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The patho-factor of pulmonary fibrosis is very complex. With the development of cytobiology and molecular biology there are much proof shows PF is a disease induced by multiple factor, multiple organ and multiple cell; and happens between cells and mesenchyma in multiple path.

肺纤维化(pulmonary fibrosis,PF)形成的病理因素十分复杂,近几年细胞生物学和分子生物学的发展为PF的形成机制提供了大量依据,证明PF是一个多因素、多器官、多细胞、多种因子之间以及细胞与间质成分之间形成的一个多层次,多步骤,多通路的疾病。

Nowadays, the study regarding the effect of growth factors on annulus fibrosis is less than that of nucleus pulpous.

但目前有关生长因子对纤维环细胞作用的研究少于髓核细胞,有待加强。

Results:(1) In clinical pathology, swelling, denatured, even necrosis and putrescence could be picked out; Collagen fibers in tendon remarkedly swelled, and tissue structure disarranged, and collagen even ruptured, broken and dissolved; Obvious denature, apoptosis and necrosis could be found in tendon cells. There appeared to be a big accumulation of inflammatory cells.

结果 (1)临床病理组织学观察发现:肌腱组织肿胀、变性、甚者坏死、腐败;肌腱内胶原纤维肿胀明显、组织结构紊乱,失去正常排列,甚者出现胶原断裂、破碎、溶解等现象;腱细胞可见明显的变性、凋亡和坏死;病变部位可见大量炎性细胞聚集。

Results The reticulin fibre proliferated in all specimen and most of them occured mega karyocytosis.The myelofibrosis was severer along with the progress of CML,while megakaryocyte counts didn′t change significantly.

结果 发现所有患者的骨髓组织均存在网硬蛋白纤维增多,且随CML进展其程度加重;大多数患者巨核细胞过度增生,在CML不同阶段中巨核细胞数比较未见显著差异。

Line (HSC-T6): a new cell model for the study of retinoid metabolism in vitro.

肝星状细胞及相关细胞因子在肝纤维化形成中的作用。

Methods Constructed the model of fetal scarless wound healing and investigated the expression of collagen in fetal and adult rat wounds by immunohistochemistry and in situ hybridization.

染色,Ⅰ、Ⅲ型胶原免疫组化,Ⅰ、Ⅲ型胶原原位杂交。结果胎鼠伤口愈合快,组织结构再生完全,没有瘢痕形成,胶原呈网状正常排列,Ⅰ、Ⅲ型胶原蛋白及表达均增多,同时伴细胞数增多,Ⅲ型胶原首先形成网状排列;成年伤口胶原纤维沉积慢,平行排列的胶原逐渐呈束状填塞伤口以致瘢痕形成,伤口内Ⅰ、Ⅲ型前胶原mRNA表达均增多,细胞数目增多不明显。

Acute diffuse lung injury were identified in toxication control group, intra-pul

结果 中毒组大鼠肺的病理学改变为急性弥漫性肺损伤,表现为肺泡腔内出血、渗出、炎性细胞浸润,肺泡隔炎性细胞浸润及纤维组织增生,⌒秃廷⑿蜕掀は赴坏死脱落。

The second, many coccus in kidney, heart and pancreas were found besides liver cell degeneration, congestion of liver, epithelium cell degeneration, necrosis of tubuli tenales, kidney hemorrhage, cardiac muscle cell degeneration, heart hemorrhage.

病例2,肝细胞变性,肺淤血,肾小管上皮细胞变性、坏死,间质出血,心肌纤维变性,间质出血,肾、心、胰脏均可见到散在分布的球菌。

Ca2+-ATPase and acid phosphatase of fiber in Phyllostachys edulis culms during secondary wall formation were studied. Early, intact double karyotheca remained in fiber nucleus, while nuclear chromatin agglutinated.

利用显微和细胞化学方法,对毛竹茎秆纤维次生壁形成过程中超微结构变化以及ATP酶、Ca2+-ATPase和酸性磷酸酶的超微细胞化学定位进行了研究。

Methods The disorder of myofibrils,swelling of mitochondria with broken cristae and decrease of cytochrome C oxidase activity caused by ADR were prevented by the administration of teapol.

结果 阿霉素所造成的大鼠心肌细胞肌原纤维排列紊乱、线粒体肿胀,嵴断裂及细胞色素C氧化酶活性降低,可明显地被抗氧化剂天力体保所防止。

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