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[PMID]:29408309
[Au] Autor:Mohamed DI; Nabih ES; El-Waseef DAA; El-Kharashi OA; Abd El Samad AA
[Ad] Endereço:Department of Pharmacology, Faculty of Medicine, Ain Shams University, Cairo, Egypt.
[Ti] Título:The protective effect of pentoxifylline versus silymarin on the pancreas through increasing adenosine by CD39 in a rat model of liver cirrhosis: Pharmacological, biochemical and histological study.
[So] Source:Gene;651:9-22, 2018 Apr 20.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Impaired glucose homoeostasis due to insulin resistance and decrease sensitivity of pancreatic ß-cells is a feature of liver disease and results into hepatogenous diabetes. Decrease expression of CD39 was linked to inflammation and occurrence of diabetes. Therefore, we performed this study to explore the protective effect of pentoxifylline (PTX) and silymarin administration on the ß-cells of the pancreas in a rat model of thioacetamide induced liver cirrhosis. Biochemical, histological and immunohistochemistry studies of the liver and pancreas were performed and provided an evidence on the protective effect of PTX to pancreatic ß-cells compared to silymarin. Also, silymarin induced a significant improvement of liver cirrhosis compared to PTX. In conclusion, the potential protective effect of PTX against ß-cells deterioration could be attributed to increasing pancreatic CD39 expression and the subsequent increase of adenosine.
[Mh] Termos MeSH primário: Adenosina/metabolismo
Antígenos CD/metabolismo
Apirase/metabolismo
Cirrose Hepática Experimental/tratamento farmacológico
Pâncreas/efeitos dos fármacos
Pentoxifilina/uso terapêutico
Substâncias Protetoras/uso terapêutico
Silimarina/uso terapêutico
[Mh] Termos MeSH secundário: Amilases/sangue
Animais
Modelos Animais de Doenças
Células Secretoras de Insulina/efeitos dos fármacos
Fígado/patologia
Cirrose Hepática Experimental/metabolismo
Cirrose Hepática Experimental/patologia
Testes de Função Hepática
Masculino
Pâncreas/patologia
Ratos
Ratos Wistar
Fator de Crescimento Transformador beta1/metabolismo
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens, CD); 0 (Protective Agents); 0 (Silymarin); 0 (Transforming Growth Factor beta1); EC 3.2.1.- (Amylases); EC 3.6.1.5 (Apyrase); EC 3.6.1.5 (CD39 antigen); K72T3FS567 (Adenosine); SD6QCT3TSU (Pentoxifylline)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180207
[St] Status:MEDLINE


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[PMID]:28456646
[Au] Autor:Ng WY; Migotto A; Ferreira TS; Lopes LB
[Ad] Endereço:Department of Pharmaceutical Sciences, Albany College of Pharmacy and Health Sciences, Albany, NY, USA.
[Ti] Título:Monoolein-alginate beads as a platform to promote adenosine cutaneous localization and wound healing.
[So] Source:Int J Biol Macromol;102:1104-1111, 2017 Sep.
[Is] ISSN:1879-0003
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Alginate beads containing the polar lipid monoolein were developed as a strategy to manage wet wounds by providing improved uptake of excess exudate while releasing adenosine locally for promotion of healing. To obtain monoolein-containing beads, the lipid was mixed with almond oil (2:1w/w), and emulsified within the alginate aqueous dispersion, followed by ionotropic gelation in CaCl solution. Compared to alginate-only, monoolein-alginate systems were 1.44-fold larger, their swelling ability was 1.40-fold higher and adenosine cumulative release was approximately 1.30-fold lower (at 24h). Monoolein-alginate beads were considered safe for topical application as demonstrated by the absence of changes on the viability of reconstructed skin equivalents compared to PBS. Smaller amounts of adenosine were delivered by the beads into and across damaged porcine skin (created by an incisional wound) compared to the drug aqueous solution, and cutaneous localization was favored. More specifically, the beads increased the viable skin layer/receptor phase delivery ratio by approximately 4-fold at 12h post-application. Considering the wide range of adenosine physiological effects and the importance of skin localization for its use in wound healing, these results demonstrate the potential of monoolein-containing beads for localized drug delivery and management of wet wounds.
