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Drugs R D ; 2021 Apr 19.
Artículo en Inglés | MEDLINE | ID: mdl-33876394


INTRODUCTION: Opioids are potent painkillers but can have severe adverse effects in the intensive care unit (ICU). The aim of this study was to compare the outcomes of fentanyl and morphine use among patients at risk for and with acute respiratory distress syndrome (ARDS). METHODS: We developed a dataset of real-world data to enable the comparison of the effectiveness and safety of opioids and the associated outcomes from the Multiparameter Intelligent Monitoring in Intensive Care (MIMIC)-III database and the eICU Collaborative Research Database. Patients who were admitted to the ICU with a diagnosis of or at risk for ARDS and received mechanical ventilation for at least 12 h were included. Patients were enrolled sequentially into one of six groups in three cohorts: treated with fentanyl or not; treated with morphine or not; and treated with fentanyl or morphine. Propensity score matching and multivariable analyses were performed. RESULTS: Fentanyl was associated with higher in-hospital mortality in the propensity score-matched model but not in the linear regression model. The use of morphine was associated with a higher in-hospital mortality in both models. Both fentanyl and morphine were associated with longer duration of mechanical ventilation, ICU stay, and hospitalization and a decreased likelihood of being discharged home in both models. Notably, compared with morphine, fentanyl was associated with a lower mortality and an increased likelihood of being discharged home. CONCLUSIONS: Both fentanyl and morphine were independent risk factors for worse outcomes in patients with or at risk for ARDS. Compared with morphine, fentanyl may be preferred in these patients.

Chin J Cancer ; 35: 32, 2016 Mar 24.
Artículo en Inglés | MEDLINE | ID: mdl-27013185


The stromal interaction molecule (STIM)-calcium release-activated calcium channel protein (ORAI) and inositol 1,4,5-trisphosphate receptors (IP3Rs) play pivotal roles in the modulation of Ca(2+)-regulated pathways from gene transcription to cell apoptosis by driving calcium-dependent signaling processes. Increasing evidence has implicated the dysregulation of STIM-ORAI and IP3Rs in tumorigenesis and tumor progression. By controlling the activities, structure, and/or expression levels of these Ca(2+)-transporting proteins, malignant cancer cells can hijack them to drive essential biological functions for tumor development. However, the molecular mechanisms underlying the participation of STIM-ORAI and IP3Rs in the biological behavior of cancer remain elusive. In this review, we summarize recent advances regarding STIM-ORAI and IP3Rs and discuss how they promote cell proliferation, apoptosis evasion, and cell migration through temporal and spatial rearrangements in certain types of malignant cells. An understanding of the essential roles of STIM-ORAI and IP3Rs may provide new pharmacologic targets that achieve a better therapeutic effect by inhibiting their actions in key intracellular signaling pathways.

Canales de Calcio Activados por la Liberación de Calcio/metabolismo , Receptores de Inositol 1,4,5-Trifosfato/metabolismo , Neoplasias/patología , Antineoplásicos/farmacología , Antineoplásicos/uso terapéutico , Apoptosis , Movimiento Celular/efectos de los fármacos , Proliferación Celular/efectos de los fármacos , Humanos , Invasividad Neoplásica , Neoplasias/metabolismo , Transducción de Señal/efectos de los fármacos
Oncol Rep ; 34(2): 755-62, 2015 Aug.
Artículo en Inglés | MEDLINE | ID: mdl-26062728


Multidrug resistance (MDR) remains a formidable challenge in the use of chemotherapy and represents a powerful obstacle to the treatment of leukemia. ATP-binding cassette subfamily B member 1 (ABCB1) is a recognized factor which causes MDR and is closely related to poor outcome and relapse in leukemia. Ongoing research concerning the strategy for inhibiting the abnormally high activity of the ABCB1 transporter is critically needed. In the present study, we sought to elucidate the interaction between ABCB1 transporter and butorphanol. Our results showed that butorphanol significantly antagonized ABCB1-mediated drug efflux and increased the intracellular drug concentration by inhibiting the transport activity of ABCB1 in leukemia cells. Mechanistic investigations demonstrated that butorphanol did not alter the protein expression or localization of ABCB1 in HL60/VCR and K562/ADR cells. Furthermore, homology modeling indicated that butorphanol could fit into the large drug-binding cavity of ABCB1 and form a binding conformation. In conclusion, butorphanol reversed the ABCB1-mediated MDR in leukemia cells by directly suppressing the efflux activity of ABCB1.

Butorfanol/administración & dosificación , Resistencia a Antineoplásicos/efectos de los fármacos , Leucemia/tratamiento farmacológico , Subfamilia B de Transportador de Casetes de Unión a ATP/antagonistas & inhibidores , Subfamilia B de Transportador de Casetes de Unión a ATP/genética , Antineoplásicos/administración & dosificación , Línea Celular Tumoral , Doxorrubicina/administración & dosificación , Resistencia a Múltiples Medicamentos/genética , Humanos , Leucemia/genética , Leucemia/patología , Proteínas de Neoplasias/biosíntesis , Paclitaxel/administración & dosificación