Assuntos
Angioplastia com Balão , Artéria Femoral , Doença Arterial Periférica , Placa Aterosclerótica , Artéria Poplítea , Ultrassonografia de Intervenção , Humanos , Artéria Femoral/diagnóstico por imagem , Artéria Poplítea/diagnóstico por imagem , Angioplastia com Balão/efeitos adversos , Angioplastia com Balão/instrumentação , Doença Arterial Periférica/diagnóstico por imagem , Doença Arterial Periférica/terapia , Doença Arterial Periférica/cirurgia , Masculino , Idoso , FemininoRESUMO
Pheochromocytoma multisystem crisis is a rare and life-threatening disease that is associated with numerous symptoms and which is also difficult to diagnose. We herein report an autopsy case of a 61-year-old man who died due to pheochromocytoma multisystem crisis. The patient complained of vomiting and breathlessness. Computed tomography showed a shadow-like region with a similar appearance to interstitial pneumonia. The patient was diagnosed with takotsubo cardiomyopathy induced by severe lung disease based on the results of echocardiography and coronary angiography. The patient was treated for interstitial pneumonia. However, his condition rapidly deteriorated and he died 6 hours after arrival. We were later informed of his extremely high catecholamine serum levels. We found pheochromocytoma with hemorrhage at autopsy. The patient's lungs showed acute passive congestion with edema and extravasation.
Assuntos
Neoplasias das Glândulas Suprarrenais/diagnóstico , Feocromocitoma/diagnóstico , Neoplasias das Glândulas Suprarrenais/complicações , Neoplasias das Glândulas Suprarrenais/patologia , Autopsia , Diagnóstico Diferencial , Dispneia/etiologia , Ecocardiografia , Evolução Fatal , Humanos , Doenças Pulmonares Intersticiais/diagnóstico , Doenças Pulmonares Intersticiais/diagnóstico por imagem , Masculino , Pessoa de Meia-Idade , Feocromocitoma/complicações , Feocromocitoma/patologia , Cardiomiopatia de Takotsubo/diagnóstico , Cardiomiopatia de Takotsubo/diagnóstico por imagem , Tomografia Computadorizada por Raios XRESUMO
OBJECTIVE: Although psychological and/or physiological stress has been well documented to influence immune responses, the precise mechanism for immunomodulation remains to be elucidated. The present work describes the role of the hypothalamic-pituitary-adrenal (HPA) axis in the mechanism of stress-mediated enhanced-resistance to lethality after lipopolysaccharide (LPS) injection. METHODS/RESULTS: Preconditioning with restraint stress (RS) resulted in enhanced activation of the HPA axis in response to LPS injection and suppressed LPS-induced release of proinflammatory cytokines and nitric oxide metabolites. Melanocortin 2 receptor-deficient mice (MC2R(-/-)) failed to increase plasma levels of glucocorticoids in response to LPS injection, and exhibited high sensitivity to LPS-induced lethality with enhanced release of proinflammatory cytokines as compared with MC2R(+/-) mice. Real-time PCR analysis revealed that RS induced upregulation of uncoupling protein-2 (UCP2) in macrophages in the lung and the liver of MC2R(+/-), but not of MC2R(-/-), mice. In addition, RS increased UCP2-dependent uncoupling activity of isolated mitochondria from the liver of MC2R(+/-), but not of MC2R(-/-), mice. In vitro study revealed that corticosterone and dexamethasone directly increased UCP2 expression in mouse RAW 264.7 macrophages and suppressed the generation of LPS-induced mitochondrial reactive oxygen species (ROS) and TNF-α production. Knockdown of UCP2 by small interfering RNA blunted the dexamethasone action for suppressing LPS-induced mitochondrial ROS and TNF-α production. CONCLUSION: The present work suggests that RS enhances activation of the HPA axis to release glucocorticoids and upregulation of UCP2 in macrophages, thereby increasing the resistance to endotoxin-induced systemic inflammation and death.
Assuntos
Glucocorticoides/metabolismo , Canais Iônicos/metabolismo , Proteínas Mitocondriais/metabolismo , Estresse Psicológico/metabolismo , Regulação para Cima/fisiologia , Hormônio Adrenocorticotrópico/metabolismo , Animais , Linhagem Celular Transformada , Corticosterona/metabolismo , Citocinas/metabolismo , Modelos Animais de Doenças , Lipopolissacarídeos/farmacologia , Macrófagos/efeitos dos fármacos , Macrófagos/metabolismo , Masculino , Camundongos , Camundongos Endogâmicos C57BL , Camundongos Transgênicos , Mitocôndrias/efeitos dos fármacos , Mitocôndrias/metabolismo , Óxido Nítrico/metabolismo , RNA Interferente Pequeno/genética , RNA Interferente Pequeno/metabolismo , Receptor Tipo 2 de Melanocortina/deficiência , Receptor Tipo 2 de Melanocortina/genética , Proteína Desacopladora 2 , Regulação para Cima/efeitos dos fármacosRESUMO
Cells adhering onto implant surfaces are subjected to oxidative stress during wound healing processes. Although titanium and its alloys are among the most frequently used biomaterials in orthopedic and dental implants, titanium surfaces do not have antioxidant properties, and cells grown on these surfaces can show permanent oxidative stress. The present study assessed the antioxidant property and osteogenic properties of titanium samples with or without oxidation treatments. A thick rutile TiO2 film was observed on thermally oxidized titanium surfaces, while amorphous anatase TiO2 formed on anodically oxidized titanium surfaces prepared by discharging in 1 M Na2HPO4. A resistance to the depletion of reduced glutathione in adherent osteoblasts, which correlates with antioxidant behavior, occurred on anodically oxidized titanium. Enhanced osteogenic gene expressions and nano-biomechanical properties of mineralized tissue were achieved on anodically oxidized titanium, in comparison with thermally oxidized or untreated titanium. Thus, anodic oxidation by discharging in electrolyte is expected to be a useful surface modification for titanium implants.