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1.
A A Case Rep ; 8(11): 279-281, 2017 Jun 01.
Artigo em Inglês | MEDLINE | ID: mdl-28181944

RESUMO

We report a case of deliberate intrathecal catheter insertion and removal in the setting of continuous dual-antiplatelet therapy with clopidogrel and aspirin. A patient with recently sited bare metal intracerebral stents developed severe symptomatic hydrocephalus and required temporary cerebrospinal fluid diversion. The risks of intracerebral in-stent thrombosis or delayed intervention precluded following guidelines for the management of clopidogrel in neuraxial procedures. Options to mitigate the risk of and facilitate the early detection of epidural hematoma are discussed when neuraxial instrumentation is indicated in the setting of clopidogrel and aspirin therapy.


Assuntos
Aspirina/uso terapêutico , Cateteres de Demora , Remoção de Dispositivo , Drenagem/instrumentação , Procedimentos Endovasculares/instrumentação , Hidrocefalia/terapia , Aneurisma Intracraniano/terapia , Inibidores da Agregação Plaquetária/uso terapêutico , Stents , Ticlopidina/análogos & derivados , Clopidogrel , Drenagem/efeitos adversos , Drenagem/métodos , Quimioterapia Combinada , Procedimentos Endovasculares/efeitos adversos , Hematoma Epidural Espinal/etiologia , Humanos , Hidrocefalia/líquido cefalorraquidiano , Hidrocefalia/diagnóstico por imagem , Aneurisma Intracraniano/complicações , Aneurisma Intracraniano/diagnóstico , Trombose Intracraniana/etiologia , Trombose Intracraniana/prevenção & controle , Masculino , Metais , Pessoa de Meia-Idade , Desenho de Prótese , Fatores de Risco , Hemorragia Subaracnóidea/etiologia , Ticlopidina/uso terapêutico , Resultado do Tratamento
2.
Gastroenterology ; 140(3): 987-97, 2011 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-21111739

RESUMO

BACKGROUND & AIMS: Endoplasmic reticulum (ER) stress responses (collectively known the unfolded protein response [UPR]) have important roles in several human disorders, but their contribution to alcoholic pancreatitis is not known. We investigated the role of X-box binding protein 1 (XBP1), a UPR regulator, in prevention of alcohol-induced ER stress in the exocrine pancreas. METHODS: Wild-type and Xbp1(+/-) mice were fed control or ethanol diets for 4 weeks. Pancreatic tissue samples were then examined by light and electron microscopy to determine pancreatic alterations; UPR regulators were analyzed biochemically. RESULTS: In wild-type mice, ethanol activated a UPR, increasing pancreatic levels of XBP1 and XBP1 targets such as protein disulfide isomerase (PDI). In these mice, pancreatic damage was minor. In ethanol-fed Xbp1(+/-) mice, XBP1 and PDI levels were significantly lower than in ethanol-fed wild-type mice. The combination of XBP1 deficiency and ethanol feeding reduced expression of regulators of ER function and the up-regulation of proapoptotic signals. Moreover, ethanol feeding induced oxidation of PDI, which might compromise PDI-mediated disulfide bond formation during ER protein folding. In ethanol-fed Xbp1(+/-) mice, ER stress was associated with disorganized and dilated ER, loss of zymogen granules, accumulation of autophagic vacuoles, and increased acinar cell death. CONCLUSIONS: Long-term ethanol feeding causes oxidative ER stress, which activates a UPR and increases XBP1 levels and activity. A defective UPR due to XBP1 deficiency results in ER dysfunction and acinar cell pathology.


