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[PMID]:27248569
[Au] Autor:Fast BJ; Galan MP; Schafer AC
[Ad] Endereço:a Dow AgroSciences LLC , Indianapolis , IN , USA.
[Ti] Título:Event DAS-444Ø6-6 soybean grown in Brazil is compositionally equivalent to non-transgenic soybean.
[So] Source:GM Crops Food;7(2):79-83, 2016 Apr 02.
[Is] ISSN:2164-5701
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Soybean event DAS-444Ø6-6 is tolerant to the herbicides 2,4-D, glyphosate, and glufosinate. An investigation of potential unintended adverse compositional changes in a genetically modified crop is required to meet government regulatory requirements in various geographies. A study to meet these requirements in Brazil was completed demonstrating compositional equivalency between DAS-444Ø6-6 and non-transgenic soybean. This study supplements the extensive literature supporting transgenesis as less disruptive of crop composition compared with traditional breeding methods.
[Mh] Termos MeSH primário: Biotecnologia/legislação & jurisprudência
Engenharia Genética/legislação & jurisprudência
Resistência a Herbicidas
Herbicidas/farmacologia
Plantas Geneticamente Modificadas/efeitos dos fármacos
Feijão de Soja/efeitos dos fármacos
[Mh] Termos MeSH secundário: Ácido 2,4-Diclorofenoxiacético/farmacologia
Ácido 4-Acetamido-4'-isotiocianatostilbeno-2,2'-dissulfônico/análogos & derivados
Ácido 4-Acetamido-4'-isotiocianatostilbeno-2,2'-dissulfônico/farmacologia
Agricultura/legislação & jurisprudência
Aminobutiratos/farmacologia
Brasil
Cruzamento
Produtos Agrícolas
Glicina/análogos & derivados
Glicina/farmacologia
Feijão de Soja/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aminobutyrates); 0 (Herbicides); 2577AQ9262 (2,4-Dichlorophenoxyacetic Acid); 27816-59-7 (4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid); 4632WW1X5A (glyphosate); 51276-47-2 (phosphinothricin); 81-11-8 (amsonic acid); TE7660XO1C (Glycine)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170601
[Lr] Data última revisão:
170601
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160602
[St] Status:MEDLINE
[do] DOI:10.1080/21645698.2016.1184815


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[PMID]:26543230
[Au] Autor:Gray AL; Coleman DT; Castore RF; Mohyeldin MM; El Sayed KA; Cardelli JA
[Ad] Endereço:Louisiana State University Health Sciences Center - Shreveport, Shreveport, LA, USA.
[Ti] Título:Isothiocyanatostilbenes as novel c-Met inhibitors.
[So] Source:Oncotarget;6(38):41180-93, 2015 Dec 01.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The hepatocyte growth factor receptor (HGFR or c-Met) is a driver of multiple cancer subtypes. While there are several c-Met inhibitors in development, few have been approved for clinical use, warranting the need for continued research and development of c-Met targeting therapeutic modalities. The research presented here demonstrates a particular class of compounds known as isothiocyanatostilbenes can act as c-Met inhibitors in multiple cancer cell lines. Specifically, we found that 4,4'-Diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) and 4,4'-Diisothiocyanatodihydrostilbene-2,2'-disulfonic acid (H2DIDS) had c-Met inhibitory effective doses in the low micromolar range while 4-acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid (SITS) and 4,4'-dinitrostilbene-2, 2'-disulfonic acid (DNDS) exhibited IC50s 100 to 1000 fold higher. These compounds displayed much greater selectivity for inhibiting c-Met activation compared to similar receptor tyrosine kinases. In addition, DIDS and H2DIDS reduced hepatocyte growth factor (HGF)-induced, but not epidermal growth factor (EGF)-induced, cell scattering, wound healing, and 3-dimensional (3D) proliferation of tumor cell spheroids. In-cell and cell-free assays suggested that DIDS and H2DIDS can inhibit and reverse c-Met phosphorylation, similar to SU11274. Additional data demonstrated that DIDS is tolerable in vivo. These data provide preliminary support for future studies examining DIDS, H2DIDS, and derivatives as potential c-Met therapeutics.
