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[PMID]:29318581
[Au] Autor:Vietto V; Franco JV; Saenz V; Cytryn D; Chas J; Ciapponi A
[Ad] Endereço:Family and Community Medicine Service, Hospital Italiano de Buenos Aires, Buenos Aires, Argentina.
[Ti] Título:Prostanoids for critical limb ischaemia.
[So] Source:Cochrane Database Syst Rev;1:CD006544, 2018 01 10.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Peripheral arterial occlusive disease (PAOD) is a common cause of morbidity and mortality due to cardiovascular disease in the general population. Although numerous treatments have been adopted for patients at different disease stages, no option other than amputation is available for patients presenting with critical limb ischaemia (CLI) unsuitable for rescue or reconstructive intervention. In this regard, prostanoids have been proposed as a therapeutic alternative, with the aim of increasing blood supply to the limb with occluded arteries through their vasodilatory, antithrombotic, and anti-inflammatory effects. This is an update of a review first published in 2010. OBJECTIVES: To determine the effectiveness and safety of prostanoids in patients with CLI unsuitable for rescue or reconstructive intervention. SEARCH METHODS: For this update, the Cochrane Vascular Information Specialist searched the Specialised Register (January 2017) and the Cochrane Central Register of Controlled Trials (CENTRAL; 2017, Issue 1). In addition, we searched trials registries (January 2017) and contacted pharmaceutical manufacturers, in our efforts to identify unpublished data and ongoing trials. SELECTION CRITERIA: Randomised controlled trials describing the efficacy and safety of prostanoids compared with placebo or other pharmacological control treatments for patients presenting with CLI without chance of rescue or reconstructive intervention. DATA COLLECTION AND ANALYSIS: Two review authors independently selected trials, assessed trials for eligibility and methodological quality, and extracted data. We resolved disagreements by consensus or by consultation with a third review author. MAIN RESULTS: For this update, 15 additional studies fulfilled selection criteria. We included in this review 33 randomised controlled trials with 4477 participants; 21 compared different prostanoids versus placebo, seven compared prostanoids versus other agents, and five conducted head-to-head comparisons using two different prostanoids.We found low-quality evidence that suggests no clear difference in the incidence of cardiovascular mortality between patients receiving prostanoids and those given placebo (risk ratio (RR) 0.81, 95% confidence interval (CI) 0.41 to 1.58). We found high-quality evidence showing that prostanoids have no effect on the incidence of total amputations when compared with placebo (RR 0.97, 95% CI 0.86 to 1.09). Adverse events were more frequent with prostanoids than with placebo (RR 2.11, 95% CI 1.79 to 2.50; moderate-quality evidence). The most commonly reported adverse events were headache, nausea, vomiting, diarrhoea, flushing, and hypotension. We found moderate-quality evidence showing that prostanoids reduced rest-pain (RR 1.30, 95% CI 1.06 to 1.59) and promoted ulcer healing (RR 1.24, 95% CI 1.04 to 1.48) when compared with placebo, although these small beneficial effects were diluted when we performed a sensitivity analysis that excluded studies at high risk of bias. Additionally, we found evidence of low to very low quality suggesting the effects of prostanoids versus other active agents or versus other prostanoids because studies conducting these comparisons were few and we judged them to be at high risk of bias. None of the included studies assessed quality of life. AUTHORS' CONCLUSIONS: We found high-quality evidence showing that prostanoids have no effect on the incidence of total amputations when compared against placebo. Moderate-quality evidence showed small beneficial effects of prostanoids for rest-pain relief and ulcer healing when compared with placebo. Additionally, moderate-quality evidence showed a greater incidence of adverse effects with the use of prostanoids, and low-quality evidence suggests that prostanoids have no effect on cardiovascular mortality when compared with placebo. None of the included studies reported quality of life measurements. The balance between benefits and harms associated with use of prostanoids in patients with critical limb ischaemia with no chance of reconstructive intervention is uncertain; therefore careful assessment of therapeutic alternatives should be considered. Main reasons for downgrading the quality of evidence were high risk of attrition bias and imprecision of effect estimates.
