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[PMID]:29251976
[Au] Autor:Arger CA; Heil SH; Sigmon SC; Tidey JW; Stitzer ML; Gaalema DE; Durand HJ; Bunn JY; Ruggieri EK; Higgins ST
[Ad] Endereço:Vermont Center on Tobacco Regulatory Science, Department of Psychiatry, University of Vermont.
[Ti] Título:Preliminary validity of the modified Cigarette Evaluation Questionnaire in predicting the reinforcing effects of cigarettes that vary in nicotine content.
[So] Source:Exp Clin Psychopharmacol;25(6):473-478, 2017 12.
[Is] ISSN:1936-2293
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Validity studies evaluating self-report measures in relation to behavioral preference of cigarettes varying in nicotine content are needed. The current study examined the relationship between ratings on the modified Cigarette Evaluation Questionnaire (mCEQ) and the relative reinforcing effects of Spectrum research cigarettes (15.8, 5.2, 2.4, 0.4 mg per gram of tobacco). Data for this secondary analysis were obtained from a double-blind study (Higgins et al., 2017) evaluating the subjective and reinforcing effects of Spectrum cigarettes under acute smoking abstinence. Current smokers (N = 26) were recruited from three vulnerable smoking populations (economically disadvantaged women of reproductive age, opioid-maintained individuals, individuals with affective disorders). In Phase 1 (five sessions), the mCEQ (Satisfaction, Psychological Reward, Enjoyment of Respiratory Tract Sensations, Craving Reduction, Aversion subscales) was administered following ad lib smoking of Spectrum cigarettes and subscale differences scores were calculated by subtracting ratings of the 15.8 mg/g cigarette from ratings of the reduced nicotine content cigarettes. In Phase 2 (six sessions), participants completed six 2-dose concurrent choice tests. The relationship between mCEQ subscale difference scores from Phase 1 and nicotine dose choice from Phase 2 was examined using mixed-model repeated-measures analyses of variance. Higher Satisfaction and lower Aversion subscale difference scores were associated with choosing the 15.8 mg/g cigarette more than the 5.2, 2.4, and 0.4 mg/g cigarettes. Scores on the other mCEQ subscales were not associated with nicotine choice. These results provide support for validity of the mCEQ Satisfaction and Aversion subscales predicting the relative reinforcing effects and abuse liability of varying nicotine content cigarettes. (PsycINFO Database Record
[Mh] Termos MeSH primário: Nicotina/administração & dosagem
Agonistas Nicotínicos/administração & dosagem
Abandono do Hábito de Fumar
Fumar/psicologia
Inquéritos e Questionários
Produtos do Tabaco/efeitos adversos
[Mh] Termos MeSH secundário: Adulto
Relação Dose-Resposta a Droga
Método Duplo-Cego
Feminino
Seres Humanos
Masculino
Avaliação de Resultados (Cuidados de Saúde)
Satisfação Pessoal
Valor Preditivo dos Testes
Reforço (Psicologia)
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Nicotinic Agonists); 6M3C89ZY6R (Nicotine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180224
[Lr] Data última revisão:
180224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171219
[St] Status:MEDLINE
[do] DOI:10.1037/pha0000145


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[PMID]:29232312
[Au] Autor:Karam-Hage M; Kypriotakis G; Robinson JD; Green CE; Mann G; Rabius V; Wippold R; Blalock JA; Mouhayar E; Tayar J; Chaftari P; Cinciripini PM
[Ti] Título:Improvement of Smoking Abstinence Rates With Increased Varenicline Dosage: A Propensity Score-Matched Analysis.
[So] Source:J Clin Psychopharmacol;38(1):34-41, 2018 Feb.