[Mh] Termos MeSH primário: Movimento Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-met/metabolismo
Estilbenos/farmacologia
[Mh] Termos MeSH secundário: Ácido 4,4'-Di-Isotiocianoestilbeno-2,2'-Dissulfônico/análogos & derivados
Ácido 4,4'-Di-Isotiocianoestilbeno-2,2'-Dissulfônico/farmacologia
Ácido 4-Acetamido-4'-isotiocianatostilbeno-2,2'-dissulfônico/farmacologia
Animais
Western Blotting
Linhagem Celular Tumoral
Relação Dose-Resposta a Droga
Feminino
Fator de Crescimento de Hepatócito/farmacologia
Seres Humanos
Camundongos Nus
Neoplasias/tratamento farmacológico
Neoplasias/metabolismo
Neoplasias/patologia
Fosforilação/genética
Fatores de Tempo
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Stilbenes); 27816-59-7 (4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid); 61481-03-6 (dihydro-DIDS); 67256-21-7 (Hepatocyte Growth Factor); 6ND7PC82E2 (4,4'-dinitro-2,2'-stilbenedisulfonic acid); EC 2.7.10.1 (Proto-Oncogene Proteins c-met); Q1O6DSW23R (4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151107
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.5748


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[PMID]:25394471
[Au] Autor:Kao L; Azimov R; Abuladze N; Newman D; Kurtz I
[Ad] Endereço:Division of Nephrology, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California; and.
[Ti] Título:Human SLC4A11-C functions as a DIDS-stimulatable H⁺(OH⁻) permeation pathway: partial correction of R109H mutant transport.
[So] Source:Am J Physiol Cell Physiol;308(2):C176-88, 2015 Jan 15.
[Is] ISSN:1522-1563
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The SLC4A11 gene mutations cause a variety of genetic corneal diseases, including congenital hereditary endothelial dystrophy 2 (CHED2), Harboyan syndrome, some cases of Fuchs' endothelial dystrophy (FECD), and possibly familial keratoconus. Three NH2-terminal variants of the human SLC4A11 gene, named SLC4A11-A, -B, and -C are known. The SLC4A11-B variant has been the focus of previous studies. Both the expression of the SLC4A11-C variant in the cornea and its functional properties have not been characterized, and therefore its potential pathophysiological role in corneal diseases remains to be explored. In the present study, we demonstrate that SLC4A11-C is the predominant SLC4A11 variant expressed in human corneal endothelial mRNA and that the transporter functions as an electrogenic H(+)(OH(-)) permeation pathway. Disulfonic stilbenes, including 4,4'-diisothiocyano-2,2'-stilbenedisulfonate (DIDS), 4,4'-diisothiocyanatodihydrostilbene-2,2'-disulfonate (H2DIDS), and 4-acetamido-4'-isothiocyanato-stilbene-2,2'-disulfonate (SITS), which are known to bind covalently, increased SLC4A11-C-mediated H(+)(OH(-)) flux by 150-200% without having a significant effect in mock-transfected cells. Noncovalently interacting 4,4'-diaminostilbene-2,2'-disulfonate (DADS) was without effect. We tested the efficacy of DIDS on the functionally impaired R109H mutant (SLC4A11-C numbering) that causes CHED2. DIDS (1 mM) increased H(+)(OH(-)) flux through the mutant transporter by ∼40-90%. These studies provide a basis for future testing of more specific chemically modified dilsulfonic stilbenes as potential therapeutic agents to improve the functional impairment of specific SLC4A11 mutant transporters.
[Mh] Termos MeSH primário: Ácido 4,4´-Di-Isotiocianoestilbeno-2,2´-Dissulfônico/farmacologia
Proteínas de Transporte de Ânions/metabolismo
Antiporters/metabolismo
Hidróxidos/metabolismo
Permeabilidade/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Ácido 4,4'-Di-Isotiocianoestilbeno-2,2'-Dissulfônico/análogos & derivados
Ácido 4-Acetamido-4'-isotiocianatostilbeno-2,2'-dissulfônico/análogos & derivados
Ácido 4-Acetamido-4'-isotiocianatostilbeno-2,2'-dissulfônico/farmacologia
Proteínas de Transporte de Ânions/genética
Antiporters/genética
Transporte Biológico/fisiologia
Linhagem Celular
Córnea/efeitos dos fármacos
Córnea/metabolismo
Células Endoteliais/efeitos dos fármacos
Células Endoteliais/metabolismo
Células HEK293
Seres Humanos
Mutação/genética
RNA Mensageiro/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anion Transport Proteins); 0 (Antiporters); 0 (Hydroxides); 0 (RNA, Messenger); 0 (SLC4A11 protein, human); 27816-59-7 (4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid); 61481-03-6 (dihydro-DIDS); 81-11-8 (amsonic acid); 9159UV381P (hydroxide ion); Q1O6DSW23R (4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid)
[Em] Mês de entrada:1503
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141115
[St] Status:MEDLINE
[do] DOI:10.1152/ajpcell.00271.2014


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[PMID]:25123669
[Au] Autor:Kant S; Kumar A; Singh SM
[Ad] Endereço:School of Biotechnology, Banaras Hindu University, Varanasi, 221005, India.
