Author: "QING-TAO MENG" - Searchworks@Jio Institute Digital Library Search Results

108 results on '"QING-TAO MENG"'

1. Comparison of the levels of depression and anxiety in elderly aortic stenosis patients treated with surgical or transcatheter aortic valve replacement

Author: Jiao Sun, Qing-Tao Meng, Yu-Wei Wang, Wei-Long Zhao, Feng-Zhi Sun, Ji-Hong Liu, and Ji-Yi Liu
Subjects: Aortic stenosis, TAVR, SAVR, Depression, Anxiety, Quality of life, Surgery, RD1-811, Anesthesiology, RD78.3-87.3
Abstract: Abstract Objective Currently, only a few studies have been conducted on the mental status recovery in elderly aortic stenosis (AS) patients after treatment. How transcatheter aortic valve replacement (TAVR) and surgical aortic valve replacement (SAVR) differentially impinge on the mental status of elderly AS patients is completely unknown. The present prospective study aims to investigate this question by comparing the post-treatment levels of depression and anxiety, quality of life and frailty. Methods A total of 120 elderly patients (age above 70) with symptomatic AS were included, where 78 of them were treated with TAVR and 42 of them were treated with SAVR. Levels of depression and anxiety, quality of life and frailty were assessed by the Chinese version of Hospital Anxiety and Depression Scale (HADS), World Health Organization Quality of Life Instrument-Older Adults Module (WHOQOL-OLD) and clinical frailty scale, respectively. Scores were recorded and compared at admission, 1 month, 4 months and 8 months after treatment. Results Before treatment, both patient groups had similar baseline characteristics and all mental parameters. During the follow-up period, patients in the TAVR group demonstrated significant improvement in all assessed mental parameters to certain extent compared to the SAVR group. Specifically, frailty was significantly improved in the TAVR-treated patients at all three follow-up time points. Levels of depression and anxiety were significantly improved 8 months after treatment, although the remaining patient number is limited. Quality of life was only significantly improved 1 month after treatment. Conclusion TAVR may provide a better mental recovery outcome in elderly AS patients.
Published: 2022
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2. BNP facilitates NMB-encoded histaminergic itch via NPRC-NMBR crosstalk

Author: Qing-Tao Meng, Xian-Yu Liu, Xue-Ting Liu, Juan Liu, Admire Munanairi, Devin M Barry, Benlong Liu, Hua Jin, Yu Sun, Qianyi Yang, Fang Gao, Li Wan, Jiahang Peng, Jin-Hua Jin, Kai-Feng Shen, Ray Kim, Jun Yin, Ailin Tao, and Zhou-Feng Chen
Subjects: itch, BNP, NPRC, NPRA, GRP, spinal cord, Medicine, Science, Biology (General), QH301-705.5
Abstract: Histamine-dependent and -independent itch is conveyed by parallel peripheral neural pathways that express gastrin-releasing peptide (GRP) and neuromedin B (NMB), respectively, to the spinal cord of mice. B-type natriuretic peptide (BNP) has been proposed to transmit both types of itch via its receptor NPRA encoded by Npr1. However, BNP also binds to its cognate receptor, NPRC encoded by Npr3 with equal potency. Moreover, natriuretic peptides (NP) signal through the Gi-couped inhibitory cGMP pathway that is supposed to inhibit neuronal activity, raising the question of how BNP may transmit itch information. Here, we report that Npr3 expression in laminae I-II of the dorsal horn partially overlaps with NMB receptor (NMBR) that transmits histaminergic itch via Gq-couped PLCβ-Ca2+ signaling pathway. Functional studies indicate that NPRC is required for itch evoked by histamine but not chloroquine (CQ), a nonhistaminergic pruritogen. Importantly, BNP significantly facilitates scratching behaviors mediated by NMB, but not GRP. Consistently, BNP evoked Ca2+ responses in NMBR/NPRC HEK 293 cells and NMBR/NPRC dorsal horn neurons. These results reveal a previously unknown mechanism by which BNP facilitates NMB-encoded itch through a novel NPRC-NMBR cross-signaling in mice. Our studies uncover distinct modes of action for neuropeptides in transmission and modulation of itch in mice.
Published: 2021
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3. Ischemic Postconditioning-Mediated DJ-1 Activation Mitigate Intestinal Mucosa Injury Induced by Myocardial Ischemia Reperfusion in Rats Through Keap1/Nrf2 Pathway

Author: Rong Chen, Wei Li, Zhen Qiu, Qin Zhou, Yuan Zhang, Wen-yuan Li, Ke Ding, Qing-tao Meng, and Zhong-yuan Xia
Subjects: intestinal barrier injury, ischemic postconditioning, DJ-1, myocardial ischemia reperfusion, nuclear factor (erythroid-derived 2)-like 2, Biology (General), QH301-705.5
Abstract: Intestinal mucosal barrier dysfunction induced by myocardial ischemia reperfusion (IR) injury often leads to adverse cardiovascular outcomes after myocardial infarction. Early detection and prevention of remote intestinal injury following myocardial IR may help to estimate and improve prognosis after acute myocardial infarction (AMI). This study investigated the protective effect of myocardial ischemic postconditioning (IPo) on intestinal barrier injury induced by myocardial IR and the underlying cellular signaling mechanisms with a focus on the DJ-1. Adult SD rats were subjected to unilateral myocardial IR with or without ischemic postconditioning. After 30 min of ischemia and 120 min of reperfusion, heart tissue, intestine, and blood were collected for subsequent examination. The outcome measures were (i) intestinal histopathology, (ii) intestinal barrier function and inflammatory responses, (iii) apoptosis and oxidative stress, and (iv) cellular signaling changes. IPo significantly attenuated intestinal injury induced by myocardial IR. Furthermore, IPo significantly increased DJ-1, nuclear Nrf2, NQO1, and HO-1 expression in the intestine and inhibited IR-induced apoptosis and oxidative stress. The protective effect of IPo was abolished by the knockdown of DJ-1. Conversely, the overexpression of DJ-1 provided a protective effect similar to that of IPo. Our data indicate that IPo protects the intestine against myocardial IR, which is likely mediated by the upregulation of DJ-1/Nrf2 pathway.
Published: 2021
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4. Dexmedetomidine preconditioning protects against lung injury in hemorrhagic shock rats

