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[PMID]:28601540
[Au] Autor:Rojas-Perez-Ezquerra P; Noguerado-Mellado B; Morales-Cabeza C; Zambrano Ibarra G; Datino Romaniega T
[Ad] Endereço:Allergy Department, Hospital General Universitario Gregorio Marañón, Madrid, Spain. Electronic address: patricia.rojas@salud.madrid.org.
[Ti] Título:Atrial Fibrillation in Anaphylaxis.
[So] Source:Am J Med;130(9):1114-1116, 2017 Sep.
[Is] ISSN:1555-7162
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The relationship between anaphylaxis and cardiovascular events has been reported in the past. While skin and respiratory symptoms are usually the most common and the first to appear, cardiovascular complications play a key role and represent the leading cause of death in anaphylaxis. METHODS: We report 3 episodes of atrial fibrillation triggered by anaphylaxis. Allergy and cardiology studies were performed. In both patients, the etiological agent was identified: Anisakis simplex hypersensitivity and food allergy. RESULTS: The heart is the source and target of chemical mediators released during an allergic reaction. In the heart, there are plenty of mast cells, and they are predominantly located around the coronary adventitia and in close contact with small vessels in the muscle wall. The release of mediators can influence ventricular function, heart rate, and coronary artery tone. Anaphylaxis can trigger any kind of arrhythmia. In these cases, the very interesting point of discussion was: which should be first, treating anaphylaxis or cardiac events? The other controversial point was the use of epinephrine, the first line of treatment for anaphylaxis. Recommendations about epinephrine in cardiac patients during an anaphylactic event are still a major dilemma. CONCLUSIONS: We emphasize the importance of the priority of establishing protocols between cardiologist and allergist in treatment of cardiac complications during anaphylaxis, and we warn about the correct diagnosis of arrhythmias in anaphylaxis in order to treat them as soon as possible, to prevent other consequences and complications.
[Mh] Termos MeSH primário: Anafilaxia/complicações
Atenolol/administração & dosagem
Fibrilação Atrial/etiologia
Clorfeniramina/administração & dosagem
Epinefrina/uso terapêutico
Hipersensibilidade Alimentar/complicações
Metilprednisolona/uso terapêutico
Urticária/complicações
[Mh] Termos MeSH secundário: Actinidia/efeitos adversos
Actinidia/imunologia
Administração Intravenosa
Adulto
Idoso de 80 Anos ou mais
Anafilaxia/tratamento farmacológico
Anafilaxia/etiologia
Animais
Anisakis/imunologia
Anisakis/parasitologia
Antiarrítmicos/administração & dosagem
Antiarrítmicos/imunologia
Antiarrítmicos/uso terapêutico
Anti-Inflamatórios/administração & dosagem
Anti-Inflamatórios/uso terapêutico
Arachis/efeitos adversos
Arachis/imunologia
Atenolol/imunologia
Atenolol/uso terapêutico
Fibrilação Atrial/tratamento farmacológico
Broncodilatadores/administração & dosagem
Broncodilatadores/uso terapêutico
Clorfeniramina/uso terapêutico
Quimioterapia Combinada
Epinefrina/administração & dosagem
Hipersensibilidade Alimentar/diagnóstico
Hipersensibilidade Alimentar/tratamento farmacológico
Hipersensibilidade Alimentar/etiologia
Gadiformes/imunologia
Gadiformes/parasitologia
Antagonistas dos Receptores Histamínicos H1/administração & dosagem
Antagonistas dos Receptores Histamínicos H1/uso terapêutico
Seres Humanos
Hipodermóclise
Masculino
Metilprednisolona/administração & dosagem
Urticária/etiologia
Urticária/imunologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 0 (Anti-Inflammatory Agents); 0 (Bronchodilator Agents); 0 (Histamine H1 Antagonists); 3Q9Q0B929N (dexchlorpheniramine); 3U6IO1965U (Chlorpheniramine); 50VV3VW0TI (Atenolol); X4W7ZR7023 (Methylprednisolone); YKH834O4BH (Epinephrine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170919
[Lr] Data última revisão:
170919
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170612
[St] Status:MEDLINE


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[PMID]:28250021
[Au] Autor:Finlin BS; Zhu B; Confides AL; Westgate PM; Harfmann BD; Dupont-Versteegden EE; Kern PA
[Ad] Endereço:Department of Medicine, Division of Endocrinology, and the Barnstable Brown Diabetes and Obesity Center, University of Kentucky, Lexington, KY.
