Base de dados : MEDLINE
Pesquisa : D02.886.778.370 [Categoria DeCS]
Referências encontradas : 1111 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 112 ir para página                         

  1 / 1111 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28659489
[Au] Autor:Morrison J; Rathore APS; Mantri CK; Aman SAB; Nishida A; St John AL
[Ad] Endereço:Center for Infection and Immunity, Mailman School of Public Health, Columbia University, New York, New York, USA jmm2105@cumc.columbia.edu ashley.st.john@duke-nus.edu.sg.
[Ti] Título:Transcriptional Profiling Confirms the Therapeutic Effects of Mast Cell Stabilization in a Dengue Disease Model.
[So] Source:J Virol;91(18), 2017 Sep 15.
[Is] ISSN:1098-5514
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:There are no approved therapeutics for the treatment of dengue disease despite the global prevalence of dengue virus (DENV) and its mosquito vectors. DENV infections can lead to vascular complications, hemorrhage, and shock due to the ability of DENV to infect a variety of immune and nonimmune cell populations. Increasingly, studies have implicated the host response as a major contributor to severe disease. Inflammatory products of various cell types, including responding T cells, mast cells (MCs), and infected monocytes, can contribute to immune pathology. In this study, we show that the host response to DENV infection in immunocompetent mice recapitulates transcriptional changes that have been described in human studies. We found that DENV infection strongly induced metabolic dysregulation, complement signaling, and inflammation. DENV also affected the immune cell content of the spleen and liver, enhancing NK, NKT, and CD8 T cell activation. The MC-stabilizing drug ketotifen reversed many of these responses without suppressing memory T cell formation and induced additional changes in the transcriptome and immune cell composition of the spleen, consistent with reduced inflammation. This study provides a global transcriptional map of immune activation in DENV target organs of an immunocompetent host and supports the further development of targeted immunomodulatory strategies to treat DENV disease. Dengue virus (DENV), which causes febrile illness, is transmitted by mosquito vectors throughout tropical and subtropical regions of the world. Symptoms of DENV infection involve damage to blood vessels and, in rare cases, hemorrhage and shock. Currently, there are no targeted therapies to treat DENV infection, but it is thought that drugs that target the host immune response may be effective in limiting symptoms that result from excessive inflammation. In this study, we measured the host transcriptional response to infection in multiple DENV target organs using a mouse model of disease. We found that DENV infection induced metabolic dysregulation and inflammatory responses and affected the immune cell content of the spleen and liver. The use of the mast cell stabilization drug ketotifen reversed many of these responses and induced additional changes in the transcriptome and immune cell repertoire that contribute to decreased dengue disease.
[Mh] Termos MeSH primário: Antialérgicos/administração & dosagem
Vírus da Dengue/imunologia
Dengue/tratamento farmacológico
Dengue/patologia
Perfilação da Expressão Gênica
Cetotifeno/administração & dosagem
Mastócitos/imunologia
[Mh] Termos MeSH secundário: Animais
Dengue/imunologia
Modelos Animais de Doenças
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Allergic Agents); X49220T18G (Ketotifen)
[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:170630
[St] Status:MEDLINE