[Is] ISSN:1533-712X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE/BACKGROUND: It is unclear whether increasing the dose of varenicline beyond the standard dose of 2 mg/d would improve smoking abstinence. METHODS: We examined the effect of 3 mg/d of varenicline on smoking abstinence among smokers who had reduced their smoking by 50% or more in response to 2 mg/d for at least 6 weeks but had not quit smoking. Of 2833 patients treated with varenicline, dosage of a subset of 73 smokers was increased to 3 mg/d after 6 weeks. We used a propensity score analysis involving multiple baseline covariates to create a comparative sample of 356 smokers who remained on 2 mg/d. All smokers received concurrent and similar smoking-cessation counseling. RESULTS: At 3 months, we found higher 7-day point prevalence smoking-abstinence rate in the 3-mg group (26%) than in the 2-mg group (11.5%, χ = 10.60, P < 0.001; risk ratio [RR], 2.3; 95% confidence interval [CI], 1.4-3.6). The difference in abstinence rates remained significant at the 6-month (P < 0.001; RR, 2.6; 95% CI, 1.6-3.9) and 9-month follow-up (P < 0.001; RR, 2.2; 95% CI, 1.4-3.3). CONCLUSIONS: A relatively small increase in the daily dose of varenicline seems to offer a benefit for those who are not able to achieve total abstinence after approximately 6 weeks of 2 mg/d.
[Mh] Termos MeSH primário: Agonistas Nicotínicos/administração & dosagem
Abandono do Hábito de Fumar/métodos
Fumar/epidemiologia
Vareniclina/administração & dosagem
[Mh] Termos MeSH secundário: Aconselhamento/métodos
Relação Dose-Resposta a Droga
Feminino
Seguimentos
Seres Humanos
Masculino
Meia-Idade
Pontuação de Propensão
Estudos Retrospectivos
Abandono do Hábito de Fumar/estatística & dados numéricos
Fatores de Tempo
Produtos para o Abandono do Uso de Tabaco
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nicotinic Agonists); W6HS99O8ZO (Varenicline)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE
[do] DOI:10.1097/JCP.0000000000000829


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[PMID]:27775852
[Au] Autor:Pardo M; Beurel E; Jope RS
[Ad] Endereço:Department of Psychiatry and Behavioral Sciences, Miller School of Medicine, University of Miami, Miami, FL, 33136, USA.
[Ti] Título:Cotinine administration improves impaired cognition in the mouse model of Fragile X syndrome.
[So] Source:Eur J Neurosci;45(4):490-498, 2017 Feb.
[Is] ISSN:1460-9568
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Cotinine is the major metabolite of nicotine and has displayed some capacity for improving cognition in mouse models following chronic administration. We tested if acute cotinine treatment is capable of improving cognition in the mouse model of Fragile X syndrome, Fmr1 knockout mice, and if this is related to inhibition by cotinine treatment of glycogen synthase kinase-3ß (GSK3ß), which is abnormally active in Fmr1 mice. Acute cotinine treatment increased the inhibitory serine-phosphorylation of GSK3ß and the activating phosphorylation of AKT, which can mediate serine-phosphorylation of GSK3ß, in both wild-type and Fmr1 mouse hippocampus. Acute cotinine treatment improved cognitive functions of Fmr1 mice in coordinate and categorical spatial processing, novel object recognition, and temporal ordering. However, cotinine failed to restore impaired cognition in GSK3ß knockin mice, in which a serine9-to-alanine9 mutation blocks the inhibitory serine phosphorylation of GSK3ß, causing GSK3ß to be hyperactive. These results indicate that acute cotinine treatment effectively repairs impairments of these four cognitive tasks in Fmr1 mice, and suggest that this cognition-enhancing effect of cotinine is linked to its induction of inhibitory serine-phosphorylation of GSK3. Taken together, these results show that nicotinic receptor agonists can act as cognitive enhancers in a mouse model of Fragile X syndrome and highlight the potential role of inhibiting GSK3ß in mediating the beneficial effects of cotinine on memory.