[Ti] Título:Mast Cells Promote Seasonal White Adipose Beiging in Humans.
[So] Source:Diabetes;66(5):1237-1246, 2017 May.
[Is] ISSN:1939-327X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Human subcutaneous (SC) white adipose tissue (WAT) increases the expression of beige adipocyte genes in the winter. Studies in rodents suggest that a number of immune mediators are important in the beiging response. We studied the seasonal beiging response in SC WAT from lean humans. We measured the gene expression of various immune cell markers and performed multivariate analysis of the gene expression data to identify genes that predict UCP1. Interleukin (IL)-4 and, unexpectedly, the mast cell marker CPA3 predicted UCP1 gene expression. Therefore, we investigated the effects of mast cells on UCP1 induction by adipocytes. TIB64 mast cells responded to cold by releasing histamine and IL-4, and this medium stimulated UCP1 expression and lipolysis by 3T3-L1 adipocytes. Pharmacological block of mast cell degranulation potently inhibited histamine release by mast cells and inhibited adipocyte UCP1 mRNA induction by conditioned medium (CM). Consistently, the histamine receptor antagonist chlorpheniramine potently inhibited adipocyte UCP1 mRNA induction by mast cell CM. Together, these data show that mast cells sense colder temperatures, release factors that promote UCP1 expression, and are an important immune cell type in the beiging response of WAT.
[Mh] Termos MeSH primário: Adipócitos/metabolismo
Tecido Adiposo Bege/metabolismo
Tecido Adiposo Branco/metabolismo
Mastócitos/metabolismo
RNA Mensageiro/metabolismo
Estações do Ano
Proteína Desacopladora 1/genética
[Mh] Termos MeSH secundário: Células 3T3-L1
Adipócitos/efeitos dos fármacos
Adulto
Animais
Carboxipeptidases A/genética
Degranulação Celular
Clorfeniramina/farmacologia
Temperatura Baixa
Feminino
Regulação da Expressão Gênica
Histamina/metabolismo
Antagonistas dos Receptores Histamínicos H1/farmacologia
Seres Humanos
Interleucina-4/genética
Interleucina-4/metabolismo
Lipólise
Masculino
Proteínas de Membrana/genética
Camundongos
Análise Multivariada
Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/genética
RNA Mensageiro/efeitos dos fármacos
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Gordura Subcutânea/metabolismo
Coxa da Perna
Proteína Desacopladora 1/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histamine H1 Antagonists); 0 (IL4 protein, human); 0 (Membrane Proteins); 0 (PPARGC1A protein, human); 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha); 0 (RNA, Messenger); 0 (TMEM26 protein, human); 0 (UCP1 protein, human); 0 (Ucp1 protein, mouse); 0 (Uncoupling Protein 1); 207137-56-2 (Interleukin-4); 3U6IO1965U (Chlorpheniramine); 820484N8I3 (Histamine); EC 3.4.17.1 (CPA3 protein, human); EC 3.4.17.1 (Carboxypeptidases A)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170818
[Lr] Data última revisão:
170818
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170303
[St] Status:MEDLINE
[do] DOI:10.2337/db16-1057


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[PMID]:28131782
[Au] Autor:Kim J; Song JH
[Ad] Endereço:Department of Pharmacology, College of Medicine, Chung-Ang University, 84 Heukseok-Ro, Dongjak-Gu, Seoul 06974, Republic of Korea.