  2 / 1111 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28336398
[Au] Autor:Faustino-Rocha AI; Gama A; Oliveira PA; Vanderperren K; Saunders JH; Pires MJ; Ferreira R; Ginja M
[Ad] Endereço:Faculty of Veterinary Medicine, Lusophone University of Humanities and Technologies, Lisbon, Portugal; Center for the Research and Technology of Agro-Environmental and Biological Sciences (CITAB), University of Trás-os-Montes and Alto Douro (UTAD), Vila Real, Portugal. Electronic address: anafaustin
[Ti] Título:Modulation of mammary tumor vascularization by mast cells: Ultrasonographic and histopathological approaches.
[So] Source:Life Sci;176:35-41, 2017 May 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: The inhibition of mast cells' degranulation may be an approach to prevent the formation of new vessels during the mammary carcinogenesis. MATERIALS AND METHODS: Female Sprague-Dawley rats were randomly divided into five experimental groups. Mammary tumors were induced by intraperitoneal injection of N-methyl-N-nitrosourea (MNU). Animals from group II were treated with ketotifen for 18weeks immediately after the MNU administration, while animals from group III only received the ketotifen after the development of the first mammary tumor. Mammary tumors vascularization was assessed by ultrasonography (Doppler, B Flow and contrast-enhanced ultrasound) and immunohistochemistry (vascular endothelial growth factor-A). KEY FINDINGS AND SIGNIFICANCE: Similar to what occurs in women with breast cancer, the majority of MNU-induced mammary tumors exhibited a centripetal enhancement order of the contrast agent, clear margin and heterogeneous enhancement. Ultrasonographic and immunohistochemical data suggest that the inhibition of mast cells' degranulation did not change the mammary tumors vascularization.
[Mh] Termos MeSH primário: Neoplasias Mamárias Animais
Mastócitos/metabolismo
Metilnitrosoureia/toxicidade
Neovascularização Patológica
Ultrassonografia
[Mh] Termos MeSH secundário: Animais
Feminino
Cetotifeno/farmacologia
Neoplasias Mamárias Animais/irrigação sanguínea
Neoplasias Mamárias Animais/induzido quimicamente
Neoplasias Mamárias Animais/diagnóstico por imagem
Neoplasias Mamárias Animais/metabolismo
Neovascularização Patológica/diagnóstico por imagem
Neovascularização Patológica/metabolismo
Neovascularização Patológica/patologia
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
684-93-5 (Methylnitrosourea); X49220T18G (Ketotifen)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170428
[Lr] Data última revisão:
170428
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170325
[St] Status:MEDLINE


  3 / 1111 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:28314259
[Au] Autor:Faustino-Rocha AI; Gama A; Neuparth MJ; Oliveira PA; Ferreira R; Ginja M
[Ad] Endereço:Department of Veterinary Sciences, School of Agrarian and Veterinary Sciences, University of Trás-os-Montes and Alto Douro, Vila Real, Portugal anafaustino.faustino@sapo.pt.
[Ti] Título:Mast Cells in Mammary Carcinogenesis: Host or Tumor Supporters?
[So] Source:Anticancer Res;37(3):1013-1021, 2017 03.
[Is] ISSN:1791-7530
[Cp] País de publicação:Greece
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIM: The effects of mast cells on carcinogenesis is not yet fully understood. This work aimed to disclose the role of mast cells in mammary carcinogenesis in a rat model. MATERIALS AND METHODS: Mammary tumors were induced by the administration of N-methyl-N-nitrosourea (MNU) in three groups of rats. Animals from one group were treated with ketotifen immediately after MNU administration, and animals from another only received ketotifen after the development of the first mammary tumor. The biochemical profile was determined. Mammary tumors were evaluated by histopathology and immunohistochemistry. RESULTS: Animals from ketotifen-treated groups developed fewer mammary tumors, higher number of mammary lesions and had lower histamine levels when compared to non-treated animals. Animals treated with ketotifen immediately after MNU exhibited the lowest proliferative and apoptotic indexes. CONCLUSION: The mainly positive effect of the inhibition of mast cell degranulation seems to be the reduction of tumor proliferation when the mast cell degranulation was inhibited before tumor development.
[Mh] Termos MeSH primário: Neoplasias Mamárias Animais/fisiopatologia
Neoplasias Mamárias Experimentais/fisiopatologia
Mastócitos/citologia
[Mh] Termos MeSH secundário: Animais
Proliferação Celular
Transformação Celular Neoplásica
Feminino
Imuno-Histoquímica
Cetotifeno/química
Neoplasias Mamárias Animais/induzido quimicamente
Neoplasias Mamárias Experimentais/induzido quimicamente
Metilnitrosoureia/química
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
684-93-5 (Methylnitrosourea); X49220T18G (Ketotifen)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170411
[Lr] Data última revisão:
170411
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170319
[St] Status:MEDLINE