[Mh] Termos MeSH primário: Isquemia/tratamento farmacológico
Perna (Membro)/irrigação sanguínea
Doenças Vasculares Periféricas/tratamento farmacológico
Prostaglandinas/uso terapêutico
[Mh] Termos MeSH secundário: Alprostadil/uso terapêutico
Amputação/estatística & dados numéricos
Epoprostenol/uso terapêutico
Seres Humanos
Iloprosta/uso terapêutico
Isquemia/mortalidade
Perna (Membro)/cirurgia
Úlcera da Perna/tratamento farmacológico
Nafronil/uso terapêutico
Ácidos Nicotínicos/uso terapêutico
Pentoxifilina/uso terapêutico
Prostaglandinas/efeitos adversos
Ensaios Clínicos Controlados Aleatórios como Assunto
Vasodilatadores/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Nicotinic Acids); 0 (Prostaglandins); 0 (Vasodilator Agents); 42H8PQ0NMJ (Nafronyl); A99MK953KZ (Inositol Niacinate); DCR9Z582X0 (Epoprostenol); F5TD010360 (Alprostadil); JED5K35YGL (Iloprost); SD6QCT3TSU (Pentoxifylline)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180301
[Lr] Data última revisão:
180301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180111
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD006544.pub3


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[PMID]:27773805
[Au] Autor:Camilleri M; Sellin JH; Barrett KE
[Ad] Endereço:Clinical Enteric Neuroscience Translational and Epidemiological Research, Division of Gastroenterology and Hepatology, Department of Medicine, Mayo Clinic, Rochester, Minnesota. Electronic address: camilleri.michael@mayo.edu.
[Ti] Título:Pathophysiology, Evaluation, and Management of Chronic Watery Diarrhea.
[So] Source:Gastroenterology;152(3):515-532.e2, 2017 Feb.
[Is] ISSN:1528-0012
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chronic watery diarrhea poses a diagnostic and therapeutic challenge and is often a disabling condition for patients. Although acute diarrhea is likely to be caused by infection, the causes of chronic diarrhea (>4 weeks in duration) are more elusive. We review the pathophysiology, diagnosis, and treatment of chronic diarrhea. Drawing on recent insights into the molecular mechanisms of intestinal epithelial transport and barrier function, we discuss how diarrhea can result from a decrease in luminal solute absorption, an increase in secretion, or both, as well as derangements in barrier properties. We also describe the various extraepithelial factors that activate diarrheal mechanisms. Finally, clinical evaluation and tests used in the assessment of patients presenting with chronic diarrhea are reviewed, and an algorithm guiding therapeutic decisions and pharmacotherapy is presented.
[Mh] Termos MeSH primário: Diarreia/metabolismo
Absorção Intestinal
Secreções Intestinais
Intestinos/metabolismo
[Mh] Termos MeSH secundário: Proteína C-Reativa/metabolismo
Cromograninas/metabolismo
Doença Crônica
Diarreia/diagnóstico
Diarreia/fisiopatologia
Diarreia/terapia
Fezes/química
Motilidade Gastrointestinal
Seres Humanos
Inflamação
Intestinos/fisiopatologia
Síndrome do Intestino Irritável/metabolismo
Lactoferrina/metabolismo
Complexo Antígeno L1 Leucocitário/metabolismo
Concentração Osmolar
Permeabilidade
Prostaglandinas/metabolismo
Serotonina/metabolismo
Substância P/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Chromogranins); 0 (Leukocyte L1 Antigen Complex); 0 (Prostaglandins); 333DO1RDJY (Serotonin); 33507-63-0 (Substance P); 9007-41-4 (C-Reactive Protein); EC 3.4.21.- (Lactoferrin)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:180201
[Lr] Data última revisão:
180201
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


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[PMID]:29202670
[Au] Autor:Walker C; Biasucci LM
[Ad] Endereço:a Global Product Director , Pfizer , Walton Oaks , UK.