Author: Lei Zhang, Wei Wang, Qian-Qian Qiao, Xue-Shan Bu, Ling-Hua Tang, Yi-Fan Jia, Zhong-Yuan Xia, and Qing-Tao Meng
Subjects: Dexmedetomidine, Hemorrhagic shock, Preconditioning, Lung injury, Rat, Anesthesiology, RD78.3-87.3
Abstract: Abstract Background and objectives: Dexmedetomidine has demonstrated protective effects against lung injury in vitro. Here, we investigated whether dexmedetomidine preconditioning protected against lung injury in hemorrhagic shock rats. Methods: Male Sprague-Dawley rats were randomly divided into four groups (n = 8): control group, hemorrhagic shock group, 5 ug.kg-1 dexmedetomidine (DEX1) group, and 10 ug.kg-1 dexmedetomidine (DEX2) group. Saline or dexmedetomidine were administered over 20 min. 30 min after injection, hemorrhage was initiated in the hemorrhagic shock, DEX1 and DEX2 group. Four hours after resuscitation, protein and cellular content in bronchoalveolar lavage fluid, and the lung histopathology were measured. The malondialdehyde, superoxide dismutase, Bcl-2, Bax and caspase-3 were also tested in the lung tissue. Results: Compare with hemorrhagic shock group, 5 ug.kg-1 dexmedetomidine pretreatment reduced the apoptosis (2.25 ± 0.24 vs. 4.12 ± 0.42%, p < 0.05), histological score (1.06 ± 0.12 vs. 1.68 ± 0.15, p < 0.05) and protein (1.92 ± 0.38 vs. 3.95 ± 0.42 mg.mL-1, p < 0.05) and WBC (0.42 ± 0.11 vs. 0.92 ± 0.13 × 109/L, p < 0.05) in bronchoalveolar lavage fluid. Which is correlated with increased superoxide dismutase activity (8.35 ± 0.68 vs. 4.73 ± 0.44 U.mg-1 protein, p < 0.05) and decreased malondialdehyde (2.18 ± 0.19 vs. 3.28 ± 0.27 nmoL.mg-1 protein, p < 0.05). Dexmedetomidine preconditioning also increased the Bcl-2 level (0.55 ± 0.04 vs. 0.34 ± 0.05, p < 0.05) and decreased the level of Bax (0.46 ± 0.03 vs. 0.68 ± 0.04, p < 0.05), caspase-3 (0.49 ± 0.03 vs. 0.69 ± 0.04, p < 0.05). However, we did not observe any difference between the DEX1 and DEX2 groups for these (p > 0.05). Conclusion: Dexmedetomidine preconditioning has a protective effect against lung injury caused by hemorrhagic shock in rats. The potential mechanisms involved are the inhibition of cell death and improvement of antioxidation. But did not show a dose-dependent effect.
Published: 2019
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5. Corrigendum: Mechanism and Management of Fentanyl-Induced Cough

Author: Rong Chen, Ling-hua Tang, Tao Sun, Zi Zeng, Yun-yan Zhang, Ke Ding, and Qing-tao Meng
Subjects: adverse drug reactions, opioids, pharmacology, prevention, therapeutics, Therapeutics. Pharmacology, RM1-950
Published: 2020
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6. Gastrointestinal Symptoms Associated With Unfavorable Prognosis of COVID-19 Patients: A Retrospective Study

Author: Rong Chen, Yan-li Yu, Wei Li, Ya Liu, Jing-xiao Lu, Fangyue Chen, Qin Zhou, Zhong-yuan Xia, Ling Gao, Qing-tao Meng, and Daqing Ma
Subjects: gastrointestinal symptoms, COVID-19, prognosis, SARS-CoV-2 (COVID-19), ARDS (acute respiratory distress syndrome), Medicine (General), R5-920
Abstract: Background and Aim: The global pandemic of COVID-19 has posed an enormous threat to the economy and people's lives across various countries. Patients with COVID-19 most commonly present with respiratory symptoms. However, gastrointestinal (GI) symptoms can also occur. We aimed to study the relationship between GI symptoms and disease prognosis in patients with COVID-19.Methods: In a single-center and retrospective cohort study, the outcomes in COVID-19 patients with or without GI symptoms were compared. The propensity score is a conditional probability of having a particular exposure (COVID-19 patients with GI symptoms vs. without GI symptoms) given a set of baseline measured covariates. Survival was estimated using the Kaplan-Meier method, and any differences in survival were evaluated with a stratified log-rank-test. To explore the GI symptoms associated with ARDS, non-invasive ventilator treatment, tracheal intubation, tracheotomy, and CRRT, univariable and multivariable COX regression models were used.Results: Among 1,113 eligible patients, 359 patients with GI symptoms and 718 without GI symptoms had similar propensity scores and were included in the analyses. Patients with GI symptoms, as compared with those without GI symptoms, were associated with a similar risk of death, but with higher risks of ARDS, non-invasive mechanical ventilation in COVID-19 patients, respectively.Conclusions: The presence of GI symptoms was associated with a high risk of ARDS, non-invasive mechanical ventilation and tracheal intubation in patients with COVID-19 but not mortality.
Published: 2020
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7. Mechanism and Management of Fentanyl-Induced Cough