  4 / 1111 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28190755
[Au] Autor:Kanamitsu K; Nozaki Y; Nagaya Y; Sugiyama Y; Kusuhara H
[Ad] Endereço:Laboratory of Molecular Pharmacokinetics, Graduate School of Pharmaceutical Sciences, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan; Tokushima Research Institute, Otsuka Pharmaceutical Co., Ltd., 463-10 Kagasuno, Kawauchi-cho, Tokushima-shi, Tokushima, 771-0192, Japan.
[Ti] Título:Quantitative prediction of histamine H1 receptor occupancy by the sedative and non-sedative antagonists in the human central nervous system based on systemic exposure and preclinical data.
[So] Source:Drug Metab Pharmacokinet;32(2):135-144, 2017 Apr.
[Is] ISSN:1880-0920
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Significant histamine H1 receptor occupation in the central nervous system (CNS) is associated with sedation. Here we examined the time profiles of the H1 receptor occupancy (RO) in the CNS using sedative (diphenhydramine and ketotifen) and non-sedative (bepotastine and olopatadine) antagonists at their therapeutic doses by integrating in vitro and animal data. A pharmacokinetic model was constructed to associate plasma concentrations and receptor binding in the brain. Dissociation and association rate constants with the H1 receptor and plasma and brain unbound fractions were determined in vitro. Passive and active clearances across the blood-brain barrier (BBB) were estimated based on physicochemical properties and microdialysis studies in mice and monkeys. The estimated RO values were comparable with the reported values determined at time to maximum concentration (T ) of plasma by positron-emission tomography in humans. The simulation suggested that the predicted maximum ROs by bepotastine and olopatadine were greater than the reported values. Sensitivity analysis showed that active transport across BBB had a significant impact on the RO duration of the H1 antagonists examined. The present study demonstrated that modeling and simulation permits a reasonable RO estimation in the human CNS. Our findings will facilitate the development of CNS-acting drugs.
[Mh] Termos MeSH primário: Sistema Nervoso Central/efeitos dos fármacos
Antagonistas dos Receptores Histamínicos H1/farmacologia
Receptores Histamínicos H1/metabolismo
[Mh] Termos MeSH secundário: Animais
Encéfalo/metabolismo
Sistema Nervoso Central/metabolismo
Difenidramina/sangue
Difenidramina/farmacologia
Antagonistas dos Receptores Histamínicos H1/sangue
Seres Humanos
Cetotifeno/sangue
Cetotifeno/farmacologia
Macaca fascicularis
Masculino
Camundongos
Camundongos Endogâmicos
Cloridrato de Olopatadina/sangue
Cloridrato de Olopatadina/farmacologia
Piperidinas/sangue
Piperidinas/farmacologia
Tomografia por Emissão de Pósitrons
Piridinas/sangue
Piridinas/farmacologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Histamine H1 Antagonists); 0 (Piperidines); 0 (Pyridines); 0 (Receptors, Histamine H1); 2XG66W44KF (Olopatadine Hydrochloride); 8GTS82S83M (Diphenhydramine); HYD2U48IAS (bepotastine); X49220T18G (Ketotifen)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170505
[Lr] Data última revisão:
170505
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170214
[St] Status:MEDLINE


  5 / 1111 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28095628
[Au] Autor:Smets K; Werbrouck J; Goossens A; Gilissen L
[Ad] Endereço:Department of Dermatology, University Hospitals KU Leuven, 3000, Leuven, Belgium.
[Ti] Título:Sensitization from ketotifen fumarate in eye drops presenting as chronic conjunctivitis.
[So] Source:Contact Dermatitis;76(2):124-126, 2017 Feb.
[Is] ISSN:1600-0536
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Antialérgicos/efeitos adversos
Conjuntivite Alérgica/induzido quimicamente
Cetotifeno/efeitos adversos
[Mh] Termos MeSH secundário: Adulto
Doença Crônica
Feminino
Seres Humanos
Testes do Emplastro
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Allergic Agents); 0 (ketotifen fumarate ophthalmic solution); X49220T18G (Ketotifen)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170614
[Lr] Data última revisão:
170614
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170118
[St] Status:MEDLINE
[do] DOI:10.1111/cod.12695