[Ti] Título:Bicarbonate transport inhibitor SITS modulates pH homeostasis triggering apoptosis of Dalton's lymphoma: implication of novel molecular mechanisms.
[So] Source:Mol Cell Biochem;397(1-2):167-78, 2014 Dec.
[Is] ISSN:1573-4919
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Bicarbonate transporter (BCT) plays a crucial role in maintaining pH homeostasis of tumor cells by import of HCO3(-). This helps the tumor cells in manifesting extracellular tumor acidosis, accompanied by a relative intracellular alkalinization, which in turn promotes tumor progression. Therefore, blocking BCT-mediated HCO3(-) transport is envisaged as a promising anticancer therapeutic approach. Thus, using a murine model of a T cell lymphoma, designated as Dalton's lymphoma (DL), in the present in vitro investigation the antitumor consequences of blocking BCT function by its inhibitor 4-acetamido-4-isothiocyanostilbene-2,2-disulfonate (SITS) were explored. Treatment of DL cells with SITS resulted in an increase in the extracellular pH, associated with a decline in DL cell survival and augmented induction of apoptosis. BCT inhibition also elevated the expression of cytochrome c, caspase-9, caspase-3, Bax, reactive oxygen species, and nitric oxide along with inhibition of HSP-70 and Bcl2, which regulate tumor cell survival and apoptosis. SITS-treated DL cells displayed upregulated production of IFN-γ and IL-6 along with a decline of IL-10. Treatment of DL cells with SITS also inhibited the expression of fatty acid synthase, which is crucial for membrane biogenesis in neoplastic cells. The expression of lactate transporter MCT-1 and multidrug resistance regulating protein MRP-1 got inhibited along with hampered uptake of glucose and lactate production in SITS-treated DL cells. Thus, the declined tumor cell survival following inhibition of BCT could be the consequence of interplay of several inter-connected regulatory molecular events. The outcome of this study indicates the potential of BCT inhibition as a novel therapeutic approach for treatment of hematological malignancies.
[Mh] Termos MeSH primário: Ácido 4-Acetamido-4´-isotiocianatostilbeno-2,2´-dissulfônico/farmacologia
Proteínas de Transporte de Ânions/antagonistas & inibidores
Apoptose/efeitos dos fármacos
Homeostase/efeitos dos fármacos
Linfoma de Células T/tratamento farmacológico
Proteínas de Neoplasias/metabolismo
Neoplasias Experimentais/tratamento farmacológico
Simportadores/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Proteínas de Transporte de Ânions/genética
Proteínas de Transporte de Ânions/metabolismo
Apoptose/genética
Proteínas Reguladoras de Apoptose/genética
Proteínas Reguladoras de Apoptose/metabolismo
Bicarbonatos/metabolismo
Citocinas/genética
Citocinas/metabolismo
Homeostase/genética
Concentração de Íons de Hidrogênio
Linfoma de Células T/genética
Linfoma de Células T/metabolismo
Linfoma de Células T/patologia
Camundongos
Camundongos Endogâmicos BALB C
Proteínas de Neoplasias/antagonistas & inibidores
Proteínas de Neoplasias/genética
Neoplasias Experimentais/genética
Neoplasias Experimentais/metabolismo
Neoplasias Experimentais/patologia
Simportadores/genética
Simportadores/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anion Transport Proteins); 0 (Apoptosis Regulatory Proteins); 0 (Bicarbonates); 0 (Cytokines); 0 (Neoplasm Proteins); 0 (Slc4a11 protein, mouse); 0 (Symporters); 27816-59-7 (4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid)
[Em] Mês de entrada:1506
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140816
[St] Status:MEDLINE
[do] DOI:10.1007/s11010-014-2184-2


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[PMID]:24714077
[Au] Autor:Giambelluca MS; Ciancio MC; Orlowski A; Gende OA; Pouliot M; Aiello EA
[Ad] Endereço:Centro de Investigaciones Cardiovasculares, CCT La Plata, CONICET. Facultad de Ciencias Médicas, Universidad Nacional de La Plata, La Plata, Argentina.
[Ti] Título:Characterization of the Na/HCO3(-) cotransport in human neutrophils.
[So] Source:Cell Physiol Biochem;33(4):982-90, 2014.