[Ti] Título:Cardiovascular safety of non-steroidal anti-inflammatory drugs revisited.
[So] Source:Postgrad Med;130(1):55-71, 2018 Jan.
[Is] ISSN:1941-9260
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Non-steroidal anti-inflammatory drugs (NSAIDs) have been widely used to treat inflammatory pain for decades. More recently, newer NSAIDs were developed to target the inducible isoform of cyclooxygenase (COX), COX-2, with the aim of reducing gastrointestinal toxicity. While the COX-2 selective inhibitors were effective in reducing pain and gastrointestinal harm, they soon were associated with an increased risk of adverse cardiovascular events. Initially, the view emerged that selective inhibition of COX-2, and sparing of COX-1, was responsible for the increased cardiovascular harm observed. However, as more data from different human populations has become available this view has begun to be challenged. This review examines the current understanding of the role of prostaglandins and COX-1 and COX-2, particularly in platelets, the vasculature, and the kidney together with an overview of the cardiovascular and renal safety of both traditional NSAIDs and COX-2 selective inhibitors. Available data from active comparator randomized controlled trials, including the data from the PRECISION trial investigating the long term cardiovascular safety of patients exclusively with elevated baseline cardiovascular risk, are presented. The data, when considered holistically, support the idea that all NSAIDs carry some level of cardiovascular risk, be they traditional NSAIDs or COX-2 selective agents. There is also some evidence of heterogeneity of effect with NSAIDs particularly in relation to effects on blood pressure, with no clear demarcation based on the degree of COX-2 selectivity.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/farmacologia
Doenças Cardiovasculares/induzido quimicamente
Doenças Cardiovasculares/prevenção & controle
[Mh] Termos MeSH secundário: Seres Humanos
Prostaglandinas/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Prostaglandins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180103
[Lr] Data última revisão:
180103
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE
[do] DOI:10.1080/00325481.2018.1412799


  4 / 26597 MEDLINE  
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[PMID]:29176799
[Au] Autor:Ra S; Ayaki M; Yuki K; Tsubota K; Negishi K
[Ad] Endereço:Departments of Ophthalmology, Keio University, School of Medicine, Tokyo, Japan.
[Ti] Título:Dry eye, sleep quality, and mood status in glaucoma patients receiving prostaglandin monotherapy were comparable with those in non-glaucoma subjects.
[So] Source:PLoS One;12(11):e0188534, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Prior studies suggested that glaucoma patients suffer worse dry eye and mood and sleep disorders than non-glaucoma subjects. Prostaglandin analogues are first-line therapy for glaucoma, inducing few instillation problems and sufficient pressure-reduction effects. This study compared dry eye, sleep quality, and mood status between glaucoma patients receiving prostaglandin monotherapy and non-glaucoma subjects. METHODS: This cross-sectional study evaluated 1520 patients (579 males and 941 females) for glaucoma status and dry eye-related symptoms (dryness, eye fatigue, photophobia, pain, blurring) and signs (Schirmer test, tear break-up time, corneal staining scores). Of the total cohort, 93 patients were also evaluated by Pittsburgh sleep quality index (PSQI) and hospital anxiety and depression score (HADS). Inclusion criteria were consecutive patients ≥ 51 years of age and best-corrected visual acuity ≥ 20/25. Glaucoma patients included those treated with prostaglandin or a fixed combination including prostaglandin. Exclusion criteria were history of ocular surgery within one month. Data were analyzed using the chi-square or Mann-Whitney U tests, at 5% significance. RESULTS: There were no significant differences in dry eye-related signs and symptoms between the control (n = 1431, mean age of 66.9 years) and glaucoma groups (n = 89, 67.9 years). The psychiatric sub-analysis of the control (n = 61, 66.2 years) and glaucoma groups (n = 32, 67.3 years) revealed mean scores of 5.02 ± 3.10 and 5.16 ± 3.46 for PSQI (normal range ≤ 5), 9.47 ± 5.61 and 9.42 ± 7.36 for HADS (normal range ≤ 10), 4.84 ± 3.22 and 4.71 ± 3.45 for anxiety (normal range ≤ 5), and 4.63 ± 3.05 and 4.71 ± 4.40 for depression (normal range ≤ 5), respectively, without statistical significance. CONCLUSIONS: Our results were comparable between glaucoma patients on prostaglandin monotherapy and non-glaucoma subjects for dry eye-related clinical manifestations, sleep quality, and mood status.