[Mh] Termos MeSH primário: Adenosina/metabolismo
Alginatos/química
Portadores de Fármacos/química
Glicerídeos/química
Microesferas
Pele/metabolismo
Cicatrização/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adenosina/química
Adenosina/farmacologia
Animais
Liberação Controlada de Fármacos
Ácido Glucurônico/química
Ácidos Hexurônicos/química
Permeabilidade
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alginates); 0 (Drug Carriers); 0 (Glycerides); 0 (Hexuronic Acids); 8A5D83Q4RW (Glucuronic Acid); 8C3Z4148WZ (alginic acid); C4YAD5F5G6 (monoolein); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170501
[St] Status:MEDLINE


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[PMID]:29442034
[Au] Autor:Li J; Ma L; Fan Y; Zhang Y; Sun D; Wu B
[Ti] Título:Crosstalk between 6-OHDA-induced autophagy and apoptosis in PC12 cells is mediated by phosphorylation of Raf-1/ERK1/2.
[So] Source:Pharmazie;71(8):465-471, 2016 08 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Parkinson's disease (PD) is a degenerative brain disorder characterized by motor symptoms and loss of dopaminergic (DA) neurons in the substantia nigra. The mechanisms for DA cell death in PD have been extensively investigated using PC12 cells treated with a dopamine neurotoxin 6-hydroxydopamine (6-OHDA). 6-OHDA may induce both autophagy and apoptosis in PC12 cells. However, it remains unclear whether crosstalk occurs between autophagy and apoptosis in PC12 cells treated with 6-OHDA and whether Raf-1/ERK1/2 and their phosphorylation status play a role in autophagy. In this study, we used MDC staining assay and flow cytometry and found that 6-OHDA induced autophagy in PC12 cells. This induction was inhibited by the autophagy inhibitor 3-MA. Our electron microscopy observations also supported 6-OHDA induced autophagy in PC12 cells. Apoptosis of PC12 cells was increased with inhibition of autophagy by 3-MA. In addition, Inhibition of Raf-1 resulted in a decreased 6-OHDA-induced autophagy rate among PC12 cells. Phosphorylation levels of Raf-1 and ERK1/2 were increased in PC12 cells treated with 6-OHDA and inhibited by co-treatment with 6-OHDA and 3-MA. These data suggest that crosstalk between 6-OHDA-induced apoptosis and autophagy in PC12 cells may be regulated via the Raf-1/ERK1/2 signaling pathway. Our data suggest a mechanism for 6-OHDA toxicity in PC12 cells, contributing to our understanding of the pathogenesis of PD.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Autofagia/efeitos dos fármacos
Hidroxidopaminas/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Fosforilação/efeitos dos fármacos
Proteínas Proto-Oncogênicas c-raf/metabolismo
Receptor Cross-Talk/efeitos dos fármacos
[Mh] Termos MeSH secundário: Adenosina/análogos & derivados
Adenosina/farmacologia
Animais
Sobrevivência Celular/efeitos dos fármacos
Células PC12
Proteínas Proto-Oncogênicas c-raf/efeitos dos fármacos
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Hydroxydopamines); 72055-62-0 (3-methyladenosine); EC 2.7.11.1 (Proto-Oncogene Proteins c-raf); EC 2.7.11.1 (Raf1 protein, rat); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6586


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[PMID]:28465300
[Au] Autor:Pelletier-Galarneau M; Hunter CRRN; Ascah KJ; Beanlands RSB; Dwivedi G; deKemp RA; Chow BJW; Ruddy TD
[Ad] Endereço:Division of Nuclear Medicine, The Ottawa Hospital, Ottawa, Canada.
[Ti] Título:Randomized Trial Comparing the Effects of Ticagrelor Versus Clopidogrel on Myocardial Perfusion in Patients With Coronary Artery Disease.
