Database : MEDLINE
Search on : Quinidine [Words]
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[PMID]: 29465478
[Au] Autor:Henter ID; de Sousa RT; Zarate CA
[Ad] Address:From the Experimental Therapeutics and Pathophysiology Branch, Intramural Research Program, National Institute of Mental Health, National Institutes of Health, Bethesda, MD.
[Ti] Title:Glutamatergic Modulators in Depression.
[So] Source:Harv Rev Psychiatry;, 2018 Feb 20.
[Is] ISSN:1465-7309
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Both preclinical and clinical studies have implicated glutamatergic system dysfunction in the pathophysiology of mood disorders such as bipolar depression and major depressive disorder. In particular, rapid reductions in depressive symptoms have been noted in response to subanesthetic doses of the glutamatergic modulator ketamine in subjects with major depressive disorder or bipolar depression. These results have prompted the repurposing or development of other glutamatergic modulators, both as monotherapy or adjunctive to other therapies. Here, we highlight the evidence supporting the antidepressant effects of various glutamatergic modulators, including (1) broad glutamatergic modulators (ketamine, esketamine, dextromethorphan, dextromethorphan-quinidine [Nuedexta], AVP-786, nitrous oxide [N2O], AZD6765), (2) subunit (NR2B)-specific N-methyl-D-aspartate (NMDA) receptor antagonists (CP-101,606/traxoprodil, MK-0657 [CERC-301]), (3) glycine-site partial agonists (D-cycloserine, GLYX-13, sarcosine, AV-101), and (4) metabotropic glutamate receptor modulators (AZD2066, RO4917523/basimglurant, JNJ40411813/ADX71149, R04995819 [RG1578]).
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1097/HRP.0000000000000183

  2 / 7886 MEDLINE  
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[PMID]: 29521222
[Au] Autor:Mukkavilli R; Jadhav G; Vangala S
[Ad] Address:Georgia State University, Atlanta, GA 30303. United States.
[Ti] Title:Evaluation of Drug Transport in MDCKII-Wild Type, MDCKII-MDR1, MDCKII-BCRP and Caco-2 Cell Lines.
[So] Source:Curr Pharm Biotechnol;, 2018 Mar 07.
[Is] ISSN:1873-4316
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:BACKGROUND: Drug transporters function as gatekeepers and modulate drug access into the body and various tissues. Thus a thorough and precise understanding of transporter liability for compound uptake and efflux is critical during drug development. METHODS: In the present study, we assessed the apparent permeability (Papp) and compared the efflux ratio of various compounds in stably transfected Madin-Darby Canine Kidney (MDCKII) cells overexpressing human P-gp (MDCKII-P-gp), human BCRP (MDCKII-BCRP), wild type (MDCKII-WT), and Caco-2 cell monolayers. RESULTS: We observed that quinidine, a substrate for P-gp transporter, showed efflux ratio (Papp B-A/Papp A-B) of 838 in MDCKII-P-gp cells which plummeted to 14 in presence of verapamil, a known inhibitor of P-gp. With MDCKII-WT cells, Papp of quinidine dropped from 2 to 1, in the presence of verapamil. Caco-2 cells showed a diminutive decrease in efflux ratio of quinidine from 2.5 to 1.6 by verapamil. Prazosin and dantrolene were evaluated in MDCKII-BCRP cells and were found to have 80-fold higher efflux ratio compared to MDCKII-WT cells. In Caco-2 cells, prazosin and dantrolene showed efflux ratio of 4 and 2, respectively. Rhodamine-123, a fluorogenic probe substrate of P-gp showed efflux ratio of 4 in Caco-2 cells and BCRP substrate estrone-3-sulphate showed an efflux ratio of 7. In presence of BCRP inhibitor fumitremorgin-c, the efflux ratio of estrone-3-sulfate dropped to 1 in Caco-2 cells. CONCLUSION: The very high efflux ratios of P-gp and BCRP substrates in transfected MDCKII cells clearly demonstrate the potential usefulness of these models to provide more definitive data to evaluate the transporter involvement compared to Caco-2 or MDCKII-WT cells.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.2174/1389201019666180308091855

