Drugs online research references
J Clin Psychopharmacol. 1992 Aug;12(4):246-50.
Nortriptyline and weight change in depressed patients over 60.
Paradis CF, Stack JA, George CJ, Miller MD, Pollock BG, Rifai AH, Mazumdar S, Perel JM, Reynolds CF 3rd.
Depression Prevention Program, Western Psychiatric Institute and Clinic, Pittsburgh, PA 15213.
Weight change in pounds and body mass index was documented in 29 geriatric patients with recurrent depression successfully treated with nortriptyline over a 30-week period of acute and continuation therapy (925 patient-weeks of nortriptyline treatment). Weight before index episode as documented by physician records, and weight at three points (beginning of treatment, end of acute therapy, and end of continuation therapy) were recorded. Weight changes over the interval between these times and net weight change over the entire interval were then calculated. Only five patients (17.2%) gained a clinically significant (greater than 10 lb) amount of weight during treatment, ranging from 10 to 43 lb above premorbid weights. Seven of 29 patients (24.1%) showed a net weight loss below premorbid levels (maximum loss 12.5 lb), and 6 patients (20.7%) showed no weight change. The pattern of weight gain was variable; no correlations were found between initially high body mass index and weight gain over the entire interval. These data suggest that nortriptyline is apparently not a potent weight promoter in this group.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1527227&dopt=Abstract
J Pharmacol Exp Ther. 1991 Feb;256(2):734-40.
Pharmacological characteristics of high-affinity serotonin uptake systems established through gene transfer.
Frnka JV, Chang AS, Lam DM.
Alice McPherson Laboratory of Retina Research, Baylor College of Medicine, The Woodlands, Texas 77381.
Inactivation of a neurotransmitter, after its stimulated release, via high-affinity uptake mechanisms is an essential regulatory step of neurotransmission in both the central and peripheral nervous systems. To initiate explorations of the molecular mechanisms and the underlying biochemical architecture of high-affinity neurotransmitter uptake systems, we have used gene transfer technology to establish and identify novel cellular models that express these systems. Human genomic DNA was transfected into mouse L-M fibroblasts and two independently arising, clonal cell lines (L-S1 and L-S2) have been identified as expressing high-affinity serotonin (5-HT) uptake systems. The 5-HT uptake characteristics of L-S1 and L-S2 are essentially comparable (in terms of Na+ dependence, temperature sensitivity, imipramine antagonizability, kinetic saturability and high affinities) and those of L-S1 have been reported previously. Furthermore, competition studies utilizing catecholamine neurotransmitters and their amino acid precursors demonstrated that these systems are highly specific for 5-HT. Several known inhibitors of high-affinity 5-HT uptake systems (including amitriptyline, desipramine, fluoxetine, imipramine, nortriptyline, tryptamine, 5-methoxytryptamine and N-acetyl 5-methoxytryptamine) were assessed in terms of their respective potencies to inhibit 5-[3H]HT uptake by L-S1 and L-S2 cells. For L-S1 cells, the rank order of inhibitor potencies is imipramine greater than amitriptyline greater than fluoxetine greater than desipramine = nortriptyline greater than tryptamine greater than 5-methoxytryptamine greater than N-acetyl-5-methoxytryptamine. For L-S2, the rank order is similar to that of L-S1 except that fluoxetine is more potent than amitriptyline.(ABSTRACT TRUNCATED AT 250 WORDS)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1994003&dopt=Abstract
Mol Pharmacol. 1992 Sep;42(3):383-90.
Cloning, pharmacological characterization, and chromosome assignment of the human dopamine transporter.
Giros B, el Mestikawy S, Godinot N, Zheng K, Han H, Yang-Feng T, Caron MG.
Department of Cell Biology, Howard Hughes Medical Institute Laboratories, Duke University Medical Center, Durham, North Carolina 27710.
We have screened a human substantia nigra cDNA library with probes derived from the rat dopamine transporter. A 3.5-kilobase cDNA clone was isolated and its corresponding gene was located on the distal end of chromosome 5 (5p15.3). This human clone codes for a 620-amino acid protein with a calculated molecular weight of 68,517. Hydropathicity analysis suggests the presence of 12 putative transmembrane domains, a characteristic feature of sodium-dependent neurotransmitter carriers. The rat and the human dopamine transporters are 92% homologous. When permanently expressed in mouse fibroblast Ltk- cells, the human clone is able to induce a saturable, time- and sodium-dependent, dopamine uptake. This transport is blocked by psychostimulant drugs (cocaine, l- and d-amphetamine, and phenyclidine), neurotoxins (6-hydroxydopamine and N-methyl-4-phenylpyridine (MPP))+), neurotransmitters (epinephrine, norepinephrine, gamma-aminobutyric acid, and serotonin), antidepressants (amitriptyline, bupropion, desipramine, mazindol, nomifensine, and nortriptyline), and various uptake inhibitors (mazindol, GBR 12783, GBR 12909, and amfonelic acid). The rank orders of the Ki values of these substances at the human and the rat dopamine transporters are highly correlated (r = 0.998). The cloning of DNA human dopamine transporter gene has allowed establishment of a cell line stably expressing the human dopamine transporter and, for the first time, an extensive characterization of its pharmacology. Furthermore, these newly developed tools will help in the study of the regulation of dopamine transport in humans and in the clarification of the potential role of the dopamine transporter in a variety of disease states.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1406597&dopt=Abstract
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