[So] Source:J Am Heart Assoc;6(5), 2017 May 02.
[Is] ISSN:2047-9980
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Ticagrelor is a P2Y receptor inhibitor used in acute coronary syndromes to reduce platelet activity and to decrease thrombus formation. Ticagrelor is associated with a reduction in mortality incremental to that observed with clopidogrel, potentially related to its non-antiplatelet effects. Evidence from animal models indicates that ticagrelor potentiates adenosine-induced myocardial blood flow (MBF) increases. We investigated MBF at rest and during adenosine-induced hyperemia in patients with stable coronary artery disease treated with ticagrelor versus clopidogrel. METHODS AND RESULTS: This randomized double-blinded crossover study included 22 patients who received therapeutic interventions of ticagrelor 90 mg orally twice a day for 10 days and clopidogrel 75 mg orally once a day for 10 days, with a washout period of at least 10 days between the treatments. Global and regional MBF and myocardial flow reserve were measured using rubidium 82 positron emission tomography/computed tomography at baseline and during intermediate- and high-dose adenosine. Global MBF was significantly greater with ticagrelor versus clopidogrel (1.28±0.55 versus 1.13±0.47 mL/min per gram, =0.002) at intermediate-dose adenosine and not different at baseline (0.65±0.19 versus 0.60±0.15 mL/min per gram, =0.084) and at high-dose adenosine (1.64±0.40 versus 1.61±0.19 mL/min per gram, =0.53). In regions with impaired myocardial flow reserve (<2.5), MBF was greater with ticagrelor compared with clopidogrel during intermediate and high doses of adenosine ( <0.0001), whereas the differences were not significant at baseline. CONCLUSIONS: Ticagrelor potentiates global and regional adenosine-induced MBF increases in patients with stable coronary artery disease. This effect may contribute to the incremental mortality benefit compared with clopidogrel. CLINICAL TRIAL REGISTRATION: URL: http://www.clinicaltrials.gov. Unique identifier: NCT01894789.
[Mh] Termos MeSH primário: Adenosina/análogos & derivados
Doença da Artéria Coronariana/tratamento farmacológico
Circulação Coronária/efeitos dos fármacos
Vasos Coronários/efeitos dos fármacos
Inibidores da Agregação de Plaquetas/administração & dosagem
Ticlopidina/análogos & derivados
[Mh] Termos MeSH secundário: Adenosina/administração & dosagem
Adenosina/efeitos adversos
Administração Oral
Idoso
Doença da Artéria Coronariana/diagnóstico por imagem
Doença da Artéria Coronariana/fisiopatologia
Vasos Coronários/diagnóstico por imagem
Vasos Coronários/fisiopatologia
Estudos Cross-Over
Método Duplo-Cego
Esquema de Medicação
Feminino
Seres Humanos
Masculino
Meia-Idade
Imagem de Perfusão do Miocárdio/métodos
Ontário
Inibidores da Agregação de Plaquetas/efeitos adversos
Tomografia Computadorizada com Tomografia por Emissão de Pósitrons
Valor Preditivo dos Testes
Compostos Radiofarmacêuticos/administração & dosagem
Radioisótopos de Rubídio/administração & dosagem
Ticlopidina/administração & dosagem
Ticlopidina/efeitos adversos
Fatores de Tempo
Resultado do Tratamento
Vasodilatadores/administração & dosagem
[Pt] Tipo de publicação:CLINICAL TRIAL, PHASE II; COMPARATIVE STUDY; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Platelet Aggregation Inhibitors); 0 (Radiopharmaceuticals); 0 (Rubidium Radioisotopes); 0 (Vasodilator Agents); A74586SNO7 (clopidogrel); GLH0314RVC (Ticagrelor); K72T3FS567 (Adenosine); OM90ZUW7M1 (Ticlopidine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[Cl] Clinical Trial:ClinicalTrial
[St] Status:MEDLINE


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[PMID]:29289258
[Au] Autor:Luni FK; Khan AR; Singh H; Riaz H; Malik SA; Khawaja O; Farid T; Cummings J; Taleb M
[Ad] Endereço:Department of Cardiovascular Diseases and Department of Family Medicine, Mercy Saint Vincent Medical Center, Toledo, Ohio. Electronic address: fluni@mercy.com.