  3 / 7886 MEDLINE  
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[PMID]: 29521135
[Au] Autor:Zanelli U; Michna T; Petersson C
[Ad] Address:a Global Early Development/Quantitative Pharmacology and Drug Disposition (QPD) , Biopharma , Merck , Darmstadt , Germany.
[Ti] Title:Determination of low intrinsic clearance in vitro: the benefit of a novel internal standard in human hepatocyte incubations.
[So] Source:Xenobiotica;:1-20, 2018 Mar 09.
[Is] ISSN:1366-5928
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:1) A novel method utilizing an internal standard in hepatocytes incubations has been developed and demonstrated to decrease the variability in the determination of intrinsic clearance in this system. The reduced variability was shown to allow differentiation of lower elimination rate constants from noise. 2) The suggested method was able to compensate for a small but systematic error (0.5 µL/min/10 cells) caused by an evaporation of approximately 15% of the volume during the incubation time. 3) The approach was validated using six commercial drugs (ketoprofen, tolbutamide, phenacetin, etodolac and quinidine) which were metabolized by different pathways. 4) The suggested internal standard, MSC1815677, was extensively characterized and the acquired data suggest that it fulfils the requirements of an internal standard present during the incubation. The proposed internal standard was stable during the incubation and showed a low potential to inhibit drug metabolizing enzymes and transporters. With MSC1815677 we propose a novel simple, robust and cost-effective method to address the challenges in the estimation of low clearance in hepatocyte incubations.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1080/00498254.2018.1451010

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[PMID]: 29473523
[Au] Autor:Etchegoyen CV; Keller GA; Mrad S; Cheng S; Di Girolamo G
[Ad] Address:Universidad de Buenos Aires - Pharmacology Ciudad Autonoma de Buenos Aires, Buenos Aires. Argentina.
[Ti] Title:Drug-induced QT Interval prolongation in the Intensive Care Unit.
[So] Source:Curr Clin Pharmacol;, 2018 02 23.
[Is] ISSN:2212-3938
[Cp] Country of publication:United Arab Emirates
[La] Language:eng
[Ab] Abstract:Drug-induced QT interval prolongation is the most frequent cause of Long QT syndrome (LQTS) in the clinical practice. This electrophysiological entity, produced by an extended duration of the myocardial repolarization and reflected as a prolonged QT interval in the superficial electrocardiogram (EKG), increases the risk of polymorphic ventricular tachycardia (Torsades de Pointes) appearance and sudden death. Certain antiarrhythmic drugs such as amiodarone, sotalol, quinidine, procainamide, verapamil and diltiazem are known as drugs that, due to their mechanism of action, prolong the QT interval, demanding constant monitorization. Nevertheless there are other widely used drugs in the Intensive Care Unit (ICU) that have no cardiovascular indication but still are frequently associated with prolonged QT interval such as ondansetron, like macrolides and fluoroquinolones , typical antipsychotic such as haloperidol and thioridazine or atypical such as sertindole. Taking into consideration this unexpected association with the prolongation of the QT interval, these drugs require a closed monitorization in these critical patients. Since ICU patients are particularly vulnerable to this sort of alteration of ventricular repolarization caused by the effect of these drugs itselves or by pharmacological interaction with other medication, which can generate extension of the QT interval as well as other clinical presentation associated with the risk of developing Torsades de Point, the strict and closed control of physicians in charge must be on a daily basis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180307
[Lr] Last revision date:180307
[St] Status:Publisher
[do] DOI:10.2174/1574884713666180223123947

  5 / 7886 MEDLINE  
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[PMID]: 29501667
[Au] Autor:Bjerregaard P
[Ad] Address:Division of Cardiology, Saint Louis University, Saint Louis, Missouri, Cardiovascular Division, Washington University in Saint Louis, Saint Louis, Missouri. Electronic address: prebenbjerregaard@hotmail.com.
[Ti] Title:The diagnosis and management of short QT syndrome.
[So] Source:Heart Rhythm;, 2018 Mar 01.
[Is] ISSN:1556-3871
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Establishing a definition of SQTS including symptomatology and QT interval duration is still a work in progress. It is clear, however, that SQTS is a rare, life-threatening, inherited heart disease presenting as SCD or aborted SCD in 34% and a family history of SCD in 15%. Genetic testing is important in diagnosing the disease, but so far with a causative mutation found in less than 25%. A benign variety of the disease has been observed in children with atrial fibrillation and a KCNH2-V141M mutation, and just recently a mutation in the cardiac Cl,HCO - exchanger AE3 was found to cause SQTS. Issues related to measuring and correcting the QT interval for heart rate has made it difficult to rely entirely on QT duration for the diagnosis of SQTS. In order to establish the diagnosis on firmer grounds, symptoms, family history and genetic testing need to be considered. While the benefit of implantation of an ICD as secondary prophylaxis against SCD in a patient with SQTS is well-documented, the benefit as primary prophylaxis is controversial and not proven by solid data. In two recent similar studies involving 115 patients at an approximate 5 year follow-up, an ICD implanted in 40 patients saved the lives of 12 who had presented with cardiac arrest in 11 and syncope in one. No appropriate shocks were delivered in any patients who did not have a history of either syncope or cardiac arrest. Currently Quinidine is the only drug which has undergone any clinical testing.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180304
[Lr] Last revision date:180304
[St] Status:Publisher

