Chlorohydrin water‐swellable rubber—composed of chlorohydrin rubber (CHR), crosslinked polyacrylate (CPA), the amphiphilic compatibilizer poly(vinyl alcohol)‐g‐poly(butyl acrylate) (PVA‐g‐PBA), precipitated silica (PSA), and poly(ethylene glycol) (PEG)—was prepared. The dispersion of PEG in the blend was characterized by wide‐angle X‐ray diffraction (WAXD). The dependence of the water absorbing ratio by weight, the water‐swelling ratio by volume, and the percentage loss by weight on PEG and PSA contents were investigated. The effects of PEG and PSA on the second water‐swelling behaviors and long‐term water‐retention behaviors were also studied. Optimums for the water‐absorbing and water‐swelling abilities within the range of the experiment were obtained. © 2001 John Wiley & Sons, Inc. J Appl Polym Sci 79: 2509–2516, 2001

COX-2-dependent prostaglandin (PG) E 2 synthesis regulates macrophage MMP expression, which is thought to destabilize atherosclerotic plaques. However, the administration of selective COX-2 inhibitors paradoxically increases the frequency of adverse cardiovascular events potentially through the loss of anti-inflammatory prostanoids and/or disturbance in the balance of pro-and anti-thrombotic prostanoids. To avoid these collateral effects of COX-2 inhibition, a strategy to identify and block specific prostanoid-receptor interactions may be required. We previously reported that macrophage engagement of vascular extracellular matrix (ECM) triggers proteinase expression through a MAPK erk1/2 -dependent increase in COX-2 expression and PGE 2 synthesis. Here we demonstrate that elicited macrophages express the PGE 2 receptors EP1-4. When plated on ECM, their expression of EP2 and EP4, receptors linked to PGE 2 -induced activation of adenylyl cyclase, is strongly stimulated. Forskolin and dibutryl cyclic-AMP stimulate macrophage matrix metalloproteinase (MMP)-9 expression in a dose-dependent manner. However, an EP2 agonist (butaprost) has no effect on MMP-9 expression, and macrophages from EP2 null mice exhibited enhanced COX-2 and MMP-9 expression when plated on ECM. In contrast, the EP4 agonist (PGE 1 -OH) stimulated macrophage MMP-9 expression, which was inhibited by the EP4 antagonist ONO-AE3-208. When compared with COX-2 silencing by small interfering RNA or inhibition by celecoxib, the EP4 antagonist was as effective in inhibiting ECM-induced proteinase expression. In addition, ECM-induced MMP-9 expression was blocked in macrophages in which EP4 was silenced by small interfering RNA. Thus, COX-2-dependent ECM-induced proteinase expression is effectively blocked by selective inhibition of EP4, a member of the PGE 2 family of receptors.Atherosclerosis is a chronic inflammatory disease characterized by lipid accumulation, macrophage recruitment, smooth muscle proliferation, and fibrosis (1, 2). Macrophage proteinase expression compromises the structural integrity of atherosclerotic lesions by degrading components of the extracellular matrix (ECM), 2 which contributes to lesion ulceration or rupture and subsequent sequelae of thrombosis, myocardial infarction, and stroke (3-6). A substantial body of evidence has identified cyclooxygenase (COX)-2 as a targetable component of the signaling pathway responsible for increased proteinase expression by macrophages in atherosclerotic lesions. COX metabolizes arachidonic acid to an unstable endoperoxide, which is then converted to the principal prostaglandins (PG) by specific synthases (7,8). COX-2 expression is elevated in atherosclerotic lesions (9 -14). PGE 2 , an important mediator of the inflammatory response, stimulates proteinase expression by a variety of cells including macrophages (15-18). Both PGE synthase and matrix metalloproteinase (MMP) activities are elevated in regions of symptomatic plaques rich in macrophages and susceptible to rupture (13,19). Moreover, tr...

The present studies compared the antiproliferative effects of diallyl trisulfide (DATS) and diallyl disulfide (DADS) on cultured human neoplastic (A549) and nonneoplastic (MRC-5) lung cells. Addition of 10 microM DATS reduced A549 growth by 47%, whereas 10 microM DADS decreased growth by only 20%. DATS treatment (10 microM) did not alter MRC-5 cell growth. DATS (10 microM) caused a marked and progressive increase in intracellular Ca2+ in A549 cells during the first four hours after treatment. Intracellular Ca2+ in A549 cells exposed to DATS returned to near control levels within one hour after refeeding complete medium without DATS. Exposure to 1 microM DATS for 24 hours significantly induced apoptosis, as indicated by increased DNA fragmentation. The ability of DATS and DADS to suppress neoplastic growth is consistent with increasing evidence that several garlic components have anticarcinogenic and antitumorigenic properties.

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