[Mh] Termos MeSH primário: Cognição/efeitos dos fármacos
Cotinina/uso terapêutico
Síndrome do Cromossomo X Frágil/tratamento farmacológico
Agonistas Nicotínicos/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Cotinina/administração & dosagem
Cotinina/farmacologia
Proteína do X Frágil de Retardo Mental/genética
Síndrome do Cromossomo X Frágil/genética
Glicogênio Sintase Quinase 3 beta/genética
Glicogênio Sintase Quinase 3 beta/metabolismo
Hipocampo/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Mutação de Sentido Incorreto
Agonistas Nicotínicos/administração & dosagem
Agonistas Nicotínicos/farmacologia
Fosforilação
Processamento de Proteína Pós-Traducional
Proteínas Proto-Oncogênicas c-akt/metabolismo
Percepção Espacial
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Fmr1 protein, mouse); 0 (Nicotinic Agonists); 139135-51-6 (Fragile X Mental Retardation Protein); EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); K5161X06LL (Cotinine)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1111/ejn.13446


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[PMID]:29227073
[Au] Autor:Uspenska KR; Gergalova GL; Lykhmus OY; Skok MV
[Ti] Título:The effect of amixin and agmatine on cytochrome C release from isolated mitochondria
[So] Source:Ukr Biochem J;88(1):5-10, 2016 Jan-Feb.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:Mitochondrial nicotinic acetylcholine receptors (nAChRs) control permeability transition pore formation and cytochrome c release in the presence of apoptogenic factors. This study demonstrates that pharmacological agents amixin and agmatine affect mitochondrial nAChR functioning: they slightly suppress cytochrome c release from mouse brain and liver mitochondria stimulated with apoptogenic dose of Са2+ and prevent the effect of α7 nAChR agonist PNU282987. We conclude that mitochondria may be one of therapeutic targets of amixin and agmatine.
[Mh] Termos MeSH primário: Agmatina/farmacologia
Indutores de Interferon/farmacologia
Mitocôndrias/efeitos dos fármacos
Tilorona/farmacologia
Receptor Nicotínico de Acetilcolina alfa7/metabolismo
[Mh] Termos MeSH secundário: Animais
Benzamidas/antagonistas & inibidores
Benzamidas/farmacologia
Encéfalo/efeitos dos fármacos
Compostos Bicíclicos com Pontes/antagonistas & inibidores
Compostos Bicíclicos com Pontes/farmacologia
Cálcio/farmacologia
Fracionamento Celular
Citocromos c/antagonistas & inibidores
Citocromos c/secreção
Fígado/efeitos dos fármacos
Fígado/metabolismo
Camundongos
Camundongos Endogâmicos C57BL
Mitocôndrias/metabolismo
Agonistas Nicotínicos/farmacologia
Especificidade de Órgãos
Receptor Nicotínico de Acetilcolina alfa7/agonistas
Receptor Nicotínico de Acetilcolina alfa7/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzamides); 0 (Bridged Bicyclo Compounds); 0 (Interferon Inducers); 0 (Nicotinic Agonists); 0 (PNU-282987); 0 (alpha7 Nicotinic Acetylcholine Receptor); 70J407ZL5Q (Agmatine); 9007-43-6 (Cytochromes c); O6W7VEW6KS (Tilorone); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.01.005


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[PMID]:27778062
[Au] Autor:Tutka P; Kondrat-Wróbel MW; Zaluska K; Zólkowska D; Florek-Luszczki M; Luszczki JJ
[Ad] Endereço:Department of Pharmacology, University of Rzeszów, Al. Rejtana 16c, 35-959, Rzeszów, Poland. tutka@umlub.pl.
[Ti] Título:Cytisine inhibits the protective activity of various classical and novel antiepileptic drugs against 6 Hz-induced psychomotor seizures in mice.
[So] Source:Psychopharmacology (Berl);234(2):281-291, 2017 Jan.
[Is] ISSN:1432-2072
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Cytisine (CYT) is a partial agonist of brain α4ß2 nicotinic acetylcholine receptors widely used in Central/Eastern Europe for smoking cessation. OBJECTIVES: This study evaluated the effect of CYT on the ability of classical and novel antiepileptic drugs to prevent seizures evoked by the 6-Hz test, a model of psychomotor seizures in mice thought as a model of drug-resistant seizures. RESULTS: CYT administered intraperitoneally (i.p.) in a dose of 2 mg kg significantly inhibited the anticonvulsant activity of lacosamide, levetiracetam, and pregabalin, increasing their median effective doses 50 (ED ) values from 6.88 to 10.52 mg kg (P < 0.05) for lacosamide, from 22.08 to 38.26 mg kg (P < 0.05) for levetiracetam, and from 40.48 to 64.61 mg kg (P < 0.01) for pregabalin, respectively. There were no significant changes in total brain concentrations of lacosamide, levetiracetam, and pregabalin following CYT i.p. administration. CYT administered in a dose of 2 mg kg failed to change the protective action of clobazam, clonazepam, phenobarbital, tiagabine, and valproate in the 6-Hz test. Neither CYT (2 mg kg ) alone nor its combination with the anticonvulsant drugs (at their ED values from the 6-Hz test) affected motor coordination; skeletal muscular strength and long-term memory, as determined in the chimney; and grip strength and passive avoidance tests, respectively. CONCLUSION: CYT-evoked alterations in the protection provided by some antiepileptic drugs against seizures can be of serious concern for epileptic smokers, who might demonstrate therapeutic failure to lacosamide, levetiracetam, and pregabalin, resulting in possible breakthrough seizure attacks.
