1
The high glucose environment increased cytoplasmic ROS accumulation in cultured DRG neurons.
2
More high glucose-cultured CTLs are prone to necrosis after execution of killing.
3
However, several days of exposure to high glucose were required before their appearance.
4
The proliferation and migration ability of BMSCs were suppressed under high glucose conditions.
5
However, the bone regeneration ability of BMSCs is inhibited in high glucose microenvironments.
6
Carnosine protects against the adverse effects of high glucose levels on renal cells.
7
Hence, we examined how Shh expression in the sclerotome was affected under high glucose.
8
We found that high glucose treatment significantly inhibited Shh expression.
9
MRP8 knockdown by shRNA significantly restored EC function after exposure to high glucose concentrations.
10
Reduced autophagy may result in limited renal cell function during exposure to high glucose conditions.
11
Purpose: To explore the effect of high glucose on migration of BMSCs through inhibiting CXCR-4.
12
We have previously reported that high glucose conditions impair the function of osteoblast-like MG-63 cells.
13
Caldesmon protein isoforms were quantified both under normal and high glucose conditions by two-dimensional electrophoresis.
14
Using oligonucleotide microarrays we analyzed isolated intact human islets incubated at low and high glucose.
15
Basal glucagon release was inhibited by ambient high glucose in control and STZ rats alike.
16
However, the detailed cellular mechanisms leading to retinal AC dysfunction under high glucose conditions remain unclear.
