Cyclooxygenase 2 (COX-2) mRNA, protein, and activity are transiently induced after infection of human fibroblasts with human cytomegalovirus. Prostaglandin E 2, the product of COX-2 activity, is transiently increased by a factor of >50 in cultures of virusinfected fibroblasts. Both specific (BMS-279652, 279654, and 279655) and nonspecific (indomethacin) COX-2 inhibitors can abrogate the virus-mediated induction of prostaglandin E2 accumulation. Levels of COX-2 inhibitors that completely block the induction of COX-2 activity, but do not compromise cell viability, reduce the yield of human cytomegalovirus in human fibroblasts by a factor of >100. Importantly, the yield of infectious virus can be substantially restored by the addition of prostaglandin E 2 together with the inhibitory drug. This finding argues that elevated levels of prostaglandin E 2 are required for efficient replication of human cytomegalovirus in fibroblasts. H uman cytomegalovirus (HCMV) is a ubiquitous member of the herpesvirus family. HCMV infection of healthy adults is generally subclinical. However, the virus is a major infectious cause of birth defects, and it is an adventitious pathogen that causes disease and mortality in immunocompromised individuals (1).HCMV infection dramatically alters the steady state levels of many cellular mRNAs (2-4). The quantity of 1,425 cellular mRNAs, of Ϸ12,600 assayed, changed by a factor of Ն3 during the first 48 h after infection of human fibroblasts (3).The mRNAs encoding several constituents of the pathway that produces prostaglandin H 2 (PGH 2 ) from arachidonic acid are among those modulated by HCMV infection (2, 3). The mRNAs encoding cytosolic phospholipase A2 (cPLA2) and cyclooxygenase 2 (COX-2) increase, and the mRNA encoding lipocortin 1, also known as annexin 1, decreases after infection. When activated by phosphorylation, cPLA2 cleaves and releases arachidonic acid from membranes (5, 6), which can then be converted by COX-2 to PGH 2 . Lipocortin 1 binds to cPLA2 and inhibits its activation (7-9), blocking the release of arachidonic acid that can serve as a substrate for COX-2. If mRNA levels reflect enzymatic activity, then one would expect that the production of PGH 2 and its metabolites is strongly induced after HCMV infection. Consistent with this prediction, arachidonic acid release (10-12) and prostaglandin E 2 synthesis (PGE 2 is made from PGH 2 by PGE 2 synthase) are induced after infection of monocytes with HCMV (10, 13). Prostaglandins serve as second messages that elicit a wide range of physiological responses in cells and tissues. They have the potential to exert profound effects on HCMV replication and pathogenesis, given their ability to modulate gene expression and immune function.A specific inhibitor of COX-2 has been shown to block the accumulation of PGE 2 after HCMV infection (13), and nonspecific inhibitors of the enzyme, i.e., compounds that affect COX-2, as well as other targets, reduce virus yields in cultured cells (13,14). The mechanism for this inhibition is not clear, ...

When used for staged breast reconstruction, this unique, sterile ADM seems to induce less inflammation. Moreover, the significantly decreased presence of myofibroblasts in this material supports the observed clinical findings of decreased capsular contracture in ADM-assisted breast reconstruction.

Our study serves as a guide for umbilical positioning with mean measurements for men and women, and categorized by sex and race.

There are clear physiologic differences in single muscle fibers from cleft palates and normal palates: cleft palate fibers are physiologically fast, have greater fatigability, and have greater power production. Detection of functional and/or fiber type differences in muscles of cleft palates may provide preoperative identification of a patient's susceptibility to velopharyngeal inadequacy and permit early surgical intervention to correct this clinical condition.