Publications by authors named "Shanglong Yao"

136 Publications

Death-Associated Protein Kinase 1 Promotes Alveolar Epithelial Cell Apoptosis and Ventilator-Induced Lung Injury Through P53 Pathway.

Shock 2021 Jul 8. Epub 2021 Jul 8.

Department of Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277, Jiefang Ave, Wuhan, 430022, Hubei, China Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277, Jiefang Ave, Wuhan, 430022, Hubei, China.

Objectives: Mechanical stretch induced alveolar epithelial cell (AEC) apoptosis participates in the onset of ventilator induced lung injury (VILI). In this study, we explored whether death associated protein kinase 1 (DAPK1) mediated cyclic stretch (CS) induced AEC apoptosis and VILI though P53 pathway.

Materials And Methods: AEC apoptosis was induced by CS using the FX-5000T Flexercell Tension Plus system. C57BL/6 mouse received high tidal volume ventilation to build VILI model. DAPK1 inhibitor, P53 inhibitor or DAPK1 plasmid was used to regulate the expression of DAPK1 and P53, respectively. Flow cytometery was performed to assay cell apoptosis and the changes of mitochondrial membrane potential (MMP); Immunoblotting was adopted to analyse related protein expression; The binding of related proteins was detected by coimmunoprecipitation; AEC apoptosis in vivo was determined by immunohistochemistry assay.

Results: CS promoted AEC apoptosis, increased DAPK1 and P53 expression and induced the binding of DAPK1 and P53; inhibition of DAPK1 or P53 reduced CS induced AEC apoptosis, suppressed the expression of Bax, increased Bcl-2 level and stabilized MMP; AEC apoptosis and the level of P53 were both increased after overexpressing of DAPK1. Moreover, DAPK1 plasmid transfection also promoted the expression of Bax and the change of MMP, but decreased the level of Bcl-2. Inhibition of DAPK1 or P53 in vivo alleviated high tidal volume ventilation induced AEC apoptosis and lung injury.

Conclusions: DAPK1 contributes to AEC apoptosis and the onset of VILI though P53 and its intrinsic pro-apoptotic pathway. Inhibition of DAPK1 or P53 alleviates high tidal volume ventilation induced lung injury and AEC apoptosis.
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http://dx.doi.org/10.1097/SHK.0000000000001831DOI Listing
July 2021

Pretreatment with valproic acid alleviates pulmonary fibrosis through epithelial-mesenchymal transition inhibition in vitro and in vivo.

Lab Invest 2021 Jun 24. Epub 2021 Jun 24.

Anesthetics, Pain Medicine and Intensive Care, Department of Surgery and Cancer, Faculty of Medicine, Imperial College London, Chelsea & Westminster Hospital, London, UK.

Epithelial-mesenchymal transition (EMT) plays a crucial role in the development of pulmonary fibrosis. This study aims to investigate the effects of valproic acid (VPA) on EMT in vitro and in vivo. In vitro, EMT was induced by the administration of transforming growth factor-β1 (TGF-β1) in a human alveolar epithelial cell line (A549). The dose effects of VPA (0.1-3 mM) on EMT were subsequently evaluated at different timepoints. VPA (1 mM) was applied prior to the administration of TGF-β1 and the expression of E-cadherin, vimentin, p-Smad2/3 and p-Akt was assessed. In addition, the effects of a TGF-β type I receptor inhibitor (A8301) and PI3K-Akt inhibitor (LY294002) on EMT were evaluated. In vivo, the effects of VPA on bleomycin-induced lung fibrosis were evaluated by assessing variables such as survival rate, body weight and histopathological changes, whilst the expression of E-cadherin and vimentin in lung tissue was also evaluated. A8301 and LY294002 were used to ascertain the cellular signaling pathways involved in this model. The administration of VPA prior to TGF-β1 in A549 cells prevented EMT in both a time- and concentration-dependent manner. Pretreatment with VPA downregulated the expression of both p-Smad2/3 and p-Akt. A8301 administration increased the expression of E-cadherin and reduced the expression of vimentin. LY294002 inhibited Akt phosphorylation induced by TGF-β1 but failed to prevent EMT. Pretreatment with VPA both increased the survival rate and prevented the loss of body weight in mice with pulmonary fibrosis. Interestingly, both VPA and A8301 prevented EMT and facilitated an improvement in lung structure. Overall, pretreatment with VPA attenuated the development of pulmonary fibrosis by inhibiting EMT in mice, which was associated with Smad2/3 deactivation but without Akt cellular signal involvement.
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http://dx.doi.org/10.1038/s41374-021-00617-2DOI Listing
June 2021

Efficacy and safety of ciprofol for the sedation/anesthesia in patients undergoing colonoscopy: Phase IIa and IIb multi-center clinical trials.

Eur J Pharm Sci 2021 Sep 8;164:105904. Epub 2021 Jun 8.

Department of Anesthesiology, West China Hospital, Sichuan University & The Research Units of West China (2018RU012), Chinese Academy of Medical Sciences, Chengdu, China. Electronic address:

Objective: Ciprofol is a new intravenous anesthetic agent similar to propofol that has the pharmacodynamic characteristics of a rapid rate of onset and recovery in pre-clinical experiments. The aims of the present clinical trials were to compare the efficacy and safety of ciprofol emulsion for sedation or general anesthesia during colonoscopy and to define optimal doses for a subsequent phase III clinical trial.

Methods: A phase IIa multi-center, open-label, non-randomized, positive control, dose-escalating study was performed to determine a recommended phase IIb dose (RP2D) of ciprofol to induce sedation or anesthesia in patients undergoing colonoscopy. Phase IIb was also a multi-center clinical trial, but the patients were randomized into 3 groups at a ratio of 1:1:1. It was a double-blinded, propofol controlled study that administered ciprofol 0.4 mg/kg (n = 31) and 0.5 mg/kg (n = 32) or propofol at 2.0 mg/kg (n = 31), with the aim of establishing the optimal dose of ciprofol. The primary endpoint was the colonoscopy success rate. Secondary endpoints were the duration of colonoscope insertion, recovery time, number of top-up doses needed, and the total dose of ciprofol or propofol required to maintain adequate sedation or anesthesia. In addition, we evaluated the satisfaction of sedation/anesthesia from the endoscopists, anesthetists and patients' points of view. Safety was assessed according to the incidence of AEs including serious AEs and drug related AEs and the assessment of vital signs, a 12-lead ECG and laboratory tests.