  6 / 7886 MEDLINE  
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[PMID]: 29365273
[Au] Autor:Srisomboon Y; Zaidman NA; Maniak PJ; Deachapunya C; O'Grady SM
[Ad] Address:Department of Physiology, Srinakharinwirot University.
[Ti] Title:P2Y receptor regulation of K2P channels that facilitate K secretion by human mammary epithelial cells.
[So] Source:Am J Physiol Cell Physiol;, 2018 Jan 24.
[Is] ISSN:1522-1563
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:The objective of this study was to determine the molecular identity of ion channels involved in K secretion by the mammary epithelium and to examine their regulation by purinoceptor agonists. Apical membrane voltage clamp experiments were performed on human mammary epithelial cells where the basolateral membrane was exposed to the pore-forming antibiotic amphotericin B dissolved in a solution with intracellular-like ionic composition. Addition of the Na channel inhibitor benzamil reduced the basal current, consistent with inhibition of Na uptake across the apical membrane whereas the K 3.1 channel blocker TRAM-34 produced an increase in current resulting from inhibition of basal K efflux. Treatment with K2P channel blockers quinidine, bupivacaine and a selective TASK1/TASK3 inhibitor (PK-THPP) all produced concentration-dependent inhibition of apical K efflux. qRT-PCR experiments detected mRNA expression for nine K2P channel subtypes. Western blot analysis of biotinylated apical membranes and confocal immunocytochemistry revealed that at least five K2P subtypes (TWIK1, TREK1, TREK2, TASK1 and TASK3) are expressed in the apical membrane. Apical UTP also increased the current, but pretreatment with the PKC inhibitor GF109203X blocked the response. Similarly, direct activation of PKC with phorbol 12-myristate 13-acetate produced a similar increase in current as observed with UTP. These results support the conclusion that the basal level of K secretion involves constitutive activity of apical K 3.1 channels and multiple K2P channel subtypes. Apical UTP evoked a transient increase in K 3.1 channel activity, but over time caused persistent inhibition of K2P channel function leading to an overall decrease in K secretion.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180302
[Lr] Last revision date:180302
[St] Status:Publisher
[do] DOI:10.1152/ajpcell.00342.2016

  7 / 7886 MEDLINE  
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[PMID]: 29491217
[Au] Autor:Jo K; Choi HS; Jeon S; Ahn CW; Suh HJ
[Ad] Address:Department of Public Health Science, Korea University.
[Ti] Title:Nelumbo nucifera Seed Extract Promotes Sleep in Drosophila melanogaster.
[So] Source:Biol Pharm Bull;41(3):399-408, 2018.
[Is] ISSN:1347-5215
[Cp] Country of publication:Japan
[La] Language:eng
[Ab] Abstract:The sleep-promoting effects of the water extract of Nelumbo nucifera seeds (NNE) were investigated in an invertebrate model. The effects of NNE on the subjective nighttime activity, sleep episodes, and sleep time were determined using Drosophila melanogaster and locomotor activity monitoring systems in basal and caffeine-induced arousal conditions. The movements of fruit flies were analyzed using the Noldus EthoVision-XT system, and the levels of neuromodulators were analyzed using HPLC. Expression of neuromodulator receptors was analyzed using real-time PCR. NNE was shown to contain neurotransmission-related components; γ-aminobutyric acid (GABA) (2.33±0.22 mg/g), tryptophan (2.00±0.06 mg/g), quinidine (0.55±0.33 mg/g), and neferine (0.16±0.01 mg/g). The total activity of flies during nighttime was decreased by 52% with 1.0% NNE treatment. In the individual and collective conditions, the subjective nighttime activities (45/38%) and sleep bouts (20/14%) of flies was significantly decreased with NNE treatment, while total sleep times (10/27%) were significantly increased. This sleep-promoting effect is more pronounced in caffeine-treated conditions; the nighttime activity of flies was reduced by 53%, but total sleep time was increased by 60%. Our video-tracking analysis showed a significant decrease of the moving distance and velocity of flies by NNE. This NNE-mediated sleep-promoting effect was associated with up-regulation of GABA /GABA and serotonin receptors. The NNE-mediated increase of GABA content was identified in flies. These results demonstrate that NNE effectively promotes sleep in flies by regulating the GABAergic/serotonergic neuromodulators, and could be an alternative agent for sleep promotion.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180301
[Lr] Last revision date:180301
[St] Status:In-Process
[do] DOI:10.1248/bpb.b17-00763

