云南树Qu肝脏结构的光,电镜观察

本文报告了树Ｑｕ肺脏的一般结构和超微结构。与人和灵长目相似,其肺实质也是由导气部和呼吸部构成。但不同的是其细支气管粘膜形成很高的皱襞。在电镜下Ｃｌａｒａ细胞电子密度高,顶部胞质中含有大量膜包颗粒,这些结构与大白鼠和家兔的结构相似。许多毛细血管外方都包绕状基膜和肺泡Ｉ型上皮细胞的胞质。气血屏障由肺泡上皮细胞、融合的基膜和内皮细胞胞质构成。说明树Ｑｕ肺脏不但是呼吸器官,也是一些激素和介质产生及代谢的重     

黑熊肺脏光,电镜观察

本文采用光镜,扫描及透射电镜对成体黑熊肺脏组织进行观察。结果表明：黑熊肺脏和其它哺动物肺脏结构基本相似,亦由支气管各级分支,肺小叶及小叶间结缔组织构成,每个细支气管连同它的各级分支和肺泡组成一个肺小叶,肺泡是支气管树的终末部分,呈多面囊形泡,肺泡壁有Ｉ,ＩＩ两种类型上皮细胞。气－血屏障由肺泡上皮,上皮基膜,内皮基膜和内皮四层结构组成,厚约０．５μｍ。     

胡子鲇、月鳢、泥鳅具气呼吸作用器官呼吸上皮的电镜观察

应用扫描电子显微镜与透射电子显微镜技术观察了具气呼吸作用的胡子鲇树枝状鳃上器、月鳢耳片状鳃上器和泥鳅的肠等器官 ,证实 3种淡水鱼类具气呼吸作用的器官表面均被覆一层高度毛细血管化的呼吸上皮。胡子鲇的呼吸上皮表面形态呈玉米棒状 ,月鳢的鳃上器表面为半圆形鹅卵石状 ,泥鳅肠内壁表面如云朵状。这 3种器官的呼吸上皮细胞均为同一种类型 ,是一类特化的扁平上皮细胞 ,兼有哺乳类肺泡Ⅰ型和Ⅱ型上皮细胞的细微结构特征。同时 ,构成气血屏障的三部分即呼吸上皮细胞、毛细血管内皮细胞胞质薄层和两者之间的基底膜与其他脊椎动物的呼吸器官极为相似。     

牦牛胎儿肺脏发育的形态学研究

本实验选取40份不同胎龄的牦牛肺脏样本,通过组织学和组织化学的方法对牦牛肺发育过程进行研究,旨在为发育生物学提供形态学资料.结果表明,牦牛胚胎肺发育可分为5个时期:(1)胚胎期(30～50 d),胚胎出现肺芽,其分支形成主支气管,进一步分出叶支气管,上皮均为假复层柱状上皮; (2)假腺期(50～120 d),支气管树发育明显,末端终蕾结构似腺体,为假复层柱状上皮;(3)小管期(120 ～180 d),呼吸部发育明显,终蕾腺泡样结构消失,可见多处管状分支,上皮为单层柱状或单层立方;(4)囊状期(180 ～220d),终囊管壁由较厚肺泡隔及原始肺泡组成,少数原始肺泡上皮分化为扁平的肺泡Ⅰ型细胞和立方形的肺泡Ⅱ型细胞;(5)肺泡期(220 ～ 260 d),形成肺泡,大部分上皮细胞分化为扁平的肺泡Ⅰ型细胞和立方形的肺泡Ⅱ型细胞.胚胎期和假腺期支气管和终蕾上皮的糖原含量丰富,从小管期开始,上皮细胞糖原含量开始急剧减少.之后的几个时期,只有导气部个别上皮细胞PAS反应呈阳性.实验结果表明:牦牛胎儿的肺脏发育的特点与普通牛的基本相似,主要不同点是牦牛的囊状期较短,肺泡期较长,即牦牛胎儿的肺脏更早发育成熟.     