[Mh] Termos MeSH primário: Alcaloides/toxicidade
Anticonvulsivantes/uso terapêutico
Eletrochoque/efeitos adversos
Agonistas Nicotínicos/toxicidade
Convulsões/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Anticonvulsivantes/farmacologia
Azocinas/toxicidade
Relação Dose-Resposta a Droga
Masculino
Memória de Longo Prazo/efeitos dos fármacos
Memória de Longo Prazo/fisiologia
Camundongos
Fenobarbital/antagonistas & inibidores
Fenobarbital/farmacologia
Fenobarbital/uso terapêutico
Piracetam/análogos & derivados
Piracetam/antagonistas & inibidores
Piracetam/farmacologia
Piracetam/uso terapêutico
Quinolizinas/toxicidade
Convulsões/etiologia
Convulsões/psicologia
Ácido Valproico/antagonistas & inibidores
Ácido Valproico/farmacologia
Ácido Valproico/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alkaloids); 0 (Anticonvulsants); 0 (Azocines); 0 (Nicotinic Agonists); 0 (Quinolizines); 230447L0GL (etiracetam); 53S5U404NU (cytisine); 614OI1Z5WI (Valproic Acid); YQE403BP4D (Phenobarbital); ZH516LNZ10 (Piracetam)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171205
[Lr] Data última revisão:
171205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1007/s00213-016-4461-0


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[PMID]:28450546
[Au] Autor:Sun Y; Yang Y; Galvin VC; Yang S; Arnsten AF; Wang M
[Ad] Endereço:Department of Neurology, Peking University First Hospital, Beijing 100034.
[Ti] Título:Nicotinic α4ß2 Cholinergic Receptor Influences on Dorsolateral Prefrontal Cortical Neuronal Firing during a Working Memory Task.
[So] Source:J Neurosci;37(21):5366-5377, 2017 May 24.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The primate dorsolateral prefrontal cortex (dlPFC) subserves top-down regulation of attention and working memory abilities. Depletion studies show that the neuromodulator acetylcholine (ACh) is essential to dlPFC working memory functions, but the receptor and cellular bases for cholinergic actions are just beginning to be understood. The current study found that nicotinic receptors comprised of α4 and ß2 subunits (α4ß2-nAChR) enhance the task-related firing of delay and fixation cells in the dlPFC of monkeys performing a working memory task. Iontophoresis of α4ß2-nAChR agonists increased the neuronal firing and enhanced the spatial tuning of delay cells, neurons that represent visual space in the absence of sensory stimulation. These enhancing effects were reversed by coapplication of a α4ß2-nAChR antagonist, consistent with actions at α4ß2-nAChR. Delay cell firing was reduced when distractors were presented during the delay epoch, whereas stimulation of α4ß2-nAChR protected delay cells from these deleterious effects. Iontophoresis of α4ß2-nAChR agonists also enhanced the firing of fixation cells, neurons that increase firing when the monkey initiates a trial, and maintain firing until the trial is completed. These neurons are thought to contribute to sustained attention and top-down motor control and have never before been the subject of pharmacological inquiry. These findings begin to build a picture of the cellular actions underlying the beneficial effects of ACh on attention and working memory. The data may also help to explain why genetic insults to α4 subunits are associated with working memory and attentional deficits and why α4ß2-nAChR agonists may have therapeutic potential. The acetylcholine (ACh) arousal system in the brain is needed for robust attention and working memory functions, but the receptor and cellular bases for its beneficial effects are poorly understood in the newly evolved primate brain. The current study found that ACh stimulation of nicotinic receptors comprised of α4 and ß2 subunits (α4ß2-nAChR) enhanced the firing of neurons in the primate prefrontal cortex that subserve top-down attentional control and working memory. α4ß2-nAChR stimulation also protected neuronal responding from the detrimental effects of distracters presented during the delay epoch, when information is held in working memory. These results illuminate how ACh strengthens higher cognition and help to explain why genetic insults to the α4 subunit weaken cognitive and attentional abilities.
