Comparison of the effectiveness of high-flow nasal oxygen vs. standard facemask oxygenation for pre- and apneic oxygenation during anesthesia induction: a systematic review and meta-analysis.

BACKGROUND: In recent years, high flow nasal oxygen (HFNO) has been widely used in clinic, especially in perioperative period. Many studies have discussed the role of HFNO in pre- and apneic oxygenation, but their results are controversial. Our study aimed to examine the effectiveness of HFNO in pre- and apneic oxygenation by a meta-analysis of RCTs. METHODS: EMBASE, PUBMED, and COCHRANE LIBRARY databases were searched from inception to July 2021 for relevant randomized controlled trails (RCTs) on the effectiveness of HFNO versus standard facemask ventilation (FMV) in pre- and apenic oxygenation. Studies involving one of the following six indicators: (1) Arterial oxygen partial pressure (PaO2), (2) End expiratory oxygen concentration (EtO2), (3) Safe apnoea time, (4) Minimum pulse oxygen saturation (SpO2min), (5) Oxygenation (O2) desaturation, (6) End expiratory carbon dioxide (EtCO2) or Arterial carbon dioxide partial pressure(PaCO2) were included. Due to the source of clinical heterogeneity in the observed indicators in this study, we adopt random-effects model for analysis, and express it as the mean difference (MD) or risk ratio (RR) with a confidence interval of 95% (95%CI). We conducted a risk assessment of bias for eligible studies and assessed the overall quality of evidence for each outcome. RESULTS: Fourteen RCTs and 1012 participants were finally included. We found the PaO2 was higher in HFNO group than FMV group with a MD (95% CI) of 57.38 mmHg (25.65 to 89.10; p = 0.0004) after preoxygenation and the safe apnoea time was significantly longer with a MD (95% CI) of 86.93 s (44.35 to 129.51; p < 0.0001) during anesthesia induction. There were no significant statistical difference in the minimum SpO2, CO2 accumulation, EtO2 and O2 desaturation rate during anesthesia induction between the two groups. CONCLUSIONS: This systematic review and meta-analysis suggests that HFNO should be considered as an oxygenation tool for patients during anesthesia induction. Compared with FMV, continuous use of HFNO during anesthesia induction can significantly improve oxygenation and prolong safe apnoea time in surgical patients.

Stabilization of the histone acetyltransferase Tip60 by deubiquitinating enzyme USP7 stimulates the release of pro-inflammatory mediators in acute lung injury.

Acute lung injury (ALI) is often associated with inflammation. Increasing evidence has identified the role for ubiquitin-specific protease 7 (USP7) in activating the expression of inflammatory factors in macrophages. The present study evaluated whether USP7 also mediates histone acetyltransferase Tat-interactive protein 60 (Tip60) in the development of ALI inflammation. An ALI mouse model was induced by intratracheal lipopolysaccharide (LPS) administration. Next, lung myeloperoxidase (MPO) activity and the ratio of dry weight/wet weight of lung were examined to evaluate tissue damage. In addition, RAW 264.7 cells were treated with LPS to induce an in vitro LPS-induced inflammatory cell model. ELISA was performed to measure expression of IL-1ß, TNF-α, IL-6, and IL-8 in cells and tissues. TUNEL was used to detect LPS-induced cell apoptosis. Furthermore, the interaction between USP7 and Tip60 was identified by IP, Western blot analysis, and cycloheximide (CHX) treatment. The enrichment of Tip60 and H3K27ac in the promoter region of IL-6 and IL-8 was assessed by ChIP. USP7 was highly expressed in LPS-endotoxin-induced ALI mouse models and silencing of USP7 delayed the progression of ALI in mice. Silencing of USP7 protected RAW 264.7 cells against LPS-induced inflammation and apoptosis by downregulating IL-1ß, TNF-α, IL-6, and IL-8. USP7 enhanced Tip60 protein stability, and Tip60 increased the enrichment of H3K27ac on IL-6 and IL-8 promoter region and activated NF-κB p65 to increase IL-6 and IL-8 expression. These findings reveal a new post-transcriptional role for USP7 in inflammation by stabilizing Tip60 and increasing the release of the pro-inflammatory cytokines, and implicate USP7 inhibitors as potential therapeutic agents for ALI. KEY MESSAGES: USP7 expresses highly in an acute lung injury (ALI) mouse models. Silencing of USP7 inhibits inflammation and cell apoptosis in ALI mouse. USP7 stabilizes Tip60 to boost the release of IL-6 and IL-8. Tip60 increases IL-6 and IL-8 expression by acetylating NF-κB p65. Silencing of USP7 alleviates ALI by repressing NF-κB p65 and Tip60.

