Isolation and differentiation of nestin positive cells from rat oral mucosal lamina propria

2010 ◽  
Vol 79 (1) ◽  
pp. 9-14 ◽  
Author(s):  
Rui Dong ◽  
Xiaoliang Liu ◽  
Mingwen Fan ◽  
Ling Yang ◽  
Lin Peng ◽  
...  
1979 ◽  
Vol 16 (3) ◽  
pp. 292-309 ◽  
Author(s):  
N. F. Cheville

Stomachs of four dogs with uremia and four normal dogs were examined. Uremic stomachs represented four types of disease: atrophic, amyloidotic, ulcerative and necrotic gastropathy. Pathologic changes common to all uremic stomachs were expansion of the lamina propria, atrophy of gastric glands, and submucosal arteriopathy; lesions were limited to body and fundic zones. Lamina propria was markedly expanded by edema, mastocytosis, deposition of acidic mucosubstances, fibroplasia and mineralization. Capillaries in lamina propria had swollen endothelium and calcium salts were present extracellularly as amorphous granular laminae. Gastric glands were distorted and irregular and had fewer cells per unit of tissue. Parietal cells were swollen and had fragmentation of cytocavitary network and mitochondrial swelling with calcification. Chief cells were shrunken, agranular and atrophic with foci of glycogen and dilation of endoplasmic reticulum. Argentaffin cell content was diminished. Muscular arteries of submucosae had segmental degenerative lesions characterized by myocyte necrosis, calcification, and deposition of acidic mucosubstances and fibrin; thrombosis and obstructive arteriopathy were common. These studies suggest that uremic gastropathy is a disease of mucosal lamina propria and that lesions were due to anoxia caused by diffuse vascular injury and to altered parietal cell function.


2015 ◽  
Vol 4 (11) ◽  
pp. 1283-1293 ◽  
Author(s):  
Emma Board-Davies ◽  
Rachael Moses ◽  
Alastair Sloan ◽  
Phil Stephens ◽  
Lindsay C. Davies

Author(s):  
John H. L. Watson ◽  
C. N. Sun

That the etiology of Whipple's disease could be bacterial was first suggested from electron micrographs in 1960. Evidence for binary fission of the bacteria, their phagocytosis by histiocytes in the lamina propria, their occurrence between and within the cells of the epithelium and on the brush border of the lumen were reported later. Scanning electron microscopy has been applied by us in an attempt to confirm the earlier observations by the new technique and to describe the bacterium further. Both transmission and scanning electron microscopy have been used concurrently to study the same biopsy specimens, and transmission observations have been used to confirm those made by scanning.The locations of the brush borders, the columnar epithelial cells, the basement membrane and the lamina propria beneath it were each easily identified by scanning electron microscopy. The lamina propria was completely filled with the wiener-shaped bacteria, Fig. 1.


Author(s):  
D.S. Friend ◽  
N. Ghildyal ◽  
M.F. Gurish ◽  
K.F. Austen ◽  
R.L. Stevens

Trichinella spiralis induces a profound mastocytosis and eosinophilia in the small intestine of the infected mouse. Mouse mast cells (MC) store in their granules various combinations of at least five chymotryptic chymases [designated mouse MC protease (mMCP) 1 to 5], two tryptic proteases designated mMCP-6 and mMCP-7 and an exopeptidase, carboxypeptidase A (mMC-CPA). Using antipeptide, protease -specific antibodies to these MC granule proteases, immunohistochemistry was done to determine the distribution, number and protease phenotype of the MCs in the small intestine and spleen 10 to >60 days after Trichinella infection of BALB/c and C3H mice. TEM was performed to evaluate the granule morphology of the MCs between intestinal epithelial cells and in the lamina propria (mucosal MCs) and in the submucosa, muscle and serosa of the intestine (submucosal MCs).As noted in the table below, the number of submucosal MCs remained constant throughout the study. In contrast, on day 14, the number of MCs in the mucosa increased ~25 fold. Increased numbers of MCs were observed between epithelial cells in the mucosal crypts, in the lamina propria and to a lesser extent, between epithelial cells of the intestinal villi.


Author(s):  
Shaopeng Hu ◽  
Jianhua Wang ◽  
Zhen Li ◽  
Huei Chen ◽  
Fei Cu ◽  
...  

Gastritis from returning bile is a common disease, but the reason for the disease is not clear. As the pathologic ultrastructure research progresses, it has drawn attention to the ultrastructural change of cells in gastric mucosa by clinical workers. We observed gastric mucosa tissues of 15 patients suffering from gastritis with a transmission electron microscope (TEM) and a scanning electron microscope (SEM). It is the first report in China that fungus exists in the lamina propria of gastric mucosa tissue. The result is as follows.The gastric mucosa tissues of 15 patients suffering from gastritis were acquired by stomachoscopy. Both TEM and SEM specimens were prepared by the usual methods. Under the TEM, the epithelial surface became higher and larger. Mitochondria of the cells were swollen and cristae were disrupted. There were vacuoles in the cells. The nucleus showed disorder, heterochromatin became darker, and nucleolae could be observed.


Author(s):  
R. B. Moyes ◽  
R. E. Droleskey ◽  
M. H. Kogut ◽  
J. R. DeLoach

Salmonella enteritidis (SE) is of great concern to the poultry industry due to the organism's ability to penetrate the intestinal mucosa of the laying hen and subsequently colonize the ovaries and yolk membrane. The resultant subclinical infection can lead to SE infection of raw eggs and egg products. Interference with the ability of the organism to invade has been linked to the activation and recruitment of inflammatory polymorphonuclear cells, heterophils, to the lamina propria of the intestinal tract.Recently it has been established that heterophil activation and increased resistance to SE organ invasion can be accomplished by the administration of SE-immune lymphokines (SE-ILK) obtained from supernatants of concanavalin-A stimulated SE immune T lymphocytes from SE hyperimmunized hens. Invasion of SE into the lamina propria provides a secondary signal for directing activated heterophils to the site of SE invasion.


2001 ◽  
Vol 120 (5) ◽  
pp. A135-A135
Author(s):  
S FIORUCCI ◽  
A MENCARELLI ◽  
B PALAZZETTI ◽  
E DISTRUTTI ◽  
J WALLACE ◽  
...  

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