[Ti] Título:Identification and Ablation of Dormant Conduction in Atrial Fibrillation Using Adenosine.
[So] Source:Am J Med Sci;355(1):27-36, 2018 Jan.
[Is] ISSN:1538-2990
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Ablation is used for treatment of atrial fibrillation (AF) but recurrence is common. Dormant conduction is hypothesized to be responsible for these recurrences, and the role of adenosine in identification and ablation of these pathways is controversial with conflicting results on AF recurrence. MATERIALS AND METHODS: We conducted a meta-analysis for studies evaluating AF ablation and adenosine use. Included in the meta-analysis were human studies that compared ablation using adenosine or adenosine triphosphate (ATP) and reported freedom from AF in patients beyond a minimum follow-up of 6 months. RESULTS: Our analysis suggests that the use of adenosine leads to a decrease in recurrence of AF compared to the cohort which did not utilize adenosine. Subgroup analysis showed no difference in the recurrence of AF with the modality used for ablation (cryoablation vs. radiofrequency ablation) or with the preparation of adenosine used (ATP vs. adenosine). There was a significant benefit in delayed administration of ATP over early administration. Pooling results of only randomized control trials did not show any significant difference in AF recurrence. CONCLUSIONS: Adenosine-guided identification and ablation of dormant pathways may lead to a decrease in recurrence of AF.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/uso terapêutico
Adenosina/uso terapêutico
Antiarrítmicos/uso terapêutico
Fibrilação Atrial/diagnóstico
Fibrilação Atrial/terapia
Ablação por Cateter/métodos
[Mh] Termos MeSH secundário: Adenosina/farmacologia
Trifosfato de Adenosina/farmacologia
Antiarrítmicos/farmacologia
Fibrilação Atrial/fisiopatologia
Ablação por Cateter/tendências
Seguimentos
Sistema de Condução Cardíaco/efeitos dos fármacos
Sistema de Condução Cardíaco/fisiopatologia
Seres Humanos
Estudos Observacionais como Assunto/métodos
Ensaios Clínicos Controlados Aleatórios como Assunto/métodos
Recidiva
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 8L70Q75FXE (Adenosine Triphosphate); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180101
[St] Status:MEDLINE


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[PMID]:29390379
[Au] Autor:Choi S; Song M
[Ti] Título:Successful coronary stenting in a patient with factor V deficiency in the absence of fresh frozen plasma transfusion: Case report.
[So] Source:Medicine (Baltimore);96(50):e9274, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Drug-eluting stent (DES) implantation in a patient with factor V deficiency (F5D) is very complex. No antithrombotic therapy study has been reported for F5D patients who undergo a coronary stenting procedure. PATIENT CONCERNS: A 73-year-old woman presented with chest discomfort and exertional dyspnea. Coronary stenting was performed successfully using DES stents. DIAGNOSES: The D-dimer, prothrombin time, and partial thromboplastin time prolongation persisted from admission until 24 hours after coronary stenting. Epistaxis and blood-tinged sputum occurred on day 3. The antiplatelet therapy measured using a Multiplate Analyzer was adequate, and other laboratory findings except factor V activity (14%) were within normal ranges; she was diagnosed with F5D based on low factor V activity. INTERVENTIONS: While taking 90 mg of ticagrelor and 100 mg of aspirin daily, the patient revisited due to recurrent epistaxis, hemoptysis, and coughing on day 26. Epistaxis and hemoptysis stopped after the aspirin was discontinued. Finally, the daily maintenance dose was reduced to 90 mg of ticagrelor once. OUTCOMES: She led healthy life for 9 months without any recurrent symptoms and the test results also were stabilized. LESSONS: We report a case of an F5D patient who underwent coronary stenting in the absence of frozen fresh plasma transfusion who received successful maintenance therapy using a single antiplatelet agent (90 mg of ticagrelor/day) with recurrent multiple mucosal bleeding events after coronary stenting.
