1
Ventricular hydroxyproline content was found to be unchanged among the experimental groups.
2
Interference from protein of collagenous origin was excluded by hydroxyproline determinations.
3
Fasting calcium and hydroxyproline excretion are related to fasting sodium excretion in postmenopausal women.
4
The hydroxyproline content and histopathological findings supported this result.
5
Tissue samples were taken from the incision line for histopathological evaluation and hydroxyproline content measurement.
6
We postulate that calcium excretion is sodium dependent and that hydroxyproline excretion is calcium dependent.
7
The long-term effect of mepindolol on left ventricular hydroxyproline concentration was assessed 21 days post-coronary occlusion.
8
No changes in hydroxyproline levels were seen.
9
Despite the increased tissue hydroxyproline levels in group IV, erythropoietin failed to show any effects in group III.
10
Therefore, we sought to lower urinary hydroxyproline, which is a marker of bone resorption, by lowering urinary sodium.
11
Apstatin analogues lacking the L-alanine or having hydroxyproline in place of the proline in the second position had reduced affinity.
12
There was no statistical difference between the groups with small and large infarcts in regard to myocardial concentration of hydroxyproline.
13
Collagenolytic activity of the cells was determined by measuring the amount of hydroxyproline released into the medium from degraded collagen.
14
Urinary hydroxyproline was an inverse function of alpha and a positive function of fasting urinary calcium in the osteoporotic group.
15
The fibrosis degree was determined pathologically by using the Ashcroft scoring method and biochemically by hydroxyproline assay in lung tissue.
16
A significant decrease of urinary calcium and hydroxyproline excretion and a significant increase of PTH accompanied Ca normalization in both groups.