苏氏(鱼芒)鲇鳔的组织学及呼吸上皮的超微结构的研究

本文首次报道了苏氏(鱼芒)鲇的具有气呼吸作用的鳔的组织学和呼吸上皮的超微结构。鳔由浆膜、纤维层、粘膜上皮三层构成,纤维层的胶原纤维向鳔腔内突入衍生出密集的泡囊状小室,并在鳔腔中心汇合为中轴。泡囊小室的内表面被覆高度毛细血管化的上皮(即呼吸上皮)。呼吸上皮细胞是一类同型特化的扁平上皮细胞,电镜观察证明具有哺乳类肺泡上皮Ⅰ型和Ⅱ型细胞的结构。上皮细胞基底面与单层的毛细血管壁细胞联接形成胞质薄层的血-气屏障。研究结果证实鳔是苏氏(鱼芒)鲇的重要副呼吸器官,具有强的空气呼吸作用。     

苏氏mang鲇鳔的组织学及呼吸上皮的超微结构的研究

本文首次报道了苏氏mang鲇的具有气呼吸作用的鳔的组织学和呼吸上皮的超微结构。鳔由浆膜、纤维层。粘膜上皮三层构成,纤维层的胶原纤维向鳔腔内突人衍生出密集的泡囊状小室,并在鳔腔中心汇合为中轴。泡囊小室的内表面被覆高度毛细血管化的上皮(即呼吸上皮)。呼吸上皮细胞是一类同型特化的扁平上皮细胞,电镜观察证明具有哺乳类肺泡上皮Ⅰ型和Ⅱ型细胞的结构。上皮细胞基底面与单层的毛细血管壁细胞联接形成胞质薄层的血一气屏障。研究结果证实鳔是苏氏mang鲇的重要副呼吸器官,具有强的空气呼吸作用。     

丹顶鹤肺脏组织结构光镜及扫描电镜观察

本文对1例成熟,正常丹顶鹤肺脏进行了光镜及扫描电子显微镜观察。丹顶鹤肺脏由各级支气管和无数肺小叶及小叶间结缔组织组成。肺小叶呈六面棱柱形,由副支气管、肺房、漏斗和大量呼吸毛细管组成。呼吸毛细管含相当丰富的毛细血管。毛细血管内皮细胞,呼吸毛细管的上皮细胞,连同其间少量的结缔组织共同组成生理上的气-血屏障。在肺房表面可观察到两种上皮细胞,一种扁平而光滑,另一种表面有微绒毛并有胞质突起。     

珠江口池养梭鱼鳃的光镜、扫描和透射电镜观察

应用光学显微镜、扫描电镜和透射电镜对珠江口池塘养殖梭鱼Liza haematocheila鳃的组织结构、表面形态特征及鳃小片超微结构进行了观察。结果表明梭鱼具有4对鳃,每个鳃由鳃弓、鳃丝、鳃小片和鳃耙组成。梭鱼鳃丝和鳃小片的表面结构和超微结构与其他硬骨鱼类的基本相似,鳃丝表面分布有众多规则或不规则的环形微嵴、沟、坑、孔等结构。鳃丝分为呼吸区和非呼吸区,呼吸区较为平滑,上皮细胞表面无微嵴,呈皱褶状;非呼吸区分布有沟、坑、孔等结构,上皮细胞有较规则的指纹状微嵴。鳃小片是最主要的呼吸场所,由基膜、上皮细胞、内皮细胞、柱细胞和毛细血管网组成。泌氯细胞主要分布在鳃小片基部,并有开口通往外界。本文还探讨了梭鱼鳃的结构与其功能的密切关系。     