  8 / 7886 MEDLINE  
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[PMID]: 29352276
[Au] Autor:Osadchii OE
[Ad] Address:Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark.
[Ti] Title:Arrhythmogenic drugs can amplify spatial heterogeneities in the electrical restitution in perfused guinea-pig heart: An evidence from assessments of monophasic action potential durations and JT intervals.
[So] Source:PLoS One;13(1):e0191514, 2018.
[Is] ISSN:1932-6203
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Non-uniform shortening of the action potential duration (APD90) in different myocardial regions upon heart rate acceleration can set abnormal repolarization gradients and promote arrhythmia. This study examined whether spatial heterogeneities in APD90 restitution can be amplified by drugs with clinically proved proarrhythmic potential (dofetilide, quinidine, procainamide, and flecainide) and, if so, whether these effects can translate to the appropriate changes of the ECG metrics of ventricular repolarization, such as JT intervals. In isolated, perfused guinea-pig heart preparations, monophasic action potentials and volume-conducted ECG were recorded at progressively increased pacing rates. The APD90 measured at distinct ventricular sites, as well as the JTpeak and JTend values were plotted as a function of preceding diastolic interval, and the maximum slopes of the restitution curves were determined at baseline and upon drug administration. Dofetilide, quinidine, and procainamide reverse rate-dependently prolonged APD90 and steepened the restitution curve, with effects being greater at the endocardium than epicardium, and in the right ventricular (RV) vs. the left ventricular (LV) chamber. The restitution slope was increased to a greater extent for the JTend vs. the JTpeak interval. In contrast, flecainide reduced the APD90 restitution slope at LV epicardium without producing effect at LV endocardium and RV epicardium, and reduced the JTpeak restitution slope without changing the JTend restitution. Nevertheless, with all agents, these effects translated to the amplified epicardial-to-endocardial and the LV-to-RV non-uniformities in APD90 restitution, paralleled by the increased JTend vs. JTpeak difference in the restitution slope. In summary, these findings suggest that arrhythmic drug profiles are partly attributable to the accentuated regional heterogeneities in APD90 restitution, which can be indirectly determined through ECG assessments of the JTend vs. JTpeak dynamics at variable pacing rates.
[Mh] MeSH terms primary: Anti-Arrhythmia Agents/adverse effects
Arrhythmias, Cardiac/chemically induced
Arrhythmias, Cardiac/physiopathology
[Mh] MeSH terms secundary: Action Potentials/drug effects
Action Potentials/physiology
Animals
Electrophysiological Phenomena
Female
Flecainide/adverse effects
Guinea Pigs
In Vitro Techniques
Perfusion
Phenethylamines/adverse effects
Procainamide/adverse effects
Quinidine/adverse effects
Sulfonamides/adverse effects
[Pt] Publication type:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Anti-Arrhythmia Agents); 0 (Phenethylamines); 0 (Sulfonamides); ITX08688JL (Quinidine); K94FTS1806 (Flecainide); L39WTC366D (Procainamide); R4Z9X1N2ND (dofetilide)
[Em] Entry month:1802
[Cu] Class update date: 180226
[Lr] Last revision date:180226
[Js] Journal subset:IM
[Da] Date of entry for processing:180121
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191514