Results: In the phase IIa trial, the colonoscopy success rates in the 0.2-0.5 mg/kg ciprofol and propofol 2.0 mg/kg groups were 100% and all doses were safe and well tolerated. Ciprofol doses of 0.4 mg/kg and 0.5 mg/kg are recommended for subsequent IIb phases. In the phase IIb trial, a 100% success rate was reconfirmed in all the dosage groups. The mean time of colonoscope insertion in the ciprofol 0.4 mg/kg, ciprofol 0.5 mg/kg and propofol 2.0 mg/kg groups were 1.9, 1.5 and 1.5 min, the mean recovery times from colonoscope withdrawal were 6.1, 5.1, and 4.3 min, and the times to discharge were 11.8, 11.2 and 10.6 min, respectively. The satisfaction ratings of anesthetists in the ciprofol 0.5 mg/kg group (9.5 ± 0.8) were higher than in the ciprofol 0.4 mg/kg (9.2 ± 1.0) and propofol 2.0 mg/kg (9.2 ± 0.9) groups. The incidence of sedation and anesthesia-related AEs was highest in the propofol 2.0 mg/kg group (25.8%), followed by the ciprofol 0.5 mg/kg group (21.9%), and was least in the ciprofol 0.4 mg/kg group (16.1%) (P = 0.750).

Conclusions: Ciprofol was safe and well tolerated at doses ranging from 0.1 mg/kg to 0.5 mg/kg. Ciprofol 0.4-0.5 mg/kg induced equivalent sedation/anesthesia and had a similar safety profile to propofol 2.0 mg/kg during colonoscopy without producing serious AEs.
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http://dx.doi.org/10.1016/j.ejps.2021.105904DOI Listing
September 2021

[Application progress of ultrasound monitoring of diaphragm function in clinic].

Zhonghua Wei Zhong Bing Ji Jiu Yi Xue 2021 May;33(5):638-640

Department of Anesthesiology, Wuhan Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, Hubei, China.

In recent years, point of care ultrasound (POCUS) has developed rapidly in the fields of anesthesia and critical care. POCUS is widely used in clinic to monitor the function of human tissues and organs such as the heart, lungs, and diaphragm due to its visual, non-invasive, portable, and repeatable characters at the bedside. Diaphragm is an important structure to maintain respiratory function. Diaphragm paralysis or dysfunction can cause a significant decrease in inspiratory function. The patient's diaphragm function can be assessed through monitoring diaphragm thickness and activity by POCUS, and combined with other clinical indicators, the patient's recovery of respiratory function can be comprehensively evaluated, and rapidly identify the pathological conditions, such as diaphragm paralysis, diaphragm atrophy, diaphragmatic hypoplasia and amyotrophic lateral sclerosis. Dynamic evaluation of the process from diaphragmatic dysfunction to recovery can provide guidance for weaning and extubation, and real-time feedback on the treatment effect. This article reviews the ultrasound evaluation methods and clinical applications to the diaphragm, in order to guide clinicians to use relevant indicators to comprehensively evaluate the structure and function of the diaphragm, and then diagnose and treat diaphragm dysfunction, which may help making clinical decision.
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http://dx.doi.org/10.3760/cma.j.cn121430-20200824-00591DOI Listing
May 2021

The Initial Response to a Pandemic: Anesthesiology Experiences from China at the Onset of COVID-19.

Anesthesiol Clin 2021 Jun 11;39(2):255-264. Epub 2021 Feb 11.

Department of Anesthesiology and Critical Care, Perelman School of Medicine at the University of Pennsylvania, Center of Penn Global Health Scholar, 336 John Morgan Building, 3620 Hamilton Walk, Philadelphia, PA 19104, USA. Electronic address:

This article documents experiences from frontline anesthesia providers in Wuhan, China, mainly from the anesthesiologists in Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China. Those experiences offer valuable insight into the processes used to optimize the emergency response system, and the medical resources and emergency allocation, as well as providing information on the role anesthesiologists played in managing the pandemic.
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http://dx.doi.org/10.1016/j.anclin.2021.02.002DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7877230PMC
June 2021

Inactivation of TOPK Caused by Hyperglycemia Blocks Diabetic Heart Sensitivity to Sevoflurane Postconditioning by Impairing the PTEN/PI3K/Akt Signaling.

Oxid Med Cell Longev 2021 23;2021:6657529. Epub 2021 Apr 23.

Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 Jiefang Avenue, Wuhan 430022, China.

The cardioprotective effect of sevoflurane postconditioning (SPostC) is lost in diabetes that is associated with cardiac phosphatase and tensin homologue on chromosome 10 (PTEN) activation and phosphoinositide 3-kinase (PI3K)/Akt inactivation. T-LAK cell-originated protein kinase (TOPK), a mitogen-activated protein kinase- (MAPKK-) like serine/threonine kinase, has been shown to inactivate PTEN (phosphorylated status), which in turn activates the PI3K/Akt signaling (phosphorylated status). However, the functions of TOPK and molecular mechanism underlying SPostC cardioprotection in nondiabetes but not in diabetes remain unknown. We presumed that SPostC exerts cardioprotective effects by activating PTEN/PI3K/Akt through TOPK in nondiabetes and that impairment of TOPK/PTEN/Akt blocks diabetic heart sensitivity to SPostC. We found that in the nondiabetic C57BL/6 mice, SPostC significantly attenuated postischemic infarct size, oxidative stress, and myocardial apoptosis that was accompanied with enhanced p-TOPK, p-PTEN, and p-Akt. These beneficial effects of SPostC were abolished by either TOPK kinase inhibitor HI-TOPK-032 or PI3K/Akt inhibitor LY294002. Similarly, SPostC remarkably attenuated hypoxia/reoxygenation-induced cardiomyocyte damage and oxidative stress accompanied with increased p-TOPK, p-PTEN, and p-Akt in H9c2 cells exposed to normal glucose, which were canceled by either TOPK inhibition or Akt inhibition. However, either in streptozotocin-induced diabetic mice or in H9c2 cells exposed to high glucose, the cardioprotective effect of SPostC was canceled, accompanied by increased oxidative stress, decreased TOPK phosphorylation, and impaired PTEN/PI3K/Akt signaling. In addition, TOPK overexpression restored posthypoxic p-PTEN and p-Akt and decreased cell death and oxidative stress in H9c2 cells exposed to high glucose, which was blocked by PI3K/Akt inhibition. In summary, SPostC prevented myocardial ischemia/reperfusion injury possibly through TOPK-mediated PTEN/PI3K/Akt activation and impaired activation of this signaling pathway may be responsible for the loss of SPostC cardioprotection by SPostC in diabetes.
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http://dx.doi.org/10.1155/2021/6657529DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8093075PMC
May 2021

GYY4137 alleviates sepsis-induced acute lung injury in mice by inhibiting the PDGFRβ/Akt/NF-κB/NLRP3 pathway.

Life Sci 2021 Apr 10;271:119192. Epub 2021 Feb 10.

Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China; Institute of Anesthesia and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. Electronic address:

Aims: GYY4137 [GYY, morpholin-4-ium-4-methoxyphenyl (morpholino) phosphinodithioate] is a novel and perfect hydrogen sulfide (HS) donor that is stable in vivo and in vitro. HS, along with CO and NO, has been recognized as the third physiological gas signaling molecule that plays an active role in fighting various lung infections. However, the mechanism by which GYY4137 affects cecal ligation and puncture (CLP)-induced acute lung injury (ALI) is not understood. This study aimed to investigate whether GYY4137 inhibits the activation of the pyrin domain-containing protein 3 (NLRP3) inflammasome by inhibiting the PDGFRβ/Akt/NF-κB pathway.

Main Methods: The model of CLP-induced ALI was established in vivo. The mice were subsequently treated with GYY4137 (25 μg/g and 50 μg/g) to simulate the realistic conditions of pathogenesis. Western blotting and immunohistochemical staining were used to examine protein expression, hematoxylin and eosin staining was used for the histopathological analysis, and the levels of inflammatory factors were determined using enzyme-linked immunosorbent assays (ELISAs).

Key Findings: GYY4137 significantly increased the 7-day survival of mice with septic peritonitis and protected against CLP-induced ALI, including decreasing neutrophil infiltration, improving sepsis-induced lung histopathological changes, diminishing lung tissue damage, and attenuating the severity of lung injury in mice. The protective effect of GYY4137 was undoubtedly dose-dependent. We discovered that GYY4137 reduced the levels of the p-PDGFRβ, p-NF-κB, ASC, NLRP3, caspase-1, and p-Akt proteins in septic mouse lung tissue. Akt regulates the generation of proinflammatory cytokines in endotoxemia-associated ALI by enhancing the nuclear translocation of NF-κB.

Significance: These results indicate a new molecular mechanism explaining the effect of GYY4137 on the treatment of CLP-induced ALI in mice.
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http://dx.doi.org/10.1016/j.lfs.2021.119192DOI Listing
April 2021

Ethnic disparities in postpartum hemorrhage after cesarean delivery: a retrospective case-control study.

J Anesth 2021 04 28;35(2):197-205. Epub 2021 Jan 28.

Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Purpose: To explore the relationship of ethnicity and postpartum hemorrhage (PPH) for women who underwent cesarean delivery (CD) and examine the risk factors for PPH in distinct ethnic groups in China.

Methods: We conducted case-control studies with the maternity data from the 11,778 CD cases, in Xinjiang Uygur Autonomous Region. Initially, multivariable logistic regression was used to estimate the disparity of race-ethnicity on the risk of PPH in ethnic Han, Uygur, Hui and Kazakh. Then, we performed case-control studies within two major ethnic groups, identifying the specific risk factors for PPH.

Results: Ethnic Uygur were associated with a statistically significant increased odds [adjusted odds ratios (aOR) 2.05; 95% confidence interval (CI) 1.26-3.33] of PPH compared with ethnic Han. For subgroup analyses, in Uygur subgroup, general anesthesia (aOR 7.78; 95% CI 2.31-26.20); placenta previa (aOR 11.18; 95% CI 3.09-40.45); prenatal anemia (aOR 4.84; 95% CI 2.44-9.60); emergency surgery (aOR 4.22; 95% CI 1.95-9.13) were independently associated with PPH. In Han subgroup, general anesthesia (aOR 5.70; 95% CI 1.89-17.26); placenta previa (aOR 20.08; 95% CI 6.35-63.46); multiple pregnancy (aOR 7.21; 95% CI 1.61-32.37); body mass index (aOR 1.19; 95% CI 1.07-1.31) were the risk factors to PPH.

Conclusion: Uygur have more tendency to PPH compared to Han, and risk factors for PPH in Uygur and Han groups may differ. Knowing these differences may be meaningful when planning interventions and resources for high-risk patients undergoing cesarean delivery, and we need more research aimed at risk factors for PPH.
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http://dx.doi.org/10.1007/s00540-021-02899-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7969550PMC
April 2021

MicroRNA-155: Regulation of Immune Cells in Sepsis.

Mediators Inflamm 2021 8;2021:8874854. Epub 2021 Jan 8.

Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.

MicroRNAs are small noncoding RNAs which regulate gene expression at the posttranscriptional level. miR-155 is encoded by the miR-155 host gene (miR155HG), also known as the noncoding B cell integration cluster (BIC). MicroRNAs are widely expressed in various hematopoietic cells and are involved in regulating the immune system. In this review, we summarized how miR-155 modulates specific immune cells and the regulatory role of miR-155 in sepsis. miR-155 is expressed by different populations of innate and adaptive immune cells and is involved in the regulation of development, proliferation, and function in these cells. Sepsis is associated with uncontrollable inflammatory responses, accompanied by unacceptably high mortality. Due to the inadequacy of diagnostic markers as well as treatment strategies, treating sepsis can be a huge challenge. So far, a large number of experiments have shown that the expression of miR-155 is increased at an early stage of sepsis and that this increase is positively correlated with disease progression and severity. In addition, by blocking the proinflammatory effects of miR-155, it can effectively improve sepsis-related organ injury, providing novel insights to identify potential biomarkers and therapeutic targets for sepsis. However, since most of the current research is limited to animal experiments, further clinical research is required to determine the function of miR-155 and its mechanism related to sepsis.
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http://dx.doi.org/10.1155/2021/8874854DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7810547PMC
January 2021

The impact of carbon monoxide on years of life lost and modified effect by individual- and city-level characteristics: Evidence from a nationwide time-series study in China.

Ecotoxicol Environ Saf 2021 Mar 8;210:111884. Epub 2021 Jan 8.

Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. Electronic address:

Ambient carbon monoxide (CO) has been linked with mortality and morbidity. Little evidence is available regarding the relation between CO and years of life lost (YLL). Using data from 48 major cities in China from 2013 to 2017, we applied generalized additive models and random effects meta-analyses to explore the effects of CO on YLL from various diseases. Stratified analyses and meta-regression were performed to estimate potential effect modifications of demographic factors, regions, meteorological factors, co-pollutants, urbanization rate, economic level and health service level. Additional life gains due to avoidable YLL under certain scenario were also evaluated. Results indicated that a 1-mg/m³ increase of CO concentrations (lagged over 0-3 d), was associated with 2.08% (95% confidence interval [CI], 1.35%, 2.80%), 2.35% (95% CI: 1.39%, 3.30%), 1.47% (95% CI: -0.01%, 2.93%), 2.28% (95% CI: 1.09%, 3.47%), 2.42% (95% CI: 1.31%, 3.54%), 2.09% (95% CI: 0.47%, 3.72%) increments in daily YLL from non-accidental causes, cardiovascular diseases, respiratory diseases, coronary heart disease, stroke and chronic obstructive pulmonary disease, respectively. These associations were robust to the adjustment of co-pollutants and varied substantially by geography and demographic characteristics. Associations were stronger in the elder people (≥65 years), females, population with low education attainment, and lived in south region, than younger people, males, high educated populations and those lived in north region. Moreover, the harmful impact of increasing CO concentration could be attenuated by city-level characteristics, including the growth of urbanization rate, gross domestic product (GDP), GDP per capita, number of hospital beds, doctors and hospitals. Finally, an estimated life of 0.081 (95% CI: -0.027, 0.190) years would be gained per deceased people if CO concentration could fall to 1 mg/m. In conclusions, this nationwide analysis showed significant associations between short-term CO exposure and cause-specific YLL. The heterogeneity of both individual- and city-level characteristics should be considered for relevant intervention. These findings may have significant public health implications for the reduction of CO-attributed disease burden in China.
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http://dx.doi.org/10.1016/j.ecoenv.2020.111884DOI Listing
March 2021

Association Between Intermediate-Acting Neuromuscular-Blocking Agents and Short-Term Postoperative Outcomes in Patients with Gastric Cancer.

Cancer Manag Res 2020 6;12:11391-11402. Epub 2020 Nov 6.

Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, Hubei, People's Republic of China.

Purpose: This study examined whether different neuromuscular-blocking agents (NMBAs) work differently on the short-term outcomes of gastric cancer patients in terms of laboratory test results and severity of postoperative illness, and whether the effect is dose-related.

Patients And Methods: Data of 1643 adult patients receiving gastric cancer surgery were analyzed by employing generalized linear models (GLMs), to explore the effects of different NMBAs on neutrophil-lymphocyte ratio (NLR), platelet-lymphocyte ratio (PLR), lymphocyte-monocyte ratio (LMR) at postoperative day 1 (POD1), POD3, POD7, and return to intended oncologic therapy (RIOT), among others. We adjusted multiple covariants, including patient-, anesthesia-, and surgical complexity-related risk factors.

Results: Without adjusting dosage of NMBAs, POD1NLR, POD1PLR ( < 0.05), POD3NLR, POD7NLR, POD3 lymphocytes, POD7LMR ( < 0.01) in gastric cancer patients administered with benzylisoquinoline NMBAs worsened, and the administration of aminosteroidal NMBAs was associated with less risk of transfer to ICU ( < 0.01); without adjusting the types of NMBAs, the highest dose of NMBAs postponed the RIOT ( < 0.05) and was negatively associated with POD3NLR, POD7NLR and POD7LMR ( < 0.01), and increased risk of postoperative transfer to ICU ( < 0.01). When patients given benzylisoquinolines were re-divided in terms of five equal quintiles, from low to high dose, RIOT was delayed and POD7LMR decreased significantly in the fourth and fifth quintile groups as compared to the first quintile group. A higher risk for postoperative transfer to ICU was found in the fifth quintile group as compared to the first quintile group.

Conclusion: Patients with gastric cancer given benzylisoquinoline NMBAs had more unfavorable short-term outcomes, such as more severe inflammation and increased risk of transfer to ICU than their counterparts administered aminosteroidal NMBAs, and the effect of benzylisoquinolines was dose-related. The effect of aminosteroids on short-term outcomes was not dose-related in the dosage range we used.
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http://dx.doi.org/10.2147/CMAR.S258016DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7654551PMC
November 2020

Clinical data of early COVID-19 cases receiving extracorporeal membrane oxygenation in Wuhan, China.

J Clin Anesth 2021 02 14;68:110044. Epub 2020 Sep 14.

Department of Anaesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. Electronic address:

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http://dx.doi.org/10.1016/j.jclinane.2020.110044DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7489925PMC
February 2021

Plasma Proteomics Identify Biomarkers and Pathogenesis of COVID-19.

Immunity 2020 11 20;53(5):1108-1122.e5. Epub 2020 Oct 20.

State Key Laboratory of Virology, Wuhan Institute of Virology, Center for Biosafety Mega-Science, Chinese Academy of Sciences (CAS), Wuhan, Hubei 430071, China; Center for Translational Medicine, Wuhan Jinyintan Hospital, Wuhan, Hubei 430023, China; Joint Laboratory of Infectious Diseases and Health, Wuhan Institute of Virology & Wuhan Jinyintan Hospital, CAS, Wuhan, Hubei 430023, China; University of Chinese Academy of Sciences, Beijing 100049, China. Electronic address:

The coronavirus disease 2019 (COVID-19) pandemic is a global public health crisis. However, little is known about the pathogenesis and biomarkers of COVID-19. Here, we profiled host responses to COVID-19 by performing plasma proteomics of a cohort of COVID-19 patients, including non-survivors and survivors recovered from mild or severe symptoms, and uncovered numerous COVID-19-associated alterations of plasma proteins. We developed a machine-learning-based pipeline to identify 11 proteins as biomarkers and a set of biomarker combinations, which were validated by an independent cohort and accurately distinguished and predicted COVID-19 outcomes. Some of the biomarkers were further validated by enzyme-linked immunosorbent assay (ELISA) using a larger cohort. These markedly altered proteins, including the biomarkers, mediate pathophysiological pathways, such as immune or inflammatory responses, platelet degranulation and coagulation, and metabolism, that likely contribute to the pathogenesis. Our findings provide valuable knowledge about COVID-19 biomarkers and shed light on the pathogenesis and potential therapeutic targets of COVID-19.
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http://dx.doi.org/10.1016/j.immuni.2020.10.008DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7574896PMC
November 2020

Efficacy and Safety of Neuromuscular Blockade in Overweight Patients Undergoing Nasopharyngeal Surgery.

Med Sci Monit 2020 Sep 16;26:e926452. Epub 2020 Sep 16.

Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China (mainland).

BACKGROUND Adequate muscle relaxation and rapid recovery of neuromuscular function are essential in the perioperative period. We therefore compared various anesthetic regimens of neuromuscular blockers and antagonists administered to overweight patients undergoing nasopharyngeal surgery. MATERIAL AND METHODS This prospective, randomized, double-blind study was conducted in overweight patients undergoing nasopharyngeal surgery. We randomly assigned 102 patients into 3 groups (each n=34) treated with various muscle relaxant agents and antagonists: rocuronium and sugammadex (Group RS), rocuronium and neostigmine (Group RN), and cisatracurium and neostigmine (Group CN). Then, we compared the efficacy and safety indexes of the 3 groups. RESULTS Onset times of muscular relaxation in Group RS and Group RN (110 s and 120 s) were shorter than in Group CN (183 s). Time from administration of antagonist to recovery of the TOF ratio to 0.9 was shorter in Group RS (3.3 min) than in other groups (20.7 min and 19.1 min, respectively). The incidence of postoperative residual curarization (PORC) was significantly lower in Group RS (5.9%) than in the other 2 groups (both 41.2%). The hemodynamic parameter changes before extubation were significantly higher in Group RN and Group CN than in Group RS. The postoperative pain scores were lowest in Group RS. CONCLUSIONS For overweight patients undergoing nasopharyngeal surgery, the use of rocuronium with sugammadex had the shortest onset time of neuromuscular relaxation, accelerated the reversion of neuromuscular blockade, effectively reduced the occurrence of PORC, relieved postoperative pain, and maintained hemodynamic stability before extubation. The combination of rocuronium and sugammadex may be the best anesthetic regimen for overweight patients undergoing nasopharyngeal surgery.
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http://dx.doi.org/10.12659/MSM.926452DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7519943PMC
September 2020

Death-associated Protein Kinase 1 Mediates Ventilator-induced Lung Injury in Mice by Promoting Alveolar Epithelial Cell Apoptosis.

Anesthesiology 2020 10;133(4):905-918

Background: Alveolar epithelial cell apoptosis is implicated in the onset of ventilator-induced lung injury. Death-associated protein kinase 1 (DAPK1) is associated with cell apoptosis. The hypothesis was that DAPK1 participates in ventilator-induced lung injury through promoting alveolar epithelial cell apoptosis.

Methods: Apoptosis of mouse alveolar epithelial cell was induced by cyclic stretch. DAPK1 expression was altered (knockdown or overexpressed) in vitro by using a small interfering RNA or a plasmid, respectively. C57/BL6 male mice (n = 6) received high tidal volume ventilation to establish a lung injury model. Adeno-associated virus transfection of short hairpin RNA and DAPK1 inhibitor repressed DAPK1 expression and activation in lungs, respectively. The primary outcomes were alveolar epithelial cell apoptosis and lung injury.

Results: Compared with the control group, the 24-h cyclic stretch group showed significantly higher alveolar epithelial cell apoptotic percentage (45 ± 4% fold vs. 6 ± 1% fold; P < 0.0001) and relative DAPK1 expression, and this group also demonstrated a reduced apoptotic percentage after DAPK1 knockdown (27 ± 5% fold vs. 53 ± 8% fold; P < 0.0001). A promoted apoptotic percentage in DAPK1 overexpression was observed without stretching (49 ± 6% fold vs. 14 ± 3% fold; P < 0.0001). Alterations in B-cell lymphoma 2 and B-cell lymphoma 2-associated X are associated with DAPK1 expression. The mice subjected to high tidal volume had higher DAPK1 expression and alveolar epithelial cell apoptotic percentage in lungs compared with the low tidal volume group (43 ± 6% fold vs. 4 ± 2% fold; P < 0.0001). Inhibition of DAPK1 through adeno-associated virus infection or DAPK1 inhibitor treatment appeared to be protective against lung injury with reduced lung injury score, resolved pulmonary inflammation, and repressed alveolar epithelial cell apoptotic percentage (47 ± 4% fold and 48 ± 6% fold; 35 ± 5% fold and 34 ± 4% fold; P < 0.0001, respectively).

Conclusions: DAPK1 promotes the onset of ventilator-induced lung injury by triggering alveolar epithelial cell apoptosis through intrinsic apoptosis pathway in mice.

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http://dx.doi.org/10.1097/ALN.0000000000003464DOI Listing
October 2020

Simple and Effective Primary Assessment of Emergency Patients in a COVID-19 Outbreak Area: A Retrospective, Observational Study.

Risk Manag Healthc Policy 2020 20;13:1253-1260. Epub 2020 Aug 20.

Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, People's Republic of China.

Background: The rapid spread of COVID-19 has expanded into a pandemic, for which the main containment strategies to reduce transmission are social distancing and isolation of ill persons. Thousands of medical staff have been infected worldwide. Coronavirus testing kits have been in short supply, and early diagnostic reagents did not have high sensitivity. The aim of this study was to describe the characteristics of patients requiring emergency surgery in a COVID-19 outbreak area.

Methods: We assessed medical data regarding all patients who underwent emergency surgery at the main campus of Wuhan Union Hospital from January 23, 2020, to February 15, 2020. We classified patients based on suspicion of COVID-19 infection (suspected vs not suspected) before they were admitted to the operating room. We used descriptive statistics to analyze the data. Outcomes included the incidence of confirmed COVID-19 infection and length of stay, which were followed until March 25, 2020.

Results: Among the 88 emergency patients included in this study, the mean age was 37 years. Twenty-five patients presented with abnormalities observed on chest CT scans and 16 presented with fever. The median wait time for surgery was one day. The median preparation time and median time until short orientation memory concentration test (SOMCT) recovery from anesthesia were 44.0 min and 23.0 min, respectively. The median postoperative length of stay was five days. Compared with patients not suspected of COVID-19 infection, six patients were confirmed to be infected with COVID-19 in the suspected group. No health care workers were infected during this study period.

Conclusion: Simple identification using temperature screening of patients, respiratory symptoms, and chest CT scans before being admitted for emergency surgery was rapid and effective. Shortened contact times might reduce the risk of infection. Additional investigations with larger samples and improved designs are needed to confirm these observations.
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http://dx.doi.org/10.2147/RMHP.S263950DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7445534PMC
August 2020

Maresin1 ameliorates sepsis-associated lung injury by inhibiting the activation of the JAK2/STAT3 and MAPK/ NF-κB signaling pathways.

Microb Pathog 2020 Nov 29;148:104468. Epub 2020 Aug 29.

Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China; Institute of Anesthesia and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. Electronic address:

Sepsis-associated acute lung injury (ALI) is a clinically critical disease that carries a high mortality rate. The pathogenesis of sepsis-associated ALI has not yet been precisely elucidated and there is a lack of effective treatment. As a new endogenous docosahexaenoic acid (DHA)-derived lipid mediators, Maresin1 has a significant dual role of anti-inflammatory and promoting inflammation regression. In this study, we established the sepsis model by the cecal ligation and puncture method (CLP) to explore the effect of Maresin1 on sepsis-induced lung injury. We found that the intervention of Maresin1 could significantly attenuate the sepsis-induced inflammatory responses, characterized by the down-regulation of the level of IL-1β, IL-6, TNF-α, MPO, etc. Maresin1 could also significantly decrease the number of neutrophils in lung tissue, thus improving the related lung injury indicators. Our experiment clarified that the protective effect of Maresin1 on sepsis-associated lung injury is closely related to its inhibition function of JAK2/STAT3 and MAPK/NF-κB signaling pathways. Our findings provide new research directions and therapeutic targets for sepsis-associated ALI.
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http://dx.doi.org/10.1016/j.micpath.2020.104468DOI Listing
November 2020

Protectin DX ameliorates inflammation in sepsis-induced acute lung injury through mediating PPARγ/NF-κB pathway.

Immunol Res 2020 10 26;68(5):280-288. Epub 2020 Aug 26.

Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.

Previous reports have demonstrated that the newly identified lipid mediator protectin DX (PDX) could effectively attenuate multiple organ injuries in sepsis. The aim of our study was to clarify whether PDX could improve acute lung injury (ALI) induced by sepsis and elucidate the relevant potential mechanism. After inducing sepsis by the cecal ligation and puncture approach, mice were treated with a high or low dose of PDX. Pathological changes in the pulmonary tissue were analyzed by hematoxylin-eosin staining, and lung injury score was evaluated. Lung permeability and edema were assessed by lung wet/dry ratio, and protein and cellular load of the bronchoalveolar lavage fluid (BALF). Inflammatory cytokine levels in BALF were measured by ELISA and the expression of PPARγ in the lung tissue was analyzed by immunoblotting. The results suggested that PDX could diminish the inflammatory response in lung tissue after sepsis by upregulating PPARγ and inhibiting the phosphorylation and activation of NF-κB p65. PDX treatment lowered the levels of pro-inflammation cytokines IL-1β, IL-6, TNF-α, and MCP-1, and the levels of anti-inflammatory cytokine IL-10 was increased in the BALF. It also improved lung permeability and reduced lung injury. Furthermore, the protective effect of PDX on lung tissue could be reversed by GW9662, a specific PPAR-γ antagonist. Taken together, our study indicated that PDX could ameliorate the inflammatory response in ALI by activating the PPARγ/NF-κB pathway in a mouse model of sepsis.
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http://dx.doi.org/10.1007/s12026-020-09151-7DOI Listing
October 2020

[Research progress on the mechanism of pro-inflammatory regression mediators promoting inflammation regression by regulating immune cells].

Zhonghua Wei Zhong Bing Ji Jiu Yi Xue 2020 Jul;32(7):873-876

Department of Anesthesiology, Institute of Anesthesia and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, Hubei, China. Corresponding author: Xia Haifa, Email:

Inflammatory response is an effective host defense mechanism to eliminate pathogens at the site of infection. The regression phase of inflammation mainly maintains the stable environment in tissues. Pro-inflammatory regression mediators (SPMs) are endogenous anti-inflammatory molecules, which play an important role in reducing excessive tissue damage and chronic inflammation. This paper reviews the interaction between SPMs and immune cells in inflammatory sites. By reviewing the relevant literature, it was found that SPMs regulate the components of innate and adaptive immune system, including neutrophils, macrophages, innate lymphocytes, natural killer cells and T cells.
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http://dx.doi.org/10.3760/cma.j.cn121430-20200224-00196DOI Listing
July 2020

SIRT1 is a key regulatory target for the treatment of the endoplasmic reticulum stress-related organ damage.

Biomed Pharmacother 2020 Oct 9;130:110601. Epub 2020 Aug 9.

Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science Technology, Wuhan, 430022, China; Institute of Anesthesia and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science Technology, Wuhan, 430022, China. Electronic address:

Endoplasmic reticulum (ER) stress is an evolutionarily conserved adaptive response that contributes to deal with the misfolded or unfolded protein in the lumen of the ER and restore the ER homeostasis. However, excessive and prolonged ER stress can trigger the cell-death signaling pathway which causes cell death, usually in the form of apoptosis. It is generally accepted that inappropriate cellular apoptosis and a series of the subsequent inflammatory response and oxidative stress can cause disturbance of normal physiological functions and organ damage. A lot of evidence shows that the excessive activation of the ER stress contributes to the pathogenesis of many kinds of diseases and inhibiting the inappropriate stress is of great significance for maintaining the normal physiological function. In recent years, Sirtuin1 (SIRT1) has become a research hotspot on ER stress. As a master regulator of ER stress, increasing evidence suggests that SIRT1 plays a positive role in a variety of ER stress-induced organ damage via multiple mechanisms, including inhibiting cellular apoptosis and promoting autophagy. Furthermore, a lot of factors have shown effective regulation of SIRT1, which indicates the feasibility of treating SIRT1 as a target for the treatment of ER stress-related diseases. We summarize and reveal the molecular mechanisms underlying the protective effect of SIRT1 in multiple ER stress-mediated organ damage in this review. We also summed up the possible adjustment mechanism of SIRT1, which provides a theoretical basis for the treatment of ER stress-related diseases.
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http://dx.doi.org/10.1016/j.biopha.2020.110601DOI Listing
October 2020

Role of Anesthesia Nurses in the Treatment and Management of Patients With COVID-19.

J Perianesth Nurs 2020 10 30;35(5):453-456. Epub 2020 May 30.

Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

As the backbone for the treatment of patients with coronavirus disease 2019 (COVID-19), nurses have been playing key roles in cabin hospitals, isolation wards, and intensive care units for critical cases. Anesthesia nurses have their own professional specialties, such as airway management, the use and maintenance of life support equipment, including ventilators, and the use of high-flow oxygen equipment. With rich experience in emergency responses and nursing, anesthesia nurses, along with emergency nurses and critical care nurses, play important roles during the treatment of patients with COVID-19. In our hospital, 27 of 34 anesthesia nurses participated in the front-line fight against COVID-19 and did an excellent job. Anesthesia care by nurses is relatively new in China, and the role of anesthesia nurses during a disaster response has not been fully appreciated. Given their specialty, anesthesia nurses have played important roles in the treatment of patients with COVID-19. We hope that authorities will consider including anesthesia nurses in national disaster response medical rescue teams.
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http://dx.doi.org/10.1016/j.jopan.2020.05.007DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7260532PMC
October 2020

Specialized pro-resolving mediators: It's anti-oxidant stress role in multiple disease models.

Mol Immunol 2020 10 1;126:40-45. Epub 2020 Aug 1.

Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China; Institute of Anesthesia and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. Electronic address:

Oxidative stress-related injury is a negative state caused by the imbalance between oxidation and antioxidant effects in the internal environment of the body. Oxidative stress has been confirmed to be an important factor in aging and a variety of diseases and the inhibition of inappropriate oxidative stress responses are important for maintaining normal physiological functions. Recently, considerable attention has been focused on specialized pro-resolving mediators(SPMs). SPMs are endogenous mediators derived from polyunsaturated fatty acids, which have multiple protective effects such as anti-inflammation, pro-resolution, and promoting tissue damage repair, etc. Moreover, the role of SPMs on oxidative stress has been extensively researched and provides a possible treatment method. In the current study, we review the positive role of SPMs in oxidative stress-related disease and outline the possible involved mechanism, thus providing the theoretical support for a better understanding of the roles of SPMs in oxidative stress and the theoretical basis for finding targets for the oxidative stress-related diseases.
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http://dx.doi.org/10.1016/j.molimm.2020.07.017DOI Listing
October 2020

Anxiety persists after recovery from acquired COVID-19 in anaesthesiologists.

J Clin Anesth 2020 Dec 7;67:109984. Epub 2020 Jul 7.

Department of Anesthesiology and Critical Care, Perelman School of Medicine at the University of Pennsylvania, PA, USA. Electronic address:

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http://dx.doi.org/10.1016/j.jclinane.2020.109984DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7340014PMC
December 2020

Corrigendum to Resolvin D1 Attenuates Lipopolysaccharide Induced Acute Lung Injury Through CXCL-12/CXCR4 Pathway [J Surg Res. 2014 May 1;188(1):213-221].

J Surg Res 2020 08;252:285

Department of Anesthesiology and Critical Care, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

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http://dx.doi.org/10.1016/j.jss.2020.03.049DOI Listing
August 2020

Practical workflow recommendations for emergency endotracheal intubation in critically ill patients with COVID-19 based on the experience of Wuhan Union Hospital.

J Clin Anesth 2020 11 28;66:109940. Epub 2020 May 28.

Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277, Jiefang Avenue, Wuhan 430022, China. Electronic address:

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http://dx.doi.org/10.1016/j.jclinane.2020.109940DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7253997PMC
November 2020

LncRNAMORT is upregulated in myocardial infarction and promotes the apoptosis of cardiomyocyte by downregulating miR-93.

BMC Cardiovasc Disord 2020 05 25;20(1):247. Epub 2020 May 25.

Department of Anesthesiology, Institute of Anesthesiology and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No.1277 Jiefang Avenue, Wuhan City, Hubei Province, 430000, People's Republic of China.

Background: Myocardial infarction (MI) affects the expression of a large number of lncRNAs, while the functions of those dysregulated lncRNAs are mostly unclear.

Materials And Methods: Expression of MORT and miR-93 in hearth tissues and plasma of both MI mice and Sham mice and both MI patients and healthy controls was detected by RT-qPCR. Correlations of expression levels of MORT and miR-93 between hear tissues and plasma of MI mice were explored by performing linear regression.

Results: In the present study we found that MORT expression levels were higher, while expression levels of miR-93 were lower in both plasma and heart tissues of mice MI mice models compared with Sham mice. Plasma levels of MORT and miR-93 were largely consistent with expression levels of MORT and miR-93 in heart tissue of MI mice. MORT expression levels were also higher, while levels of miR-93 were also lower in plasma of MI patients compared with healthy controls. MORT and miR-93 were inversely correlated in MI patients but not in healthy controls. MORT overexpression resulted in inhibited miR-93 expression in cardiomyocytes (AC16 cell line), while miR-93 overexpression did not significantly affect MORT expression. MORT overexpression promoted cardiomyocyte apoptosis, while miR-93 overexpression played and opposite role and attenuated the effects of MORT overexpression.

Conclusion: Therefore, lncRNA MORT is upregulated in myocardial infarction and promotes the apoptosis of cardiomyocyte by downregulating miR-93.
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http://dx.doi.org/10.1186/s12872-020-01522-0DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7249308PMC
May 2020

Maresin1 ameliorates acute lung injury induced by sepsis through regulating Th17/Treg balance.

Life Sci 2020 Aug 11;254:117773. Epub 2020 May 11.

Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China; Institute of Anesthesia and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. Electronic address:

The disturbance of the immune homeostasis caused by infection is decisive for multiple organ dysfunction caused by sepsis. Both the th17 cell and the regulatory cell(Tregs) are important components of the immune system and play a crucial role in maintaining immune homeostasis. In this study, we explored the effect of Maresin1, an emerging specific pro-inflammatory mediator, on the balance of Th17/Treg in sepsis, and investigated the underlying mechanism. We used the male C57BL/6 mice to establish the model of sepsis-induced lung injury by cecal ligation and puncture to verify the protective effect of Maresin1. Our study showed that Maresin1 could significantly inhibit the excessive inflammatory response and promote the inflammation regression in the process of sepsis-induced acute lung injury, thereby reducing lung damage and improving lung function. These effects were accompanied with the regulation of Maresin1 on the Th17/Treg balance in the early stages of sepsis. We demonstrated that Maresin1 has a certain effect on increasing the number of Treg and decreasing the number of Th17 cells in the early stages of sepsis, which is consistent with its effect on STAT3/RORγt and STAT5/Foxp3 signal pathways. Our study elucidated for the first time the relationship between Maresin1 and Th17/Treg balance in sepsis-induced acute lung injury.
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http://dx.doi.org/10.1016/j.lfs.2020.117773DOI Listing
August 2020

Regulatory T cells are a double-edged sword in pulmonary fibrosis.

Int Immunopharmacol 2020 Jul 22;84:106443. Epub 2020 Apr 22.

Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China; Institute of Anesthesia and Critical Care Medicine, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. Electronic address:

Pulmonary fibrosis (PF) is a chronic progressive interstitial lung disease. The pathogenesis of PF has not been clearly elucidated, and there is no obvious effective treatment to arrest the progression of PF to date. A long-term chronic inflammatory response and inappropriate repair process after lung injury are important causes and pathological processes of PF. As an influential type of the body's immune cells, regulatory T cells (Tregs) play an irreplaceable role in inhibiting the inflammatory response and promoting the repair of lung tissue. However, the exact roles of Tregs in the process of PF have not been clearly established, and the available literature concerning the roles of Tregs in PF are contradictory. First, Tregs can advance the progression of pulmonary fibrosis by secreting platelet-derived growth factor (PDGF), transforming growth factor-β (TGF-β) and other related factors, promoting epithelial-mesenchymal transition (EMT) and affecting the Th1 and Th2 balance, etc. Second, Tregs can inhibit PF by promoting the repair of epithelial cell damage, inhibiting the accumulation of fibroblasts, and strongly inhibiting the production and function of other related pro-inflammatory factors and pro-inflammatory cells. Accordingly, in this review, we focus on the multiple roles of Tregs in different models and different pulmonary fibrosis phases, thereby providing theoretical support for a better understanding of the multiple roles of these cells in PF and a theoretical basis for identifying targets for PF therapy.
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http://dx.doi.org/10.1016/j.intimp.2020.106443DOI Listing
July 2020

Emergency tracheal intubation in 202 patients with COVID-19 in Wuhan, China: lessons learnt and international expert recommendations.

Br J Anaesth 2020 07 10;125(1):e28-e37. Epub 2020 Apr 10.

Department of Anaesthesia and Intensive Care Medicine, St James's Hospital, Dublin, Ireland.

Tracheal intubation in coronavirus disease 2019 (COVID-19) patients creates a risk to physiologically compromised patients and to attending healthcare providers. Clinical information on airway management and expert recommendations in these patients are urgently needed. By analysing a two-centre retrospective observational case series from Wuhan, China, a panel of international airway management experts discussed the results and formulated consensus recommendations for the management of tracheal intubation in COVID-19 patients. Of 202 COVID-19 patients undergoing emergency tracheal intubation, most were males (n=136; 67.3%) and aged 65 yr or more (n=128; 63.4%). Most patients (n=152; 75.2%) were hypoxaemic (Sao <90%) before intubation. Personal protective equipment was worn by all intubating healthcare workers. Rapid sequence induction (RSI) or modified RSI was used with an intubation success rate of 89.1% on the first attempt and 100% overall. Hypoxaemia (Sao <90%) was common during intubation (n=148; 73.3%). Hypotension (arterial pressure <90/60 mm Hg) occurred in 36 (17.8%) patients during and 45 (22.3%) after intubation with cardiac arrest in four (2.0%). Pneumothorax occurred in 12 (5.9%) patients and death within 24 h in 21 (10.4%). Up to 14 days post-procedure, there was no evidence of cross infection in the anaesthesiologists who intubated the COVID-19 patients. Based on clinical information and expert recommendation, we propose detailed planning, strategy, and methods for tracheal intubation in COVID-19 patients.
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http://dx.doi.org/10.1016/j.bja.2020.03.026DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7151238PMC
July 2020

Anesthetic Management of Patients Undergoing Aortic Dissection Repair With Suspected Severe Acute Respiratory Syndrome COVID-19 Infection.

J Cardiothorac Vasc Anesth 2020 06 16;34(6):1402-1405. Epub 2020 Mar 16.

Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. Electronic address:

Severe acute respiratory syndrome coronavirus-2 is still active in Wuhan, China, and is spreading to the rest of the world. Recently, perioperative anesthetic management in patients with suspected or confirmed coronavirus-2 has been reported. However, little has been reported on the anesthetic management of patients undergoing aortic dissection repair in patients with suspected severe acute respiratory syndrome coronavirus-2 infection. During the outbreak in Wuhan, the authors' team completed 4 cases of aortic dissection repair successfully in patients with suspected severe acute respiratory syndrome coronavirus-2 infection. The purpose of the present report is to summarize current knowledge and experiences on anesthetic management in this patient population and to provide clinical practice guidelines on anesthetic management and infection prevention and control in these critically ill patients.
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http://dx.doi.org/10.1053/j.jvca.2020.03.021DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102517PMC
June 2020
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