斑衣蜡蝉雌性生殖系统超微结构

【目的】明确斑衣蜡蝉Lycorma delicatula雌成虫生殖系统整体形态及超微结构特征,为蜡蝉总科昆虫分类及系统发育探讨提供更多形态学证据。【方法】采用光学显微镜与透射电子显微镜,观察斑衣蜡蝉雌成虫生殖系统整体形态和各主要器官的超微结构。【结果】斑衣蜡蝉雌成虫生殖系统主要包括1对卵巢、1个中输卵管、1个交配囊、1个交配囊管、1个前阴道、1个后阴道、1个受精囊、1个受精管和2根受精囊附腺。卵巢为端滋式,由14根卵巢小管组成,卵室由固有膜、滤泡细胞和卵细胞组成,卵巢小管中的滋养细胞清晰可见;中输卵管位于前阴道基部,由中输卵管腔、上皮细胞、肌肉鞘和基膜组成;交配囊膨大呈圆球状,囊壁由上皮细胞、肌肉层和基膜组成;交配囊管呈圆柱状,连接交配囊和后阴道,由肌肉鞘、上皮细胞层和管腔组成;前、后阴道超微结构相似,主要由肌肉鞘、基膜、上皮细胞和管腔组成,但后阴道上皮细胞细胞核周围存在分泌颗粒,且管腔内有大量微绒毛,而前阴道壁内包含有大量囊泡结构;受精管从中输卵管末端延伸至受精囊,由基膜、厚层肌肉鞘和管腔组成;受精囊为受精管近末端略膨大的囊状结构,由肌肉鞘、基膜、上皮细胞和囊腔构成;雌性受精囊附腺着生于受精囊末端,为均匀的螺旋管状,主要由肌肉层、上皮细胞层和附腺中心管腔组成。【结论】斑衣蜡蝉雌性生殖系统与已报道的蜡蝉总科其他类群的雌性生殖系统结构相似,但卵巢小管数目有差异;蝉亚目中不同总科雌成虫雌性附腺与受精囊附腺的形态特征存在明显区别;斑衣蜡蝉雌性生殖系统超微结构与叶蝉总科和沫蝉总科昆虫也存在部分差异。这些差异是否可以作为头喙亚目高级阶元的划分依据仍有待于进一步研究。     

肺多潜能上皮干细胞在肺损伤修复中的作用

肺作为一个复杂的多功能器官,对人类生存至关重要。肺上皮细胞对维持肺脏功能和修复肺脏损伤具有重要作用。近年来研究认为,位于细支气管与肺泡交界处有一种肺干细胞,即支气管肺泡干细胞(bronchioalveolar stem cells, BASCs),但由于体内示踪BASCs的技术瓶颈,该干细胞是否具有再生为肺脏上皮细胞的能力一直存在争论。中国科学院生物化学与细胞生物学研究所周斌研究团队及其合作者的最新研究成果利用双同源重组系统(Cre-loxP和Dre-rox)特异性标记和示踪BASCs,并结合不同小鼠肺脏损伤模型揭示,BASCs在体内具有再生肺脏的能力,为肺脏的修复和再生研究提供了新的理论基础及研究方向。     

Differences in basement membrane-associated microdomains of type I and type II pneumocytes in the rat and rabbit lung

The basement membrane-associated microdomains of type I pneumocytes in rat and rabbit pulmonary alveoli were found to be uniquely different from those of type II pneumocytes in the specific distribution of cytochemically detectable sulfate esters as demonstrated with the high iron diamine (HID) technique at the electron microscopic level. Aldehyde-fixed frozen or Vibratome sections of neonatal and adult lungs were treated with a mixture of the meta and para isomers of N,N-dimethyl-phenylenediamine-HCl in the presence of ferric chloride, which at low pH (1.0) has been previously shown to be highly specific for sulfate esters of glycosaminoglycans and glycoproteins. Reaction product was subsequently enhanced with a thiocarbohydrazide-silver proteinate, postembedding sequence for electron microscopy. Samples of lung parenchyma treated in this fashion were observed to have discrete, electron-dense silver grains associated with the various microanatomical components of pulmonary basement membranes. In the region of the alveolar basement membrane, the lamina rara externa associated with type I cells was observed to contain an abundance of regularly disposed, cytochemically detectable sulfate esters, while the lamina densa and lamina rara interna were diffusely and sparsely reactive by comparison. Quantitatively, 62% of all reactive sites found in the basement membrane region of type I cells were localized in the lamina rara externa. By contrast, the lamina rara externa of type II cells had less than half as many reactive foci indicative of sulfate esters as the same region of type I cell basement membranes. HID-reactive sulfate esters were found evenly distributed within the laminae associated with the basement membrane of type II cells. This cytochemically detectable difference in the sulfate ester composition of basement membrane-associated sulfate ester composition of basement membrane-associated microdomains of type I compared with that of type II pneumocytes may be highly significant when considering known patterns of epithelial renewal in pulmonary alveoli. Since type II cells are known to divide and either remain type II cells or differentiate into type I cells, regional differences in the molecular composition of the alveolar basement membranes and their associated structures may be key determinants of cell-specific processes of cytodifferentiation in the pulmonary alveolus.     