  9 / 7886 MEDLINE  
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[PMID]: 29477412
[Au] Autor:Hammond FM; Sauve W; Ledon F; Davis C; Formella AE
[Ad] Address:Indiana University School of Medicine, Indianapolis, IN, US. Electronic address: Flora.hammond@rhin.com.
[Ti] Title:Safety, Tolerability, and Effectiveness of Dextromethorphan/Quinidine for Pseudobulbar Affect Among Study Participants With Traumatic Brain Injury: Results From the PRISM-II Open Label Study.
[So] Source:PM R;, 2018 Feb 22.
[Is] ISSN:1934-1563
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:BACKGROUND: Dextromethorphan 20mg /quinidine 10mg (DM/Q) was approved to treat pseudobulbar affect (PBA) based upon phase 3 trials conducted in participants with amyotrophic lateral sclerosis or multiple sclerosis. PRISM II evaluated DM/Q effectiveness, safety and tolerability for PBA following stroke, dementia or traumatic brain injury (TBI). OBJECTIVE: To report results from the TBI cohort of PRISM II, including a TBI-specific functional scale. DESIGN: Open-label trial evaluating twice daily DM/Q over 90 days. STUDY PARTICIPANTS: Adults (n=120) with a clinical diagnosis of PBA secondary to non-penetrating TBI; stable psychiatric medications were allowed. METHODS: PRISM II was an open-label, 12-week trial enrolling adults with PBA secondary to dementia, stroke, or TBI. All study participants received DM/Q 20/10 mg twice daily. Study visits occurred at baseline and at day 30 and day 90. SETTING: 150 US centers. MAIN OUTCOME MEASUREMENTS: Primary endpoint was change in Center for Neurologic Study-Lability Scale (CNS-LS) score from baseline to day 90. Secondary outcomes included PBA episode count, Clinical and Patient Global Impression of Change (CGI-C; PGI-C), Quality of Life-Visual Analog Scale (QOL-VAS), treatment satisfaction, Neurobehavioral Functioning Inventory (NFI), Patient Health Questionnaire (PHQ-9), and Mini Mental State Examination (MMSE). RESULTS: DM/Q-treated participants showed significant mean (SD) reductions in CNS-LS from baseline (day 30, -5.6 [5.2]; day 90, -8.5 [5.2]; both, P<.001). Compared with baseline, PBA episodes were reduced by 61.3% and 78.5% at days 30 and 90 (both, P<.001). At day 90, 78% and 73% of study participants had "much improved" or "very much improved" on the CGI-C and PGI-C. QOL-VAS scores were significantly reduced from baseline (-3.7 [3.3]; P<.001). Mean (SD) PHQ-9 scores improved compared to baseline at day 30 (-3.2 [5.3], P<.001) and 90 (-5.2 [6.4], P<.001). NFI T-scores were significantly improved (P<.001), while MMSE scores were unchanged. Adverse events (AEs) were consistent with the known DM/Q safety profile; the most common AE was diarrhea (8.3%). CONCLUSIONS: DM/Q was well tolerated and significantly reduced PBA episodes in study participants with TBI. Changes in CNS-LS and PBA episode count were similar to changes with DM/Q in phase 3 trials.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180225
[Lr] Last revision date:180225
[St] Status:Publisher

  10 / 7886 MEDLINE  
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[PMID]: 29474194
[Au] Autor:Berkovich RR; Sokolov AY; Togasaki DM; Yakupova AA; Cesar PH; Sahai-Srivastava S
[Ti] Title:Dextromethorphan/Quinidine in Migraine Prophylaxis: An Open-label Observational Clinical Study.
[So] Source:Clin Neuropharmacol;, 2018 Feb 22.
[Is] ISSN:1537-162X
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:OBJECTIVE: This study aimed to assess potential efficacy and safety of dextromethorphan/quinidine (DMQ) in prophylactic treatment of migraine in patients with multiple sclerosis (MS) with superimposed pseudobulbar affect (PBA). METHODS: Multiple sclerosis patients with superimposed PBA and comorbid migraine were enrolled into this open-label observational study at the University of Southern California Comprehensive MS Center. The baseline characteristics included, among other data, frequency and severity of acute migraine attacks and use of migraine relievers. The DMQ was used exclusively per its primary indication - PBA symptoms control - 20/10 mg orally, twice a day for the mean of 4.5 months (the shortest exposure registered was 3 months and the longest, 6 months). To determine whether treatment caused an effect on migraine frequency and severity, the baseline and posttreatment values were compared using nonparametric sign test. RESULTS: Thirty-three MS subjects with PBA, who also suffered from migraines, were identified. Twenty-nine subjects had improvement in headache frequency, 4 had no change, and none had worsening (P < 0.001 as compared with the baseline). Twenty-eight subjects had improvement in headache severity, 5 had no change, and none had worsening (P < 0.001). CONCLUSIONS: Our pilot study results provide evidence that DMQ shows promise as a candidate for larger clinical studies evaluating its efficacy for the prevention of migraine headaches.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180223
[Lr] Last revision date:180223
[St] Status:Publisher
[do] DOI:10.1097/WNF.0000000000000272


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