[Mh] Termos MeSH primário: Afeto
Síndromes do Olho Seco/fisiopatologia
Glaucoma/fisiopatologia
Prostaglandinas/uso terapêutico
Sono
[Mh] Termos MeSH secundário: Idoso
Feminino
Glaucoma/tratamento farmacológico
Seres Humanos
Masculino
Meia-Idade
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Prostaglandins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188534


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[PMID]:29215850
[Au] Autor:Samodelkin EI; Mercucheva NG; Kosareva PV; Nesterova LY
[Ti] Título:[The role of prostaglandins and Cyclooxygenase in pathogenesis of chronic endometritis].
[So] Source:Patol Fiziol Eksp Ter;61(2):98-100, 2017 Apr-Jun.
[Is] ISSN:0031-2991
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:The purpose: to present the modern data of cyclooxygenase role (COX) in the development of chronic endometritis.106 references on the role of COX-1 and COX-2 in the development of chronic endometritis in patients of reproductive age, published in the Medline database, Pubmed, Scopus were analyzed; 14 sources are included in this review. Prostaglandins (PG) play an important role in maintaining inflammatory process in the endometrium. Nevertheless, the production of PG and leukotrienes (LTS) - lipid mediators, which, along with PG, play a major role in the inflammatory process of the inflamed uterus, is not fully understood. Cyclooxygenase-2, the enzyme having various physiological functions, is involved in reproduction, where its role is polyfunctional. It has been established that the inhibition of cyclooxygenase pathways, blocking the synthesis of prostaglandins, eliminates the effects of many pro-inflammatory cytokine involved in the pathogenesis of chronic endometritis. Conclusion. The role of cyclooxygenase in the development of chronic endometritis is interesting; on the basis of the acquired knowledge, we can plan the use of drugs that inhibit the cyclooxygenase pathway (NSAIDs) in the treatment of chronic endometritis - as a method of pathogenetic therapy. The issue is not fully understood. Further research is needed in this sphere.
[Mh] Termos MeSH primário: Anti-Inflamatórios não Esteroides/uso terapêutico
Ciclo-Oxigenase 1/metabolismo
Ciclo-Oxigenase 2/metabolismo
Endometrite
Prostaglandinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Endometrite/tratamento farmacológico
Endometrite/metabolismo
Endometrite/patologia
Feminino
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents, Non-Steroidal); 0 (Prostaglandins); EC 1.14.99.1 (Cyclooxygenase 1); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (PTGS1 protein, human); EC 1.14.99.1 (PTGS2 protein, human)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171221
[Lr] Data última revisão:
171221
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171208
[St] Status:MEDLINE


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[PMID]:28910408
[Au] Autor:Karlsson J; Gouveia-Figueira S; Alhouayek M; Fowler CJ
[Ad] Endereço:Department of Pharmacology and Clinical Neuroscience, Pharmacology Unit, Umeå University, Umeå, Sweden.
[Ti] Título:Effects of tumour necrosis factor α upon the metabolism of the endocannabinoid anandamide in prostate cancer cells.