Repopulation of a human alveolar matrix by adult rat type II pneumocytes in vitro : A novel system for type II pneumocyte culture

This paper describes the preparation of lung acellular alveolar matrix fragments and culture of rat type II pneumocytes directly on the alveolar epithelial basement membrane, thereby permitting study of the effect of lung basement membrane on the morphology and function of type II cells. Collagen types I, III, IV and V, laminin and fibronectin were located by immunofluorescence in the lung matrix with the same patterns as those described for the normal human lung. Transmission electron microscopy (TEM) of the fragments revealed intact epithelial and endothelial basement membranes. The matrix maintained the normal three-dimensional alveolar architecture. Glycosaminoglycans were still present by Alcian Blue staining. Isolated adult rat type II pneumocytes cultured on 150 micron thick fragments of acellular human alveolar extracellular matrix undergo gradual cytoplasmic flattening, with loss of lamellar bodies, mitochondria, and surface microvilli. These changes are similar to the in vivo differentiation of type II pneumocytes into type I pneumocytes. The type II pneumocyte behaviour on the lung epithelial basement membrane contrasted sharply with that of the same cell type cultured on a human amnionic basement membrane. On the latter surface the cells retained their cuboidal shape, lamellar bodies and surface microvilli for up to 8 days. These observations suggest that the basement membranes from different organ systems exert differing influences on the morphology and function of type II pneumocytes and that the alveolar and amnionic basement membranes may have differing three-dimensional organizations. The technique of direct culture of type II cells on the lung basement membrane provides a useful tool for studying the modulating effect of the basement membrane on alveolar epithelial cells.     

Interleukin-1β and tumor necrosis factor-α have opposite effects on fibroblasts and epithelial cells during basement membrane formation

Interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) are typical proinflammatory cytokines that influence various cellular functions, including metabolism of the extracellular matrix. We examined the roles of IL-1beta and TNF-alpha in basement membrane formation in an in vitro model of alveolar epithelial tissue composed of alveolar epithelial cells and pulmonary fibroblasts. Formation of the basement membrane by immortalized rat alveolar type II epithelial (SV40-T2) cells, which ordinarily do not form a continuous basement membrane, was dose-dependently upregulated in the presence of 2 ng/ml IL-1beta or 5 ng/ml TNF-alpha. IL-1beta or TNF-alpha alone induced increased secretion of type IV collagen, laminin-1, and nidogen-1/entactin, all of which contributed to this upregulation. In contrast, while SV40-T2 cells cultured with a fibroblasts-embedded type I collagen gel were able to form a continuous basement membrane, they failed to form a continuous basement membrane in the presence of IL-1beta or TNF-alpha. Fibroblasts treated with IL-1beta or TNF-alpha secreted matrix metalloproteinase (MMP)-9 and MMP-2, and these MMPs inhibited basement membrane formation and degraded the basement membrane architecture. Neither IL-1beta- nor TNF-alpha-treated SV40-T2 cells increased the secretion of MMP-9 and MMP-2. These results suggest that IL-1beta participates in basement membrane formation in two ways. One is the induction of MMP-2 and MMP-9 secretion by fibroblasts, which inhibits basement membrane formation, and the other is induction of basement membrane component secretion from alveolar epithelial cells to enhance basement membrane formation.     