[Mh] Termos MeSH primário: Adenosina/análogos & derivados
Estenose Coronária/tratamento farmacológico
Stents Farmacológicos
Deficiência do Fator V/complicações
Antagonistas do Receptor Purinérgico P2Y/uso terapêutico
[Mh] Termos MeSH secundário: Adenosina/uso terapêutico
Idoso
Testes de Coagulação Sanguínea
Estenose Coronária/diagnóstico
Feminino
Seres Humanos
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Purinergic P2Y Receptor Antagonists); GLH0314RVC (Ticagrelor); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009274


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[PMID]:29273417
[Au] Autor:Cherukupalli S; Hampannavar GA; Chinnam S; Chandrasekaran B; Sayyad N; Kayamba F; Reddy Aleti R; Karpoormath R
[Ad] Endereço:Department of Pharmaceutical Chemistry, College of Health Sciences, University of KwaZulu-Natal, Durban 4000, South Africa.
[Ti] Título:An appraisal on synthetic and pharmaceutical perspectives of pyrazolo[4,3-d]pyrimidine scaffold.
[So] Source:Bioorg Med Chem;26(2):309-339, 2018 01 15.
[Is] ISSN:1464-3391
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Pyrazolo[4,3-d]pyrimidine, a fused heterocycle bearing pyrazole and pyrimidine portions has gained a significant attention in the field of bioorganic and medicinal chemistry. Pyrazolo[4,3-d]pyrimidine derivatives have demonstrated numerous pharmacological activities particularly, anti-cancer, anti-infectious, phosphodiesterase inhibitors, adenosine antagonists and cytokinin antagonists etc. This review extensively unveils the synthetic and pharmacological diversity with special emphasis on structural variations around pyrazolo[4,3-d]pyrimidine scaffold. This endeavour has thus uncovered the medicinal worthiness of pyrazolo[4,3-d]pyrimidine framework. To the best of our knowledge this review is the first compilation on synthetic, medicinal and structure activity relationship (SAR) aspects of pyrazolo[4,3-d]pyrimidines since 1956.
[Mh] Termos MeSH primário: Anti-Infecciosos/farmacologia
Antineoplásicos/farmacologia
Inibidores Enzimáticos/farmacologia
Neoplasias/tratamento farmacológico
Pirazóis/farmacologia
Pirimidinas/farmacologia
[Mh] Termos MeSH secundário: Adenosina/antagonistas & inibidores
Adenosina/metabolismo
Anti-Infecciosos/síntese química
Anti-Infecciosos/química
Antineoplásicos/síntese química
Antineoplásicos/química
Citocininas/antagonistas & inibidores
Citocininas/metabolismo
Inibidores Enzimáticos/síntese química
Inibidores Enzimáticos/química
Seres Humanos
Estrutura Molecular
Diester Fosfórico Hidrolases/metabolismo
Pirazóis/síntese química
Pirazóis/química
Pirimidinas/síntese química
Pirimidinas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Anti-Infective Agents); 0 (Antineoplastic Agents); 0 (Cytokinins); 0 (Enzyme Inhibitors); 0 (Pyrazoles); 0 (Pyrimidines); 271-80-7 (pyrazolo(3,4-d)pyrimidine); EC 3.1.4.- (Phosphoric Diester Hydrolases); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171224
[St] Status:MEDLINE


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[PMID]:28742222
[Au] Autor:Lanser AJ; Rezende RM; Rubino S; Lorello PJ; Donnelly DJ; Xu H; Lau LA; Dulla CG; Caldarone BJ; Robson SC; Weiner HL
[Ad] Endereço:Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
[Ti] Título:Disruption of the ATP/adenosine balance in CD39 mice is associated with handling-induced seizures.