[Ti] Título:Inhibitory effects of antihistamines, diphenhydramine and chlorpheniramine, on proton currents in BV2 microglial cells.
[So] Source:Eur J Pharmacol;798:122-128, 2017 Mar 05.
[Is] ISSN:1879-0712
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Microglial NADPH oxidase is a major source of toxic reactive oxygen species produced during chronic neuroinflammation. Voltage-gated proton channel (H 1) functions to maintain the intense activity of NADPH oxidase, and channel inhibition alleviates the pathology of neurodegenerative diseases such as ischemic stroke and multiple sclerosis associated with oxidative neuroinflammation. Antagonists of histamine H receptors have beneficial effects against microglia-mediated oxidative stress and neurotoxicity. We examined the effects of the H antihistamines, diphenhydramine and chlorpheniramine, on proton currents in BV2 microglial cells recorded using the whole-cell patch clamp technique. Diphenhydramine and chlorpheniramine reduced the proton currents with almost the same potency, yielding IC values of 42 and 43µM, respectively. Histamine did not affect proton currents, excluding the involvement of histamine receptors in their action. Neither drug shifted the voltage-dependence of activation or the reversal potential of the proton currents, even though diphenhydramine slowed the activation and deactivation kinetics. The inhibitory effects of the two antihistamines on proton currents could be utilized to develop therapeutic agents for neurodegenerative diseases and other diseases associated with H 1 proton channel abnormalities.
[Mh] Termos MeSH primário: Clorfeniramina/farmacologia
Difenidramina/farmacologia
Antagonistas dos Receptores Histamínicos/farmacologia
Microglia/efeitos dos fármacos
Microglia/metabolismo
Prótons
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Canais Iônicos/antagonistas & inibidores
Canais Iônicos/metabolismo
Cinética
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histamine Antagonists); 0 (Hv1 proton channel, mouse); 0 (Ion Channels); 0 (Protons); 3U6IO1965U (Chlorpheniramine); 8GTS82S83M (Diphenhydramine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170515
[Lr] Data última revisão:
170515
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170130
[St] Status:MEDLINE


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[PMID]:28040476
[Au] Autor:Hishinuma S; Kosaka K; Akatsu C; Uesawa Y; Fukui H; Shoji M
[Ad] Endereço:Department of Pharmacodynamics, Meiji Pharmaceutical University, 2-522-1 Noshio, Kiyose, Tokyo 204-8588, Japan. Electronic address: hishi@my-pharm.ac.jp.
[Ti] Título:Asp73-dependent and -independent regulation of the affinity of ligands for human histamine H receptors by Na .
[So] Source:Biochem Pharmacol;128:46-54, 2017 Mar 15.
[Is] ISSN:1873-2968
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The affinity of ligands for G-protein-coupled receptors (GPCRs) is allosterically regulated by Na via a highly conserved aspartate residue (Asp ) in the second transmembrane domain of GPCRs. In the present study, we examined the Na -mediated regulation of the affinity of ligands for G -protein-coupled human histamine H receptors in Chinese hamster ovary cells. The affinities of 3 agonists and 20 antihistamines were evaluated by their displacement curves against the binding of [ H]-mepyramine to membrane preparations in the presence or absence of 100mM NaCl. The affinities of most drugs including histamine, an agonist, and d-chlorpheniramine, a first-generation antihistamine, were reduced by NaCl, with the extent of NaCl-mediated changes varying widely between drugs. In contrast, the affinities of some second-generation antihistamines such as fexofenadine were increased by NaCl. These changes were retained in intact cells. The mutation of Asp (Asp73) to asparagine abrogated NaCl-induced reductions in affinities for histamine and d-chlorpheniramine, but not NaCl-induced increases in the affinity for fexofenadine. Quantitative structure-activity relationship (QSAR) analyses showed that these Na -mediated changes were explained and predicted by a combination of the molecular energies and implicit solvation energies of the compounds. These results suggest that Na diversely regulates the affinity of ligands for H receptors from the extracellular sites of receptors via Asp73-dependent and -independent mechanisms in a manner that depends on the physicochemical properties of ligands. These results may contribute to a deeper understanding of the fundamental mechanisms by which the affinity of ligands for their receptors is allosterically regulated by Na .
