一例疑似黏膜病死亡麋鹿消化及主要免疫器官病理组织学观察

应用常规石蜡切片,H.E染色,对临床初步诊断为黏膜病的一例死亡麋鹿（Elaphodus davidianus）的消化系统及脾、淋巴结进行病理组织学观察。结果表明,消化道的病变主要在黏膜层,黏膜上皮细胞脱落、坏死,固有层内毛细血管充血,炎性细胞浸润 脾主要表现为急性败血型,红髓充血、出血严重,白髓几乎完全消失 淋巴结坏死严重,组织结构被破坏,界限不明显,仅见淋巴细胞弥漫性分布于整个淋巴结内。病理组织学观察为临床诊断提供了形态学依据。     

嗜麦芽寡养单胞菌胞外产物对斑点叉尾损伤的病理学研究

采用硫酸铵盐析从嗜麦芽假单胞菌培养物中提取其胞外产物,通过腹腔注射方式,进行了嗜麦芽假单胞菌(P.maltophilia)胞外产物对斑点叉尾(Ictalurus punctatus)损伤的系统病理学研究。结果表明,嗜麦芽假单胞菌胞外产物具有较强的毒力,对斑点叉尾(42.5±4.4)g的半致死剂量(LD50)为3.21mg蛋白/kg体重。病鱼出现神经症状,腹部和下颌充血、出血,腹部膨大,腹腔内充满大量淡黄色或带血的腹水,胃肠道黏膜充血、出血,肠套叠,肝、脾、肾肿大等临床病变。组织学病变主要表现为全身多组织、器官水肿,出血、变性、坏死以及炎症反应,特别是脑、骨骼肌、肝、脾、肾和胃肠道的损伤较为严重。超微结构观察发现病鱼肝、脾、肾和骨骼肌等器官的细胞的超微结构均有较为严重的破坏,线粒体肿胀,嵴断裂或溶解消失,呈空囊状,内质网扩张,细胞核变形,染色质溶解或固缩;研究中还发现嗜麦芽假单胞菌胞外产物可致淋巴细胞凋亡,脾和肾间质内淋巴细胞均表现为细胞核染色质浓缩边移,或核固缩成一个或数个团块凝聚在核膜周边,形成凋亡小体。       

乙酸诱导建立大鼠急性直肠黏膜损伤模型的形态学观察

目的通过形态学观察评价乙酸诱导建立急性直肠黏膜损伤模型的效果。方法将含有4%乙酸溶液的棉签经SD大鼠肛门置入直肠1 min,置入深度为3 cm,诱导大鼠形成急性直肠黏膜损伤,并于损伤后0.5 h和1、4、6 d分别解剖大鼠,对直肠进行大体形态观察和组织病理学分析。结果损伤后大鼠6 d内全部存活,模型成功率为100%。损伤后0.5 h~1 d,大鼠直肠黏膜大体形态由充血、水肿和溃疡到合并出血,镜下形态见黏膜层由上皮组织坏死伴出血到黏膜组织全层坏死,腺体由部分留存到全无,黏膜下层由水肿到合并充血、出血,间质内由血管扩张充血到炎细胞浸润;损伤后4~6 d,直肠黏膜大体形态仍可见部分水肿和血丝,镜下形态见黏膜上皮有部分留存,损伤部位有炎性肉芽组织增生,黏膜充血、出血减轻。结论 4%乙酸作用于直肠1 min能成功诱导建立大鼠急性直肠黏膜损伤模型,该模型操作方便、成功率高、重复性好,损伤维持时间6 d以上,适合作为快速筛选直肠外用药物疗效的动物模型。     