Propofol Target-controlled Infusion in Anesthesia Induction during Painless Gastroscopy.

OBJECTIVE: To investigate the feasibility of using the eyelash reflex as an indicator to calculate the individualised optimal target concentration in anesthesia induction during painless gastroscopy. STUDY DESIGN: Experimental study. PLACE AND DURATION OF STUDY: China-Japan Union Hospital of Jilin University, China, from January to December in 2016. METHODOLOGY: A total of 180 patients, who were scheduled to receive painless fibergastroscopic examination or treatment in the last three months, were enrolled in this study. All patients were randomly divided into three groups, according to the doctor visiting order (n=60, each). During the induction of anesthesia using propofol target-controlled infusion, the effectsite concentration upon the disappearance of the eyelash reflex (C0) was recorded first. Then, one ug/kg of fentanyl was injected. At the same time, the target effect-site concentration induced by propofol was determined: the effect-site concentration in group A was 1.5 times of C0, the effect-site concentration in group B was two times of C0, and the effectsite concentration in group C was 2.5 times of C0. RESULTS: During anesthesia induction, the incidence of motor responses was higher in group A than in groups B and C (p<0.05), and the incidence of hypoxemia was significantly higher in group C than in groups A and B (p<0.01). CONCLUSION: In the anesthesia option of fentanyl combined with propofol target-controlled infusion, the effect-site concentration of propofol can be set to two times of that at the time the eyelash reflex disappears. This study provides a new pre-assessment method for the induction dose of propofol in painless gastroscopy.

Prophylactic treatment with MSC-derived exosomes attenuates traumatic acute lung injury in rats.

The mesenchymal stem cell (MSC) is a potential strategy in the pretreatment of traumatic acute lung injury (ALI), a disease that causes inflammation and oxidative stress. This study aimed to investigate whether MSC-exosomal microRNA-124-3p (miR-124-3p) affects traumatic ALI. Initially, a traumatic ALI rat model was established using the weight-drop method. Then, exosomes were obtained from MSCs of Sprague-Dawley rats, which were injected into the traumatic ALI rats. We found that miR-124-3p was abundantly-expressed in MSCs-derived exosomes and could directly target purinergic receptor P2X ligand-gated ion channel 7 (P2X7), which was overexpressed in traumatic ALI rats. After that, a loss- and gain-of-function study was performed in MSCs and traumatic ALI rats to investigate the role of miR-124-3p and P2X7 in traumatic ALI. MSC-derived exosomal miR-124-3p or silenced P2X7 was observed to increase the survival rate of traumatic ALI rats and enhance the glutathione/superoxide dismutase activity in their lung tissues. However, the wet/dry weight of lung tissues, activity of methylenedioxyamphetamine and H2O2, and levels of inflammatory factors (TNF-a, IL-6, and IL-8) were reduced. Similarly, the numbers of total cells, macrophages, neutrophils, and lymphocytes in bronchoalveolar lavage fluid were also reduced when treated with exosomal miR-124-3p or silenced P2X7. In conclusion, the results provide evidence that miR-124-3p transferred by MSC-derived exosomes inhibited P2X7 expression, thus improving oxidative stress injury and suppressing inflammatory response in traumatic ALI, highlighting a potential pretreatment for traumatic ALI.

MicroRNA-485 Modulates the TGF-ß/ Smads Signaling Pathway in Chronic Asthmatic Mice by Targeting Smurf2.