[Mh] Termos MeSH primário: Ácido Aspártico/genética
Receptores Histamínicos H1/fisiologia
Cloreto de Sódio/farmacologia
[Mh] Termos MeSH secundário: Animais
Células CHO
Cátions Monovalentes
Clorfeniramina/farmacologia
Cricetulus
Histamina/farmacologia
Agonistas dos Receptores Histamínicos/farmacologia
Antagonistas dos Receptores Histamínicos H1/farmacologia
Seres Humanos
Ligantes
Mutação
Relação Quantitativa Estrutura-Atividade
Ensaio Radioligante
Receptores Histamínicos H1/genética
Terfenadina/análogos & derivados
Terfenadina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cations, Monovalent); 0 (Histamine Agonists); 0 (Histamine H1 Antagonists); 0 (Ligands); 0 (Receptors, Histamine H1); 30KYC7MIAI (Aspartic Acid); 3U6IO1965U (Chlorpheniramine); 451W47IQ8X (Sodium Chloride); 7BA5G9Y06Q (Terfenadine); 820484N8I3 (Histamine); E6582LOH6V (fexofenadine)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170502
[Lr] Data última revisão:
170502
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170102
[St] Status:MEDLINE


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[PMID]:27923888
[Au] Autor:Beshir L; Kaballo B; Young D
[Ad] Endereço:1 Department of Internal Medicine, Omdurman Military Hospital, Khartoum, Sudan.
[Ti] Título:Attempted suicide by ingestion of hair dye containing p-phenylenediamine: a case report.
[So] Source:Ann Clin Biochem;54(4):507-510, 2017 Jul.
[Is] ISSN:1758-1001
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Para-phenylenediamine is widely used as a chemical in hair dyes and in combination with henna. This dye is used to paint the body for decorative reasons, to speed the processing time of henna and to intensify the results. Para-phenylenediamine is widely used in the Middle East, North Africa and India. Several reports have been published of the fatal ingestion of hair dye containing para-phenylenediamine. Here, we describe the case of a 14-year-old girl who ingested the compound but whose prompt treatment prevented her death. Ingestion of para-phenylenediamine produces a typical triad of angioneurotic oedema, rhabdomyolysis and acute tubular necrosis. Awareness of signs of these associated conditions in our patient, together with a comprehensive history, facilitated appropriate treatment to be instituted. We document the steps we took to enable her complete physical recovery.
[Mh] Termos MeSH primário: Lesão Renal Aguda/prevenção & controle
Angioedema/prevenção & controle
Tinturas para Cabelo/envenenamento
Fenilenodiaminas/envenenamento
Rabdomiólise/tratamento farmacológico
Tentativa de Suicídio/prevenção & controle
[Mh] Termos MeSH secundário: Lesão Renal Aguda/induzido quimicamente
Lesão Renal Aguda/diagnóstico
Lesão Renal Aguda/patologia
Adolescente
Angioedema/induzido quimicamente
Angioedema/diagnóstico
Angioedema/patologia
Clorfeniramina/uso terapêutico
Feminino
Hidratação
Furosemida/uso terapêutico
Seres Humanos
Hidrocortisona/análogos & derivados
Hidrocortisona/uso terapêutico
Naftoquinonas/envenenamento
Respiração Artificial
Rabdomiólise/induzido quimicamente
Rabdomiólise/diagnóstico
Rabdomiólise/patologia
Tentativa de Suicídio/psicologia
Traqueostomia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hair Dyes); 0 (Naphthoquinones); 0 (Phenylenediamines); 0388G963HY (hydrocortisone sodium phosphate); 3U6IO1965U (Chlorpheniramine); 7LXU5N7ZO5 (Furosemide); TLH4A6LV1W (lawsone); U770QIT64J (4-phenylenediamine); WI4X0X7BPJ (Hydrocortisone)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170707
[Lr] Data última revisão:
170707
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161208
[St] Status:MEDLINE
[do] DOI:10.1177/0004563216685117


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[PMID]:27528108
[Au] Autor:Fernandes CE; Serafim KR; Gianlorenço AC; Mattioli R
[Ad] Endereço:Laboratory of Neuroscience, Physiotherapy Department, Center of Biological Sciences and Health, Federal University of Sao Carlos, Rod. Washington Luis, Km 235, 13565-905 Sao Carlos, Brazil. Electronic address: ceduardomonici@hotmail.com.