[Is] ISSN:1421-9778
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Bicarbonate transport has crucial roles in regulating intracellular pH (pHi) in a variety of cells. The purpose of this study was to evaluate its participation in the regulation of pHi in resting and stimulated human neutrophils. METHODS: Freshly isolated human neutrophils acidified by an ammonium prepulse were used in this study. RESULTS: We demonstrated that resting neutrophils have a bicarbonate transport mechanism that prevents acidification when the Na(+)/H(+) exchanger is blocked by EIPA. Neutrophils acidified by an ammonium prepulse showed an EIPA-resistant recovery of pHi that was inhibited by the blocker of the anionic transporters SITS or the Na(+)/HCO3(-) cotransporter (NBC) selective inhibitor S0859, and abolished when sodium was removed from the extracellular medium. In western blot and RT-PCR analysis the expression of NBCe2 but not NBCe1 or NBCn1 was detected in neutrophils Acidified neutrophils increased the EIPA-insensitive pHi recovery rate when its activity was stimulated with fMLF/ cytochalasin B. This increase in the removal of acid equivalents was insensitive to the blockade of the NADPH oxidase with DPI. CONCLUSION: It is concluded that neutrophils have an NBC that regulates basal pHi and is modulated by chemotactic agents.
[Mh] Termos MeSH primário: Neutrófilos/metabolismo
Simportadores de Sódio-Bicarbonato/metabolismo
[Mh] Termos MeSH secundário: Ácido 4-Acetamido-4'-isotiocianatostilbeno-2,2'-dissulfônico/farmacologia
Amilorida/análogos & derivados
Amilorida/farmacologia
Cloreto de Amônio/farmacologia
Benzamidas/farmacologia
Bicarbonatos/farmacologia
Citocalasina B/farmacologia
Células HEK293
Seres Humanos
Concentração de Íons de Hidrogênio
Transporte de Íons/efeitos dos fármacos
N-Formilmetionina Leucil-Fenilalanina/farmacologia
NADPH Oxidases/antagonistas & inibidores
NADPH Oxidases/metabolismo
Neutrófilos/efeitos dos fármacos
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
RNA Mensageiro/metabolismo
Simportadores de Sódio-Bicarbonato/genética
Trocadores de Sódio-Hidrogênio/metabolismo
Sulfonamidas/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Benzamides); 0 (Bicarbonates); 0 (Protein Isoforms); 0 (RNA, Messenger); 0 (S 0859 compound); 0 (Sodium-Bicarbonate Symporters); 0 (Sodium-Hydrogen Exchangers); 0 (Sulfonamides); 01Q9PC255D (Ammonium Chloride); 27816-59-7 (4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid); 3CHI920QS7 (Cytochalasin B); 59880-97-6 (N-Formylmethionine Leucyl-Phenylalanine); 7DZO8EB0Z3 (Amiloride); EC 1.6.3.- (NADPH Oxidases); VW50CE070T (ethylisopropylamiloride)
[Em] Mês de entrada:1501
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140410
[St] Status:MEDLINE
[do] DOI:10.1159/000358669


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[PMID]:23902890
[Au] Autor:Zheng XB; Wang R; Yang HL; Sun XL
[Ad] Endereço:Department of Geriatric Medicine, China-Japan Union Hospital, Jilin University, Changchun 130033, China.
[Ti] Título:[Effects of chloride ion channel and its blockers on myocardial ischemia reperfusion arrhythmias in rabbits].
[So] Source:Zhonghua Yi Xue Za Zhi;93(15):1168-73, 2013 Apr 16.