[Mh] Termos MeSH primário: Potenciais Evocados
Memória de Curto Prazo
Neurônios/metabolismo
Córtex Pré-Frontal/metabolismo
Receptores Nicotínicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Macaca mulatta
Masculino
Neurônios/efeitos dos fármacos
Neurônios/fisiologia
Agonistas Nicotínicos/farmacologia
Córtex Pré-Frontal/citologia
Córtex Pré-Frontal/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nicotinic Agonists); 0 (Receptors, Nicotinic); 0 (nicotinic receptor alpha4beta2)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171124
[Lr] Data última revisão:
171124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.0364-17.2017


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[PMID]:29049178
[Au] Autor:Zhou C; Wu L; Liu Q; An H; Jiang B; Zuo F; Zhang L; He Y
[Ad] Endereço:aDepartment of Respiration, Chinese PLA General Hospital bDepartment of Epidemiology, Institute of Geriatrics cCentral Laboratory of Navy General Hospital dDepartment of Acupuncture eDepartment of Rehabilitation, Chinese PLA General Hospital, Beijing, China.
[Ti] Título:Evaluation of smoking cessation intervention in patients with chronic diseases in smoking cessation clinics.
[So] Source:Medicine (Baltimore);96(42):e7459, 2017 Oct.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study aimed to evaluate the effects of psychological intervention and psychological plus drug intervention on smoking cessation among male smokers with single chronic diseases.A total of 509 male smokers were divided into psychological group (n = 290) and psychological plus drugs (n = 219) groups according to their will. The physicians provided free individual counseling and follow-up interviews with brief counseling for all the subjects. In addition to mental intervention, patients in psychological plus drug group also received bupropion hydrochloride or varenicline tartrate to quit smoking. Outcomes were self-reported, regarding the 7-day point prevalence on abstinence rate and continuous abstinence rates at 1-, 3-, and 6-month follow-up period. Data analyses were performed using intention-to-treat analysis and per protocol analysis.With regards to the 3 follow-up time points, 7-day point-prevalence abstinence rate in psychological plus drugs group was all higher than that in the psychological intervention group. Additionally, the 3-month continuous abstinence rate (21.4%) of the 6-month follow-up in the psychological group was not significantly higher than that (26.9%) in the psychological plus drugs group (P >.05 for all). Fagerström test score, stage of quitting smoking, perceived confidence or difficulty in quitting, and chronic disease types were independently correlated with 3-month continuous abstinence in the 6-month follow up (P <.05 for all). The results were similar between intentional analysis and protocol analysis.The psychological intervention and psychological plus drugs intervention exerted good effects on smoking cessation in a short time (1 month). Nevertheless, the advantages did not appear during long-time (6 months) follow-up.
[Mh] Termos MeSH primário: Doença Crônica/psicologia
Aconselhamento/métodos
Agonistas Nicotínicos/uso terapêutico
Abandono do Hábito de Fumar/métodos
Fumar/terapia
[Mh] Termos MeSH secundário: Adulto
Bupropiona/uso terapêutico
Terapia Combinada
Seguimentos
Seres Humanos
Análise de Intenção de Tratamento
Masculino
Meia-Idade
Fumar/psicologia
Abandono do Hábito de Fumar/psicologia
Resultado do Tratamento
Vareniclina/uso terapêutico
[Pt] Tipo de publicação:EVALUATION STUDIES; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Nicotinic Agonists); 01ZG3TPX31 (Bupropion); W6HS99O8ZO (Varenicline)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171122
[Lr] Data última revisão:
171122
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171020
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000007459


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[PMID]:28885019
[Au] Autor:Quadri M; Stokes C; Gulsevin A; Felts ACJ; Abboud KA; Papke RL; Horenstein NA
[Ad] Endereço:Department of Chemistry, University of Florida , P.O. Box 117200, Gainesville, Florida 32611-7200, United States.
