Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.1.21 (CPT)
 4,580 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Intravenous (I.V.) cocaine (0.03-3 mg/kg) produced dose-dependent, rapid, and brief increases in blood pressure (BP) in conscious rats pretreated with the dopamine receptor antagonist, SCH 23390. Monoamine uptake inhibitors structurally analogous to cocaine (cocaethylene, CFT, betaCIT, CPT, (+)-cocaine, norcocaine, and benztropine) also produced this rapid pressor response, whereas structurally unrelated uptake inhibitors with diverse monoamine transporter selectivities (BTCP, indatraline, GBR 12935, mazindol, nomifensine, and zimeldine) either did not produce a rapid pressor response or produced only a small pressor response. At nonconvulsant doses, the sodium channel blockers acetylprocainamide, dibucaine, dyclonine, prilocaine, proparacaine, quinidine, and tetracaine produced a small pressor response or no increase in BP. In rats implanted with telemetric devices, cocaine and its analog, CFT, produced a biphasic pharmacological response that consisted of an initial brief and abrupt behavioral arousal associated with a rapid, large increase in BP followed by prolonged, parallel increases in BP and locomotor activity. Pretreatment with SCH 23390 prevented the prolonged but not the initial rapid and brief pressor and activity responses to both cocaine and CFT administration. The present data suggest that the inhibition of dopamine, norepinephrine, or serotonin transporter functions, either alone or in combination, does not mediate the rapid pressor response to cocaine. The sodium channel-blocking action of cocaine per se does not appear to be involved in the rapid pressor response to cocaine. Finally, the present results confirm previous findings that dopaminergic mechanisms mediate the prolonged increases in BP and locomotor activity produced by cocaine.
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PMID:Monoamine transporter and sodium channel mechanisms in the rapid pressor response to cocaine. 947 74

The aim of this study is to evaluate Protein Z (PTZ) and protein C (PTC) levels in newborns suffering from RDS, healthy preterm and full term newborns and to compare PTZ serum levels in RDS preterm infants with healthy preterm before and after recovery. Sixty newborn infants, recruited from the neonatal unit, were enrolled in the study and divided into 3 groups: Group (I): 20 preterm with RDS, Group (II): 20 healthy preterm control newborns (CPT) and Group (III): 20 healthy full term control newborns (CFT). Protein Z and C were measured using ELISA kits. The results of the study showed lower levels of protein Z were obtained in RDS group compared to preterm controls whose levels were significantly lower than in full-term controls. A significant increase in PTZ levels in RDS' group after recovery, when compared to preterm controls. In RDS, no significant correlations existed between PTZ levels (before and after recovery) and routine investigations except for a significant negative correlation with platelets count. No significant differences were found in PTC levels between the 3 studied groups. To conclude: premature newborns suffering from RDS showed decreased serum protein Z levels than normal preterm control newborns with further increase in its pattern after recovery. Further studies are recommended to evaluate the role of PTZ on outcome in premature newborns with RDS and to evaluate the relationship between protein PTZ and PTC and other coagulation factors incriminated in the development of RDS.
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PMID:Role of protein Z and protein C in neonates with respiratory distress syndrome in Egypt (experience of one centre). 2018 Mar 21