[Is] ISSN:0376-2491
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To explore the impact of chloride ion channel and its blockers 4, 4'-diisothiocyanostilbene-2, 2'-disulfonic acid (DIDS), cyanato-stilbene-2, 2'-disulfonic acid (SITS) and 5-nitro-2-(3-phenyl-propylamino) benzoic acid (NPPB) on arrhythmias caused by myocardial ischemia reperfusion. METHODS: A total of 40 rabbits were divided into control, ischemia reperfusion, DIDS low-dose, DIDS high-dose, SITS low-dose, SITS high-dose, NPPB low-dose and NPPB high-dose groups. Myocardial ischemia reperfusion model was established by ligation of anterior descending coronary artery. And standard limb lead II of electrocardiogram (ECG) was continuously monitored during the experimental process. Then comparisons of heart rate, ECG P wave, R wave, T wave, ST segment changes and arrhythmias score were made between the above groups. RESULTS: During 30-minute ischemia, compared with the control group, all other groups showed significantly decreased heart rate ((199.8 ± 4.0) - (253.6 ± 2.1) vs (267.0 ± 3.4), all P < 0.01), elevated ECG P wave ((0.216 ± 0.019) - (0.356 ± 0.024) vs (0.186 ± 0.019), all P < 0.01), R wave ((0.564 ± 0.017) - (1.138 ± 0.048) vs (0.506 ± 0.018), all P < 0.01), T wave ((0.542 ± 0.013) - (0.856 ± 0.045) vs (0.278 ± 0.015), all P < 0.01) and ST segment ((0.326 ± 0.027) - (0.668 ± 0.054) vs (0.024 ± 0.023), all P < 0.01) and increased arrhythmia score ((1.4 ± 0.5) - (4.6 ± 0.5) vs (0.4 ± 0.5), all P < 0.01). Compared with the ischemia reperfusion group, the above indices significantly improved in the intervention groups (heart rate: (214.8 ± 3.4) - (246.8 ± 4.0) vs (199.8 ± 4.0), all P < 0.01; P wave: (0.216 ± 0.019) - (0.316 ± 0.011) vs (0.356 ± 0.024), all P < 0.01; R wave: (0.564 ± 0.017) - (0.980 ± 0.035) vs (1.138 ± 0.048), all P < 0.01; T wave: (0.542 ± 0.013) - (0.792 ± 0.026) vs (0.856 ± 0.045), all P < 0.01; ST segment: (0.326 ± 0.027) - (0.596 ± 0.018) vs (0.668 ± 0.054), all P < 0.01; arrhythmia score: (1.4 ± 0.5) - (3.8 ± 0.4) vs (4.6 ± 0.5), all P < 0.01). Among which, the DIDS group was the best, followed by the SITS group and then the NPPB group. And the high-dose subgroups were better than those of the low-dose subgroups. During 60-minute reperfusion, the decreased heart rate upswing significantly in each group and the elevated P wave, R wave, T wave and ST segment fell back gradually. The DIDS group showed the most obvious amplitude change, followed by the SITS group and then the NPPB group. And the high-dose subgroups were better than those of the low-dose subgroups. The arrhythmia score during reperfusion showed the same trend. CONCLUSION: Chloride ion channel is involved in the generation of myocardial ischemia reperfusion arrhythmia.Early application of chloride ion channel blockers DIDS, SITS and NPPB may improve the ECG manifestations and reduce the degree of reperfusion arrhythmia.
[Mh] Termos MeSH primário: Arritmias Cardíacas/fisiopatologia
Canais de Cloreto
Isquemia Miocárdica/fisiopatologia
Traumatismo por Reperfusão Miocárdica/fisiopatologia
[Mh] Termos MeSH secundário: Ácido 4,4'-Di-Isotiocianoestilbeno-2,2'-Dissulfônico/farmacologia
Ácido 4-Acetamido-4'-isotiocianatostilbeno-2,2'-dissulfônico/farmacologia
Animais
Antiarrítmicos/farmacologia
Canais de Cloreto/antagonistas & inibidores
Nitrobenzoatos/farmacologia
Coelhos
[Pt] Tipo de publicação:ENGLISH ABSTRACT; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 0 (Chloride Channels); 0 (Nitrobenzoates); 27816-59-7 (4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid); 3A35O9G3YZ (5-nitro-2-(3-phenylpropylamino)benzoic acid); Q1O6DSW23R (4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid)
[Em] Mês de entrada:1401
[Cu] Atualização por classe:130801
[Lr] Data última revisão:
130801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130802
[St] Status:MEDLINE


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[PMID]:22514656
[Au] Autor:Shen B; Li X; Wang F; Yao X; Yang D
[Ad] Endereço:Department of Physiology, The Chinese University of Hong Kong, Shatin, Hong Kong, China.
[Ti] Título:A synthetic chloride channel restores chloride conductance in human cystic fibrosis epithelial cells.
[So] Source:PLoS One;7(4):e34694, 2012.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mutations in the gene-encoding cystic fibrosis transmembrane conductance regulator (CFTR) cause defective transepithelial transport of chloride (Cl(-)) ions and fluid, thereby becoming responsible for the onset of cystic fibrosis (CF). One strategy to reduce the pathophysiology associated with CF is to increase Cl(-) transport through alternative pathways. In this paper, we demonstrate that a small synthetic molecule which forms Cl(-) channels to mediate Cl(-) transport across lipid bilayer membranes is capable of restoring Cl(-) permeability in human CF epithelial cells; as a result, it has the potential to become a lead compound for the treatment of human diseases associated with Cl(-) channel dysfunction.
