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Unless the sonographer has spent time studying normal peritoneal thickness, this finding could easily be missed.
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To identify molecular markers associated with adhesion and normal peritoneal tissue using microarray expression profiling.
To determine the response of adhesion and normal peritoneal fibroblasts to interferon-γ (IFN-γ) under normal and hypoxic conditions.
To determine whether the COX-2 gene is expressed in human fibroblasts isolated from normal peritoneal and adhesion tissues.
To determine whether docosahexaenoic acid (DHA) reduces adhesion marker mRNA levels in normal peritoneal and adhesion fibroblasts.
To determine the mechanism by which hypoxia increases expression of iNOS in human normal peritoneal and adhesion fibroblasts.
To determine whether α smooth muscle cell actin (αSMCA) is expressed in human fibroblasts isolated from normal peritoneal and adhesion tissues.
To determine the levels of COX-1, COX-2, and prostaglandin (PG) E2 in human fibroblasts isolated from normal peritoneal and adhesion tissues.
To determine whether normal peritoneal and adhesion fibroblasts express tissue plasminogen activator (tPA) and plasminogen activator inhibitor (PAI-I) and whether their expression is regulated by oxygen.
Fig. 1 a Normal peritoneal stripe (white arrow) in a patient without pneumoperitoneum in right hypochondrium scan with linear probe.
When added simultaneously with LPS at culture initiation, 10 to 100 microM cortisone increased the viability of normal peritoneal macrophages as determined by trypan blue exclusion.
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