[Ti] Título:Sulfonium as a Surrogate for Ammonium: A New α7 Nicotinic Acetylcholine Receptor Partial Agonist with Desensitizing Activity.
[So] Source:J Med Chem;60(18):7928-7934, 2017 Sep 28.
[Is] ISSN:1520-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Weak partial agonists that promote a desensitized state of the α7 nicotinic acetylcholine receptor (nAChR) have been associated with anti-inflammatory effects. Exemplar compounds feature a tertiary or quaternary ammonium group. We report the synthesis, structure, and electrophysiological evaluation of 1-ethyl-4-phenylthiomorpholin-1-ium triflate, a weak partial agonist with a sulfonium isostere of the ammonium pharmacophore. These results offer new insights in understanding nAChR-ligand interactions and provide a new chemical space to target the α7 nAChR.
[Mh] Termos MeSH primário: Morfolinas/química
Morfolinas/farmacologia
Agonistas Nicotínicos/química
Agonistas Nicotínicos/farmacologia
Oniocompostos/química
Oniocompostos/farmacologia
Compostos de Sulfônio/química
Compostos de Sulfônio/farmacologia
Receptor Nicotínico de Acetilcolina alfa7/agonistas
[Mh] Termos MeSH secundário: Compostos de Amônio/síntese química
Compostos de Amônio/química
Compostos de Amônio/farmacologia
Animais
Seres Humanos
Modelos Moleculares
Morfolinas/síntese química
Agonistas Nicotínicos/síntese química
Oniocompostos/síntese química
Compostos de Sulfônio/síntese química
Xenopus laevis
Receptor Nicotínico de Acetilcolina alfa7/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (1-ethyl-4-phenylthiomorpholin-1-ium); 0 (Ammonium Compounds); 0 (Morpholines); 0 (Nicotinic Agonists); 0 (Onium Compounds); 0 (Sulfonium Compounds); 0 (alpha7 Nicotinic Acetylcholine Receptor)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jmedchem.7b00875


  9 / 6662 MEDLINE  
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[PMID]:28842382
[Au] Autor:Koga M; Kanaoka Y; Sugiyama K; Ohishi K; Ejima Y; Hisanaga M; Kataoka Y; Yamauchi A
[Ad] Endereço:Department of Pharmaceutical Care and Health Sciences, Faculty of Pharmaceutical Sciences, Fukuoka University, Fukuoka 814-0180, Japan.
[Ti] Título:Varenicline promotes endothelial cell migration by lowering vascular endothelial-cadherin levels via the activated α7 nicotinic acetylcholine receptor-mitogen activated protein kinase axis.
[So] Source:Toxicology;390:1-9, 2017 Sep 01.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Varenicline is a widely used and effective drug for smoking cessation. Despite its efficacy, varenicline increases the risk of cardiovascular disease. We previously demonstrated that varenicline aggravates atherosclerotic plaque formation in apolipoprotein E knockout mice. However, little is known about its effects in vascular endothelial cells. Therefore, we examined whether varenicline promotes migration of human umbilical vein endothelial cells (HUVECs) using the Boyden chamber assay. Varenicline (100µM) markedly promoted migration of HUVECs and decreased expression of vascular endothelial (VE)-cadherin, an endothelial adhesion molecule. Extracellular signal-regulated kinase (ERK), p38 and c-Jun N-terminal kinase (JNK) signaling were markedly activated by varenicline. Methyllycaconitine (MLA; 100nM), an α7 nicotinic acetylcholine receptor (nAChR) antagonist, but not dihydro-ß-erythroidine hydrobromide (DHßE; 20µM) blocked varenicline-stimulated migration and varenicline-activated ERK, p38 and JNK signaling in HUVECs. MLA (100nM), PD98059 (an ERK inhibitor; 20µM), SB203580 (a p38 inhibitor; 20µM) and SP600125 (a JNK inhibitor; 20µM) also blocked cell migration and varenicline-induced downregulation of VE-cadherin expression in HUVECs. These findings suggest that varenicline promotes HUVEC migration by lowering VE-cadherin expression due to activated ERK/p38/JNK signaling through α7 nAChR. These processes probably contribute to varenicline-aggravated atherosclerotic plaque. Hence, an increased risk of cardiovascular events upon varenicline treatment might occur and must be considered in patients with cardiovascular diseases.
