U.S. Senate Special Committee on Aging. 1991, September ; . The Drug Manufacturing Industry: A Prescription for Profits. [Staff report]. Washington, D.C. U.S. Government Printing Office. Vogenberg, F. 2000, July ; . How to Convince Payers of the Value of Pharmaceuticals. Drug Benefit Trends. Vol. 12. No. 7. pp. 57-58. Wade, V., Mansfield P., & McDonald P. 1989 ; . Drug Companies Evidence to Justify Advertising. Lancet. Vol. 2. pp. 1261-1264. Waltermire, R. 1998, October ; . Direct to Consumer Advertising of Rx Drugs Can be Harmful to Your Health. Drug Benefit Trends. Vol. 10. No. 10. pp. 60-61. Wazana, A. 2000, January 19 ; . Physicians and the Pharmaceutical Industry. Is a Gift Ever Just a Gift? JAMA. Vol. 283. No 3. pp. 373-380. Wilkes M., Bell, R., & Kravitz, R. 2000, March April ; . `Direct-to-Consumer Prescription Drug Advertising: Trends, Impact, and Implications. Health Affairs. Vol. 19. No. 2. pp. 110-127. Winslow, C., et al. 1988, March 24 ; . The Appropriateness of Carotid Endarterectomy. New England Journal of Medicine. Vol. 318, No. 12. pp. 721-727. World Health Organization WHO ; . 1993 ; . Clinical Pharmacological Evaluation in Drug Control. EUR ICP DSE 173. Copenhagen, Denmark. As quoted in Blurring the Boundaries. New Trends in Drug Promotion by Barbara Mintzes. HAI-Europe, 1998. Wurtzbacher, J. 1999, December 6 ; . Controlling Spiraling Pharmacy Budgets. In a Presentation at the 34th ASHP Midyear Clinical Meeting. American Society of Health-System Pharmacists. Wyeth-Ayerst Laboratories. 1998, September ; . Latest Trends in Prescription Benefit Cost and Design. Pharmacy Benefit Management Institute: Author. Ziegler, M., Lew, P., & Singer, B. 1995, April 26 ; . The Accuracy of Drug Information from Pharmaceutical Sales Representatives. JAMA. Vol 273. No. 16. pp. 1296-1298. Zuger, A. 1999, January 11 ; . Fever Pitch: Getting Doctors to Prescribe is Big Business. New York Times.
Interviewees noted that the availability of ART reduces the burden imposed by HIV AIDS on general health facilities by reducing numbers of opportunistic infections and hospitalisations. On the other hand, some facilities reported increases in patient numbers, with no corresponding increase in staff. In others, for example where a new ARV treatment clinic was set up, additional physical infrastructure and health care workers allocated to the ART programme allowed for general health staff to focus on other health concerns. In the case of many of the earliest ART sites, this also brings challenges for integration. Here, the ART programme remains separate from general health services and functions as a special unit catering solely to patients requiring ART. Doctors involved in ART may not be involved with patients seeking care for possibly AIDS-related conditions, which can generate a time-consuming referral process for both staff and patients. Some recently developed ART sites were found to be more closely integrated with general health services and here, interviewees expressed considerable satisfaction with the extent to which the ART programme had alleviated the general health burden of the hospital. Making the transition towards greater integration with general health services remains a challenge for the early sites, for example, prozac.
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With the untreated control culture at 24, 48, and 72 h. However, the effect of cocaine on DC-SIGN gene expression was not significantly different at all the time points studied, for both IDC and MDC, although a slight increase in DC-SIGN expression was observed at 48 h IDC. Fig. 1C shows the effect of cocaine on DC-SIGN expression by MDC as analyzed by flow cytometry using PE labeled DC-SIGNspecific Ab. These results demonstrate that cocaine at 10 6, 10 and 10 12 M significantly up-regulates the percentage of DC-SIGN-positive cells: 10.3% p 0.0001 ; , 7.4% p 0.01 ; , 7.1% p 0.01 ; , and 6.4% p 0.05 ; , respectively, compared with the untreated control culture 4.7% ; . These results are consistent with the effect of cocaine on the gene expression of DCSIGN by MDC Fig. 1B ; . Data presented in Fig. 1D show the stimulatory effect of cocaine on HIV replication in MDC. MDC were infected with a dual tropic HIV-1 strain ASM-54; National Institutes of Health reagent catalog no. 2794 ; and treated with or without cocaine. The HIV-LTRR U5 region was amplified by real-time quantitative PCR using primers specific for a 180-bp fragment of the region as described 32, 33 ; . This method is designed to detect early stages of reverse transcription of HIV. Our results demonstrate that cocaine at 10 6 TAI 1.25, p 0.05 ; and 10 8 M TAI 1.53, p 0.01 ; significantly up-regulated the HIV-LTR-R U5 region compared with the untreated HIV-infected control culture TAI 1.0 ; . Data presented in Fig. 1E show the levels of p24 Ag in the culture supernatants of MDC infected with HIV-1Ba-L in the presence or absence of cocaine 10 6 M ; MDC infected with HIV-1Ba-L in the absence of cocaine produced 20.3 pg ml p24 Ag, whereas MDC infected with HIV-1Ba-L in the presence of cocaine significantly up-regulated the production of p24 Ag 46.7 pg ml, p 0.012 ; . Although MDC showed only low level of infection with HIVBa-L, which is consistent with other studies 34, 35 ; , the production of p24 Ag was significantly up-regulated by cocaine and thus supports the LTR amplification as presented in Fig. 1D. This suggests that cocaine can enhance HIV LTR-R U5 transcript expression as well as p24 Ag production by infected MDC. Cocaine increases DC-SIGN and DC-SIGNR gene expression by HIV-infected MDC Data presented in Fig. 2A show the effect of treatment of HIV-1 dual tropic strain, ASM-54; National Institutes of Health reagent catalog no. 2794 ; -infected MDC in vitro with different concentrations of cocaine on the gene expression of DC-SIGN and DCSIGNR as analyzed by real-time quantitative PCR. These results demonstrate that cocaine at 10 6 TAI 2.35, p 0.001 ; and 10 8 M TAI 1.4, p 0.05 ; significantly up-regulate DC-SIGN gene expression compared with the untreated HIV-infected control and zestoretic.
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Funding Support: This study was supported by the National Institute of Child Health and Human Development, Bethesda, Md, through cooperative agreements U10 HD 21397, U01 HD 2367902, U10 HD 213853, U10 HD 214154, U10 HD 279045, and U01 HD 198977 ; , as well as intra-agency agreements with the National Institute on Drug Abuse, Bethesda; Administration on Children, Youth, and Families, Washington, DC; and the Center for Substance Abuse Treatment, Washington. Acknowledgment: We thank Elisabeth Ravelo for the preparation of this manuscript and Abik Das and W. Kenneth Poole of Research Triangle Institute for their assistance and review of the manuscript and ziac.
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