Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.16.2 (PCP)
 3,761 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The binding of neuropeptide Y (NPY) and peptide YY (PYY) to sigma and phencyclidine (PCP) receptors in brain membranes was studied. NPY and PYY at up to 500 nM did not bind to sigma or PCP receptors under different binding conditions including different temperatures, membrane preparations, protease inhibitor and sources of the peptides. These findings are in contrast with the reported potent affinities of NPY and PYY for sigma and PCP receptors by Roman et al. (1989, European J. Pharmacol. 174, 301).
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PMID:Neuropeptide Y and peptide YY do not bind to brain sigma and phencyclidine binding sites. 164 26

The present study addressed the hypothesis that the DA transporter ligand, [3H]mazindol, labels multiple sites/states associated with the dopamine (DA) transporter in striatal membranes. Incubations with [3H]mazindol proceeded for 18-24 hr at 4 degrees C in 55.2 mM sodium phosphate buffer, pH 7.4, with a protease inhibitor cocktail. In order to obtain data suitable for quantitative curve fitting, it was necessary to repurify the [3H]mazindol by HPLC before a series of experiments. Under these conditions, we observed greater than 80% specific binding. The method of binding surface analysis was used to characterize the interaction of GBR12935, BTCP, mazindol, and CFT with binding site/sites labeled by [3H]mazindol. A one site model fit the data as well as the two site model: Bmax = 16911 fmol/mg protein, Kd of [3H]mazindol = 75 nM, Ki of GBR12935 = 8.1 nM, Ki of CFT = 50 nM and Ki of BTCP = 44 nM. The inhibitory mechanism (competitive or noncompetitive) of several drugs (GBR12935, CFT, BTCP, cocaine, cis-flupentixol, nomifensine, WIN35,065-2, bupropion, PCP, and benztropine) was determined. All drugs inhibited [3H]mazindol binding by a competitive mechanism. Although the ligand-selectivity of the [3H]mazindol binding site indicates that it is the uptake inhibitor recognition site of the classic DA transporter, the quantitative differences among the ligand-selectivities of different radioligands for the same site suggest that each radioligand labels different overlapping domains of the DA uptake inhibitor recognition site. It is likely that development of domain-selective drugs may further our understanding of the DA transporter.
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PMID:Studies of the biogenic amine transporters. 1. Dopamine reuptake blockers inhibit [3H]mazindol binding to the dopamine transporter by a competitive mechanism: preliminary evidence for different binding domains. 818 30

As the decade draws to a close, physicians can be cautiously optimistic about the prevention and treatment of opportunistic infections in children with HIV disease. As more children receive therapy with powerful antiretroviral regimens, fewer are likely to be at risk for opportunistic pathogens. The widespread use of protease inhibitor combination therapies has already resulted in a dramatic decrease in morbidity and mortality in the population of HIV-infected adults. The same effect has been seen at pediatric care centers throughout the United States. Clinicians caring for HIV-infected children are now considering the safety of discontinuing prophylactic therapies for children with sustained immunologic improvement on antiretroviral therapy. For children who remain at risk, prophylactic regimens for PCP and MAC have been shown to decrease the risk for these infections. Preventive regimens for several other opportunistic infections are also available. The understanding of the pathogenesis of HIV and many of the opportunistic pathogens has led to the development of a variety of efficacious therapies for these infections. Despite these advances, physicians can anticipate that HIV-infected children will continue to develop opportunistic infections and other related complications. Some children fail to respond to antiretroviral therapies, whereas others are unable to tolerate the complex medication regimens. Prophylactic therapies are not 100% protective and, despite improved treatments, few opportunistic infections are cured. Most require lifelong maintenance therapy in the absence of immune reconstitution. Drug interactions, complex dosing schedules, adverse side effects, and high costs further limit the efficacy of these therapies. The prophylaxis, diagnosis, and treatment of opportunistic infections are likely to remain integral components of HIV care for the near and distant future.
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PMID:Opportunistic infections and other clinical manifestations of HIV disease in children. 1069 43

A new study to be presented at the 12th World AIDS Conference demonstrates that IL-2 dramatically restores immune function in people with AIDS. The study group included patients with fewer than 200 CD4-cells and a history of severe AIDS-related complications including CMV retinitis, PCP, wasting syndrome, KS, and Cryptococcal meningitis. In the study, CD4 counts rose 96 percent when IL-2 was added to protease inhibitor therapy. The increases were sustained, and naive cells increased as well. Most common side effects included fever, fatigue, sinus congestion, and headache; most side effects stopped within 24 hours of completing the treatment cycle. The findings represent new hope for people whose immune systems are substantially compromised. Contact information is provided.
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PMID:New data on IL-2. 1136 33