[Ti] Título:Cholinergic agonist reverses H1-induced memory deficit in mice.
[So] Source:Prog Neuropsychopharmacol Biol Psychiatry;72:16-22, 2017 Jan 04.
[Is] ISSN:1878-4216
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:This study investigated the effects of bilateral intraamygdalar microinjections of PNU-282987, a nicotinic cholinergic agonist, on anxiety and the reversal of amnesia induced by chlorpheniramine (CPA), an H1 histaminergic antagonist, in mice subjected to the elevated plusmaze (EPM). Two experiments were performed with seventy-nine adult male Swiss mice. The isolated microinjections of PNU-282987 did not produce effects on emotional memory; however, the combined microinjections of PNU-282987 and CPA were able to reverse the deficit in memory induced by CPA (ANOVA, p<0.05). Taken together, these results suggest that intraamygdalar injections of PNU-282987 did not induce effects on anxiety and emotional memory per se; however, concurrent microinjections of PNU-282987 and CPA-reverse amnesia induced-CPA which is suggestive of an interaction between the histaminergic and cholinergic systems in the modulation of emotion memory acquisition in mice.
[Mh] Termos MeSH primário: Benzamidas/uso terapêutico
Compostos Bicíclicos com Pontes/uso terapêutico
Clorfeniramina/toxicidade
Antagonistas dos Receptores Histamínicos H1/toxicidade
Transtornos da Memória/induzido quimicamente
Transtornos da Memória/tratamento farmacológico
Agonistas Nicotínicos/uso terapêutico
[Mh] Termos MeSH secundário: Tonsila do Cerebelo/efeitos dos fármacos
Tonsila do Cerebelo/fisiologia
Análise de Variância
Animais
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Masculino
Aprendizagem em Labirinto/efeitos dos fármacos
Camundongos
Microinjeções
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzamides); 0 (Bridged Bicyclo Compounds); 0 (Histamine H1 Antagonists); 0 (Nicotinic Agonists); 0 (PNU-282987); 3U6IO1965U (Chlorpheniramine)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170830
[Lr] Data última revisão:
170830
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160817
[St] Status:MEDLINE


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[PMID]:27756965
[Au] Autor:Ösken A; Yelgeç NS; Zehir R; Öz TK; Yaylaci S; Akdemir R; Gündüz H
[Ad] Endereço:Department of Cardiology, Siyami Ersek Thoracic and Cardiovascular Surgery Center, Training and Research Hospital, Istanbul, Turkey.
[Ti] Título:Torsades de pointes induced by concomitant use of chlorpheniramine and propranolol: An unusual presentation with no QT prolongation.
[So] Source:Indian J Pharmacol;48(4):462-465, 2016 Jul-Aug.