[So] Source:Immunology;152(4):589-601, 2017 12.
[Is] ISSN:1365-2567
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Seizures are due to excessive, synchronous neuronal firing in the brain and are characteristic of epilepsy, the fourth most prevalent neurological disease. We report handling-induced and spontaneous seizures in mice deficient for CD39, a cell-surface ATPase highly expressed on microglial cells. CD39 mice with handling-induced seizures had normal input-output curves and paired-pulse ratio measured from hippocampal slices and lacked microgliosis, astrogliosis or overt cell loss in the hippocampus and cortex. As expected, however, the cerebrospinal fluid of CD39 mice contained increased levels of ATP and decreased levels of adenosine. To determine if immune activation was involved in seizure progression, we challenged mice with lipopolysaccharide (LPS) and measured the effect on microglia activation and seizure severity. Systemic LPS challenge resulted in increased cortical staining of Iba1/CD68 and gene array data from purified microglia predicted increased expression of interleukin-8, triggering receptor expressed on myeloid cells 1, p38, pattern recognition receptors, death receptor, nuclear factor-κB , complement, acute phase, and interleukin-6 signalling pathways in CD39 versus CD39 mice. However, LPS treatment did not affect handling-induced seizures. In addition, microglia-specific CD39 deletion in adult mice was not sufficient to cause seizures, suggesting instead that altered expression of CD39 during development or on non-microglial cells such as vascular endothelial cells may promote the seizure phenotype. In summary, we show a correlation between altered extracellular ATP/adenosine ratio and a previously unreported seizure phenotype in CD39 mice. This work provides groundwork for further elucidation of the underlying mechanisms of epilepsy.
[Mh] Termos MeSH primário: Trifosfato de Adenosina/imunologia
Adenosina/imunologia
Apirase/deficiência
Córtex Cerebral/imunologia
Hipocampo/imunologia
Convulsões/imunologia
[Mh] Termos MeSH secundário: Adenosina/genética
Trifosfato de Adenosina/genética
Animais
Antígenos CD/imunologia
Apirase/imunologia
Proteínas de Ligação ao Cálcio/genética
Proteínas de Ligação ao Cálcio/imunologia
Córtex Cerebral/patologia
Hipocampo/patologia
Lipopolissacarídeos/toxicidade
Camundongos
Camundongos Knockout
Proteínas dos Microfilamentos/genética
Proteínas dos Microfilamentos/imunologia
Convulsões/genética
Convulsões/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aif1 protein, mouse); 0 (Antigens, CD); 0 (Calcium-Binding Proteins); 0 (Lipopolysaccharides); 0 (Microfilament Proteins); 8L70Q75FXE (Adenosine Triphosphate); EC 3.6.1.5 (Apyrase); EC 3.6.1.5 (CD39 antigen); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.1111/imm.12798


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[PMID]:27778525
[Au] Autor:Brice AE; Hernandez GA; Sanchez M; Haynick M; Mendoza CE
[Ad] Endereço:a Division of Cardiology, Jackson Memorial Hospital , University of Miami Miller School of Medicine , Miami , FL , USA.
[Ti] Título:In-stent thrombosis when switching ticagrelor to clopidogrel after percutaneous coronary intervention.
[So] Source:Platelets;28(3):305-309, 2017 May.
[Is] ISSN:1369-1635
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Dual antiplatelet therapy with aspirin and a P2Y12 receptor blocker has been proven to reduce subsequent cardiovascular events and in-stent thrombosis in patients undergoing percutaneous coronary intervention. Newer P2Y12 antagonists with faster onset and greater inhibition of platelet activity have improved cardiovascular outcomes but have created uncertainty with the appropriate dosing when switching between agents. Currently, there are no evidence-based guidelines to aid clinicians when switching between P2Y12 receptor blockers. Here we describe two patients that developed in-stent thrombosis when switching from ticagrelor to clopidogrel using a 300 mg clopidogrel loading dose. Both patients presented with ST elevation myocardial infarction and underwent stent placement but then developed in-stent thrombosis 48 hours after switching from ticagrelor to clopidogrel. These cases illustrate the severe consequences of suboptimal platelet inhibition and the need for prospective trials thoroughly powered to assess clinical outcomes in order to determine the most appropriate strategy when switching from ticagrelor to clopidogrel.
