Publications by authors named "Qiushi Gao"

Aims: Mid-gestational sevoflurane exposure may induce notable long-term neurocognitive impairment in offspring. This study was designed to investigate the role and potential mechanism of ferroptosis in developmental neurotoxicity induced by sevoflurane in the second trimester.

Methods: Pregnant rats on day 13 of gestation (G13) were treated with or without 3.

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Background: Pneumoperitoneum is a risk factor for perioperative atelectasis in infants. This research aimed to investigate whether lung recruitment manoeuvres guided by ultrasound are more effective for young infants (<3 months) during laparoscopy under general anaesthesia.

Methods: Young infants (<3 months) undergoing general anaesthesia during laparoscopic surgery (>2 h) were randomised to either conventional lung recruitment (control group) or ultrasound-guided lung recruitment (ultrasound group) once per hour.

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Aims: Hypoxic-ischemic brain injury (HIBI) often results in cognitive impairments. Herein, we investigated the roles of ferroptosis in HIBI and the underlying signaling pathways.

Methods: Ferrostatin-1 (Fer-1) or resveratrol (Res) treatments were administered intracerebroventricularly 30 min before HIBI in 7-day-old rats.

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Post-conditioning with sevoflurane, a volatile anesthetic, has been proved to be neuroprotective against hypoxic-ischemic brain injury (HIBI). Our previous research showed that autophagy is over-activated in a neonatal HIBI rat model, and inhibition of autophagy confers neuroprotection. There is increasing recognition that autophagy can be stimulated by activating endoplasmic reticulum (ER) stress.

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Sevoflurane postconditioning (SPC) has been widely reported to attenuate brain injury after hypoxia-ischemia encephalopathy (HIE) by inhibiting neural necrosis and autophagy. Moreover, recent reports revealed that sevoflurane facilitated hippocampal reconstruction via regulating migration. Yet, it remains unclear whether the promotion of neural migration by SPC repairs the hippocampal injury after HIE.

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With the increase in fetal surgeries, the effect of maternal anesthesia on progeny has attracted much attention. Our previous studies have demonstrated that 3.5% sevoflurane maternal exposure resulted in over-activated autophagy and cognitive impairment in the offspring.

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Background: Hypoxic-ischemic brain injury (HIBI) is a major cause of mortality in neonates and can cause long-term neurological sequelae. Excessive autophagy caused by HI may cause neuronal death. Dexmedetomidine was reported neuroprotective against HIBI.

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Article Synopsis
  • Previous research indicates that sevoflurane postconditioning offers neuroprotective benefits and enhances learning and memory in newborn rats following brain injury due to lack of oxygen.
  • In an experiment using the Rice-Vannucci model, rats treated with sevoflurane showed improved cognitive functions and reduced brain damage effects such as astrogliosis and glial scars.
  • The mechanism behind these effects involves changes in protein expressions, particularly decreased hypoxia-inducible factor-1α and increased DJ-1, suggesting sevoflurane helps stabilize brain function post-injury.
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General anaesthesia may impose significant neurocognitive risks on the developing brain. As brain injury in preterm neonates has a particular predilection for cerebral white matter, we aimed to evaluate the effects of sevoflurane on oligodendrocyte maturation and myelination in a preterm-equivalent rat model. Two-day-old postnatal (P2) Sprague-Dawley rats were exposed to 3.

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Article Synopsis
  • Microglia/macrophages show different polarization patterns after ischemic events, which can influence recovery based on the disease context; this study focuses on how sevoflurane post-conditioning affects these immune cells following hypoxic-ischemic brain injury (HIBI) in neonatal rats.
  • Using a HIBI model, researchers examined the impact of sevoflurane on microglial/macrophage polarization and identified mechanisms linked to autophagy and the enzyme cathepsin B, analyzing various cell markers to assess neuroprotection and neuronal health.
  • Results indicated that sevoflurane treatment reduced inflammatory markers and neuronal cell death after HIBI, leading to improved long-term cognitive outcomes
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Background: Dexmedetomidine (Dex) is a highly selective α2-adrenoceptor agonist used as an off-label medication for pediatric sedation and analgesia. Recently, Dex was reported to exhibit neuroprotective efficacy in several brain injury models. Here we investigate whether neonatal Dex administration promotes hippocampal neurogenesis and enhances hippocampus-dependent spatial learning and memory under physiological conditions.

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Article Synopsis
  • The study examines the effects of sevoflurane post-conditioning (SPC) on hypoxic-ischemic brain injury (HIBI) in neonatal rats, focusing on autophagy's role and the Ezh2-regulated Pten/Akt/mTOR pathway.
  • Inhibition of excessive autophagy was found to provide neuroprotection, as evidenced by improved neuronal density and morphology following SPC treatment.
  • The research concluded that SPC protects against HIBI by modulating the Pten/Akt/mTOR signaling pathway through Ezh2, which helps reduce over-activated autophagy in the hippocampus.
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The CrS/NbC Co-based self-lubricating composite coatings were successfully fabricated on Cr12MoV steel surface by laser clad Stellite 6, WS₂, and NbC mixed powders. The phase composition, microstructure, and tribological properties of the coatings ware investigated by means of X-ray diffraction (XRD), scanning electron microscopy (SEM), and energy dispersive spectrometer (EDS), as well as dry sliding wear testing. Based on the experimental results, it was found reactions between WS₂ and Co-based alloy powder had occurred, which generated solid-lubricant phase CrS, and NbC play a key role in improving CrS nuclear and refining microstructure of Co-based composite coating during laser cladding processing.

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