐水组，促胰液素细胞则没有变化。     

细胞外基质蛋白对先天性牙发育畸形的影响及机制

先天性牙发育畸形是指在胚胎发育期间或出生后,牙齿形态或结构异常的一类牙齿疾病。这类畸形可能会对牙齿的生长、咀嚼功能和美观等方面产生影响,严重的还可能影响患者的口腔健康和生活质量。先天性牙发育畸形病因及致病机制复杂,影响牙齿发育的多种因素都可能导致牙发育畸形。细胞外基质蛋白是一类存在于牙齿的细胞外基质中的蛋白质,对牙齿的生长、发育和维持牙齿的健康具有重要作用。本文对细胞外基质蛋白在先天性牙发育畸形中的作用及影响机制进行阐述,为深入理解先天性牙发育畸形的病因、致病机制及防治提供依据。     

肠道营养支持对烧伤大鼠肠粘膜屏障功能的保护作用及其机理

观察不同营养支持途径地严重烧伤所致肠粘膜屏障功能损害的影响并探讨其机制。采用30％体表面积Ⅲ度烧伤大鼠模型,随机分成正常对照（Control),静脉营养（PN）及肠道营养（EN）组,观察了烧伤后肠粘膜屏障功能的变化及PN和EN对其的影响,结果显示,烧伤后肠粘膜通透性,血浆二胺氧化酶（DAO）活性明显高于对照组（P＜0．01）,而肠上皮细胞增殖指数,肠三叶因子（ITF）含量,肠粘液层厚度及己糖和唾液酸的含量则明显降低（P＜0．05）,同PN相比,EN对上述指标均有一定的逆转作用,提示EN较PN更有利于减轻肠粘膜受损程度,促进肠粘膜修复。     

神经元来源细胞外囊泡促进神经干细胞的神经生成

背景：已有研究表明,神经干细胞能够分化为神经元、星形胶质细胞和少突胶质细胞等。间充质干细胞来源细胞外囊泡被证实能够透过血脑屏障到达中枢神经损伤部位,促进神经修复。然而,神经元来源细胞外囊泡是否促进神经干细胞向有益于神经生成的方向分化,帮助神经修复,还不是很明确。目的：探究神经元来源细胞外囊泡是否有利于神经干细胞向神经生成的方向分化。方法：用胰酶消化法从新生SD大鼠大脑皮质中提取神经元和神经干细胞。收集培养神经元的细胞上清,提取神经元来源细胞外囊泡。将培养10 d的神经干细胞与神经元来源细胞外囊泡或PBS共培养7 d,采用免疫印迹、免疫荧光和RT-qPCR技术分别检测神经元、神经干细胞、少突胶质细胞和星形胶质细胞特异性标志蛋白的表达。结果与结论：神经干细胞与神经元来源细胞外囊泡共培养后,高表达神经元特异性蛋白β3微管蛋白、神经丝蛋白200和少突胶质细胞特异性蛋白髓鞘碱性蛋白,低表达星形胶质细胞特异性标志蛋白胶质纤维酸性蛋白。这些结果说明,神经元来源细胞外囊泡能够促进神经干细胞向神经元和少突胶质细胞分化,抑制其向星形胶质细胞分化。     

科学家们将肠道干细胞诱导分化成为不同类型的成熟肠道细胞

<正>据Xiaolei Yin 2013年12月1日(Nat Methods,2013.doi:10.1038/nmeth2737.)报道,美国布莱根妇女医院等的研究者通过研究,使得肠道干细胞不断生长增殖,进而诱导其分化成为不同类型的成熟的肠道组织。对于胃肠道病症,比如克罗恩病及溃疡症等,一般的疗法只能通过药物或者膳食改变来缓解不适的症状,但是如果有一天科学家们开发了一种新型疗法,使用新的肠道组织来替换掉原先炎性的病灶组织,那么对于治疗胃肠道疾病来说将是非常大的进     

Some indices of resistance to hyperthermia in the course of acute radiation sickness

Three hours after irradiation in a dose of 800 rd rats were found to be less resistant to subsequent hyperthermia (45°C) than control animals. An increase in resistance to acute hyperthermia was found at the end of the 3rd day after irradiation. At the climax of radiation sickness (end of the 5th day) the time of onset of heat stroke and the duration of subsequent survival of the rats were indistinguishable from the corresponding values in the control. The dynamics of the response to hyperthermia correlated to some degree with the dynamics of thyroid and adrenal gland function in the irradiated animals.Departments of Pathophysiology and Biochemistry, Smolensk Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR A. P. Avtsyn.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 84, No. 8, pp. 162–164, August, 1977.     

