Sentences with phrase «corneal endothelium»

Iris to cornea PPMs cause opacities on the cornea due to their ability to damage the corneal endothelium (the inner lining of the cornea).

The corneal endothelium is a single cell layer that forms a barrier between the aqueous humor and the corneal stroma.

Because the laser has already spliced the lens, there's less need to make use of the ultrasound probe, which can in some cases create too much heat, damaging the corneal endothelium and other surrounding tissue.

Our data show that both p53 and TAp63 were found to be more highly expressed in the central than in the peripheral human corneal endothelium.

Since these proteins are known to be involved in the regulation of cell division, this study seeks information about their influence in regulating cell proliferation in the human corneal endothelium.

ΔNp63, a stem cell marker, was not detected in the corneal endothelium.

ΔNp63 and all isoforms of p73 were not detected in either central or peripheral corneal endothelium.

This investigation showed the expression patterns of p53 protein family members in the reluctantly dividing cells of the human corneal endothelium.

Although the corneal endothelium has historically been thought to be nondividing, recent data suggests that endothelial cells may be induced to divide by certain factors [1 - 3].

We have also shown that ΔNp63, a stem cell marker, is not expressed in the human corneal endothelium.

Central human corneal endothelium («central tissue») was collected from the button cut by a 8 mm (diameter) circular trephine.

BrdU fluorescent stainingin a niche of posterior limbal cells spreads to the human corneal endothelium following mechanical wounding.

In order to further indicate signs of cell division in the periphery of the corneal endothelium, the relative expressions of the p53 family of proteins in the periphery were compared with those in the central endothelium.

Studies have shown that there is a higher cell density in the peripheral corneal endothelium than in the central endothelium [17].

Telomerase activity in central, intermediate, and peripheral regions of human corneal endothelium

Evidence suggests that cells from this area migrate (perhaps as transient amplifying cells) to the endothelial periphery and, perhaps, to wounded areas of the corneal endothelium when needed.

Direct and indirect determination of nonuniform cell density distribution in human corneal endothelium.

Without wounding, minimal autofluorescence was observed in the corneal endothelium (Figure 6A).

TGFβ has been reported to act as an inhibitor of the G1 phase of cell division in the corneal endothelium by Joyce et al. [1].

Purpose: Replacing diseased corneal endothelium with a preparation of Descemet membrane carrying functional endothelium and no stroma may be a feasible method for treating corneal endothelial decompensation.

Investigators have already pointed out that the limited cellular division in the corneal endothelium is facilitated by younger donors [2,4,8].

This has more recently been supported by quantitative data obtained by Amann et al. [18] in which a nearly 10 % average increase in cell density was recorded in the peripheral regions of the human corneal endothelium, particularly in the superior region.

Figure 2 shows sets of results for four areas of human corneal endothelial tissue; central endothelium (defined by endothelial cells within a 4 mm trephined boundary), central - intermediate endothelium (defined by endothelial cells within an 8 mm trephined boundary), intermediate - peripheral endothelium (defined by endothelial cells between the 4 mm trephine edge and 12 mm from the center of the corneal endothelium), and the peripheral endothelium (defined by the 8 mm trephined edge and 12 mm from the center of the corneal endothelium).

Mechanisms of mitotic inhibition in corneal endothelium: contact inhibition and TGF - beta2.

Daus W, Volcker HE, Meysen H, Bundschuh W. [Vital staining of the corneal endothelium — increased possibilities of diagnosis].

When BrdU fluorescence assays were made on corneal transverse sections with fluorescein, fluorescence occurred in an area just at and adjacent to the trabecular meshwork, but was not seen at the corneal endothelium.

In the human corneal endothelium, staining only occurred at the wound site following wounding in 10 % of the corneas tested.

The data presented in this report (telomerase activity and BrdU - linked alkaline phosphatase activity staining) suggests that cells in the corneal endothelium may be renewed by stem - like cells located in a niche at the posterior limbus.

We considered focusing our studies on the peripheral corneal endothelium and endothelial limbus after reports by Schimmelpfenning [16] and Daus et al. [17] indicated a significant increase in endothelial cell density of the peripheral corneal endothelium.

In the unwounded human tissue, no fluorescence in the corneal endothelium was an indication of a lack of cell division (Figure 6A).

These putative stem cells may supply new cells for both the corneal endothelium and the trabeculae.

Expression of cell cycle - associated proteins in human and rabbit corneal endothelium in situ.

In order to determine whether cell division occurred in either the periphery of the corneal endothelium following mechanical wounding or at the site of the wound itself, corneas were tested with the AP - BrdU assay.

In this study, the reaction for telomerase in the peripheral corneal endothelium was manifest (Figure 2).

The fluorescence extended, without interruption, from the limbus to the corneal endothelium (Figure 7B).

Therapeutic potential of AAV - mediated MMP - 3 secretion from corneal endothelium in treating glaucoma.

After wounding, BrdU fluorescence extended into the corneal endothelium.

Paull and Whikehart [7] have also shown that p53 and TAp63 (a p53 family member) are relatively elevated in the normal central human corneal endothelium suggesting that these proteins inhibit cell - cycle promotion from the G1 to S phase.

The BrdU staining (AP - BrdU assay) procedure was carried out to demonstrate cellular division at the periphery of the corneal endothelium.

It may be useful for corneal endothelium transplantation.

Researchers from Massachusetts Eye and Ear have, for the first time, identified rapidly proliferating cells (known as «neural crest - derived progenitor cells») in the corneal endothelium of specimens from normal corneas and from corneas with Fuchs» Endothelial Corneal Dystrophy (FECD), a condition in which the cells responsible for keeping the cornea clear die prematurely — often leading to blindness.

The corneal endothelium is responsible for pumping water throughout the cornea to keep vision clear, and when cells of the corneal endothelium die, they do not regenerate.

«Previously, we thought that all of the cells in the corneal endothelium were unable to divide, but we were surprised to find this small population of dormant stem cells capable of proliferating,» said principal investigator Ula Jurkunas, M.D., a corneal and refractive surgeon at Massachusetts Eye and Ear and Associate Professor of Ophthalmology at Harvard Medical School.

Corneal sections from a person with Fuchs dystrophy show the presence of ATP1B1 in the corneal endothelium.

Based on studies of other tissues, the genes very well could play an essential role in the health of the corneal endothelium, according to the study authors.

AP - BrdU staining was not seen at the periphery of human corneal endothelia either with or without wounding in the absence of EGF (data not shown).

Not exact matches

Human corneal endothelial cells expressed both p53 and TAp63; expression was greater in the central endothelium than in the peripheral endothelium (Figure 2).

In the human cornea, the endothelium is the most important layer for the maintenance of osmotic balance and the transparency of corneal tissue [1].