[Is] ISSN:1998-3751
[Cp] País de publicação:India
[La] Idioma:eng
[Ab] Resumo:Drug-induced torsades de pointes (TdP) is a rare but potentially fatal adverse effect of commonly prescribed medications including cardiac and noncardiac drugs. Importantly, many drugs have been reported to cause the characteristic Brugada syndrome-linked electrocardiography (ECG) abnormalities and/or (fatal) ventricular tachyarrhythmias. Chlorpheniramine and propranolol have the arrhythmogenic effects reported previously. A review of literature revealed a large number of case reports of chlorpheniramine or propranolol use resulting in QTc prolongation, TdP, or both. However, we wish to report the case of a patient who was treated with a combination of chlorpheniramine and propranolol, whose ECG showed no QT prolongation but who suffered from cardiac arrest due to TdP.
[Mh] Termos MeSH primário: Clorfeniramina/efeitos adversos
Parada Cardíaca/induzido quimicamente
Propranolol/efeitos adversos
Torsades de Pointes/induzido quimicamente
[Mh] Termos MeSH secundário: Adulto
Clorfeniramina/administração & dosagem
Clorfeniramina/uso terapêutico
Desfibriladores Implantáveis
Eletrocardiografia
Parada Cardíaca/diagnóstico
Parada Cardíaca/terapia
Seres Humanos
Masculino
Propranolol/administração & dosagem
Propranolol/uso terapêutico
Torsades de Pointes/diagnóstico
Torsades de Pointes/terapia
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
3U6IO1965U (Chlorpheniramine); 9Y8NXQ24VQ (Propranolol)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161021
[St] Status:MEDLINE


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[PMID]:27437787
[Au] Autor:Sakai K; Sanders KM; Youssef MR; Yanushefski KM; Jensen L; Yosipovitch G; Akiyama T
[Ad] Endereço:aDepartment of Dermatology, Temple Itch Center, Temple University, Philadelphia, PA, USA bDepartment of Microbiology and Immunology, Temple Autoimmunity Center, Temple University, Philadelphia, PA, USA cDepartment of Anatomy and Cell Biology, Temple University, Philadelphia, PA, USA.
[Ti] Título:Mouse model of imiquimod-induced psoriatic itch.
[So] Source:Pain;157(11):2536-2543, 2016 Nov.
[Is] ISSN:1872-6623
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Itch is a major indicator of psoriasis, but the underlying mechanisms behind this symptom are largely unknown. To investigate the neuronal mechanisms of psoriatic itch, we tested whether mice subjected to the imiquimod-induced psoriasis model exhibit itch-associated behaviors. Mice received daily topical applications of imiquimod to the rostral back skin for 7 days. Imiquimod-treated mice exhibited a significant increase in spontaneous scratching behavior directed to the treated area as well as touch-evoked scratching (alloknesis). To characterize this model, we measured the mRNA expression levels of pruritogens and itch-relevant receptors/channels using real-time reverse transcription PCR. The mRNA expression of MrgprA3, MrgprC11, and MrgprD decreased gradually over time in the dorsal root ganglion (DRG) cells. There was no significant change in the mRNA expression of TRPV1 or TRPA1 in DRG cells. TRPV4 mRNA expression was transiently increased in the DRG cells, whereas TRPM8 mRNA was significantly decreased. The mRNA expression levels of histidine decarboxylase and tryptophan hydroxylase 1, as well as the intensity of histamine and serotonin immunoreactivity, were transiently increased in the skin on day 2, returning to baseline by day 7. Histamine H1-receptor antagonists, chlorpheniramine and olopatadine, significantly inhibited spontaneous scratching on day 2, but not day 7. Neither chlorpheniramine nor olopatadine affected alloknesis on day 2 or day 7. These results may reflect the limited antipruritic effects of histamine H1-receptor antagonists on human psoriasis. The imiquimod-induced psoriasis model seems to be useful for the investigation of itch and its sensitization in psoriasis.