Author: Rong Chen, Ling-hua Tang, Tao Sun, Zi Zeng, Yun-yan Zhang, Ke Ding, and Qing-tao Meng
Subjects: adverse drug reactions, opioids, pharmacology, prevention, therapeutics, Therapeutics. Pharmacology, RM1-950
Abstract: Fentanyl-induced cough (FIC) often occurs after intravenous bolus administration of fentanyl analogs during induction of general anesthesia and analgesia procedure. The cough is generally benign, but sometimes it causes undesirable side effects, including elevated intra-abdominal, intracranial or intraocular pressure. Therefore, understanding the related mechanisms and influencing factors are of great significance to prevent and treat the cough. This paper reviews the molecular mechanism, influencing factors and preventive administration of FIC, focusing on the efficacy and side effects of various drugs in inhibiting FIC to provide some medical reference for anesthesiologists.
Published: 2020
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8. Role of adiponectin in diabetes myocardial ischemia-reperfusion injury and ischemic postconditioning

Author: Chen Cao, Hui-min Liu, Wei Li, Yang Wu, Yan Leng, Rui Xue, Rong Chen, Ling-hua Tang, Qian Sun, Zhongyuan Xia, Qi-zhu Tang, Di-fei Shen, and Qing-tao Meng
Subjects: Adiponectin, Diabetes, Reperfusion Injury, Ischemic Postconditioning, Surgery, RD1-811
Abstract: Abstract Purpose Patients with diabetes are vulnerable to myocardial I/R (ischaemia/reperfusion) injury, but are not responsive to IPO (ischaemic post-conditioning). We hypothesized that decreased cardiac Adiponectin (APN) is responsible for the loss of diabetic heart sensitivity to IPO cardioprotecton. Methods Diabetic rats were subjected to I/R injury (30 min of LAD occlusion followed by 120 min of reperfusion). Myocardial infarct area was determined by TTC staining. Cardiac function was monitored by a microcatheter. ANP, 15-F2t-isoprostane, nitrotyrosine and MDA were measured by assay kits. Levels of p-Akt, total-Akt and GAPDH were determined by Western Blot. Results Diabetic rats subjected to myocardial IR exhibited severe myocardial infarction and oxidative stress injury, lower APN in the plasma and cardiac p-Akt expression ( P
Published: 2020
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9. Non-canonical Opioid Signaling Inhibits Itch Transmission in the Spinal Cord of Mice

Author: Admire Munanairi, Xian-Yu Liu, Devin M. Barry, Qianyi Yang, Jun-Bin Yin, Hua Jin, Hui Li, Qing-Tao Meng, Jia-Hang Peng, Zhen-Yu Wu, Jun Yin, Xuan-Yi Zhou, Li Wan, Ping Mo, Seungil Kim, Fu-Quan Huo, Joseph Jeffry, Yun-Qing Li, Rita Bardoni, Michael R. Bruchas, and Zhou-Feng Chen
Subjects: Biology (General), QH301-705.5
Abstract: Summary: Chronic itch or pruritus is a debilitating disorder that is refractory to conventional anti-histamine treatment. Kappa opioid receptor (KOR) agonists have been used to treat chronic itch, but the underlying mechanism remains elusive. Here, we find that KOR and gastrin-releasing peptide receptor (GRPR) overlap in the spinal cord, and KOR activation attenuated GRPR-mediated histamine-independent acute and chronic itch in mice. Notably, canonical KOR-mediated Gαi signaling is not required for desensitizing GRPR function. In vivo and in vitro studies suggest that KOR activation results in the translocation of Ca2+-independent protein kinase C (PKC)δ from the cytosol to the plasma membrane, which in turn phosphorylates and inhibits GRPR activity. A blockade of phospholipase C (PLC) in HEK293 cells prevented KOR-agonist-induced PKCδ translocation and GRPR phosphorylation, suggesting a role of PLC signaling in KOR-mediated GRPR desensitization. These data suggest that a KOR-PLC-PKCδ-GRPR signaling pathway in the spinal cord may underlie KOR-agonists-induced anti-pruritus therapies. : Munanairi et al. show that the kappa opioid receptor (KOR) agonists inhibit nonhistaminergic itch transmission by attenuating the function of the gastrin-releasing peptide receptor (GRPR), an itch receptor in the spinal cord. KOR activation causes the translocation of PKCδ from plasma to membrane, which phosphorylates GRPR to dampen itch transmission. Keywords: KOR, GRPR, itch, PKC, phosphorylation, GPCR cross-signaling, spinal cord, mouse
Published: 2018
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10. Dexmedetomidine preconditioning protects against lipopolysaccharides-induced injury in the human alveolar epithelial cells