[So] Source:PLoS One;12(9):e0185011, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Tumour necrosis factor α (TNFα) is involved in the pathogenesis of prostate cancer, a disease where disturbances in the endocannabinoid system are seen. In the present study we have investigated whether treatment of DU145 human prostate cancer cells affects anandamide (AEA) catabolic pathways. Additionally, we have investigated whether cyclooxygenase-2 (COX-2) can regulate the uptake of AEA into cells. Levels of AEA synthetic and catabolic enzymes were determined by qPCR. AEA uptake and hydrolysis in DU145 and RAW264.7 macrophage cells were assayed using AEA labeled in the arachidonic and ethanolamine portions of the molecule, respectively. Levels of AEA, related N-acylethanolamines (NAEs), prostaglandins (PG) and PG-ethanolamines (PG-EA) in DU145 cells and medium were quantitated by ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) analysis. TNFα treatment of DU145 cells increased mRNA levels of PTSG2 (gene of COX-2) and decreased the mRNA of the AEA synthetic enzyme N-acyl-phosphatidylethanolamine selective phospholipase D. mRNA levels of the AEA hydrolytic enzymes fatty acid amide hydrolase (FAAH) and N-acylethanolamine-hydrolyzing acid amidase were not changed. AEA uptake in both DU145 and RAW264.7 cells was inhibited by FAAH inhibition, but not by COX-2 inhibition, even in RAW264.7 cells where the expression of this enzyme had greatly been induced by lipopolysaccharide + interferon γ treatment. AEA and related NAEs were detected in DU145 cells, but PGs and PGE2-EA were only detected when the cells had been preincubated with 100 nM AEA. The data demonstrate that in DU145 cells, TNFα treatment changes the relative expression of the enzymes involved in the hydrolytic and oxygenation catabolic pathways for AEA. In RAW264.7 cells, COX-2, in contrast to FAAH, does not regulate the cellular accumulation of AEA. Further studies are necessary to determine the extent to which inflammatory mediators are involved in the abnormal endocannabinoid signalling system in prostate cancer.
[Mh] Termos MeSH primário: Amidoidrolases/genética
Ácidos Araquidônicos/análise
Ciclo-Oxigenase 2/genética
Endocanabinoides/análise
Alcamidas Poli-Insaturadas/análise
Neoplasias da Próstata/metabolismo
Fator de Necrose Tumoral alfa/farmacologia
[Mh] Termos MeSH secundário: Amidoidrolases/metabolismo
Animais
Linhagem Celular Tumoral
Cromatografia Líquida de Alta Pressão
Ciclo-Oxigenase 2/metabolismo
Regulação Neoplásica da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Lipopolissacarídeos/efeitos adversos
Masculino
Camundongos
Prostaglandinas/análise
Neoplasias da Próstata/genética
Células RAW 264.7
Espectrometria de Massas em Tandem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Arachidonic Acids); 0 (Endocannabinoids); 0 (Lipopolysaccharides); 0 (Polyunsaturated Alkamides); 0 (Prostaglandins); 0 (Tumor Necrosis Factor-alpha); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (PTGS2 protein, human); EC 3.5.- (Amidohydrolases); EC 3.5.1.- (fatty-acid amide hydrolase); UR5G69TJKH (anandamide)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171012
[Lr] Data última revisão:
171012
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185011


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[PMID]:28888848
[Au] Autor:Shibata S; Furuta K; Oh-Hashi K; Ueda H; Kiuchi K; Hirata Y
[Ad] Endereço:Department of Chemistry and Biomolecular Science, Faculty of Engineering, Gifu University, Yanagido, Gifu 501-1193, Japan.
[Ti] Título:Prevention of oxytosis-induced c-Raf down-regulation by (arylthio)cyclopentenone prostaglandins is neuroprotective.
[So] Source:Toxicology;390:83-87, 2017 Sep 01.