Epithelial laminin alpha5 is necessary for distal epithelial cell maturation, VEGF production, and alveolization in the developing murine lung

Laminin alpha5 is prominent in the basement membrane of alveolar walls, airways, and pleura in developing and adult lung. Targeted deletion of laminin alpha5 in mice causes developmental defects in multiple organs, but embryonic lethality has precluded examination of the latter stages of lung development. To identify roles for laminin alpha5 in lung development, we have generated an inducible lung epithelial cell-specific Lama5 null (SP-CLama5(fl/-)) mouse through use of the Cre/loxP system, the human surfactant protein C promoter, and the reverse tetracycline transactivator. SP-CLama5(fl/-) embryos exposed to doxycycline from E6.5 died a few hours after birth. Compared to control littermates, SP-CLama5(fl/-) lungs had dilated, enlarged distal airspaces, but basement membrane ultrastructure was preserved. Distal epithelial cell differentiation was perturbed, with a marked reduction of alveolar type II cells and a virtual absence of type I cells. Cell proliferation was reduced and apoptosis was increased. Capillary density was diminished, and this was associated with a decrease in total lung VEGF production. Overall, these findings indicate that epithelial laminin alpha5, independent of its structural function, is necessary for murine lung development, and suggest a role for laminin alpha5 in signaling pathways that promote alveolar epithelial cell differentiation and VEGF expression.     

The connective tissue of the rat lung: electron immunohistochemical studies

The ultrastructural distribution of specific connective-tissue components in the normal rat lung was studied by electron immunohistochemistry. Three of these components were localized: type I collagen, fibronectin and laminin. Type I collagen was present not only in major airways and vascular structures, but also in alveolar septa. Laminin was found in all basement membranes, and only in basement membranes, demonstrating once more that this glycoprotein is an intrinsic component of the basement membrane. Fibronectin was found free in the interstitium and on the surfaces of collagen fibers. The basement membranes of bronchial, glandular and endothelial cells of large vessels lacked fibronectin; however, capillary endothelial and occasionally epithelial alveolar basement membranes contained some fibronectin in an irregular, spotty distribution. This localization suggests that in the lung, as in other tissues, fibronectin is not an intrinsic component of the basement membrane, but rather a stromal and plasma protein. Only basement membranes in the alveolar parenchyma contained "trapped" plasma fibronectin.     

Immunohistochemical localization of epidermal growth factor receptor (EGF-R) in normal and diseased newborn lung tissues

The distribution of EGF receptors (EGF-R) was examined in normal, hyaline membrane diseased and pneumonic newborn lung tissues by immunohistochemical methods under the light microscope. The PAP technique with polyclonal antibodies was performed to demonstrate the EGF receptor localisation in these tissues. Strong EGF-R reactivity was observed on bronchiolar epithelium and type I and type II alveolar cells in normal newborn lung tissues; whereas, poor reactivity was observed in alveolar macrophages. On the other hand, strong immunoreactivity was detected in type I alveolar cells and alveolar macrophages in hyaline membrane disease, but no reactivity was present in type II alveolar cells. The strongest immunoreactivity was observed in alveolar macrophages of newborn pneumonic lung tissues. In conclusion, the most meaningful form of reactivity was observed in normal newborn lung tissues of airway track and respiration area. This result is related with the maturation of the lungs after birth.     

Alveolar epithelial surface area-volume relationship in isolated rat lungs.

