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Funds Mutual Vanguard       298 Faculty of Medicine Siriraj Hospital maintenance of local homeostasis in the body. Elucidation of PGE₂ involvement in the signalling molecules such as COX could lead to potential therapeutic interventions. Here, we have investigated the effects of PGE₂ on the induction of COX-2 in human umbilical vein endothelial cells (HUVEC) treated with IL-1b (1 ng/ml). COX activity was measured by the production of 6-keto-PGF_1a, PGE₂, PGF_2a and TXB₂ in the presence of exogenous arachidonic acids (10 mM for 10 min) using enzyme immunoassay (EIA). COX-1 and COX-2 protein was measured by immunoblotting using specific antibody. Untreated HUVEC contained only COX-1 protein while IL-1b treated HUVEC contained COX-1 and COX-2 protein. PGE₂ (3 mM for 24h) did not affect on COX activity and protein in untreated HUVEC. Interestingly, PGE₂ (3 mM for 24h) can inhibit COX-2 protein, but not COX-1 protein, expressed in HUVEC treated with IL-1b. This inhibition was reversed by coincubation with foskolin (100 mM). The increased COX activity in HUVEC treated with IL-1b was also inhibited by PGE₂ (0.03, 0.3 and 3 mM for 24h) in a dose dependent manner. Similarly, foskolin (10, 50 or 100 mM) can also reverse the inhibition of PGE₂ on increased COX activity in IL-1b treated HUVEC. The results suggested that i) PGE₂ can be negative feedback regulation in the induction of COX-2 elicited by IL-1b in endothelial cells, ii) the inhibition of PGE₂ on COX-2 protein and activity in IL-1b treated HUVEC was mediated by cAMP and iii) the therapeutic uses of PGE₂ in the condition which COX-2 has been involved may have roles.

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Deltastock Inc. contributes cash payments to the Fund for Compensation of Investors . The Fund shall guarantee the payment of compensation to the clients of an investment intermediary and to its subsidiaries in the host member states under the conditions and procedure of the Law on Public Offering of Securities, by the raised in the fund money, in the cases where the investment intermediary is not able to pay its liabilities to the clients, due to reasons directly linked to its financial situation .

Funds Market Money (Med. Inflam. 1999; in press.)   THE INDUCTION OF CYCLOOXYGENASE-2 IN ENDOTOXIN ACTIVEATED ENDOTHELIAL CELLS IS INHIBITED BY PROSTAGLANDIN E2. Akarasereenont P, Techatrisak K, Chotewuttakorn S, Thaworn A. Department of Pharmacology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, THAILAND.

High Yield Plus Fund Inc. (the Fund) is a diversified, end management investment company. The Fund's primary objective is to provide a high level of current income to shareholders. It seeks to achieve this objective through investment of at least 80% of its investable assets in publicly or privately offered, rated securities of comparable quality. As a secondary investment objective, the Fund will seek capital appreciation, but only when consistent with its primary objective. The Fund has agreements with, among others, Wellington Management Company, LLP (the Investment Adviser) and Prudential Investments LLC (the Administrator). The Investment Adviser makes investment decisions on behalf of the Fund.

Funds In Investing Mutual Key words : COX-2, PGE₂, endothelium

3. Subscriber agrees, as a condition to continued receipt of IBD Alerts Plus and its Content, Subscriber shall not create, sponsor or permit the trading on its exchange facilities, if any, of financial instruments or investment products (including, without limitation, derivatives, structured products, investment funds, traded funds (e.g., options on ETFs or futures on ETFs)) where the price, or performance of such instrument or product is based on, related to, or intended to track, any index published by Dow Jones or financial instrument or investment product (e.g., traded fund) linked to an index published by Dow Jones, without a separate written agreement with Dow Jones for such purpose.

Fidelity Funds Mutual                      Cyclooxygenase (COX), which exists as COX-1 and COX-2 isoforms, is the first enzyme in the pathway in which arachidonic acid is converted to prostaglandins (PGs). PGs have numerous cardiovascular and inflammatory effects. PGE₂ exerts a variety of biological activities for the maintenance of local homeostasis in the body. Elucidation of PGE₂ involvement in the signalling molecules such as COX or nitric oxide (NO) could lead to potential therapeutic interventions. Here, we have investigated the effects of PGE₂ on COX activity to produce various PGs (COX metabolites; PGI₂, PGE₂, PGF_2a and TXA₂) using enzyme immunoassay (EIA) and the isoform of COX protein expression using immunoblotting in endotoxin-activated endothelial cells. Human umbilical vein endothelial cells (HUVEC) activated with endotoxin (1 mg/ml for 24h) increased a variety of COX metabolites which the highest production is 6-keto-PGF_1a (stable metabolite of PGI₂; 14.44±1.04 ng/ml), PGE₂ (2.89±0.20 ng/ml), PGF_2a (0.98±0.01 ng/ml) and TXA₂ (0.07±0.01 ng/ml), respectively. PGE₂ (3 mM for 24h) did not affect on COX activity in untreated HUVEC. When endotoxin-treated HUVEC were coincubated with PGE₂ (0.03, 0.3 and 3 mM for 24h), the increased 6-keto-PGF_1a and PGE₂ but not PGF_2a and TXA₂ was inhibited in a dose dependent manner. At the level of COX isoform expression, untreated HUVEC contained only COX-1 protein while endotoxin-treated HUVEC contained COX-1 and COX-2 protein. Interestingly, the induction of COX-2 protein in endotoxin-treated HUVEC can inhibited by PGE₂ in a dose dependent manner while COX-1

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