BACKGROUND/AIMS: Chronic respiratory conditions continue to plague millions of people worldwide. We aimed to elucidate the detailed mechanisms of microRNA-485 (miR-485) in airway smooth muscle cell (ASMC) proliferation and apoptosis in chronic asthmatic mice. METHODS: A mouse model of chronic asthma was established. Ovalbumin was used to induce chronic asthma in the mice. The levels of transforming growth factor ß (TGF-ß), interleukin (IL)-4, IL-5, IL-13 and IL-17 in bronchoalveolar lavage fluid in mice were measured by enzyme-linked immunoassays (ELISAs). ASMCs were transfected with miR-485 mimic, miR-485 inhibitor and siRNA-Smurf2. The reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot analyses were applied to detect the mRNA and protein levels of Smurf2, α-SMA, TGF-ß1 and decapentaplegic homolog (Smads). The MTT assay was utilized for cell proliferation, while flow cytometry was conducted to assess cell cycle distribution and apoptosis. RESULTS: Lower expression of miR-485 and higher expression levels of TGF-ß1, IL-4, IL-5, IL-13 and IL-17 were detected in mice with chronic asthma. Smurf2 was identified as the target gene of miR-485. Upregulation of miR-485 mimic and downregulation of Smurf2 decreased expression levels of Smurf2, α-SMA, TGF-ß1 and Smad3, inhibited cell proliferation and increased apoptosis, while contrary results were observed in ASMCs transfected with miR-485 inhibitor. CONCLUSION: Overexpressed miR-485 inhibits cell proliferation and promotes apoptosis of ASMCs through the Smurf2-mediated TGF-ß/Smads signaling pathway in mice with chronic asthma.

MicroRNA-142 Inhibits Proliferation and Promotes Apoptosis in Airway Smooth Muscle Cells During Airway Remodeling in Asthmatic Rats via the Inhibition of TGF-ß -Dependent EGFR Signaling Pathway.

BACKGROUND/AIMS: Asthma is a heterogeneous disease characterized by chronic airway inflammation resulting from airway hyper-responsiveness to diverse stimuli. In this study, we investigated whether microRNA-142 (miR-142) expression affects proliferation and apoptosis in airway smooth muscle cells (ASMCs) during airway remodeling in asthmatic rats. METHODS: Thirty six Wistar rats were randomly classified into a control group and an model group. miR-142 mimics and inhibitors were constructed, and ASMCs were transfected using liposomes according to the following groups: blank, negative control (NC), miR-142 mimics, miR-142 inhibitors, si-TGF-ß and miR-142 inhibitors + si-TGF-ß. We verified that miR-142 targets TGF-ß using a dual-luciferase reporter assay. The expression levels of miR-142, TGF-ß, EGFR and apoptosis signaling pathway-related genes were determined using RT-qPCR and western blotting. Changes in cell proliferation, cell cycle progression and apoptosis were analyzed using MTT assays and flow cytometry. RESULTS: Rats with asthma had higher expression levels of EGFR and Akt and lower miR-142 levels. miR-142 was negatively correlated with TGF-ß expression. In ASMCs, the expression of TGF-ß, EGFR, Akt, phosphorylated-Akt (p-Akt), Bcl-2 and Bcl-xl and the rate of early apoptosis were decreased while expression of Bax and p21 and the proliferation rate were elevated with the upregulation of miR-142. The opposite results were observed with the downregulation of miR-142. Finally, the proliferative rate was decreased while the apoptosis rate was increased and expression levels of EGFR, Akt, p-Akt, Bcl-2 and Bcl-xl were reduced while Bax and p21 were elevated in the ASMCs transfected with miR-142 inhibitors and si-TGF-ß. CONCLUSION: The results of our study suggest that miR-142 inhibits proliferation and promotes apoptosis in ASMCs during airway remodeling in asthmatic rats by inhibiting TGF-ß expression via a mechanism involving the EGFR signaling pathway.

Propofol elicits autophagy via endoplasmic reticulum stress and calcium exchange in C2C12 myoblast cell line.