Author: Lei Zhang, Xian-Jin Zhou, Li-Ying Zhan, Xiao-Jing Wu, Wen-Lan Li, Bo Zhao, Qing-Tao Meng, and Zhong-Yuan Xia
Subjects: Anesthesiology, RD78.3-87.3
Abstract: Background and objectives: Dexmedetomidine (DEX) has demonstrated the preconditioning effect and shown protective effects against organize injury. In this study, using A549 (human alveolar epithelial cell) cell lines, we investigated whether DEX preconditioning protected against acute lung injury (ALI) in vitro. Methods: A549 were randomly divided into four groups (n = 5): control group, DEX group, lipopolysaccharides (LPS) group, and D-LPS (DEX + LPS) group. Phosphate buffer saline (PBS) or DEX were administered. After 2 h preconditioning, the medium was refreshed and the cells were challenged with LPS for 24 h on the LPS and D-LPS group. Then the malondialdehyde (MDA), superoxide dismutase (SOD), Bcl-2, Bax, caspase-3 and the cytochrome c in the A549 were tested. The apoptosis was also evaluated in the cells. Results: Compare with LPS group, DEX preconditioning reduced the apoptosis (26.43% ± 1.05% vs. 33.58% ± 1.16%, p
Published: 2017
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11. Ginsenoside Rb1 Attenuates Intestinal Ischemia Reperfusion Induced Renal Injury by Activating Nrf2/ARE Pathway

Author: Zhong-Yuan Xia, Qian Sun, Ying Jiang, and Qing-Tao Meng
Subjects: ginsenoside Rb1, NF-E2-related factor-2, renal injury, intestinal ischemia reperfusion, ho-1, Organic chemistry, QD241-441
Abstract: Intestinal ischemia reperfusion (IIR) is a serious clinical condition associated with simultaneous multiple organ dysfunction. The aim of this study was to investigate the effects of ginsenoside Rb1 on IIR induced renal injury in mice. An intestinal ischemia reperfusion mouse model was established by superior mesenteric artery (SMA) occlusion for 45 min, followed by reperfusion for 2 h. IIR induced renal injury characterized by increase of BUN, Cr and NGAL in serum, MDA levels and decrease of SOD levels in the renal tissues. Ginsenoside Rb1 (30, 60 mg/kg) given intraperitoneally before reperfusion attennuated renal injury, which was associated with decrease of BUN, Cr and NGAL in serum, MDA levels and increase of SOD levels in the renal tissues. Furthermore, the immunohistochemistry and Western blot data showed that ginsenoside Rb1 dramatically reversed IIR induced renal injury, associated with upregulated nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in renal tissues. Our data suggests that ginsenoside Rb1 attenuates acute renal injury induced by intestinal ischemia reperfusion by activating the Nrf2/ARE pathway.
Published: 2012
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12. Impact of renal dysfunction on mid-term outcome after transcatheter aortic valve implantation: a systematic review and meta-analysis.

Author: Chi Chen, Zhen-Gang Zhao, Yan-Biao Liao, Yong Peng, Qing-Tao Meng, Hua Chai, Qiao Li, Xiao-Lin Luo, Wei Liu, Chen Zhang, Mao Chen, and De-Jia Huang
Subjects: Medicine, Science
Abstract: There is conflicting evidence regarding the impact of preexisting renal dysfunction (RD) on mid-term outcomes after transcatheter aortic valve implantation (TAVI) in patients with symptomatic aortic stenosis (AS).Forty-seven articles representing 32,131 patients with AS undergoing a TAVI procedure were included in this systematic review and meta-analysis. Pooled analyses were performed with both univariate and multivariate models, using a fixed or random effects method when appropriate. Compared with patients with normal renal function, mid-term mortality was significantly higher in patients with preexisting RD, as defined by the author (univariate hazard ratio [HR]: 1.69; 95% confidence interval [CI]: 1.50-1.90; multivariate HR: 1.47; 95% CI: 1.17-1.84), baseline estimated glomerular filtration rate (eGFR) (univariate HR: 1.65; 95% CI: 1.47-1.86; multivariate HR: 1.46; 95% CI: 1.24-1.71), and serum creatinine (univariate HR: 1.69; 95% CI: 1.48-1.92; multivariate HR: 1.65; 95% CI: 1.36-1.99). Advanced stage of chronic kidney disease (CKD stage 3-5) was strongly related to bleeding (univariate HR in CKD stage 3: 1.30, 95% CI: 1.13-1.49; in CKD stage 4: 1.30, 95% CI: 1.04-1.62), acute kidney injure (AKI) (univariate HR in CKD stage 3: 1.28, 95% CI: 1.03-1.59; in CKD stage 4: 2.27, 95% CI: 1.74-2.96), stroke (univariate HR in CKD stage 4: 3.37, 95% CI: 1.52-7.46), and mid-term mortality (univariate HR in CKD stage 3: 1.57, 95% CI: 1.26-1.95; in CKD stage 4: 2.77, 95% CI: 2.06-3.72; in CKD stage 5: 2.64, 95% CI: 1.91-3.65) compared with CKD stage 1+2. Patients with CKD stage 4 had a higher incidence of AKI (univariate HR: 1.70, 95% CI: 1.34-2.16) and all-cause death (univariate HR: 1.60, 95% CI: 1.28-1.99) compared with those with CKD stage 3. A per unit decrease in serum creatinine was also associated with a higher mortality at mid-term follow-up (univariate HR: 1.24, 95% CI: 1.18-1.30; multivariate HR: 1.19, 95% CI: 1.08-1.30).Preexisting RD was associated with increased mid-term mortality after TAVI. Patients with CKD stage 4 had significantly higher incidences of peri-procedural complications and a poorer prognosis, a finding that should be factored into the clinical decision-making process regarding these patients.
Published: 2015
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13. Protective effect of ginsenoside Rb1 against intestinal ischemia-reperfusion induced acute renal injury in mice.