荧光假单胞菌感染大鲵的病理损伤

通过对感染荧光假单胞菌(Pseudomonas fluorescents)发病的大鲵(Andrias davidianus)主要器官进行病理剖解和病理组织学观察,以明确大鲵感染荧光假单胞菌引起的病理学损伤特点。结果表明,大鲵感染荧光假单胞菌后,主要表现为腹部极度膨胀、腹水和严重胃肠道反应,严重者可见将胃呕吐至口腔;组织器官具有典型的病理变化,其主要靶器官为肾、肝、肠道、皮肤和肌肉。分别引起坏死性肾小球肾炎、肝炎。此外,还可引起轻微肠炎及皮炎。可在肾小管管腔内、肝细胞坏死灶内、肠道固有层内及皮肤肌肉中发现数量极多的杆状细菌。     

家兔生后外周淋巴器官的组织形态学研究

本文探讨了不同发育阶段家兔淋巴结和脾的组织学年龄性变化,研究结果表明:1.初生时期淋巴结和脾脏均未达到成年水平,淋巴结皮质较薄,且呈弥散性;髓质琉松,含结缔组织较多,淋巴细胞稀少。2.具有生发中心的淋巴小结和脾小体在30日龄时出现。3.网状纤维在淋巴结主要分布于淋巴小结的外周;在脾白髓区域的网状纤维丰富而粗大。     

广东乌龟五种器官的组织学观察

利用石蜡切片法对广东乌龟的心脏、肝脏、脾脏、肺和肾脏等组织器官进行了组织结构观察.结果显示,心肌纤维束状排列,可见闰盘结构.肝脏分3叶,肝内结缔组织很少,相邻肝小叶分界不清.肝血窦内含色素细胞.脾脏分被膜和实质两部分.实质可分为白髓和红髓.白髓包括椭球周围淋巴鞘(PELS)和动脉周围淋巴鞘(PALS).红髓由脾索和脾窦组成.未发现淋巴小结和生发中心.肺为一对长形扁平囊.支气管黏膜上皮为假复层柱状纤毛上皮.细支气管的黏膜为单层柱状纤毛上皮.肺泡囊状.肾脏由肾小体、颈段、近曲小管、中间段、远曲小管、收集管等部分构成.颈段和中间段均由单层纤毛立方上皮细胞构成.近曲小管、远曲小管和收集管均由单层柱状上皮细胞构成.     

大鼠急性坏死型胰腺炎病理特征评定方法的研究

目的　以大鼠胆源性胰腺炎模型为对象 ,比较国外相关的评分标准 ,探讨这一实验模型合理、准确的病理学评定方法。方法　 4 8只SD大鼠分善宁 (16只 )、对照 (2 1只 )和假手术 (11只 )不同处理组 ,胰胆管内注射牛磺胆酸钠诱发大鼠急性坏死型胰腺炎 ,参照Schmidt等普通病理学评分标准并加以改进 ,结合电镜超微结构观察等 ,评定不同标准的病理组织学评分的准确性。结果　急性坏死型胰腺炎大鼠解剖时见大量红色腹腔渗液 ,最多者达体重的 6 % ;光镜下见胰腺组织明显出血、腺细胞坏死 ;小叶破坏 ,结构紊乱 ,小叶间隔大量红细胞 ;肝脏、心脏、肺和肾脏也出现组织充血、出血等。不同处理组的 4项组织学评分标准显示Schmidt方法不能显示组间出血的严重程度 ,炎症、水肿、坏死 3项过于繁冗。以高倍镜下间隔红细胞数平均值和分级评分比较 ,组间出血显示显著性差异。结论　 1)腹腔大量红色渗液、胰腺组织出血坏死、微血管内微血栓形成和胰外多器官损伤等是这一模型的特征 ;2 )在简化Schmidt评分标准中水肿、坏死、炎症等 3项和出血指标以及间隔红细胞数和分级统计的基础上 ,作者提出新的标准 ,以更为准确合理地评定大鼠急性坏死型胰腺炎的病理组织学特征。     

