IntroductionHemodynamic fluctuation during the induction of general anesthesia is a common event and adversely affect patients’ outcomes. The aim of this study is to investigate the impacts of different anesthesia induction agents: propofol, etomidate, and propofol-etomidate combination on patient hemodynamics and processed electroencephalography (EEG).Material and methodsSeventy-five patients undergoing elective non-cardiac surgery were randomly assigned to three groups of anesthesia induction agents: the group P received 2 mg/kg propofol, the group E received 0.3 mg/kg etomidate, and the group PE received the combination of 1mg/kg propofol plus 0.15mg/kg etomidate. Hemodynamic variables and processed EEG were measured during induction.ResultsHeart rate (HR) was significantly increased at intubation and 1 min after intubation compared with baseline in all three groups. Mean arterial pressure (MAP) decreased significantly after induction, at 5, and 10 min after intubation in group P (79.1±12.6, 77.0±14.2, 76.6±11.4 versus 93.2±9.9 mmHg; all P<0.001). MAP increased significantly at intubation and 1 min after intubation in group E (104.7±13.0, 103.8±12.8 versus 92.9±10.2; P<0.001, P=0.001 respectively). The incidence of myoclonus was lower in groups PE (4.0%) and P (4.0%) compared with that in group E (24.0%) (P=0.033). The incidence of pain at injection was higher in group P (28.0%) than that in groups PE and E (4.0% and 0.0%) (P=0.025).ConclusionsThe combination of propofol and etomidate used during induction of anesthesia provided a more stable BP profile, less pain at site of injection, and decreased myoclonic movements compared with propofol or etomidate alone.
Treatment of people with HIV (PWH) with antiretroviral therapy (ART) results in sustained suppression of viremia, but HIV persists indefinitely as integrated provirus in CD4-expressing cells. Intact persistent provirus, the "rebound competent viral reservoir" (RCVR), is the primary obstacle to achieving a cure. Most variants of HIV enter CD4+ T cells by binding to the chemokine receptor, CCR5. The RCVR has been successfully depleted only in a handful of PWH following cytotoxic chemotherapy and bone marrow transplantation from donors with a mutation in CCR5. Here we show that long-term SIV remission and apparent cure can be achieved for infant macaques via targeted depletion of potential reservoir cells that express CCR5. Neonatal rhesus macaques were infected with virulent SIVmac251, then treated with ART beginning one week after infection, followed by treatment with either a CCR5/CD3-bispecific or a CD4-specific antibody, both of which depleted target cells and increased the rate of plasma viremia decrease. Upon subsequent cessation of ART, three of seven animals treated with CCR5/CD3-bispecific antibody rebounded quickly and two rebounded 3 or 6 months later. Remarkably, the other two animals remained aviremic and efforts to detect replication-competent virus were unsuccessful. Our results show that bispecific antibody treatment can achieve meaningful SIV reservoir depletion and suggest that functional HIV cure might be achievable for recently infected individuals having a restricted reservoir.
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