[Mh] Termos MeSH primário: Adjuvantes Imunológicos/toxicidade
Aminoquinolinas/toxicidade
Modelos Animais de Doenças
Prurido/induzido quimicamente
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios não Esteroides/uso terapêutico
Antipruriginosos/uso terapêutico
Clorfeniramina/uso terapêutico
Gânglios Espinais/efeitos dos fármacos
Gânglios Espinais/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Histidina Descarboxilase/genética
Histidina Descarboxilase/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Cloridrato de Olopatadina/uso terapêutico
Medição da Dor
Prurido/tratamento farmacológico
Prurido/patologia
Distribuição Aleatória
Pele/metabolismo
Pele/patologia
Canais de Cátion TRPV/genética
Canais de Cátion TRPV/metabolismo
Triptofano Hidroxilase/genética
Triptofano Hidroxilase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adjuvants, Immunologic); 0 (Aminoquinolines); 0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Antipruritics); 0 (TRPV Cation Channels); 0 (TRPV1 protein, mouse); 2XG66W44KF (Olopatadine Hydrochloride); 3U6IO1965U (Chlorpheniramine); EC 1.14.16.4 (Tph1 protein, mouse); EC 1.14.16.4 (Tryptophan Hydroxylase); EC 4.1.1.22 (Histidine Decarboxylase); P1QW714R7M (imiquimod)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160721
[St] Status:MEDLINE


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Fotocópia
[PMID]:27436188
[Au] Autor:Bartoli F; Bruni C; Cometi L; Blagojevic J; Fiori G; Tofani L; Galluccio F; Furst DE; Matucci Cerinic M
[Ad] Endereço:Department of Experimental and Clinical Medicine, Division of Rheumatology, University of Florence, Villa Monna Tessa, Viale Pieraccini 18, 50134, Florence, Italy. francesca.bartoli19@gmail.com.
[Ti] Título:Premedication prevents infusion reactions and improves retention rate during infliximab treatment.
[So] Source:Clin Rheumatol;35(11):2841-2845, 2016 Nov.
[Is] ISSN:1434-9949
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Infliximab (IFX) is an anti-tumor necrosis factor-alpha antibody used to treat inflammatory joint diseases. Infusion reactions (IR) can occur during and after intravenous administration and often require discontinuation of IFX therapy. This retrospective study aimed at evaluating the incidence of IR in patients with joint inflammatory diseases receiving IFX with and without premedication. Clinical charts of rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis patients receiving IFX from January 2002 to December 2014 were reviewed. Patients receiving only one premedication protocol over time were enrolled and clustered based on the type of premedication as follows: group 1 received no premedication; group 2 received paracetamol, esomeprazole, hydrocortisone, and chlorpheniramine maleate; group 3 received paracetamol, hydoxyzine, ranitidine, and 6-methylprednisolone. Adverse events were recorded during the infusion, in the following hours and at control visits. The charts of 105 patients treated with IFX were selected. IR were observed in 23/51 patients of group 1, in 7/35 patients of group 2, and none of 19 patients in group 3. IR incidence was significantly lower in the second (p = 0.021) and third (p < 0.001) compared to the first group. The incidence of IR was significantly lower in group 3 than group 2 (p < 0.043). Moreover, patients in group 1 had a relative risk of developing an IR 2.5 times higher than group 2. In our experience, the use of premedication significantly reduced the number of IR to IFX. In particular, the combination of paracetamol, hydroxyzine, 6-methylprednisolone and ranitidine was more efficacious than paracetamol, esomeprazole, hydrocortisone, and chlorpheniramine maleate combination protocol.