应用绿色荧光蛋白标记迟缓爱德华菌感染斑马鱼

目的建立斑马鱼模型研究迟缓爱德华菌的致病性及感染途径。方法应用绿色荧光蛋白标记迟缓爱德华菌,追踪观察其感染斑马鱼的动力学过程及病理组织学变化。结果病理组织学检查以肝脏水肿变性,肝细胞萎缩、坏死、脱落,脾脏散在增生性结节、充血、水肿、淋巴细胞大量缺失等病变为主;感染后,该菌先后在斑马鱼肠道、鳃和皮肤中定植。结论斑马鱼可作为研究迟缓爱德华菌致病性的动物模型。肠道、鳃和皮肤可能是迟缓爱德华菌先后感染斑马鱼的主要途径。     

赛加羚羊部分器官组织学结构观察

为了解世界濒危物种、国家Ⅰ级保护野生动物赛加羚羊（Saiga tatarica）主要器官组织的结构特征,本研究利用石蜡组织切片技术,对1只因胎衣不下死亡的雌性成年赛加羚羊心、肝、脾、肺、肾的组织结构进行了观察。赛加羚羊心肌纤维发达,呈圆柱状,有分支,其胞核位于细胞边缘,各心肌纤维分支末端相互连接构成肌纤维网,闰盘明显。肝组织致密,间质少,肝小叶分界不清,切面呈不规则的多边形,肝细胞以中央静脉为中心呈放射状排列。脾的被膜较厚,脾小梁由被膜和脾门的结缔组织伸入脾实质形成,相互连接构成脾的粗支架;实质部分可明显分为白髓和红髓,白髓主要分布在脾内小动脉周围,其内部脾小结形状为圆形或椭圆形;红髓主要分布于白髓区周围,其内充满大量的红细胞。肺实质导气部主要可见细支气管和终末细支气管,其中,细支气管的管腔面富含纵行皱襞,黏膜上皮为假复层柱状纤毛上皮;呼吸部可见大量的肺泡管、肺泡囊和肺泡,肺泡结构清晰可见。肾为平滑单乳头肾,由被膜和实质构成,实质可明显分为皮质与髓质,皮质内可见大量肾小体和少量结缔组织。总体而言,与其他同类型反刍动物相比较,赛加羚羊各主要器官的组织结构未见有明显差异。     

小鼠腹腔注射硫酸铍的病理形态学观察

目的研究腹腔注射硫酸铍（BeSO4.4H2O）对小鼠主要脏器的损害作用。方法将30只6周龄昆明（KM）雄性小鼠随机分为三组,分别予以不同剂量硫酸铍生理盐水溶液腹腔注射染毒,隔日一次,染毒两周。观察主要脏器的病理组织学变化并测定脏器系数。结果与对照组比较,染毒组心、脾、肾、睾丸脏器系数无显著差异,肝、肺脏器系数差异有统计学意义（P〈0.05）;对照组肺、肝病理学组织检查未见异常,低剂量组小鼠肺组织可见淤血、出血、支气管扩张出血,肺泡腔内有少量炎性渗出物、支气管周围炎、间质性肺炎、小叶性肺炎等;高剂量组小鼠肺组织可见支气管扩张出血,支气管腔内有大量炎性渗出物,支气管周围肺泡扩张,间质性肺炎、小叶性肺炎、融合性小叶性肺炎;低剂量组肝细胞水肿,可见点状坏死和小灶性坏死;高剂量组小鼠肝组织损伤严重,肝细胞排列紊乱,多数肝细胞呈细胞水肿,肝细胞胞质成空泡状,可见明显的点状坏死和小灶性坏死,并伴有炎细胞浸润,坏死区周围肝细胞细胞质呈嗜酸性变,轻度核固缩,并且肝细胞呈不同程度的胞质疏松,肝窦以及肝中央静脉扩张有广泛变性、坏死等病理改变。睾丸、心、脾、肾未见明显异常。结论小鼠腹腔注射本试验剂量的硫酸铍后主要引起肺组织和肝脏损伤,其它脏器未见明显异常。     

