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There was no expression of PCNA protein in normal vein.
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In normal veins, the flow is continuous and spontaneous at rest and the velocity varies with respiration, increasing during inspiration, and decreasing during expiration or when a Valsalva maneuver is performed.
A significant decrease in DNA concentration was found in DV (15.5 ± 7.93 ng/mg) as compared to 244.5 ± 65.01 ng/mg of tissue in normal veins (p = 0.007).
Egr-1-positive cells were not detected in the normal vein.
Here, we have characterized the defects associated with xenicid mutation, a gene that was reported to cause Type A blisters (round, normal vein patterning) in the original wing blister screen [1].
Objectives: to examine the release of vascular endothelial growth factor (VEGF) and nitric oxide (NO) in primary varicose veins (VVs) and normal vein controls following experimentally-induced venous stasis.
When wild type EGFR is expressed in the developing wing outside the normal vein domains, it causes the formation of ectopic vein tissue (e.g., Hahn et al. 2013).
These maps show epigenetic marks in normal umbilical vein endothelial cells HUVEC, leukemic cell line K562 and normal epidermal keratinocytes Nhek.
Consistent with this suggestion we have also found a similar correlation between FHL1 expression and SM-MHC in carotid arteries and transplanted jugular veins but not in normal jugular veins of pigs (EA and PRK manuscript in preparation).
This hereditary aspect is supported by the evidence of FOXC2 gene-mutation of patients with insufficiency of the vein's valves (Mellor et al 2007) and the changes in the expression of tenascin-C of the varicose patient in comparison to patients with normal veins (Kirsch et al 1999).
However, radiolucent striation in TOS suggestive of hypertrophy of normal veins as described by Vanel et al. or extraosseous matrix mineralization reflecting osteoid-producing tumor was not detected on radiologic images in our study.
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