Author: Qian Sun, Qing-tao Meng, Ying Jiang, Hui-min Liu, Shao-qing Lei, Wa-ting Su, Wei-na Duan, Yang Wu, Zheng-yuan Xia, and Zhong-yuan Xia
Subjects: Medicine, Science
Abstract: Ginsenoside Rb1 (RB1), the most clinically effective constituent of ginseng, possesses a variety of biological activities. The objectives of this study were to investigate the protective effects of RB1 and its underlying mechanism on renal injury induced by intestinal ischemia-reperfusion (IIR) in mice. RB1 was administered prior to inducing IIR achieved by occluding the superior mesenteric artery for 45 min followed by 120 min of reperfusion. All-trans-retinoic acid (ATRA) was used as an inhibitor of NF-E2-related factor-2 (Nrf2) signaling. Adult male C57BL/6J mice were randomly divided into six groups: (1) sham group, (2) IIR group, (3) RB1 group, (4) sham + ATRA group, (5) IIR + ATRA group, and (6) RB1 + ATRA group. Intestinal histology and pathological injury score were observed. Intestinal mucosal injury was also evaluated by measuring serum diamine oxidase (DAO). Renal injury induced by IIR was characterized by increased levels of histological severity score, blood urea nitrogen (BUN), serum creatinine (Scr) and neutrophil gelatinase-associated lipocalin (NGAL), which was accompanied with elevated renal TUNEL-positive cells and the Bcl-2/Bax expression ratio. RB1 significantly reduced renal injury and apoptosis as compared with IIR group, which was reversed by ATRA treatment. Immunohistochemistry and Western blot analysis demonstrated that RB1 significantly upregulated the protein expression of heme oxygenase-1 (HO-1) and Nrf2, which were attenuated by ATRA treatment. Taken together, these results suggest that the protective effects of RB1 pretreatment against renal injury induced by IIR are associated with activation of the Nrf2/ anti-oxidant response element (ARE) pathway.
Published: 2013
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14. Dexmedetomidine preconditioning protects against lipopolysaccharides-induced injury in the human alveolar epithelial cells

Author: Lei Zhang, Xian-Jin Zhou, Li-Ying Zhan, Xiao-Jing Wu, Wen-Lan Li, Bo Zhao, Qing-Tao Meng, and Zhong-Yuan Xia
Subjects: Dexmedetomidine, Lipopolysaccharides, Preconditioning, Acute lung injury, Alveolar epithelial cell, Anesthesiology, RD78.3-87.3
Abstract: Abstract Background and objectives Dexmedetomidine (DEX) has demonstrated the preconditioning effect and shown protective effects against organize injury. In this study, using A549 (human alveolar epithelial cell) cell lines, we investigated whether DEX preconditioning protected against acute lung injury (ALI) in vitro. Methods A549 were randomly divided into four groups (n = 5): control group, DEX group, lipopolysaccharides (LPS) group, and D-LPS (DEX + LPS) group. Phosphate buffer saline (PBS) or DEX were administered. After 2 h preconditioning, the medium was refreshed and the cells were challenged with LPS for 24 h on the LPS and D-LPS group. Then the malondialdehyde (MDA), superoxide dismutase (SOD), Bcl-2, Bax, caspase-3 and the cytochrome c in the A549 were tested. The apoptosis was also evaluated in the cells. Results Compare with LPS group, DEX preconditioning reduced the apoptosis (26.43% ± 1.05% vs. 33.58% ± 1.16%, p < 0.05) in the A549, which is correlated with decreased MDA (12.84 ± 1.05 vs. 19.16 ± 1.89 nmoL.mg-1 protein, p < 0.05) and increased SOD activity (30.28 ± 2.38 vs. 20.86 ± 2.19 U.mg-1 protein, p < 0.05). DEX preconditioning also increased the Bcl-2 level (0.53 ± 0.03 vs. 0.32 ± 0.04, p < 0.05) and decreased the level of Bax (0.49 ± 0.04 vs. 0.65 ± 0.04, p < 0.05), caspase-3 (0.54 ± 0.04 vs. 0.76 ± 0.04, p < 0.05) and cytochrome c. Conclusion DEX preconditioning has a protective effect against ALI in vitro. The potential mechanisms involved are the inhibition of cell death and improvement of antioxidation.
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15. A deep learning model based on contrast-enhanced computed tomography for differential diagnosis of gallbladder carcinoma

Author: Fei Xiang, Qing-Tao Meng, Jing-Jing Deng, Jie Wang, Xiao-Yuan Liang, Xing-Yu Liu, and Sheng Yan
Subjects: Hepatology, Gastroenterology
Published: 2023

16. Perioperative intravenous S(+)-ketamine for acute postoperative pain in adults: study protocol for a multicentre, randomised, open-label, positive-controlled, pragmatic clinical trial (SAFE-SK-A trial)