  6 / 1111 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27705841
[Au] Autor:Tran PN; Tate CJ; Ridgway MC; Saliba KJ; Kirk K; Maier AG
[Ad] Endereço:Research School of Biology, The Australian National University, Canberra, ACT, 2601, Australia.
[Ti] Título:Human dihydrofolate reductase influences the sensitivity of the malaria parasite Plasmodium falciparum to ketotifen - A cautionary tale in screening transgenic parasites.
[So] Source:Int J Parasitol Drugs Drug Resist;6(3):179-183, 2016 12.
[Is] ISSN:2211-3207
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Ketotifen has recently been reported to inhibit the growth of both asexual and sexual malaria parasites. A parasite transporter, PfgABCG2, has been implicated in its mechanism of action. Human dihydrofolate reductase (hDHFR) is the most commonly used selectable marker to create transgenic Plasmodium falciparum cell lines. Growth assays using transgenic P. falciparum parasites with different selectable markers revealed that the presence of hDHFR rather than the absence of PfgABCG2 is responsible for a shift in the parasite's sensitivity to ketotifen. Employing a range of in vitro assays and liquid chromatography-mass spectrometry we show that ketotifen influences hDHFR activity, but it is not metabolised by the enzyme. Our data also highlights potential pitfalls when functionally characterising transgenic parasites.
[Mh] Termos MeSH primário: Antimaláricos/farmacologia
Cetotifeno/farmacologia
Plasmodium falciparum/efeitos dos fármacos
Tetra-Hidrofolato Desidrogenase/metabolismo
[Mh] Termos MeSH secundário: Avaliação Pré-Clínica de Medicamentos
Expressão Gênica
Seres Humanos
Testes de Sensibilidade Parasitária
Plasmodium falciparum/enzimologia
Plasmodium falciparum/genética
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Tetra-Hidrofolato Desidrogenase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antimalarials); 0 (Recombinant Proteins); EC 1.5.1.3 (Tetrahydrofolate Dehydrogenase); X49220T18G (Ketotifen)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171118
[Lr] Data última revisão:
171118
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161006
[St] Status:MEDLINE


  7 / 1111 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27382945
[Au] Autor:Shih HM; Bair MJ; Chen HL; Lin IT
[Ti] Título:Eosinophilic Gastroenteritis : Brief Review.
[So] Source:Acta Gastroenterol Belg;79(2):239-44, 2016 Apr-Jun.
[Is] ISSN:1784-3227
[Cp] País de publicação:Belgium
[La] Idioma:eng
[Ab] Resumo:Eosinophilic gastroenteritis (EGE) is a rare disease which belongs to primary eosinophilic gastrointestinal disorders (primary EGIDs), characterized by an accumulation of eosinophils in the gastrointestinal (GI) tract and is strongly associated with atopy and allergy. The clinical presentations vary depending on the site and depth of eosinophilic intestinal infiltration. Radiology pictures may show irregular thickening of the folds, but these findings can also be present in other conditions like inflammatory bowel disease and lymphoma. The endoscopic appearance is also nonspecific. The definite diagnosis requires biopsy for histological evidence of GI eosinophilic infiltration and clinicians make the diagnosis in correlation with and by exclusion of other possible causes of eosinophilic infiltration. Because EGE is a rare disease, the treatment is based on limited case reports and clinicians' experience. Corticosteroids are the mainstay of therapy. The prognosis of EGE is relatively good when patients receive timely and proper treatment.
[Mh] Termos MeSH primário: Corticosteroides/uso terapêutico
Endoscopia do Sistema Digestório
Enterite/diagnóstico
Eosinofilia/diagnóstico
Gastrite/diagnóstico
Intestino Delgado/patologia
Estômago/patologia
[Mh] Termos MeSH secundário: Acetatos/uso terapêutico
Biópsia
Cromolina Sódica/uso terapêutico
Enterite/tratamento farmacológico
Eosinofilia/tratamento farmacológico
Gastrite/tratamento farmacológico
Antagonistas dos Receptores Histamínicos H1/uso terapêutico
Seres Humanos
Fatores Imunológicos/uso terapêutico
Imunossupressores/uso terapêutico
Infliximab/uso terapêutico
Intestino Delgado/diagnóstico por imagem
Cetotifeno/uso terapêutico
Antagonistas de Leucotrienos/uso terapêutico
Mercaptopurina/uso terapêutico
Quinolinas/uso terapêutico
Estômago/diagnóstico por imagem
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Acetates); 0 (Adrenal Cortex Hormones); 0 (Histamine H1 Antagonists); 0 (Immunologic Factors); 0 (Immunosuppressive Agents); 0 (Leukotriene Antagonists); 0 (Quinolines); B72HH48FLU (Infliximab); E7WED276I5 (Mercaptopurine); MHM278SD3E (montelukast); Q2WXR1I0PK (Cromolyn Sodium); X49220T18G (Ketotifen)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160708
[St] Status:MEDLINE