Assuntos
Retículo Endoplasmático/metabolismo , Pâncreas Exócrino/metabolismo , Pancreatite Alcoólica/metabolismo , Estresse Fisiológico , Resposta a Proteínas não Dobradas , Adaptação Fisiológica , Animais , Apoptose , Proteínas Reguladoras de Apoptose/metabolismo , Proteínas de Ligação a DNA/deficiência , Proteínas de Ligação a DNA/genética , Proteínas de Ligação a DNA/metabolismo , Modelos Animais de Doenças , Retículo Endoplasmático/patologia , Etanol , Masculino , Camundongos , Camundongos Endogâmicos BALB C , Camundongos Knockout , Pâncreas Exócrino/patologia , Pancreatite Alcoólica/genética , Pancreatite Alcoólica/patologia , Pancreatite Alcoólica/prevenção & controle , Isomerases de Dissulfetos de Proteínas/metabolismo , Ratos , Ratos Wistar , Fatores de Transcrição de Fator Regulador X , Técnicas de Cultura de Tecidos , Fatores de Transcrição/deficiência , Fatores de Transcrição/genética , Fatores de Transcrição/metabolismo , Proteína 1 de Ligação a X-Box
3.
Alcohol Clin Exp Res ; 34(10): 1768-81, 2010 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-20626730

RESUMO

OBJECTIVES: The mechanisms initiating pancreatitis in patients with chronic alcohol abuse are poorly understood. Although alcohol feeding has been previously suggested to alter cholinergic pathways, the effects of these cholinergic alterations in promoting pancreatitis have not been characterized. For this study, we determined the role of the cholinergic system in ethanol-induced sensitizing effects on cerulein pancreatitis. METHODS: Rats were pair-fed control and ethanol-containing Lieber-DeCarli diets for 6 weeks followed by parenteral administration of 4 hourly intraperitoneal injections of the cholecystokinin analog, cerulein at 0.5 µg/kg. This dose of cerulein was selected because it caused pancreatic injury in ethanol-fed but not in control-fed rats. Pancreatitis was preceded by treatment with the muscarinic receptor antagonist atropine or by bilateral subdiaphragmatic vagotomy. Measurement of pancreatic pathology included serum lipase activity, pancreatic trypsin, and caspase-3 activities, and markers of pancreatic necrosis, apoptosis, and autophagy. In addition, we measured the effects of ethanol feeding on pancreatic acetylcholinesterase activity and pancreatic levels of the muscarinic acetylcholine receptors m1 and m3. Finally, we examined the synergistic effects of ethanol and carbachol on inducing acinar cell damage. RESULTS: We found that atropine blocked almost completely pancreatic pathology caused by cerulein administration in ethanol-fed rats, while vagotomy was less effective. Ethanol feeding did not alter expression levels of cholinergic muscarinic receptors in the pancreas but significantly decreased pancreatic acetylcholinesterase activity, suggesting that acetylcholine levels and cholinergic input within the pancreas can be higher in ethanol-fed rats. We further found that ethanol treatment of pancreatic acinar cells augmented pancreatic injury responses caused by the cholinergic agonist, carbachol. CONCLUSION: These results demonstrate key roles for the cholinergic system in the mechanisms of alcoholic pancreatitis.


Assuntos
Acetilcolinesterase/metabolismo , Colinérgicos/farmacologia , Etanol/farmacologia , Pancreatite Alcoólica/metabolismo , Receptor Muscarínico M1/metabolismo , Receptor Muscarínico M3/metabolismo , Amilases/metabolismo , Animais , Apoptose/efeitos dos fármacos , Autofagia/efeitos dos fármacos , Caspase 3/metabolismo , Ceruletídeo/farmacologia , Modelos Animais de Doenças , Sinergismo Farmacológico , Etanol/efeitos adversos , Lipase/sangue , Masculino , Necrose/induzido quimicamente , Pancreatite Alcoólica/sangue , Pancreatite Alcoólica/induzido quimicamente , Pancreatite Alcoólica/patologia , Ratos , Ratos Wistar , Receptor Muscarínico M1/antagonistas & inibidores , Receptor Muscarínico M3/antagonistas & inibidores , Tripsina/metabolismo , Vagotomia/métodos
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