STUDIES ON LYMPHOCYTES

Continuous extracorporeal irradiation of the circulating blood (ECIB) of from 3 to 501/2 hr duration was used to study in the calf the differential depletion of lymphocytes from spleen, lymph nodes and thymus as compared to blood and thoracic duct lymph. The cell content of tissues was measured by planimetry and/or test point analysis. Lymphocyte depletion by ECIB from various lymphoreticular organs, and from different areas within a given organ, was less than in the circulating blood or the thoracic duct lymph and varied from one site of a lymphoreticular organ to another. The degree of depletion with time followed an exponential function with at least two components. The first component corresponded to a relatively rapid fall and the second to a very slow reduction in lymphocyte content. The former is related to the elimination of an easily mobilizable pool of lymphocytes while the latter corresponds to a more sessile mass of lymphocytes which exchange with blood lymphocytes very slowly. Elimination of the easily mobilizable pool of lymphocytes by ECIB from all tissues studied was observed within 10–15 hr, indicating that the rate of exchange with blood is similar for this group of cells in various lymphoreticular tissues. The size, however, of the easily mobilizable vs the more sessile pools of lymphocytes may vary considerably, the best estimates for the former being as follows (in per cent of total lymphocyte mass): lymph node medulla, less than 10%; lymph node cortex plus paracortical zone, 18% (depletion mainly paracortical); red pulp of the spleen, 37%; densely populated white pulp of the spleen, 55%; and loosely populated white pulp of the spleen, 60%. In comparison, the approximate fractions of lymphocytes originating fromthe easily mobilizable pools in various lymphoreticular tissues plus the cells already circulating a t the onset of EClB correspond to 64% for the thoracic duct lymph and 78% for the circulating blood respectively. These findings are discussed in relation to production, recirculation and life span of lymphocytes, and immune reactions.     

Septicemic listeriosis in a reindeer calf

Septicemic listeriosis is described in a 2-day-old reindeer calf (Rangifer tarandus tarandus) from a local zoo. The gross and microscopic lesions were typical of disease caused by bacterial septicemia. Major lesions included necrosis of the liver, lung, adrenal gland, spleen, and lymph node. The diagnosis was suspected by special histopathological stains and confirmed by isolation of Listeria monocytogenes from multiple organs. This is the first report of listeriosis in a reindeer.     

Antigenic relationship between medullary thymocytes and a subpopulation of peripheral T cells in the rat: description of a masked antigen.

Using differentially absorbed rabbit antisera to rat thoracic duct cells, an antigen is described which normally is expressed on the surface of T cells in thoracic duct lymph and lymph node, but which exists in a masked form on medullary thymocytes and apparently not at all on cortical thymocytes. This antigen is termed the rat masked thymocyte antigen (RMTA). RMTA on medullary thymocytes can be unmasked mechanically by sectioning in a cryostat or enzymatically by treating with neuraminidase. Trypsin destroys or removes RMTA. Nearly all the T cells in thoracic duct lymph and lymph node are RMTA⁺, whereas only 58–66% of T cells in spleen are RMTA⁺. RMTA⁺ T cells, which are cortisone resistant, reside in the paracortex and periarteriolar sheath regions of lymph node and spleen. RMTA^? T cells, which are cortisone sensitive, appear to reside in the red pulp of spleen. The results suggest that (i) two antigenically distinct populations of T cells exist in the rat, RMTA⁺ and RMTA^? T cells, (ii) medullary thymocytes are the immediate precursors of RMTA⁺ T cells, and (iii) cortical thymocytes may be the immediate precursors of RMTA^? cells.     