  8 / 1111 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27304487
[Au] Autor:Tong F; Luo L; Liu D
[Ad] Endereço:Department of Chemistry, Medical College, Shantou University, Shantou, China.
[Ti] Título:Effect of Intervention in Mast Cell Function Before Reperfusion on Renal Ischemia-Reperfusion Injury in Rats.
[So] Source:Kidney Blood Press Res;41(3):335-44, 2016.
[Is] ISSN:1423-0143
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND/AIMS: Mast cells are sparsely distributed in the kidneys under normal conditions; however, the number of mast cells increases dramatically during renal ischemia/reperfusion injury (RI/RI). When mast cells are stimulated, numerous mediators are released, and under pathological conditions, they produce a wide range of biological effects. The aim of this study was to investigate the effect of intervention in mast cell function before reperfusion on RI/RI. METHODS: Sprague-Dawley (SD) rats (n=50) were randomized into five groups: sham group, ischemia/reperfusion (I/R) group, cromolyn sodium treatment group (CS+I/R group), ketotifen treatment group (K+I/Rgroup), and compound 48/80 treatment group (C+I/R group). I/R injury was induced by bilateral renal artery and vein occlusion for 45 min followed by 24 h of reperfusion. The agents were intravenously administered 5 min before reperfusion through the tail vein. The serum levels of blood urea nitrogen(BUN), serum creatinine (Scr) and histamine and the kidney levels of malondialdehyde (MDA), superoxide dismutase (SOD), tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6) were assessed. The expression of intracellular adhesion molecule-1 (ICAM-1) in renal tissue was also measured. RESULTS: I/R injury resulted in severe renal injury, as demonstrated by a large increase in injury scores; serum levels of BUN, Scr and histamine; and kidney levels of MDA, TNF-α, and IL-6; this was accompanied by reduced SOD activity and upregulated ICAM-1 expression. Treatment with cromolyn sodium or ketotifen markedly alleviated I/R-mediated kidney injury, whereas compound 48/80 further aggravated kidney injury. CONCLUSION: Intervention in mast cell activity prior to reperfusionhas a strong effect on RI/RI.
[Mh] Termos MeSH primário: Mastócitos/fisiologia
Traumatismo por Reperfusão/tratamento farmacológico
[Mh] Termos MeSH secundário: Animais
Antialérgicos/administração & dosagem
Antialérgicos/farmacologia
Cromolina Sódica/administração & dosagem
Cromolina Sódica/farmacologia
Cetotifeno/administração & dosagem
Cetotifeno/farmacologia
Rim/lesões
Mastócitos/efeitos dos fármacos
Mastócitos/metabolismo
Ratos
Ratos Sprague-Dawley
Traumatismo por Reperfusão/patologia
Traumatismo por Reperfusão/fisiopatologia
p-Metoxi-N-metilfenetilamina/administração & dosagem
p-Metoxi-N-metilfenetilamina/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Allergic Agents); 4091-50-3 (p-Methoxy-N-methylphenethylamine); Q2WXR1I0PK (Cromolyn Sodium); X49220T18G (Ketotifen)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170314
[Lr] Data última revisão:
170314
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160616
[St] Status:MEDLINE
[do] DOI:10.1159/000443437


