Scientific reports
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Diagnosis of sleep apnea (SA) using simple tools has the potential to improve the efficacy of cardiac implants in the prevention of cardiac arrhythmias. The aim of the present study was to validate a transthoracic impedance sensor for SA diagnosis in patients with cardiac implants. We compared the apnea-hypopnea index (AHI) obtained from polysomnography (AHIPSG) with the AHI obtained from autoscoring algorithms of the ApneaScan implantable impedance respiration sensor (AHIAS) three months after implantation of cardioverter-defibrillator (ICD) or cardiac resynchronization therapy-defibrillator (CRT-D) devices. ⋯ The mean bias was 5.4 events per hour (mean AHI: 23.3 ± 14.6 versus 29.7 ± 13.7 for AHI-PSG and AHI-AS, respectively). An optimal cutoff value for the AHIAS at 30 events/h was obtained from the Receiver Operator Characteristic (ROC) curve analysis, which yielded a sensitivity of 100%, a specificity of 80%, PPV = 67%, NPV = 100%. Using an advanced algorithm for autoscoring of transthoracic impedance included in ICDs is reliable to identify SA and has the potential to improve the management of patients with cardiac implants.
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Preterm brain injury is highly associated with inflammation, which is likely related in part to sterile responses to hypoxia-ischemia. We have recently shown that neuroprotection with inflammatory pre-conditioning in the immature brain is associated with induction of toll-like receptor 7 (TLR7). We therefore tested the hypothesis that central administration of a synthetic TLR7 agonist, gardiquimod (GDQ), after severe hypoxia-ischemia in preterm-equivalent fetal sheep would improve white and gray matter recovery. ⋯ Central infusion of GDQ was associated with a robust increase in fetal plasma concentrations of the anti-inflammatory cytokines, interferon-β (IFN-β) and interleukin-10 (IL-10), with no significant change in the concentration of the pro-inflammatory cytokine, tumor necrosis factor-α (TNF-α). In conclusion, delayed administration of the TLR7 agonist, GDQ, after severe hypoxia-ischemia in the developing brain markedly ameliorated white and gray matter damage, in association with upregulation of anti-inflammatory cytokines. These data strongly support the hypothesis that modulation of secondary inflammation may be a viable therapeutic target for injury of the preterm brain.