[Mh] Termos MeSH primário: Canais de Cloreto/síntese química
Cloretos/metabolismo
Fibrose Cística/metabolismo
Células Epiteliais/metabolismo
[Mh] Termos MeSH secundário: Ácido 4,4'-Di-Isotiocianoestilbeno-2,2'-Dissulfônico/química
Ácido 4-Acetamido-4'-isotiocianatostilbeno-2,2'-dissulfônico/química
Animais
Linhagem Celular
Eletrofisiologia
Células Epiteliais/efeitos dos fármacos
Seres Humanos
Lipopolissacarídeos/farmacologia
Camundongos
Ácido Niflúmico/química
Fator de Necrose Tumoral alfa/sangue
ortoaminobenzoatos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Chloride Channels); 0 (Chlorides); 0 (Lipopolysaccharides); 0 (Tumor Necrosis Factor-alpha); 0 (ortho-Aminobenzoates); 27816-59-7 (4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid); 4U5MP5IUD8 (Niflumic Acid); 952VN06WBB (fenamic acid); Q1O6DSW23R (4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid)
[Em] Mês de entrada:1208
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120420
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0034694


  8 / 1469 MEDLINE  
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[PMID]:22328719
[Au] Autor:Zhang X; Du XN; Zhang GH; Jia ZF; Chen XJ; Huang DY; Liu BY; Zhang HL
[Ad] Endereço:Department of Pharmacology, Hebei Medical University, Shijiazhuang, Hebei 050017, China.
[Ti] Título:Agonist-dependent potentiation of vanilloid receptor transient receptor potential vanilloid type 1 function by stilbene derivatives.
[So] Source:Mol Pharmacol;81(5):689-700, 2012 May.
[Is] ISSN:1521-0111
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transient receptor potential vanilloid type 1 (TRPV1) is a nonselective cation channel activated by capsaicin, low pH, and noxious heat and plays a key role in nociception. Understanding mechanisms for functional modulation of TRPV1 has important implications. One characteristic of TRPV1 is that channel activity induced by either capsaicin or other activators can be sensitized or modulated by factors involving different cell signaling mechanisms. In this study, we describe a novel mechanism for the modulation of TRPV1 function: TRPV1 function is modulated by 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) and its analogs. We found that, in rat dorsal root ganglion neurons, although DIDS did not induce the activation of TRPV1 per se but drastically increased the TRPV1 currents induced by either capsaicin or low pH. DIDS also blocked the tachyphylaxis of the low pH-induced TRPV1 currents. 4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic acid (SITS), a DIDS analog, failed to enhance the capsaicin-evoked TRPV1 current but increased the low pH-evoked TRPV1 currents, with an effect comparable with that of DIDS. SITS also blocked the low pH-induced tachyphylaxis. DIDS also potentiated the currents of TRPV1 channels expressed in human embryonic kidney 293 cells, with an effect of left-shifting the concentration-response curve of the capsaicin-induced TRPV1 currents. This study demonstrates that DIDS and SITS, traditionally used chloride channel blockers, can modify TRPV1 channel function in an agonist-dependent manner. The results provide new input for understanding TRPV1 modulation and developing new modulators of TRPV1 function.
[Mh] Termos MeSH primário: Estilbenos/farmacologia
Canais de Cátion TRPV/efeitos dos fármacos
[Mh] Termos MeSH secundário: Ácido 4,4'-Di-Isotiocianoestilbeno-2,2'-Dissulfônico/farmacologia
Ácido 4-Acetamido-4'-isotiocianatostilbeno-2,2'-dissulfônico/farmacologia
Animais
Ácidos Araquidônicos/farmacologia
Cálcio/metabolismo
Capsaicina/farmacologia
Células Cultivadas
Endocanabinoides
Seres Humanos
Concentração de Íons de Hidrogênio
Alcamidas Poli-Insaturadas/farmacologia
Ratos
Ratos Sprague-Dawley
Canais de Cátion TRPV/agonistas
Canais de Cátion TRPV/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Arachidonic Acids); 0 (Endocannabinoids); 0 (Polyunsaturated Alkamides); 0 (Stilbenes); 0 (TRPV Cation Channels); 0 (TRPV1 protein, human); 0 (Trpv1 protein, rat); 27816-59-7 (4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid); Q1O6DSW23R (4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid); S07O44R1ZM (Capsaicin); SY7Q814VUP (Calcium); UR5G69TJKH (anandamide)
[Em] Mês de entrada:1206
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:120214
[St] Status:MEDLINE
[do] DOI:10.1124/mol.111.076000


  9 / 1469 MEDLINE  
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[PMID]:22111710
[Au] Autor:Schutte M; Kemp G; Visser HG; Roodt A
[Ad] Endereço:Department of Chemistry, University of the Free State, P.O. Box 339, Bloemfontein 9300, South Africa.