[Is] ISSN:1879-3185
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Prolonged exposure to high concentrations of glutamate leads to cell type specific glutathione depletion and resulting oxidative stress, known as oxytosis. As a result of glutathione depletion, accumulation of reactive oxygen species and Ca influx are increased; however, the specific target of oxytosis has yet to be identified. In the present study, we focused on the effect of glutamate-induced oxidative stress on the extracellular-regulated protein kinase (ERK) pathway using the murine hippocampal HT22 cell line. Although the contribution of the ERK pathway to glutamate-induced oxytosis in HT22 cells is controversial, Western blot analysis revealed that glutamate caused down-regulation of mitogen-activated protein kinase kinase kinase (c-Raf) and a resulting decrease in the phosphorylation of c-Raf, as well as of mitogen-activated protein kinase kinase1/2 (MEK1/2) and ERK1/2, downstream components of the c-Raf/MEK/ERK pathway. Furthermore, neuroprotective (arylthio)cyclopentenone prostaglandins prevented glutamate-induced c-Raf down-regulation and consequently maintained the basal activity of c-Raf and its downstream signaling components. A pull-down assay using biotin-labeled cyclopentenone prostaglandins revealed that they preferentially bound to c-Raf relative to other signaling molecules of the ERK pathway, including Ras, MEK1/2, and ERK. These results suggest that neuroprotective (arylthio)cyclopentenone prostaglandins directly bind to c-Raf protein and protect cells from down-regulation of the c-Raf protein itself, resulting in neuroprotection against oxidative stress.
[Mh] Termos MeSH primário: Antioxidantes/farmacologia
Ciclopentanos/farmacologia
Ácido Glutâmico/toxicidade
Glutationa/metabolismo
Hipocampo/efeitos dos fármacos
Neurônios/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
Síndromes Neurotóxicas/prevenção & controle
Estresse Oxidativo/efeitos dos fármacos
Prostaglandinas/farmacologia
Proteínas Proto-Oncogênicas c-raf/metabolismo
[Mh] Termos MeSH secundário: Animais
Antioxidantes/metabolismo
Linhagem Celular
Sobrevivência Celular/efeitos dos fármacos
Ciclopentanos/metabolismo
Citoproteção
Relação Dose-Resposta a Droga
Regulação para Baixo
MAP Quinases Reguladas por Sinal Extracelular/metabolismo
Hipocampo/enzimologia
Hipocampo/patologia
MAP Quinase Quinase Quinases/metabolismo
Camundongos
Neurônios/enzimologia
Neurônios/patologia
Fármacos Neuroprotetores/metabolismo
Síndromes Neurotóxicas/etiologia
Síndromes Neurotóxicas/metabolismo
Síndromes Neurotóxicas/patologia
Fosforilação
Prostaglandinas/metabolismo
Ligação Proteica
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antioxidants); 0 (Cyclopentanes); 0 (Neuroprotective Agents); 0 (Prostaglandins); 3KX376GY7L (Glutamic Acid); EC 2.7.11.1 (Proto-Oncogene Proteins c-raf); EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases); EC 2.7.11.25 (MAP Kinase Kinase Kinases); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170911
[St] Status:MEDLINE


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[PMID]:28815606
[Au] Autor:Cui Y; Shu XO; Li HL; Yang G; Wen W; Gao YT; Cai Q; Rothman N; Yin HY; Lan Q; Xiang YB; Zheng W
[Ad] Endereço:Division of Epidemiology, Department of Medicine, Vanderbilt Epidemiology Center, Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, 2525 West End Avenue, 8th Floor, Nashville, TN.
[Ti] Título:Prospective study of urinary prostaglandin E2 metabolite and pancreatic cancer risk.
[So] Source:Int J Cancer;141(12):2423-2429, 2017 Dec 15.