Author: Hong Wang, Chong-Yang Duan, Wen-Qi Huang, Ping Zhao, Li-Zhi Zhou, Yan-Hong Liu, Cun-Ming Liu, Hai-Chen Chu, Qiang Wang, Yu-Gang Diao, Zhen Hua, Qing-Tao Meng, Hao Li, Xiao-Ying Zhang, Wei-Dong Mi, and Ping-Yan Chen
Subjects: Adult, Analgesics, Pain, Postoperative, General Medicine, Analgesics, Opioid, Anaesthesia, acute postoperative pain, esketamine, S(+)-ketamine, Humans, Multicenter Studies as Topic, Ketamine, multimodal analgesia, pragmatic clinical trial, Pain Measurement, Randomized Controlled Trials as Topic
Abstract: Introduction Postoperative pain remains incompletely controlled for decades. Recently, multimodal analgesia is emerging as a potential approach in the management of postoperative pain. Therein, S(+)-ketamine is appealing as an adjuvant drug in multimodal analgesia due to its unique pharmacological advantages. This pragmatic clinical trial (SAFE-SK-A trial) is designed to investigate the analgesic effect and safety of S(+)-ketamine for acute postoperative pain in adults and explore the optimal strategy of perioperative intravenous S(+)-ketamine in a real-world setting. Methods and analysis This multicentre, randomised, open-label, positive-controlled, pragmatic clinical trial (SAFE-SK-A study) is planned to conduct in 80 centres from China and recruit a total of 12 000 adult participants undergoing a surgical procedure under general anaesthesia. Patient recruitment started in June 2021 and will end in June 2022. Participants will be randomised in a ratio of 2:1 to either receive perioperative intravenous S(+)-ketamine plus conventional anaesthesia or conventional anaesthesia only. Given the pragmatic nature of the study, no specific restriction as to the administration dosage, route, time, synergistic regimen or basic analgesics. Primary endpoints are the area under the broken line of Numerical Rating Scale (NRS) scores for pain intensity and the total opioid consumption within 48 hours postoperative. Secondary endpoints are postoperative NRS scores, the anaesthesia recovery time, time of first rescue analgesia, the incidence of rescue analgesia, the incidence of postoperative delirium, patient questionnaire for effect, changes from baseline in cognitive function and anxiety and depression, as well as the adverse events and pharmacoeconomic outcomes. The general linear model will be used for the primary endpoint, and appropriate methods will be used for the secondary endpoints. Ethics and dissemination This trial has been approved by the local Institutional Review Board (S2021-026-02) and conducted following the Declaration of Helsinki. Results of this trial will be publicly disclosed and published in scientific journals. Trial registration number NCT04837170; Pre-results.
Published: 2021

17. Author response: BNP facilitates NMB-encoded histaminergic itch via NPRC-NMBR crosstalk

Author: Juan Liu, Xue-Ting Liu, Xian-Yu Liu, Qing-Tao Meng, Admire Munanairi, Devin M Barry, Benlong Liu, Hua Jin, Yu Sun, Qianyi Yang, Fang Gao, Li Wan, Jiahang Peng, Jin-Hua Jin, Kai-Feng Shen, Ray Kim, Jun Yin, Ailin Tao, and Zhou-Feng Chen
Published: 2021

18. Comparison of the levels of depression and anxiety in elderly aortic stenosis patients treated with surgical or transcatheter aortic valve replacement

Author: Jiao Sun, Qing-Tao Meng, Yu-Wei Wang, Wei-Long Zhao, Feng-Zhi Sun, Ji-Hong Liu, and Ji-Yi Liu
Subjects: Pulmonary and Respiratory Medicine, Heart Valve Prosthesis Implantation, Frailty, Depression, General Medicine, Aortic Valve Stenosis, Anxiety, Transcatheter Aortic Valve Replacement, Treatment Outcome, Risk Factors, Aortic Valve, Quality of Life, Humans, Surgery, Prospective Studies, Cardiology and Cardiovascular Medicine, Aged
Abstract: Objective Currently, only a few studies have been conducted on the mental status recovery in elderly aortic stenosis (AS) patients after treatment. How transcatheter aortic valve replacement (TAVR) and surgical aortic valve replacement (SAVR) differentially impinge on the mental status of elderly AS patients is completely unknown. The present prospective study aims to investigate this question by comparing the post-treatment levels of depression and anxiety, quality of life and frailty. Methods A total of 120 elderly patients (age above 70) with symptomatic AS were included, where 78 of them were treated with TAVR and 42 of them were treated with SAVR. Levels of depression and anxiety, quality of life and frailty were assessed by the Chinese version of Hospital Anxiety and Depression Scale (HADS), World Health Organization Quality of Life Instrument-Older Adults Module (WHOQOL-OLD) and clinical frailty scale, respectively. Scores were recorded and compared at admission, 1 month, 4 months and 8 months after treatment. Results Before treatment, both patient groups had similar baseline characteristics and all mental parameters. During the follow-up period, patients in the TAVR group demonstrated significant improvement in all assessed mental parameters to certain extent compared to the SAVR group. Specifically, frailty was significantly improved in the TAVR-treated patients at all three follow-up time points. Levels of depression and anxiety were significantly improved 8 months after treatment, although the remaining patient number is limited. Quality of life was only significantly improved 1 month after treatment. Conclusion TAVR may provide a better mental recovery outcome in elderly AS patients.
Published: 2021

19. Ischemic postconditioning attenuates acute kidney injury following intestinal ischemia‐reperfusion through Nrf2‐regulated autophagy, anti‐oxidation, and anti‐inflammation in mice

Author: Wei Li, Daqing Ma, Hui-min Liu, Qing-Tao Meng, Yang Wu, Yun-Yan Zhang, Zi Zeng, Chen Cao, Zhongyuan Xia, and Rong Chen
Subjects: Male, 0301 basic medicine, NF-E2-Related Factor 2, Renal function, Inflammation, Pharmacology, medicine.disease_cause, Biochemistry, Mice, 03 medical and health sciences, 0302 clinical medicine, Downregulation and upregulation, medicine.artery, Autophagy, Genetics, medicine, Animals, Superior mesenteric artery, Ischemic Postconditioning, Molecular Biology, Kidney, business.industry, Acute kidney injury, Acute Kidney Injury, medicine.disease, Intestines, Mice, Inbred C57BL, 030104 developmental biology, medicine.anatomical_structure, Reperfusion Injury, Heme Oxygenase (Decyclizing), Reperfusion, medicine.symptom, business, 030217 neurology & neurosurgery, Oxidative stress, Biotechnology
Abstract: Intestinal ischemia-reperfusion (IIR) often occurs during and following major cardiovascular or gut surgery and causes significant organ including kidney injuries. This study was to investigate the protective effect of intestinal ischemic postconditioning (IPo) on IIR-induced acute kidney injury (AKI) and the underling cellular signaling mechanisms with focus on the Nrf2/HO-1. Adult C57BL/6J mice were subjected to IIR with or without IPo. IIR was established by clamping the superior mesenteric artery (SMA) for 45 minutes followed by 120 minutes reperfusion. Outcome measures were: (i) Intestinal and renal histopathology; (ii) Renal function; (iii) Cellular signaling changes; (iv) Oxidative stress and inflammatory responses. IPo significantly attenuated IIR-induced kidney injury. Furthermore, IPo significantly increased both nuclear Nrf2 and HO-1 expression in the kidney, upregulated autophagic flux, inhibited IIR-induced inflammation and reduced oxidative stress. The protective effect of IPo was abolished by the administration of Nrf2 inhibitor (Brusatol) or Nrf2 siRNA. Conversely, a Nrf2 activator t-BHQ has a similar protective effect to that of IPo. Our data indicate that IPo protects the kidney injury induced by IIR, which was likely mediated through the Nrf2/HO-1 cellular signaling activation.
Published: 2020