[Ti] Título:Tuning the reactivity in classic low-spin d6 rhenium(I) tricarbonyl radiopharmaceutical synthon by selective bidentate ligand variation (L,L'-Bid; L,L'= N,N', N,O, and O,O' donor atom sets) in fac-[Re(CO)3(L,L'-Bid)(MeOH)]n complexes.
[So] Source:Inorg Chem;50(24):12486-98, 2011 Dec 19.
[Is] ISSN:1520-510X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A range of fac-[Re(CO)(3)(L,L'-Bid)(H(2)O)](n) (L,L'-Bid = neutral or monoanionic bidentate ligands with varied L,L' donor atoms, N,N', N,O, or O,O': 1,10-phenanthroline, 2,2'-bipydine, 2-picolinate, 2-quinolinate, 2,4-dipicolinate, 2,4-diquinolinate, tribromotropolonate, and hydroxyflavonate; n = 0, +1) has been synthesized and the aqua/methanol substitution has been investigated. The complexes were characterized by UV-vis, IR and NMR spectroscopy and X-ray crystallographic studies of the compounds fac-[Re(CO)(3)(Phen)(H(2)O)]NO(3)·0.5Phen, fac-[Re(CO)(3)(2,4-dQuinH)(H(2)O)]·H(2)O, fac-[Re(CO)(3)(2,4-dQuinH)Py]Py, and fac-[Re(CO)(3)(Flav)(CH(3)OH)]·CH(3)OH are reported. A four order-of-magnitude of activation for the methanol substitution is induced as manifested by the second order rate constants with (N,N'-Bid) < (N,O-Bid) < (O,O'-Bid). Forward and reverse rate and stability constants from slow and stopped-flow UV/vis measurements (k(1), M(-1) s(-1); k(-1), s(-1); K(1), M(-1)) for bromide anions as entering nucleophile are as follows: fac-[Re(CO)(3)(Phen)(MeOH)](+) (50 ± 3) × 10(-3), (5.9 ± 0.3) × 10(-4), 84 ± 7; fac-[Re(CO)(3)(2,4-dPicoH)(MeOH)] (15.7 ± 0.2) × 10(-3), (6.3 ± 0.8) × 10(-4), 25 ± 3; fac-[Re(CO)(3)(TropBr(3))(MeOH)] (7.06 ± 0.04) × 10(-2), (4 ± 1) × 10(-3), 18 ± 4; fac-[Re(CO)(3)(Flav)(MeOH)] 7.2 ± 0.3, 3.17 ± 0.09, 2.5 ± 2. Activation parameters (ΔH(k1)(++), kJmol(-1); ΔS(k1)(), J K(-1) mol(-1)) from Eyring plots for entering nucleophiles as indicated are as follows: fac-[Re(CO)(3)(Phen)(MeOH)](+) iodide 70 ± 1, -35 ± 3; fac-[Re(CO)(3)(2,4-dPico)(MeOH)] bromide 80.8 ± 6, -8 ± 2; fac-[Re(CO)(3)(Flav)(MeOH)] bromide 52 ± 5, -52 ± 15. A dissociative interchange mechanism is proposed.
[Mh] Termos MeSH primário: Compostos Organometálicos/síntese química
Compostos Radiofarmacêuticos/síntese química
Rênio/química
[Mh] Termos MeSH secundário: 2,2'-Dipiridil/química
Ácido 4-Acetamido-4'-isotiocianatostilbeno-2,2'-dissulfônico/análogos & derivados
Ácido 4-Acetamido-4'-isotiocianatostilbeno-2,2'-dissulfônico/química
Cristalografia por Raios X
Cinética
Ligantes
Espectroscopia de Ressonância Magnética
Metanol/química
Modelos Moleculares
Estrutura Molecular
Fenantrolinas/química
Ácidos Picolínicos/química
Espalhamento a Baixo Ângulo
Termodinâmica
Água/química
Difração de Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ligands); 0 (Organometallic Compounds); 0 (Phenanthrolines); 0 (Picolinic Acids); 0 (Radiopharmaceuticals); 059QF0KO0R (Water); 27816-59-7 (4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid); 551W113ZEP (2,2'-Dipyridyl); 7440-15-5 (Rhenium); 78543-24-5 (4-benzamido-4'-isothiocyanostilbene-2,2'-disulfonate); QZV2W997JQ (picolinic acid); UE81S5CQ0G (dipicolinic acid); W4X6ZO7939 (1,10-phenanthroline); Y4S76JWI15 (Methanol)
[Em] Mês de entrada:1204
[Cu] Atualização por classe:151119
[Lr] Data última revisão:
151119
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:111125
[St] Status:MEDLINE
[do] DOI:10.1021/ic2013792


  10 / 1469 MEDLINE  
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[PMID]:21553261
[Au] Autor:Liu D; He H; Li GL; Chen J; Yin D; Liao ZP; Tang L; Huang QR; Lai ZF; He M
[Ad] Endereço:Jiangxi Provincial Institute of Hypertension at The First Affiliated Hospital, Nanchang University, Nanchang 330006, People's Republic of China.