[Mh] Termos MeSH primário: Adenosina/análogos & derivados
Substituição de Medicamentos/efeitos adversos
Intervenção Coronária Percutânea
Inibidores da Agregação de Plaquetas/uso terapêutico
Antagonistas do Receptor Purinérgico P2Y/uso terapêutico
Trombose/diagnóstico
Ticlopidina/análogos & derivados
[Mh] Termos MeSH secundário: Adenosina/uso terapêutico
Plaquetas/efeitos dos fármacos
Plaquetas/metabolismo
Plaquetas/patologia
Esquema de Medicação
Cálculos da Dosagem de Medicamento
Feminino
Seres Humanos
Masculino
Meia-Idade
Ativação Plaquetária/efeitos dos fármacos
Agregação Plaquetária/efeitos dos fármacos
Guias de Prática Clínica como Assunto
Infarto do Miocárdio com Supradesnível do Segmento ST/sangue
Infarto do Miocárdio com Supradesnível do Segmento ST/fisiopatologia
Infarto do Miocárdio com Supradesnível do Segmento ST/cirurgia
Stents
Trombose/etiologia
Trombose/patologia
Ticlopidina/uso terapêutico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Platelet Aggregation Inhibitors); 0 (Purinergic P2Y Receptor Antagonists); A74586SNO7 (clopidogrel); GLH0314RVC (Ticagrelor); K72T3FS567 (Adenosine); OM90ZUW7M1 (Ticlopidine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180219
[Lr] Data última revisão:
180219
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161026
[St] Status:MEDLINE
[do] DOI:10.1080/09537104.2016.1235687


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[PMID]:29191553
[Au] Autor:Holien JK; Seibt B; Roberts V; Salvaris E; Parker MW; Cowan PJ; Dwyer KM
[Ad] Endereço:ACRF Rational Drug Discovery Centre, St. Vincent's Institute of Medical Research, Fitzroy, Victoria 3065, Australia. Electronic address: jholien@svi.edu.au.
[Ti] Título:AMP and adenosine are both ligands for adenosine 2B receptor signaling.
[So] Source:Bioorg Med Chem Lett;28(2):202-206, 2018 01 15.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Adenosine is considered the canonical ligand for the adenosine 2B receptor (A R). A R is upregulated following kidney ischemia augmenting post ischemic blood flow and limiting tubular injury. In this context the beneficial effect of A R signaling has been attributed to an increase in the pericellular concentration of adenosine. However, following renal ischemia both kidney adenosine monophosphate (AMP) and adenosine levels are substantially increased. Using computational modeling and calcium mobilization assays, we investigated whether AMP could also be a ligand for A R. The computational modeling suggested that AMP interacts with more favorable energy to A R compared with adenosine. Furthermore, AMPαS, a non-hydrolyzable form of AMP, increased calcium uptake by Chinese hamster ovary (CHO) cells expressing the human A R, indicating preferential signaling via the G pathway. Therefore, a putative AMP-A R interaction is supported by the computational modeling data and the biological results suggest this interaction involves preferential G activation. These data provide further insights into the role of purinergic signaling in the pathophysiology of renal IRI.
[Mh] Termos MeSH primário: Monofosfato de Adenosina/farmacologia
Adenosina/farmacologia
Receptor A2B de Adenosina/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Células CHO
Cricetulus
Relação Dose-Resposta a Droga
Seres Humanos
Ligantes
Simulação de Acoplamento Molecular
Estrutura Molecular
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ligands); 0 (Receptor, Adenosine A2B); 415SHH325A (Adenosine Monophosphate); K72T3FS567 (Adenosine)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE



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