Informativeness of clinical hematologic criteria for the early diagnosis of acute radiation sickness in pig-tailed monkeys

Research Institute of Experimental Pathology and Therapy, Academy of Medical Sciences of the USSR, Sukhumi. (Presented by Academician of the Academy of Medical Sciences of the USSR G. N. Kryzhanovskii.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 108, No. 12, pp. 676–678, December, 1989.     

电离辐射诱导造血干细胞损伤的分子机制研究进展

电离辐射(IR)诱导的造血干细胞(HSCs)损伤是IR后引发机体死亡的主要原因,其损伤机制主要涉及P53-Puma通路诱导HSCs凋亡;激活G-CSF/Stat3/BATF依赖性的分化检验点促进HSCs分化;ROS-P38通路诱导HSCs衰老以及损伤HSCs龛。近期研究为预防和治疗电离辐射引起的骨髓抑制提供了理论基础。     

Dependence of motion sickness in automobiles on the direction of linear acceleration

Summary Thirty-eight normal volunteers were tested in an ambulance car while being accelerated in one of the following positions: (1) sitting upright facing forward in the car, (2) lying supine on a stretcher head forward, (3) supine position head backward. Consecutive short periods of negative horizontal acceleration (0.7–0.95 g) were achieved by brisk braking manoeuvres of the car, followed by weak reacceleration (0.15 g). Motion sickness symptoms were observed and recorded after each experiment using a special motion sickness scaling index which was weighted according to the strength of any particular symptom. The results indicate that horizontal linear acceleration in a car, such as experienced during multiple braking manoeuvres, is an effective motion sickness provoking stimulus. Negative X-axis stimulation is more nauseogenic then acceleration in the Z-axis stimulation is more nauseogenic then acceleration in the Z-axis of the body.     

Hyperbaric oxygen treatment reduced the lung injury of type II decompression sickness

Objective: To detect the ultrastructural changes in rabbits with type II decompression sickness (DCS), and study the therapeutic effects of hyperbaric oxygen (HBO). Methods: Twenty-seven male New Zealand rabbits were randomly divided equally into the DCS group, HBO treatment group and control group. Experimental models of each group were prepared. Lung apex tissues were harvested to prepare paraffin- and EPON812-embedded tissues. Results: In the DCS group, macroscopic and histological examination revealed severe and rapid damage to lung tissue. Ultrastructural examination revealed exudation of red blood cells in the alveolar space. Type I alveolar epithelial cells exhibited retracted cell processes and swollen mitochondria, and type II cells showed highly swollen mitochondria and decrease in cytoplasmic lamellar bodies. Dilatation and congestion of capillary vessels were accompanied by swelling of endothelial cells and incomplete basement membrane. In the HBO treatment group, the findings were somewhat similar to those in the DCS group, but the extent of damage was lesser. Only a small amount of tiny bubbles could be seen in the blood vessels. Type I alveolar epithelia cells and endothelial cells of the capillaries illustrated slight shortening of cells, swollen cytoplasm and decreased cell processes. Type II alveolar epithelial cells showed slight swelling of the mitochondria, decreased vacuolar degeneration of lamellar bodies, and increase in the number of free ribosomes. Conclusions: Our microscopic and ultrastructural findings confirm that the lung is an important organ affected by DCS. We also confirmed that HBO can alleviate DCS-induced pulmonary damage.     

豚鼠胆囊胆固醇结石形成过程中肠道传输功能下降的细胞及分子机制探讨

目的探讨豚鼠胆囊胆固醇结石形成过程中肠道传输功能下降的细胞和分子机制及其与胆石形成的关系。方法健康雄性豚鼠40只,4周龄,体质量120～125g。将其随机分为实验组与对照组,每组20只。实验组给予致石饲料（胆固醇含量2%）,对照组给予正常颗粒饲料。8周造模结束后,用逆转录聚合酶链反应（RT-PCR）检测小肠组织中c-kit及scf的mRNA的表达情况,利用末端回肠全层铺片免疫荧光化学染色及激光共聚焦显微镜观察各组Cajal样间质细胞（ICCs）数量的变化。结果 RT-PCR结果显示,与对照组相比,实验组豚鼠小肠c-kit（0.316±0.056vs0.912±0.103;t=6.582,P〈0.01）和scf（0.499±0.012 vs 0.899±0.124;t=6.163,P〈0.01）的mRNA水平的表达量下降;对照组豚鼠回肠ICCs平均阳性面积为（56.24±2.68）%,实验组为（22.26±1.14）%,较对照组明显降低（t=15.256,P〈0.01）。结论饮食诱导的豚鼠胆囊胆固醇结石形成过程中,小肠c-kit和scf基因mRNA表达水平下降,ICCs数量明显减少。c-kit/scf通路抑制可能参与胆囊胆固醇结石的形成过程中肠道传输功能下降的发生。     

