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In histology, cryptitis refers to inflammation of an intestinal crypt.
Notch signaling also occurs in the intestinal crypt cells.
The mutations can be inherited or are acquired, and most probably occur in the intestinal crypt stem cell.
The subepithelial fibroblast/myofibroblast network which surround the intestinal crypts constitute the niche.
From there, the virus attacks rapidly dividing cells, notably those in the lymph nodes, intestinal crypts, and the bone marrow.
In response to bacterial antigens, Paneth cells release their secretory granules into the lumen of intestinal crypts.
There is depletion of lymphocytes in lymph nodes and necrosis and destruction of the intestinal crypts.
The high turnover rate of the intestinal lining is due to a dedicated population of stem cells found at the base of the intestinal crypt.
Pathologic processes that lead to crohn's, i.e. on-going, intestinal crypt destruction are associated with branching of the crypts.
Small intestinal crypts house stem cells that serve to constantly replenish epithelial cells that die and are lost from the villi.
Intestinal crypt cells are known to have a higher adenylate cyclase and a lower guanylate cyclase activity than differentiated villous cells.
Later studies by Christopher Potten et al. (2002), using pulse/chase experiments with tritiated thymidine, found long-term label-retaining cells in the small intestinal crypts of neonatal mice.
Cryptdins are the protein products of a related family of highly polymorphic genes that are specifically expressed by mouse Paneth cells at the base of intestinal crypts.
There, cryptdins, along with other antimicrobial peptides expressed by Paneth cells, contribute to enteric mucosal innate immunity by clearing the intestinal crypt of potential invading pathogens.
However, there is no experimental evidence to suggest that PPV either replicates extensively in the intestinal crypt epithelium or causes enteric disease as do parvoviruses of several other species.
Because CFTR messenger RNA is expressed at high levels in human and rodent intestinal crypts r14-16, mouse intestinal sections were used as controls to demonstrate probe specificity.
The EPHB2 gene is a target of the Wnt/beta-catenin signaling pathway and is important in the compartmentalization of intestinal epithelial cell proliferation to the intestinal crypts.
In histology, an intestinal crypt (also crypt of LieberkĂĽhn and intestinal gland) is a gland found in the epithelial lining of the small intestine and colon.
In the colon, a field defect probably arises by natural selection of a mutant or epigenetically altered cell among the stem cells at the base of one of the intestinal crypts on the inside surface of the colon.
Birds (storks, pink pelicans, vultures, pigeons and doves) and reptiles (vipers, turtles and tortoises) have shown toxicity associated with bone marrow suppression, intestinal crypt cell necrosis and distal villi sloughing.
Here they not only act as a regulator of the shape of the crypts and villi but also act as stem-niche cells in the intestinal crypts and as parts of atypical antigen presenting cells.
He postulated that this could be accomplished by restricting the number of stem cells for example at the base of intestinal crypts and restraining the opportunities for competition between cells by shedding differentiated intestinal cells into the gut.
Recently it has been reported that treatment of EGF-responsive, nontransformed rat intestinal crypt cell line RIE-1 cells with TGF-β resulted in an increased level of expression of HB-EGF [ 16 ] .
DEAB also exhibited in vivo efficacy as a ALDH1A1 inhibitor, as demonstrated by the toxicity to the intestinal crypt cells in mice receiving co-injections of DEAB and cyclophosphamide [ 21 ] .