In vitro studies of the alveolar epithelial response to deformation require knowledge of the in situ mechanical environment of these cells. Because of the presence of tissue folding and crumpling, previous measurements of the alveolar surface area available for gas exchange are not equivalent to the epithelial surface area. To identify epithelial deformations in uniformly inflated lungs representative of the in vivo condition, we studied isolated Sprague-Dawley rat lungs (n = 31) fixed by perfusion with glutaraldehyde on deflation after cycling three times at high lung volume (10-25 cmH2O). The epithelial basement membrane in 45 electron micrographs (x12,000)/rat was traced, digitally scanned, and analyzed. Epithelial basement membrane surface area (EBMSA) was computed from a morphometric relationship. EBMSA was found to increase 5, 16, 12, and 40% relative to EBMSA at 24% total lung capacity at lung volumes of 42, 60, 82, and 100% total lung capacity, respectively. The increases in EBMSA suggest that epithelial cells undergo significant deformations with large inflations and that alveolar basement membrane deformation may contribute to lung recoil at high lung pressures.     

Localization and quantitation of anionic charge sites in fetal and neonatal alveolar basement membranes

A method utilizing biopsy sized samples of lung for anionic charge site localization in alveolar and capillary basement membranes in human tissue is discussed. Tissue fixed in either paraformaldehyde-lysine-periodate or 1% paraformaldehyde with 0.05% glutaraldehyde, cut into 30 mu sections, and incubated with the cationic probe, polyethyleneimine, was processed for electron microscopic analysis using standard techniques. Anionic charge sites were identified and regularly distributed in increments of approximately 40-50 nm in the lamina rara externa of the alveolar basement membrane, with lesser amounts found in the lamina rara interna and lamina densa. Anionic charge sites were also demonstrated in the interstitial portion of the capillary basement membrane and on cell surfaces. These methods can be used to more broadly define the localization of anionic charge sites in human lung tissue in both normal and pathologic states.     

Basement membrane collagen requirements for attachment and growth of mammary epithelium.

In vivo mammary epithelial cells rest upon a basement membrane composed in part of type IV collagen which is synthesized by these cells. In this study, basement membrane collagen is shown to be selectively recognized by normal mammary ducts and alveoli for attachment and growth when compared to the types of collagen derived from stroma (types I or III) or cartilage (type II). Cell attachment and growth on type I collagen is inhibited by the proline analogue, cis-hydroxyproline, which blocks normal collagen production. These effects of cis-hydroxyproline are not apparent when a basement membrane collagen substratum is provided. Unlike normal mammary epithelium, mammary fibroblasts show little preference for the collagen to which they will attach. A requirement of type IV collagen synthesis for normal mammary epithelial cell attachment and growth on stromal collagen in vitro may have significance in vivo where a basement membrane scaffold may be necessary for normal mammary morphogenesis and growth.     

Expression of the immunomodulator IL-10 in type I pneumocytes of the rat: alterations of IL-10 expression in radiation-induced lung damage.

Fibrosing alveolitis is a disease with inflammatory, proliferative, and fibrotic components. In different models, it has been shown that the cytokine interleukin-10 (IL-10) plays a conflicting role in inflammation-associated fibrotic processes, inasmuch as it is an anti-inflammatory cytokine but also a TH2 cytokine with inherent pro-fibrotic effects. IL-10 is produced primarily by inflammatory cells. In this report, we show in a rat model of radiation-induced fibrosing alveolitis that IL-10 is also produced by type I alveolar epithelial cells in both normal and fibrotic lungs. The total amount of IL-10 in the lung is increased after irradiation, but type I pneumoyctes contain less IL-10. The R3/1 permanent type I pneumocyte cell line also contains IL-10, which is reduced after irradiation. Whereas in the normal lung, the entire alveolar surface is covered by IL-10-producing pneumocytes, this continuity is interrupted in fibrotic lungs, because type I pneumocytes lack full differentiation and thus full spreading over the alveolar surface. The exposure of the IL-10-negative epithelial basal membrane may allow for an easier attachment of inflammatory cells such as alveolar macrophages. These cells have the potential to act in a pro-inflammatory way by tumor necrosis factor alpha and also in a pro-fibrotic way by activating TH2 cytokines.