20. BNP facilitates NMB-encoded histaminergic itch via NPRC-NMBR crosstalk

Author: Juan Liu, Xue-Ting Liu, Xian-Yu Liu, Qing-Tao Meng, Admire Munanairi, Devin M Barry, Benlong Liu, Hua Jin, Yu Sun, Qianyi Yang, Fang Gao, Li Wan, Jiahang Peng, Jin-Hua Jin, Kai-Feng Shen, Ray Kim, Jun Yin, Ailin Tao, and Zhou-Feng Chen
Subjects: Male, Mouse, QH301-705.5, Neurokinin B, Science, NPRC, NPRA, General Biochemistry, Genetics and Molecular Biology, Mice, Ganglia, Spinal, Natriuretic Peptide, Brain, Animals, Humans, itch, Biology (General), General Immunology and Microbiology, General Neuroscience, Pruritus, spinal cord, General Medicine, Mice, Inbred C57BL, HEK293 Cells, Medicine, GRP, Receptors, Atrial Natriuretic Factor, hormones, hormone substitutes, and hormone antagonists, Histamine, Signal Transduction, Research Article, Neuroscience, BNP
Abstract: Histamine-dependent and -independent itch is conveyed by parallel peripheral neural pathways that express gastrin-releasing peptide (GRP) and neuromedin B (NMB), respectively, to the spinal cord of mice. B-type natriuretic peptide (BNP) has been proposed to transmit both types of itch via its receptor NPRA encoded by Npr1. However, BNP also binds to its cognate receptor, NPRC encoded by Npr3 with equal potency. Moreover, natriuretic peptides (NP) signal through the Gi-couped inhibitory cGMP pathway that is supposed to inhibit neuronal activity, raising the question of how BNP may transmit itch information. Here, we report that Npr3 expression in laminae I-II of the dorsal horn partially overlaps with NMB receptor (NMBR) that transmits histaminergic itch via Gq-couped PLCβ-Ca2+ signaling pathway. Functional studies indicate that NPRC is required for itch evoked by histamine but not chloroquine (CQ), a nonhistaminergic pruritogen. Importantly, BNP significantly facilitates scratching behaviors mediated by NMB, but not GRP. Consistently, BNP evoked Ca2+ responses in NMBR/NPRC HEK 293 cells and NMBR/NPRC dorsal horn neurons. These results reveal a previously unknown mechanism by which BNP facilitates NMB-encoded itch through a novel NPRC-NMBR cross-signaling in mice. Our studies uncover distinct modes of action for neuropeptides in transmission and modulation of itch in mice., eLife digest An itch is a common sensation that makes us want to scratch. Most short-term itches are caused by histamine, a chemical that is released by immune cells following an infection or in response to an allergic reaction. Chronic itching, on the other hand, is not usually triggered by histamine, and is typically the result of neurological or skin disorders, such as atopic dermatitis. The sensation of itching is generated by signals that travel from the skin to nerve cells in the spinal cord. Studies in mice have shown that the neuropeptides responsible for delivering these signals differ depending on whether or not the itch involves histamine: GRPs (short for gastrin-releasing proteins) convey histamine-independent itches, while NMBs (short for neuromedin B) convey histamine-dependent itches. It has been proposed that another neuropeptide called BNP (short for B-type natriuretic peptide) is able to transmit both types of itch signals to the spinal cord. But it remains unclear how this signaling molecule is able to do this. To investigate, Meng, Liu, Liu, Liu et al. carried out a combination of behavioral, molecular and pharmacological experiments in mice and nerve cells cultured in a laboratory. The experiments showed that BNP alone cannot transmit the sensation of itching, but it can boost itching signals that are triggered by histamine. It is widely believed that BNP activates a receptor protein called NPRA. However, Meng et al. found that the BNP actually binds to another protein which alters the function of the receptor activated by NMBs. These findings suggest that BNP modulates rather than initiates histamine-dependent itching by enhancing the interaction between NMBs and their receptor. Understanding how itch signals travel from the skin to neurons in the spinal cord is crucial for designing new treatments for chronic itching. The work by Meng et al. suggests that treatments targeting NPRA, which was thought to be a key itch receptor, may not be effective against chronic itching, and that other drug targets need to be explored.
Published: 2021

21. Ischemic post-conditioning promotes mitochondrial translocation of DJ-1 and stabilizes binding to Bcl- xL to attenuate myocardial ischemic-reperfusion injury in STZ-induced diabetic rats