人体胸腺和周围淋巴器官内T细胞亚群和NK细胞分布的研究

本文用多种Ｔ细胞和ＮＫ细胞单抗和免疫组织化学的ＡＢＣ技术,在冰冻切片上对人扁桃体、淋巴结、牌和胸腺内Ｔ细胞亚群和ＮＫ细胞的分布进行了检测。结果显示,ＣＤ５、ＣＤ８、ＣＤ４、ＣＤ３和ＡＩＧ３阳性细胞主要分布在扁桃体,淋巴结的副皮质区、脾的动脉周围淋巴鞘和胸腺,但各种抗体的反应强度不同。从各种Ｔ细胞工群的染色强度和形状看,胸腺髓质部的胸腺细胞相当于周围淋巴器官内的胸腺依赖区。胸腺内Ｔ细胞在分化过程中,质膜上的抗原也有相应变化。ＮＫ细胞主要分布在淋巴小结的生发中心,淋巴结和扁桃体的副皮质区,脾的红髓以及胸腺的筋质部。这些不同的分布,说明ＮＫ细胞不仅与淋巴小结的活动有关,可能还参与机体的免疫调节功能。     

Immunohistochemical analysis of human peripheral blood and lymphoid tissues using monoclonal antibodies immunoreactive with non-lymphoid cells

Immunoperoxidase methods were used to study human peripheral blood and lymphoid tissues using a panel of monoclonal antibodies to non-lymphoid cells. The majority of peripheral blood monocytes were immunoreactive for LeuM1, LeuM2, LeuM3 and LeuM5. Rare peripheral blood monocytes were immunoreactive for R4/23. The different antibodies showed characteristic patterns of immunoreactivity in peripheral lymphoid tissues. LeuM1 was immunoreactive with scattered cells in the paracortex of lymph node and tonsil and with many cells in the marginal zone of the spleen. LeuM2 was immunoreactive with endothelial cells in lymph node and tonsil. A few cells in the red pulp of the spleen were immunoreactive for LeuM2. LeuM3 and R4/23 showed distinctive immunoreactivity in germinal centers of secondary follicles, giving a "lacy" pattern. LeuM3 was also immunoreactive with endothelium in lymph node and tonsil and with sinus lining cells in lymph node. LeuM5 was immunoreactive with macrophages in the germinal center, fibroblastic reticulum cells in the mantle zone and interdigitating reticulum cells in the paracortex of lymph node and tonsil.     

Differential response of B cells in the lymph node and the spleen to bacterial lipopolysaccharide

In vivo polyclonal activation of B cells in the lymph nodes and the spleens of mice injected with bacterial lipopolysaccharide (LPS) was compared. The peak of anti-trinitrophenylated sheep red blood cells plaque-forming cell (PFC) response in the lymph node was reached 6-8 days after the injection of LPS while that in the spleen was reached at 2 days. The maximal increase in the total number of Ig-producing cells in the lymph node also occurred at the later stage. These differences in time courses of polyclonal activation of B cells between the lymph node and the spleen were not due to the absence of B cells in the lymph node, migration of PFC from the spleen to the lymph node, or qualitative differences of B cells. This phenomenon was dependent on the environmental difference between the lymph node and the spleen, because B cells from the lymph node could respond to LPS rapidly in the spleen. Further, the polyclonal activation of B cells was accelerated in the lymph nodes of mice receiving prior injection of LPS. In in vitro cultures of lymph node cells of those mice, a significant amount of interleukin-1 could be detected by stimulation of LPS. It was possible that the delayed activation of B cells in the lymph node was due to the time lag necessary for construction of the environmental condition suitable for activation of B cells, whereas in the spleen this condition can be provided without delay.     

3H-deoxythymidine incorporation in graft-versus-host disease in the Norway rat. II. Autoradiographic studies.