[Mh] Termos MeSH primário: Antirreumáticos/efeitos adversos
Artrite Reumatoide/tratamento farmacológico
Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/prevenção & controle
Infliximab/efeitos adversos
Pré-Medicação
[Mh] Termos MeSH secundário: Acetaminofen/uso terapêutico
Adulto
Idoso
Antirreumáticos/uso terapêutico
Artrite Psoriásica/tratamento farmacológico
Clorfeniramina/uso terapêutico
Quimioterapia Combinada
Efeitos Colaterais e Reações Adversas Relacionados a Medicamentos/etiologia
Esomeprazol/uso terapêutico
Feminino
Seres Humanos
Hidrocortisona/uso terapêutico
Hidroxizina/uso terapêutico
Infliximab/uso terapêutico
Infusões Intravenosas/efeitos adversos
Masculino
Metilprednisolona/uso terapêutico
Meia-Idade
Ranitidina/uso terapêutico
Estudos Retrospectivos
Espondilite Anquilosante/tratamento farmacológico
Resultado do Tratamento
Fator de Necrose Tumoral alfa/antagonistas & inibidores
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antirheumatic Agents); 0 (Tumor Necrosis Factor-alpha); 30S50YM8OG (Hydroxyzine); 362O9ITL9D (Acetaminophen); 3U6IO1965U (Chlorpheniramine); 884KT10YB7 (Ranitidine); B72HH48FLU (Infliximab); N3PA6559FT (Esomeprazole); WI4X0X7BPJ (Hydrocortisone); X4W7ZR7023 (Methylprednisolone)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160721
[St] Status:MEDLINE


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Texto completo
[PMID]:27344002
[Au] Autor:Serafim KR; Russo PS; Fernandes CE; Gianlorenço AC; Mattioli R
[Ad] Endereço:Laboratório de Neurociências, Departamento de Fisioterapia, Centro de Ciências Biológicas e da Sáude, Universidade Federal de São Carlos, Rod. Washington Luis, Km 235, 13565-905 Sao Carlos, Brazil. Electronic address: Kelly.serafim@hotmail.com.
[Ti] Título:Intra-amygdala microinjections of chlorpheniramine impair memory formation or memory retrieval in anxiety- and fear-mediated models.
[So] Source:Brain Res Bull;125:127-33, 2016 Jul.
[Is] ISSN:1873-2747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:H1 receptor histaminergic antagonist, chlorpheniramine (CPA) participates in cognitive performance in various animal models. However, little is known regarding the effects of CPA microinjection into the amygdala on emotional behavior. The purpose of this study was to investigate whether CPA microinjection into the amygdala has the same effect on two models, one anxiety- and the other fear-mediated, in various memory stages using the elevated plus maze (EPM) and the inhibitory avoidance task (IAT) tests. Two experiments were performed with seventy-two adult male Swiss mice. Behavioral testing was performed on two consecutive days, and in both experiments, before each trial, the animals received bilateral microinjections of saline (SAL) or CPA (0.16 nmol). The animals were re-exposed to the EPM or IAT 24h after the first trial. Four experimental groups were tested: SAL-SAL, SAL-CPA, CPA-SAL and CPA-CPA. In experiment 1, a decreased open arm exploration (% open arm entries, %OAE and% open arms time, %OAT) for SAL-SAL and SAL-CPA was showed, while these measures did not decrease for the CPA-SAL and CPA-CPA groups in Trial 2. In experiment 2, an increase of retention latency in relation to training 2 for the groups SAL-SAL and CPA-SAL and a significant decrease in latency for the group SAL-CPA was revealed. These results indicate that chlorpheniramine microinjection into the amygdala impairs emotional memory acquisition and/or consolidation in the EPM and retrieval of IAT.
[Mh] Termos MeSH primário: Tonsila do Cerebelo/efeitos dos fármacos
Ansiedade/psicologia
Clorfeniramina/toxicidade
Medo
Antagonistas dos Receptores Histamínicos H1/toxicidade
Transtornos da Memória/induzido quimicamente
Rememoração Mental/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Aprendizagem da Esquiva/efeitos dos fármacos
Modelos Animais de Doenças
Medo/psicologia
Inibição (Psicologia)
Masculino
Aprendizagem em Labirinto/efeitos dos fármacos
Camundongos
Microinjeções/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histamine H1 Antagonists); 3U6IO1965U (Chlorpheniramine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160626
[St] Status:MEDLINE



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