[Mh] Termos MeSH primário: Antígenos CD/metabolismo
Caderinas/metabolismo
Movimento Celular/efeitos dos fármacos
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Proteínas Quinases Ativadas por Mitógeno/metabolismo
Agonistas Nicotínicos/toxicidade
Vareniclina/toxicidade
Receptor Nicotínico de Acetilcolina alfa7/agonistas
[Mh] Termos MeSH secundário: Aterosclerose/induzido quimicamente
Aterosclerose/metabolismo
Aterosclerose/patologia
Células Cultivadas
Relação Dose-Resposta a Droga
Regulação para Baixo
Agonismo Parcial de Drogas
Ativação Enzimática
Células Endoteliais da Veia Umbilical Humana/metabolismo
Células Endoteliais da Veia Umbilical Humana/patologia
Seres Humanos
Fosforilação
Medição de Risco
Transdução de Sinais/efeitos dos fármacos
Fatores de Tempo
Receptor Nicotínico de Acetilcolina alfa7/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Cadherins); 0 (Chrna7 protein, human); 0 (Nicotinic Agonists); 0 (alpha7 Nicotinic Acetylcholine Receptor); 0 (cadherin 5); EC 2.7.11.24 (Mitogen-Activated Protein Kinases); W6HS99O8ZO (Varenicline)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170827
[St] Status:MEDLINE


  10 / 6662 MEDLINE  
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[PMID]:28791704
[Au] Autor:Mulcahy MJ; Lester HA
[Ad] Endereço:Department of Biology, California Institute of Technology, Pasadena, California, USA.
[Ti] Título:Granulocytes as models for human protein marker identification following nicotine exposure.
[So] Source:J Neurochem;142 Suppl 2:151-161, 2017 Aug.
[Is] ISSN:1471-4159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Nicotinic acetylcholine receptors (nAChRs) are pentameric cation channels expressed in the mammalian CNS, in the peripheral nervous system, and in skeletal muscle. Neuronal-type nAChRs are also found in several non-neuronal cell types, including leukocytes. Granulocytes are a subtype of leukocytes that include basophils, eosinophils, and neutrophils. Granulocytes, also known as polymorphonuclear leukocytes, are characterized by their ability to produce, store, and release compounds from intracellular granules. Granulocytes are the most abundant type of leukocyte circulating in the peripheral blood. Granulocyte abundance, nAChR expression, and nAChR upregulation following chronic nicotine administration makes granulocytes interesting models for identifying protein markers of nicotine exposure. Nicotinic receptor subunits and several non-nAChR proteins have been identified as protein markers of granulocyte nicotine exposure. We review methods to isolate granulocytes from human tissue, summarize present data about the expression of nAChRs in the three granulocyte cell types (basophils, eosinophils, and neutrophils), describe current knowledge of the effects of nicotine exposure on human granulocyte protein expression, and highlight areas of interest for future investigation. This is an article for the special issue XVth International Symposium on Cholinergic Mechanisms.
[Mh] Termos MeSH primário: Granulócitos/efeitos dos fármacos
Nicotina/farmacologia
Agonistas Nicotínicos/farmacologia
RNA Mensageiro/efeitos dos fármacos
Receptores Nicotínicos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Granulócitos/metabolismo
Seres Humanos
Piridinas/farmacologia
RNA Mensageiro/metabolismo
Receptores Nicotínicos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Nicotinic Agonists); 0 (Pyridines); 0 (RNA, Messenger); 0 (Receptors, Nicotinic); 6M3C89ZY6R (Nicotine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE
[do] DOI:10.1111/jnc.14010



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