Assuntos
Infecções por Citomegalovirus , Citomegalovirus/metabolismo , Herpesvirus Humano 3/metabolismo , Proteína S/metabolismo , Púrpura Fulminante , Infecção pelo Vírus da Varicela-Zoster , Adulto , Infecções por Citomegalovirus/sangue , Infecções por Citomegalovirus/patologia , Infecções por Citomegalovirus/terapia , Infecções por Citomegalovirus/virologia , Feminino , Humanos , Púrpura Fulminante/sangue , Púrpura Fulminante/patologia , Púrpura Fulminante/terapia , Púrpura Fulminante/virologia , Infecção pelo Vírus da Varicela-Zoster/sangue , Infecção pelo Vírus da Varicela-Zoster/patologia , Infecção pelo Vírus da Varicela-Zoster/terapia , Infecção pelo Vírus da Varicela-Zoster/virologiaRESUMO
In the past decades, viridans group Streptococci (VGS) have emerged as an important cause of bacteremia in neutropenic patients with cancer. The clinical course of VGS bacteremia can be devastating including septic shock and adult respiratory distress syndrome (ARDS). It has been suggested that septicemia with VGS triggers the development of noncardiogenic pulmonary edema in patients with pre-existing damage of the lungs due to aggressive cytotoxic treatment. Thus, the preemptive administration of corticosteroid to patients diagnosed with VGS bacteremia with early onset of respiratory failure has been employed to prevent ARDS. While this management strategy has been suggested in the literature, little published data are available to validate this practice. In this study, we sought to review the benefit of early administration of corticosteroid to patients who developed symptom or early signs of respiratory failure while being neutropenic with VGS bacteremia.
RESUMO
Cytosolic regions of sodium dependent neurotransmitter transporters regulate their surface density and transporting function by interconnecting themselves with intracellular signaling pathways. Here we show that calpain activation in rat brain synaptosomes leads to cleavage of both N- and C-terminal regions of GABA transporter GAT1. In the C-terminal region, calpain removes a short segment of amino acids involved in binding of GAT1 to a high-density PDZ anchoring matrix. Using a protein pull-down assay, we found that C-terminal truncation of GAT1 results in modification of its interacting proteome in vitro. Results indicate that calpain activation/inhibition in GABAergic terminals may influence the scaffolding and surface expression of GABA transporter GAT1 under normal conditions or imbalance GAT1-mediated GABAergic transmission under pathological states.
