Cell

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CELL. A small room in a prison. See Dungeon.

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Our study results confirmed that nanoemulsified methionine promoted milk protein [[alpha].sub.s2]-casein, [beta]-casein, and [kappa]-casein expression in cultured mammary epithelial cells as compared with non-emulsified methionine.
Bar: 200[micro]m; B: Columnar epithelial cells (Ep) with basophil cytoplasm (*) and nucleus with predominate decondensed chromatin.
The Panotico and Giemsa staining methods were efficient, allowing the identification of different types of vaginal epithelial cells of Santa Ines ewes during the estrus period.
It was first observed in Drosophila that microbial recognition of the receptor toll resulted in the expression of AMPs.[47] Similar to Drosophila, human toll-like receptors are present at the surface of airway epithelial cells or located in membrane-enclosed compartments.[48] Moreover, other patter recognition receptors (PRRs), such as NOD-like receptors, MDA5, and RIG-1, are located in the cell cytosol.[49] Ligation of PRRs leads to activation of cellular signaling transduction pathways such as MAPK and NF-?B.[50] This subsequently leads to expression of AMPs that are not produced at baseline conditions or only at very low levels.
When examining the conjunctival IC in all research subjects, the conjunctival epithelial cells were impressed on a filter membrane, and the goblet cells were stained red due to their glycogen granules (Figure-1 A-B).
An abundant glycocalyx that covers the epithelial cells and has previously been shown to shield human airway epithelial cells from virus-mediated gene transfer (Pickles et al., 2000) might somehow extend its protective role to macrophages.
Human lung bronchial epithelial cells (16HBE) were incubated with varied concentrations of SRM 2786 for 24 h.
Immortalization of human alveolar epithelial cells to investigate nanoparticle uptake.
PAMPs are recognized by transmembrane and cytoplasmic receptors that are expressed by a broad range of cell types, including epithelial cells. These receptors are known as pathogen-recognizing receptors (PRRs), such as Toll-like receptors (TLRs) and Nod-like receptors (NLRs), or co-receptors, such as CD14 and CD16 [37].
In order to better understand the role of signaling of AECs in modulating inflammatory responses of alveolar macrophages to an Mtb infection, the impact and molecular mechanisms of AECs on modulating Toll-like receptor- (TLR-) triggered inflammatory responses of alveolar macrophages to Mtb were interrogated in a contact-independent coculture model of A549 epithelial cells and U937 mononuclear cell-derived macrophage-like cells in the present study.
The microdots were detected in the stroma 25.2 days after the appearance of the highly reflective epithelial cells (Table 1).
Intestinal trefoil factor, Porcine intestinal epithelial cells, Endotoxin, TFF3, rhTFF3.

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