A sequential analysis was made of various areas within the lymph nodes and spleen of newborn Brown Norway (BN) rats suffering from graft-versus-host disease (GVHD) subsequent to an allogeneic injection of adult Lewis (L) lymph node cells (experimental). One micron thick autoradiographs were compared between such experimental and control littermates having received the same number of syngeneic adult BN cells. Both experimental and control animals received tritiated deoxythymidine (3HdT) one hour before killing. The autoradiographs revealed a 2.25 and 2.50 times higher thymidine labeling index of lymphocytes in the deep cortex of mesenteric lymph nodes and white pulp of the spleen, respectively, for experimental animals. The experimental effect occurred within one day. The majority of the labeled cells in experimental animals were large lymphoblasts with prominent nucleoli. The labeling index within these areas remained significantly higher than control values until day 8 in the spleen and through day 14 within the lymph nodes. However, differences in labeled cells present in high powered microscopic fields reached a peak on day 3 within compartments in experimental animals but fell significantly below control values by day 9 owing to a pronounced disappearance of both small and large lymphocytes from these areas, and a decreased intensity of individual cell labeling as the reaction progressed. In contradistinction the concentration of labeled cells present in high powered microscopic fields of lymph nodes' medulla became 3.13 times controls by day 4. Most of these labeled cells contained a more basophilic cytoplasm than those found in the deep cortex and some were distinctly plasma cell precursors. In contrast to the deep cortex their concentration remained approximately three times control values until death. The data indicates that the major proliferative events within the spleen and lymph nodes in neonatal rat GVHD are initially restricted to donor cell localization areas of these tissue compartments. Subsequently the GVHD-related events may be attributed to other areas and possibly cell types. Thus any proliferation contributing to splenomegaly in the latter stages of GVHD appears to occur in the red pulp and that contributing to lymph node enlargement a medullary response.     

Correlation of cytotoxicity with experimental allergic encephalomyelitis.

Cytotoxicity of immune lymph node cells in experimental allergic encephalomyelitis (EAE) was maximal 9 days after injection of encephalitogenic emulsion. The ability of these cells to passively transfer EAE was also maximal at this time. Immune spleen cells were more cytotoxic than lymph node cells 9 days after injection; however, these cells did not passively transfer EAE. Twelve days after injection of encephalitogenic emulsion immune spleen cells passively transferred EAE with resulting mild histopathologic lesions. At this time the spleen cells were 50% more cytotoxic than comparable lymph node cells. Cyclophosphamide suppressed the development of clinical EAE and the development of cytotoxic lymphoid cells. It also reduced clinical signs and cytotoxic activity of lymph node cells. Spleen cell cytotoxic activity was enhanced by Cyclophosphamide. It was concluded that cytotoxic activity of lymph node and spleen cells was correlated with the ability of these cells to produce EAE. Lymph node cell populations differed qualitatively and/or quantitatively from immune spleen cell populations in EAE. Capacity to passively transfer EAE coincided with the maximal Cytotoxicity of the lymphoid cells from each tissue.     

Immunohistochemical analysis of human peripheral blood and lymphoid tissues using monoclonal antibodies immunoreactive with non-lymphoid cells

Summary Immunoperoxidase methods were used to study human peripheral blood and lymphoid tissues using a panel of monoclonal antibodies to non-lymphoid cells. The majority of peripheral blood monocytes were immunoreactive for LeuM1, LeuM2, LeuM3 and LeuM5. Rare peripheral blood monocytes were immunoreactive for R4/23. The different antibodies showed characteristic patterns of immunoreactivity in peripheral lymphoid tissues. LeuM1 was immunoreactive with scattered cells in the paracortex of lymph node and tonsil and with many cells in the marginal zone of the spleen. LeuM2 was immunoreactive with endothelial cells in lymph node and tonsil. A few cells in the red pulp of the spleen were immunoreactive for LeuM2. LeuM3 and R4/23 showed distinctive immunoreactivity in germinal centers of secondary follicles, giving a lacy pattern. LeuM3 was also immunoreactive with endothelium in lymph node and tonsil and with sinus lining cells in lymph node. LeuM5 was immunoreactive with macropages in the germinal center, fibroblastic reticulum cells in the mantle zone and interdigitating reticulum cells in the paracortex of lymph node and tonsil.