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1.
Exp Mol Pathol ; 102(3): 505-514, 2017 06.
Artigo em Inglês | MEDLINE | ID: mdl-28533125

RESUMO

Due to the limited data on diabetic ketoacidosis and brain edema (DKA/BE) in children/adolescents and the lack of recent data on adults with type 1 diabetes (T1D), we addressed the question of whether neuroinflammation was present in the fatal DKA of adults. We performed immunohistochemistry (IHC) studies on the brains of two young adults with T1D and fatal DKA and compared them with two teenagers with poorly controlled diabetes and fatal DKA. C5b-9, the membrane attack complex (MAC) had significantly greater deposits in the grey and white matter of the teenagers than the young adults (p=0.03). CD59, a MAC assembly inhibitory protein was absent, possibly suppressed by the hyperglycemia in the teenagers but was expressed in the young adults despite comparable average levels of hyperglycemia. The receptor for advanced glycation end products (RAGE) had an average expression in the young adults significantly greater than in the teenagers (p=0.02). The autophagy marker Light Chain 3 (LC3) A/B was the predominant form of programmed cell death (PCD) in the teenage brains. The young adults had high expressions of both LC3A/B and TUNEL, an apoptotic cell marker for DNA fragmentation. BE was present in the newly diagnosed young adult with hyperglycemic hyperosmolar DKA and also in the two teenagers. Our data indicate that significant differences in neuroinflammatory components, initiated by the dysregulation of DKA and interrelated metabolic and immunologic milieu, are likely present in the brains of fatal DKA of teenagers when compared with young adults.


Assuntos
Biomarcadores/metabolismo , Diabetes Mellitus Tipo 1/genética , Cetoacidose Diabética/genética , Inflamação Neurogênica/genética , Adolescente , Adulto , Autofagia , Encéfalo/fisiopatologia , Edema Encefálico/diagnóstico , Edema Encefálico/etiologia , Edema Encefálico/genética , Antígenos CD59/genética , Antígenos CD59/metabolismo , Fragmentação do DNA , Diabetes Mellitus Tipo 1/complicações , Cetoacidose Diabética/complicações , Regulação da Expressão Gênica , Humanos , Imuno-Histoquímica , Marcação In Situ das Extremidades Cortadas , Mediadores da Inflamação/metabolismo , Proteínas Associadas aos Microtúbulos/genética , Proteínas Associadas aos Microtúbulos/metabolismo , Inflamação Neurogênica/etiologia , Adulto Jovem
2.
Arch Pathol Lab Med ; 137(7): 1009-14, 2013 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-23808475

RESUMO

Adrenal schwannoma is a rare type of adrenal incidentaloma, an adrenal lesion found incidentally, usually on imaging or autopsy. Computed tomography and magnetic resonance imaging are tools used to evaluate adrenal lesions. The diagnosis of adrenal schwannoma, however, cannot be made on imaging alone. Surgical resection is the primary means of management of adrenal schwannomas, as it is not possible to distinguish the schwannoma from malignant entities simply based on imaging. Histopathologic features of adrenal schwannomas are similar to those of schwannomas found at other sites. Conventional schwannomas, consisting of alternating Antoni A and Antoni B areas as well as Verocay bodies, have distinct microscopic features and can be readily distinguished from other entities. Cellular schwannomas, on the other hand, consist only of intersecting fascicles of spindle cells or Antoni A areas, resulting in a wide differential diagnosis. Ancillary studies such as immunohistochemical analysis and electron microscopy can help to provide a specific diagnosis.


Assuntos
Neoplasias das Glândulas Suprarrenais/patologia , Glândulas Suprarrenais/patologia , Achados Incidentais , Neurilemoma/patologia , Neoplasias das Glândulas Suprarrenais/metabolismo , Glândulas Suprarrenais/cirurgia , Biomarcadores Tumorais/metabolismo , Feminino , Humanos , Imuno-Histoquímica , Masculino , Microscopia Eletrônica de Transmissão , Neurilemoma/metabolismo
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