The effect of cinnarizine and cocculus indicus on simulator sickness

Pensacola Simulator Sickness Questionnaire (SSQ) is a valuable method to analyse symptoms evoked by exposure to a flight simulator environment that can also be adopted to evaluate the effectiveness of preventive tools, aiming at reducing simulator sickness (SS). In this study we analysed SSQ data in subjects undergoing a standard ground based spatial disorientation training inside a flight simulator, in order to evaluate the SS prevention obtained with two different pharmacological tools. Twelve males volunteers participated to an experimental design based on a double-blind, balanced administration of either 30 mg cinnarizine (CIN), or Cocculus Indicus 6CH (COC), or placebo (PLC) before one trial of about one hour spent inside a spatial disorientation trainer. All subjects underwent the three different conditions (CIN, COC, PLC) during 3 non-consecutive days separated by at least 2 weeks. During each experimental day, all subjects filled in SSQ. In addition, both postural instability (with the use of a static stabilometric platform), and sleepiness symptoms were evaluated. All the tests were performed before and after the simulated flight, at different times, in one-and-half-hour intervals. Results indicated a strong increase of sickness after flight simulation that linearly decreased, showing pre-simulator scores after 1.30 hours. In contrast to both PLC and COC, CIN showed significant side effects immediately following flight simulation, with no benefit at the simultaneous SSQ scores. Globally, no highly significant differences between COC and PLC were observed, although a minor degree of postural instability could be detected after COC administration. As far as the present exposure to a simulator environment is concerned, none of the pharmacological tools administered in this study resulted effective in reducing SS symptoms as detected by the SSQ. Moreover, CIN significantly increased sleepiness and postural instability in most subjects.     

Participation of endothelial cells in the development of glomerulosclerosis: a study on murine serum sickness nephritis with mitomycin C

To investigate the participation of endothelial cells in glomerulosclerosis, the study was performed in serum sickness nephritis (SSN) with administration of mitomycin C (MMC). SSN was induced in 8 week male Fisher rats by sensitizing them with albumin, chicken egg (EA). Then MMC (0.5 mg/kg bodyweight) was injected daily for 3 days and they were killed at 1, 2, 4 and 6 week intervals. Significant mesangial expansion and sclerosis were observed in the experimental mixed SSN-MMC group in comparison to the SSN or MMC control group from 1 week to 6 weeks (P < 0.05). Moreover at 1 week, double contour appearance of the glomerular capillary wall, basement membrane splitting and disruption were observed light microscopically in the mixed SSN-MMC group. Electron microscopy revealed peripheral capillary basement membrane disruption with huge subepithelial, mesangial osmiophilic deposits and epithelial foot process effacement. At 6 weeks, disappearance of the endothelial cell fenestration and subepithelial basement membrane-like material formation were observed in the MMC group. Based on these results, it is suggested that MMC induced assault on the glomerular endothelial cell produces prominent glomerular capillary basement membrane disruption at the early phase of SSN, resulting in the accumulation of huge subepithelial and mesangial deposits, mesangial cell proliferation, production of the extracelluar matrix component and initiation of glomerulosclerosis.     

Effects of glomerular macrophages on mesangial cells in rat serum sickness glomerulonephritis: A comparison of histological and co-culture studies

Effects of glomerular macrophages on mesangial cell proliferation at different stages of experimental serum sickness nephritis (SSN) in the rat were examined using a direct co-culture system. The results were compared with the manifestations of glomerular tissue at the same points in time during the course of the SSN, especially with regard to glomerular infiltration and glomerular cell proliferation. Macrophages were isolated from the glomeruli at different points in time during the course of the SSN. While the number of glomerular macrophages increased during the sensitization, the proliferating cell nuclear antigen/cyclin positivity of the glomerular tissue was increased after cessation of the antigenic sensitization. The effect of macrophages on mesangial cell proliferation was relatively diminished during the sensitization but was augmented thereafter. Proliferating cells were mostly attached by macrophages, suggesting the importance of the proximity of macrophages for mesangial proliferation. These results suggest that mesangial cell proliferation is largely influenced by macrophage function variability in the glomeruli during the course of SSN.