[Is] ISSN:1097-0215
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The cyclooxygenase 2 (COX-2) pathway is upregulated in many pancreatic cancer cells, and it is believed that carcinogenetic effects of COX-2 upregulation are largely through prostaglandin E2 (PGE2) overproduction. We tested this hypothesis by evaluating the association between urinary PGE2 metabolites (PGE-M), a biomarker of in vivo PGE2 overproduction, and pancreatic cancer risk. We conducted a case-control study with 722 subjects (239 cases and 483 controls) nested within two prospective cohort studies, the Shanghai Women's Health Study (SWHS) and Shanghai Men's Health Study (SMHS). Pre-diagnosis urine samples were measured for PGE-M using a liquid chromatography/tandem mass spectrometric method. Conditional logistic regression was used to estimate odds ratio (OR) and 95% confidence intervals (95%CI), with adjustment for potential confounders. Compared to those with the lowest urine level of PGE-M (the first quartile), individuals with higher urine levels of PGE-M had an increased risk of developing pancreatic cancer, with adjusted ORs (95%CI) of 1.63 (0.98-2.73), 1.55 (0.90-2.69) and 1.94 (1.07-3.51), for the second to the fourth quartile groups, respectively (p for trend = 0.054). This dose-response positive association was more evident among those who had BMI <25 kg/m than overweight individuals (p for interaction = 0.058). After excluding cases diagnosed in the first year of follow-up and their matched controls, this positive association persisted (p for trend = 0.037) and the interaction became statistically significant (p for interaction = 0.017). Our study adds additional evidence that the COX-2 pathway is involved in pancreatic carcinogenesis and suggests that urinary PGE-M may serve as a biomarker for predicting pancreatic cancer risk.
[Mh] Termos MeSH primário: Neoplasias Pancreáticas/epidemiologia
Prostaglandinas/urina
[Mh] Termos MeSH secundário: Adulto
Idoso
Índice de Massa Corporal
Estudos de Casos e Controles
China/epidemiologia
Cromatografia Líquida
Ciclo-Oxigenase 2/metabolismo
Feminino
Seres Humanos
Modelos Logísticos
Masculino
Meia-Idade
Razão de Chances
Neoplasias Pancreáticas/metabolismo
Neoplasias Pancreáticas/urina
Estudos Prospectivos
Espectrometria de Massas em Tandem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Prostaglandins); 73303-30-7 (7-hydroxy-5,11-dioxotetranorprostane-1,16-dioic acid); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (PTGS2 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170818
[St] Status:MEDLINE
[do] DOI:10.1002/ijc.31007


  9 / 26597 MEDLINE  
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[PMID]:28791952
[Au] Autor:Jasinska-Stroschein M; Orszulak-Michalak D
[Ad] Endereço:Zaklad Biofarmacji, Katedra Biofarmacji, Wydzial Farmaceutyczny Uniwersytetu Medycznego w Lodzi.
[Ti] Título:Novel strategies for treatment of pulmonary arterial hypertension.
[So] Source:Postepy Hig Med Dosw (Online);71(0):577-588, 2017 Jul 11.
[Is] ISSN:1732-2693
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Pulmonary hypertension (PH) is a rare disorder associated with abnormally elevated pulmonary pressures that, if untreated, leads to right heart failure and premature death. Special population include patents with pulmonary arterial hypertension (PAH). A greater understanding of the epidemiology, pathogenesis, and pathophysiology of PAH has led to significant advances over the past few years. Modern drug therapy provides a significant improvement in patient symptomatic status and a slower rate of clinical deterioration. Despite this, PAH remains a chronic disease without a cure. There is a need for the development of novel therapies and therapeutic strategies, as treatment options are neither universally available nor always effective, possibly due to the large number of mediator and signaling pathways with downstream effectors which are implicated in the pathobiology of PH, and which are not fully reversed during PAH therapy. In the following pages, we review novel strategies for treatment of PAH. For this purpose we summarized the role of specific drug therapies that involve: endothelin receptor antagonists (ERA), phosphodiesterase type 5 inhibitors (PDE-5i) and prostacyclin and prostanoids (PGI2). We focused on novel molecular mechanisms in PAH of recently approved: Guanylate cyclase stimulator and non-prostanoid IP receptor agonist. We discussed novel approach to combined therapy, as well as a new generation of investigational drugs and promising PAH-associated signaling pathways, such as, PDGF, RhoA/ROCK RAAS, HT-5 and others.