[Ti] Título:Mechanisms of chloride in cardiomyocyte anoxia-reoxygenation injury: the involvement of oxidative stress and NF-kappaB activation.
[So] Source:Mol Cell Biochem;355(1-2):201-9, 2011 Sep.
[Is] ISSN:1573-4919
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:During anoxia/reoxygenation (A/R) injury, intracellular chloride ion concentration ([Cl(-)](i)) homeostasis may play a role in maintaining the normal physiological function of cardiomyocytes. Various chloride transport systems could have influenced the concentration of chloride ion, but what kinds of chloride transport systems could play an important role in cardiomyocytes subjected to A/R injury and its mechanism are unknown. The aim of our study was to clarify the contributions of various chloride transport systems to anoxia/reoxygenation in rat neonatal cardiac myocytes and further to investigate the involved mechanisms. Oxidative stress and redox-sensitive transcription factor (NF-kappaB) activation are believed to play an important role in the A/R injury. To assess whether oxidative stress and NF-kappaB involve [Cl(-)](i) changes resulting in cardiomyocytes injury, the anoxia-reoxygenation (A/R) injury model was successfully established and administered with inhibitors of various chloride transport systems. Administration with Cl(-)-substitution and Cl(-)/HCO(3) (-) exchange inhibitor(SITS) has been shown to produce a protective effect against A/R injury by decreasing [Cl(-)](i) concentration, lipid peroxidation (malondialdehyde (MDA)) levels, and NF-kappaB activity, and by increasing antioxidant enzyme (glutathione peroxidase (GSHPx), superoxide dismutase (SOD), and catalase(CAT)) activity. However, inhibitors for the Cl(-)-channel (9-AC) and Na(+)-K(+)-2Cl(-) co-transporter (bumetanide) had no effects. Our results indicate that Cl(-)/HCO(3) (-) exchange system plays an important role in the cardiocyte A/R injury by influencing [Cl(-)](i) concentration. The protective effects of SITS and Cl(-)-substitution on cardiomyocytes may be due to the attenuation of oxidative stress and inhibition of NF-kappaB activation.
[Mh] Termos MeSH primário: Cloretos/metabolismo
Traumatismo por Reperfusão Miocárdica/metabolismo
Miócitos Cardíacos/metabolismo
NF-kappa B/metabolismo
Estresse Oxidativo
[Mh] Termos MeSH secundário: Ácido 4-Acetamido-4'-isotiocianatostilbeno-2,2'-dissulfônico/farmacologia
Animais
Antracenos/farmacologia
Apoptose
Bumetanida/farmacologia
Catalase/metabolismo
Hipóxia Celular
Sobrevivência Celular
Canais de Cloreto/antagonistas & inibidores
Canais de Cloreto/metabolismo
Antiportadores de Cloreto-Bicarbonato/metabolismo
Produtos Fermentados do Leite
Ensaios Enzimáticos
Glutationa Peroxidase/metabolismo
L-Lactato Desidrogenase/metabolismo
Peroxidação de Lipídeos
Masculino
Traumatismo por Reperfusão Miocárdica/patologia
Miócitos Cardíacos/patologia
Oxigênio/metabolismo
Cultura Primária de Células
Transporte Proteico
Ratos
Ratos Sprague-Dawley
Espécies Reativas de Oxigênio/metabolismo
Inibidores de Simportadores de Cloreto de Sódio e Potássio/farmacologia
Simportadores de Cloreto de Sódio-Potássio/metabolismo
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anthracenes); 0 (Chloride Channels); 0 (Chloride-Bicarbonate Antiporters); 0 (Chlorides); 0 (NF-kappa B); 0 (Reactive Oxygen Species); 0 (Sodium Potassium Chloride Symporter Inhibitors); 0 (Sodium-Potassium-Chloride Symporters); 0Y2S3XUQ5H (Bumetanide); 27816-59-7 (4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acid); 723-62-6 (9-anthroic acid); EC 1.1.1.27 (L-Lactate Dehydrogenase); EC 1.11.1.6 (Catalase); EC 1.11.1.9 (Glutathione Peroxidase); EC 1.15.1.1 (Superoxide Dismutase); S88TT14065 (Oxygen)
[Em] Mês de entrada:1112
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:110510
[St] Status:MEDLINE
[do] DOI:10.1007/s11010-011-0855-9



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