In this study, we investigated the relationship between propofol and autophagy and examined whether this relationship depends on ER stress, production of ROS (reactive oxygen species), and disruption of calcium (Ca2+) homeostasis. To this end, we measured C2C12 cell apoptosis in vitro, along with Ca2+ levels; ROS production; and expression of proteins and genes associated with autophagy, Ca2+ homeostasis, and ER stress, including LC3 (microtubule-associate protein 1 light chain 3), p62, AMPK (adenosine 5'-monophosphate (AMP)-activated protein kinase), phosphorylated AMPK, mTOR (the mammalian target of rapamycin), phosphorylated mTOR, CHOP (C/BEP homologous protein), and Grp78/Bip (78 kDa glucose-regulated protein). We found that propofol treatment induced autophagy, ER stress, and Ca2+ release. The ratio of phosphorylated AMPK to AMPK increased, whereas the ratio of phosphorylated mTOR to mTOR decreased. Collectively, the data suggested that propofol induced autophagy in vitro through ER stress, resulting in elevated ROS and Ca2+. Additionally, co-administration of an ER stress inhibitor blunted the effect of propofol.

Increased osteopontin protein expression may be correlated with poor prognosis in non-small-cell lung cancer: A meta analysis.

AIM: The present meta-nalysis investigates the prognostic value of osteopontin. (OPN) expression in patients with non-small-cell lung cancer. (NSCLC). MATERIALS AND METHODS: The Web of Science (1945 ~ 2013), the Cochrane Library Database (Issue 12, 2013), PubMed (1966 ~ 2013), EMBASE (1980 ~ 2013), CINAHL (1982 ~ 2013), and the Chinese Biomedical Database (CBM) (1982 ~ 2013) were searched, without language restrictions, to retrieve studies related to OPN and NSCLC. We compiled carefully selected data and a meta-analysis was conducted using STATA software (Version 12.0, Stata Corporation, and College Station, Texas USA). Hazard ratios (HR) with corresponding 95% confidence interval (95%CI) were calculated. RESULTS: Ten clinical cohort studies were selected for statistical analysis, representing a total of 1,133 NSCLC patients. The main findings of our meta-analysis are that patients who were OPN-positive had significantly shorter overall survival than OPN-negative patients. (HR = 1.47, 95%CI = 1.15. ~ 1.79,P< 0.001). Ethnicity.stratified analysis revealed a significant correlation between expression levels of OPN and poor prognosis of NSCLC patients among both Caucasians and Asians. (Asians: HR = 1.53, 95%CI = 0.95. ~ 2.11, P < 0.001; Caucasians: HR = 1.56, 95%CI = 1.08. ~ 2.03, P < 0.001; respectively). CONCLUSIONS: The present meta-analysis is consistent with the hypothesis that increased expression of OPN protein may be significantly associated with poor prognosis in patients with NSCLC.

Simultaneous electrochemical detection of catechol and hydroquinone based on gold nanoparticles@carbon nanocages modified electrode.

In the present study, carbon nanocages (CNCs) decorated with gold nanoparticles (AuNPs) with diameters of 2-5 nm were synthesized by simply mixing their solutions. The sizes of the AuNPs are small enough to diffuse into the inside of the CNCs by electrostatic incorporation and their morphologies were characterized by transmission electron microscopy, X-ray diffraction, energy dispersive spectrometry, Raman spectrometry and ultraviolet visible absorption spectra. The AuNPs@CNCs modified electrode was prepared for simultaneous highly sensitive determination of catechol (CC) and hydroquinone (HQ). This modified electrode demonstrated fantastic eletrochemical catalytic activities towards CC and HQ by cyclic voltammetry and differential pulse voltammetry. The calibration curves showed a linear response between the peak currents and the concentrations of CC and HQ. A wide dynamic detection range of 1.0-250.0 µM and 0.1-200.0 µM with a low detection limits (S/N = 3) of 0.0986 µM and 0.0254 µM can be obtained for CC and HQ respectively. The present method was successfully employed for determination of CC and HQ in a practical sample.