[Mh] Termos MeSH primário: Hipertensão Pulmonar/tratamento farmacológico
[Mh] Termos MeSH secundário: Quimioterapia Combinada
Antagonistas dos Receptores de Endotelina/uso terapêutico
Guanilato Ciclase/efeitos dos fármacos
Seres Humanos
Inibidores da Fosfodiesterase 5/uso terapêutico
Prostaglandinas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Endothelin Receptor Antagonists); 0 (Phosphodiesterase 5 Inhibitors); 0 (Prostaglandins); EC 4.6.1.2 (Guanylate Cyclase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170907
[Lr] Data última revisão:
170907
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170810
[St] Status:MEDLINE


  10 / 26597 MEDLINE  
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[PMID]:28783044
[Au] Autor:Ware JS; Wain LV; Channavajjhala SK; Jackson VE; Edwards E; Lu R; Siew K; Jia W; Shrine N; Kinnear S; Jalland M; Henry AP; Clayton J; O'Shaughnessy KM; Tobin MD; Schuster VL; Cook S; Hall IP; Glover M
[Ad] Endereço:NIHR Biomedical Research Unit in Cardiovascular Disease at Royal Brompton & Harefield, NHS Foundation Trust and Imperial College London, London, United Kingdom.
[Ti] Título:Phenotypic and pharmacogenetic evaluation of patients with thiazide-induced hyponatremia.
[So] Source:J Clin Invest;127(9):3367-3374, 2017 Sep 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thiazide diuretics are among the most widely used treatments for hypertension, but thiazide-induced hyponatremia (TIH), a clinically significant adverse effect, is poorly understood. Here, we have studied the phenotypic and genetic characteristics of patients hospitalized with TIH. In a cohort of 109 TIH patients, those with severe TIH displayed an extended phenotype of intravascular volume expansion, increased free water reabsorption, urinary prostaglandin E2 excretion, and reduced excretion of serum chloride, magnesium, zinc, and antidiuretic hormone. GWAS in a separate cohort of 48 TIH patients and 2,922 controls from the 1958 British birth cohort identified an additional 14 regions associated with TIH. We identified a suggestive association with a variant in SLCO2A1, which encodes a prostaglandin transporter in the distal nephron. Resequencing of SLCO2A1 revealed a nonsynonymous variant, rs34550074 (p.A396T), and association with this SNP was replicated in a second cohort of TIH cases. TIH patients with the p.A396T variant demonstrated increased urinary excretion of prostaglandin E2 and metabolites. Moreover, the SLCO2A1 phospho-mimic p.A396E showed loss of transporter function in vitro. These findings indicate that the phenotype of TIH involves a more extensive metabolic derangement than previously recognized. We propose one mechanism underlying TIH development in a subgroup of patients in which SLCO2A1 regulation is altered.
[Mh] Termos MeSH primário: Hiponatremia/induzido quimicamente
Inibidores de Simportadores de Cloreto de Sódio/efeitos adversos
Tiazidas/efeitos adversos
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Aquaporina 1/genética
Aquaporina 2/genética
Estudos de Coortes
Dinoprostona/metabolismo
Feminino
Estudo de Associação Genômica Ampla
Seres Humanos
Hiponatremia/genética
Masculino
Meia-Idade
Néfrons/metabolismo
Transportadores de Ânions Orgânicos/genética
Farmacogenética
Fenótipo
Polimorfismo de Nucleotídeo Único
Prostaglandinas/metabolismo
Reino Unido
Água/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AQP1 protein, human); 0 (AQP2 protein, human); 0 (Aquaporin 2); 0 (Organic Anion Transporters); 0 (Prostaglandins); 0 (SLCO2A1 protein, human); 0 (Sodium Chloride Symporter Inhibitors); 0 (Thiazides); 059QF0KO0R (Water); 146410-94-8 (Aquaporin 1); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170808
[St] Status:MEDLINE



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