  9 / 1111 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27210891
[Au] Autor:Wada Y; Ami S; Nozawa M; Goto M; Shimokawa K; Ishii F
[Ad] Endereço:Department of Pharmaceutical Sciences, Meiji Pharmaceutical University.
[Ti] Título:Generic selection criteria for safety and patient benefit [V]: Comparing the pharmaceutical properties and patient usability of original and generic nasal spray containing ketotifen fumarate.
[So] Source:Drug Discov Ther;10(2):88-92, 2016.
[Is] ISSN:1881-7831
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:The pH, osmotic pressure (cryoscopy), viscosity, squeeze force, spray angle, and spraying frequency of nasal spray containing ketotifen fumarate (1 brand-name product and 8 generic products) were measured. Based on the results of pH measurement, all products were weakly acidic (4.0 to 5.1). For all products, the osmotic pressure ratio to physiological saline was approximately 1. The viscosity of various products ranged from approximately 1.0 to 1.5 mPa·s. The spray angle of drug solution differed among the products: minimum, 46 degrees (Sawai and Fusachol); and maximum, 68.7 degrees (Sekiton). In particular, TOA, Sawai, Fusachol, and TYK showed significantly smaller angles compared to Zaditen (brand-name product). Container properties varied among the products: minimum squeeze force, 19.0 N (Sekiton); and maximum squeeze force, 43.1 N (Sawai). Based on these results, although all the above products are identical in dosage form and active ingredient, the differences in pharmaceutical properties, such as container operations and drug-solution spraying/attachment, may markedly influence patients' subjective opinions.
[Mh] Termos MeSH primário: Antialérgicos/uso terapêutico
Medicamentos Genéricos
Cetotifeno/uso terapêutico
Seleção de Pacientes
[Mh] Termos MeSH secundário: Antialérgicos/efeitos adversos
Química Farmacêutica
Embalagem de Medicamentos
Seres Humanos
Concentração de Íons de Hidrogênio
Cetotifeno/efeitos adversos
Sprays Nasais
Pressão Osmótica
Viscosidade
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Allergic Agents); 0 (Drugs, Generic); 0 (Nasal Sprays); X49220T18G (Ketotifen)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170124
[Lr] Data última revisão:
170124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160524
[St] Status:MEDLINE
[do] DOI:10.5582/ddt.2016.01019


  10 / 1111 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27178036
[Au] Autor:Maulvi FA; Mangukiya MA; Patel PA; Vaidya RJ; Koli AR; Ranch KM; Shah DO
[Ad] Endereço:Maliba Pharmacy College, Uka Tarsadia University, Surat, 394350, India. furqanmpc@gmail.com.
[Ti] Título:Extended release of ketotifen from silica shell nanoparticle-laden hydrogel contact lenses: in vitro and in vivo evaluation.
[So] Source:J Mater Sci Mater Med;27(6):113, 2016 Jun.
[Is] ISSN:1573-4838
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ketotifen an anti-allergic drug delivered via eye drops has major limitations, including poor ocular bioavailability and poor patient compliance. The objective of the research work was to fabricate ketotifen loaded microemulsion laden hydrogels and silica shell nanoparticle-laden (prepared from microemulsion using octyltrimethoxysilane) hydrogels to achieve extended ocular drug delivery. The porous silica shell membrane was synthesized at the liquid interface of microemulsion, which facilitates the prolongation of drug release duration from hydrogels. Drug encapsulated microemulsion and silica shell nanoparticles were dispersed separately in pre-monomer mixture, and fabricated to hydrogel. For comparison, hydrogel with direct drug entrapment was also fabricated. Significant loss in transmittance and physical properties was observed in hydrogels with direct drug entrapment. While, microemulsion and silica shell nanoparticle-laden hydrogels did not show significant effect on transmittance and physical properties. The in vitro drug release data showed extended release of ketotifen from hydrogels in following order: direct loading
[Mh] Termos MeSH primário: Lentes de Contato
Oftalmopatias/induzido quimicamente
Cetotifeno/farmacocinética
Nanopartículas/química
Dióxido de Silício/química
[Mh] Termos MeSH secundário: Animais
Sobrevivência Celular/efeitos dos fármacos
Preparações de Ação Retardada
Feminino
Hidrogéis
Cetotifeno/química
Cetotifeno/toxicidade
Masculino
Camundongos
Coelhos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Delayed-Action Preparations); 0 (Hydrogels); 7631-86-9 (Silicon Dioxide); X49220T18G (Ketotifen)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171021
[Lr] Data última revisão:
171021
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160515
[St] Status:MEDLINE
[do] DOI:10.1007/s10856-016-5724-3



página 1 de 112 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde