Drugs online research references
Tokai J Exp Clin Med. 1998 Dec;23(6):285-92.
PCR follow-up examination after treatment of canine leishmaniosis (CaL).
Steuber S, Moritz A, Schirrmann I, Greiner M.
Federal Institute for Health Protection of Consumers and Veterinary Medicine (BgVV), Berlin, Germany.
A study has been performed to investigate the usefulness of the polymerase chain reaction (PCR) for both the diagnosis and the follow-up after treatment of canine leishmaniosis (CaL). Blood samples (PBL) and/or bone marrow aspirates (BM) could be examined in a total of 18 confirmed cases of primary CaL. PBL was PCR-positive in 87%, whereas the BM was found to be positive in all cases (n=14) tested. PBL and BM from a total of 13 patients were submitted to PCR examinations after meglumine antimoniate (Glucantime) treatment. Only one dog showed a negative PCR after 2 treatment cycles (days 1-2: 50 mg/kg bw; days 3-10: 100 mg/kg bw). Examination of the PBL and BM after 15 months remained further PCR negative. All other dogs, from which four were pretreated with allopurinol up to 5 weeks, continued to be positive (92%) at least in the BM. Ten dogs could be monitored by means of the PCR after allopurinol treatment (2 x 10 mg/kg/bw/day/) either as a monodrug therapy in seven or as a successive combination with Glucantime in three cases. Two out of three dogs which showed good clinical improvement after daily administration for five weeks were likewise PCR negative in both the PBL and the BM. The four other dogs remained positive after the single therapy with allopurinol up to 5 weeks. A further three dogs were treated with allopurinol for 5 weeks, 6 and 20 month, respectively, after being clinically cured with Glucantime. Two of them were PCR negative in the PBL and BM after 5 weeks and 20 month, respectively. The results presented suggest that longterm treatment with allopurinol has some therapeutic benefit in CaL especially when administered following treatment with the pentavalent antimonial Glucantime.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10622624&dopt=Abstract
Biochem Pharmacol. 1993 Feb 24;45(4):893-7.
Allopurinol transport in human erythrocytes.
Razavi M, Kraupp M, Marz R.
Institute of Medical Chemistry, University of Vienna, Austria.
The mechanism of allopurinol [4-hydroxypyrazolo(3,4-d)pyrimidine] transport into human erythrocytes was investigated with an inhibitor stop assay. Allopurinol transport could be resolved into two components: (1) a saturable system and (2) a non-saturable process, which most likely represents non-facilitated diffusion. Allopurinol transport had a Km of 268 mumol/L and a Vmax of 28 pmol/microL intracellular volume/sec; the non-saturable component was 0.0195/sec. Mutual inhibition studies showed that the competitive Ki values of hypoxanthine and adenine on allopurinol transport were 120 and 3 mumol/L, respectively. These Ki values as well as the IC50 values of 100-150 mumol/L for hypoxanthine and 3-10 mumol/L for adenine were similar to the corresponding transport Km values of these bases, which are 128 and 8 mumol/L, respectively. The Ki of allopurinol on hypoxanthine transport was 274 mumol/L and thus nearly identical to its Km. Thus in erythrocytes the uricostatic agent allopurinol is an alternative substrate for the purine transport system, but lacks the exceptional high affinity it has for xanthine oxidase. This could explain the paradoxical clinical side effect of allopurinol, namely that it can provoke an attack of gout. Theophylline, a methylated purine, inhibited allopurinol transport with an IC50 of 200-400 mumol/L. Oxypurinol [4,6-dihydroxypyrazolo(3,4-d)pyrimidine], the main metabolite of allopurinol, also inhibited allopurinol transport with an IC50 of 20-40 mumol/L. This is noteworthy, since allopurinol and oxypurinol do not share the same transport system in the kidney.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8452564&dopt=Abstract
Neurosci Lett. 1996 Jul 26;213(1):37-40.
E-selectin expression on human brain microvascular endothelial cells.
Hess DC, Thompson Y, Sprinkle A, Carroll J, Smith J.
Neurology Service (127), V.A. Medical Center, Augusta, GA, USA.
E-Selectin is an endothelial adhesion molecule involved in binding and targeting of neutrophils. Little is known of its expression in the brain. We examined the expression of E-selectin on cultured human brain microvascular endothelial cells (HBMEC). There was no basal expression of E-selectin on HBMEC but with I1-1b, tumor necrosis factor (TNF), or lipopolysaccharide (LPS) stimulation there was surface expression at 4 h. The expression was quantitatively less than on cultured human umbilical vein endothelial cells (HUVEC). The cytokine-induced upregulation was partially inhibited with the glutathione donor, N-acetylcysteine (NAC), the free radical scavenger, dimethylthiourea (DMTU; 15 mM) and dexamethasone (1 microM). Allopurinol (100 microM) had no effect. TNF activated nuclear factor kappa B (NF kappa B) in HBMEC. This activation could be attenuated by prior treatment with NAC and dexamethasone. Thiol donors and corticosteroids could play a role in inhibiting potentially deleterious neutrophil-endothelial interactions in inflammatory conditions involving the brain.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8844707&dopt=Abstract
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