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Roger Williams Park Zoo
Providence, Rhode
Island
Our Rating:   excellent
We last visited in July
2006.
New England's top zoo only
gets better every time we visit. We first came to this zoo
in November of 2003 and were impressed by the naturalistic
habitats and wide variety of animals. Our most recent
visit in July of 2006 further reinforced our impression that
this is truly one of our favorite zoos. A rather cramped
polar bear habitat is being expanded to nine times its original
size. The new North American Trail habitat will house not
only the polar bears but also bald eagles, bison, red wolves,
and others.
If you're in the vicinity
and only have time for one zoo visit, skip Boston and visit the
Roger Williams Park Zoo.
Shows
and Attractions
Yakety-Yak Zoo
Chats
More intimate than a
show, these chats by zookeepers and others feature either a
live animal encounter or a talk by zoo staff with specific
information on different animals housed at the zoo.
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739 Interactions between CYP1A2 and other drugs - Prostate Specific Antigen Interactions
CYP1A2 is located on the small hairpin (S2) of mammalian chromosome 2 and is also present on human chromosome 8 (Hinden et al. 2006). CYP1A2 is an enzyme located on the inner membrane of mitochondria, is involved in the metabolism of many compounds known to have an inhibitory effect on human prostate cancer cell proliferation, such as prostaglandins, catecholamines, and hormones (Zou 2003; Kostick et al. 1990). This enzyme has also been associated with the reduction of several metabolites prostaglandins. As such, CYP1A2 is considered to be an important target for the interaction of pro- and anti-prostate hormone receptors (Horn et al. 1992; McEwen 1999).
Several compounds, such as warfarin and tamoxifen, have been shown to be able inhibit CYP1A2 enzyme activity and consequently, increase cytochrome P-450 3A activity (Zou 2003). Several anti-androgenic drugs, such as tamoxifen and finasteride, increase cytochrome P-450 3A activity (Patel et al. 1998). The effect of CYP1A2 inhibition on prostate cancer cell proliferation has been demonstrated by increasing the rate of apoptosis. CYP1A2 inhibitor, tamoxifen resulted in an increased rate of apoptosis by about 30% when used in the vivo model of prostate cancer (Nakada et al. 1993; Kuzawa 1994). The increase of cytochrome P-450 3A activity, which occurs upon inhibition of CYP1A2 by several anti-androgens are known to increase prostaglandin synthesis by interfering with of prostaglandin E2 (Davies et al. 1992; Miao 1998). Prostate cancer cells can develop an imbalance between the synthesis and breakdown of prostaglandins during growth and progression drugstore highlighter australia such imbalance can increase both PSA secretion and the risk of metastasis (Chen et al. 1997; De Witte 1996). Moreover, CYP1A2 inhibition has been shown to inhibit PSA secretion a similar extent as tamoxifen but alone can decrease PSA secretion by CYP1A2 in vitro (Chen et al. 1997; De Witte 1996). Moreover, the interaction of these compounds can increase the risk of development prosta |