Author: Yan Leng, Rui Xue, Yonghong Xiong, Wen-Yuan Li, Rong Cheng, Zhong-Yuan Xia, Wei Li, and Qing-Tao Meng
Subjects: Myocardial Ischemic Reperfusion Injury, biology, business.industry, Mitochondrial translocation, biology.protein, Post conditioning, Medicine, Bcl-xL, Pharmacology, business
Abstract: Background Ischemic post-conditioning (IPO) is a strategy in reducing myocardial ischemic-reperfusion (I/R) injury, but its specific molecular mechanism is incompletely understood. Deletions or mutations in the DJ-1 gene are directly linked to the cardiovascular system. DJ-1 plays a critical role in regulating mitochondrial homeostasis in response to stress through translocation of DJ-1 from the cytoplasm into the nucleus. Meanwhile, how the DJ-1 is removed in myocardial I/R injury and regulating apoptosis is needed to further verified. Given the discovery mentioned above, we hypothesize that DJ-1 translocate to mitochondria recover IPO induced cardioprotection in STZ-induced diabetic rats. To evaluate our hypothesis, we overexpressed the DJ-1 protein under high glucose condition, subjected IPO or not. And then measure the expression of DJ-1 in mitochondria and cytoplasm after myocardial I/R. Results We found that DJ-1 translocated to mitochondria combined with Bcl-xL was reduced cardiomyocyte injury and apoptosis in diabetic myocardial I/R heart. Additionally, the binding of DJ-1 and Bcl-xL is dependent on the oxidative state of DJ-1(oxidation of DJ-1 at Cys-106 is important for its protective effect). Conclusions If our hypothesis is correct, promote DJ-1 mitochondrial transfer may be critical with respect to restoring myocardial responsiveness to IPO in diabetes.
Published: 2021

22. Incidence and Associated Factors for Neuraxial Anaesthesia-Related Hypotension in COVID-19 Parturients Undergoing Caesarean Delivery: A Multicenter Case-Control Study

Author: Qin Zhou, Xiangdong Chen, Min Wei, Yuan Gong, Chen Cao, Hui-hui Cheng, Qing-tao Meng, Rong Chen, Zhong-yuan Xia, and Yuan Zhang
Subjects: Coronavirus disease 2019 (COVID-19), business.industry, Anesthesia, Incidence (epidemiology), Caesarean delivery, Case-control study, Medicine, business
Abstract: Background: COVID-19 continues to spread globally and results in additional challenges for perioperative management in parturients. The purpose of this study was to determine the incidence and identify associated factors for neuraxial anaesthesia-related hypotension in COVDI-19 parturients during caesarean delivery.Methods: We performed a multicenter case-control study at 3 medical institutions in Hubei province, China form 1th January to 30th May 2020. All ASA Physical Status II full termed pregnant women who received caesarean delivery under neuraxial anaesthesia were eligible for inclusion. The univariate analysis and binary logistic regression analysis were used to identified the independent predictors of neuraxial anaesthesia-related hypotension.Results: Present study included 102 COVID-19 parturients. The incidence of neuraxial anaesthesia-related hypotension was 58%. Maternal abnormal lymphocyte count (OR = 3.41, p = 0.03), full stomach (OR = 3.22, p = 0.04), baseline heart rate (OR = 1.04, p = 0.03), experience of anaesthetist (OR = 0.86, p = 0.02) and surgeon (OR = 0.76, p = 0.03), and combined spinal-epidural anaesthesia technique (OR = 3.27, p = 0.02) were associated with neuraxial anaesthesia-related hypotension. The area under the receiver operating characteristic curve achieved 0.83 which was significantly higher than 0.5 (p < 0.001). And the sensitivity, specificity and percentage correct were 75%, 79% and 75%, respectively. The Hosmer-Lemeshow test showed a good calibration of the model (H = 2.01, DF = 8, p = 0.98).Conclusions: Maternal abnormal lymphocyte count, full stomach, baseline heart rate, experience of anaesthetist and surgeon, and combined spinal-epidural anaesthesia technique were identified as the independent predictors of neuraxial anaesthesia-related hypotension.
Published: 2021

23. Dexmedetomidine preconditioning protects against lung injury in hemorrhagic shock rats

Author: Qian-Qian Qiao, Lei Zhang, Qing-Tao Meng, Zhongyuan Xia, Yi-Fan Jia, Ling-Hua Tang, Wei Wang, and Xue-Shan Bu
Subjects: Male, Resuscitation, medicine.medical_specialty, medicine.medical_treatment, Apoptosis, Preconditioning, Lung injury, Shock, Hemorrhagic, Protective Agents, lcsh:RD78.3-87.3, Rats, Sprague-Dawley, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, 030202 anesthesiology, Anesthesiology, Medicine, Animals, RD78.3-87.3, Dexmedetomidine, Saline, Lung, medicine.diagnostic_test, Dose-Response Relationship, Drug, business.industry, General Medicine, Malondialdehyde, Rats, Disease Models, Animal, Bronchoalveolar lavage, medicine.anatomical_structure, chemistry, lcsh:Anesthesiology, Anesthesia, Hemorrhagic shock, Rat, Histopathology, business, Bronchoalveolar Lavage Fluid, medicine.drug
Abstract: Background and objectives: Dexmedetomidine has demonstrated protective effects against lung injury in vitro. Here, we investigated whether dexmedetomidine preconditioning protected against lung injury in hemorrhagic shock rats. Methods: Male Sprague-Dawley rats were randomly divided into four groups (n = 8): control group, hemorrhagic shock group, 5 ug.kg−1 dexmedetomidine (DEX1) group, and 10 ug.kg−1 dexmedetomidine (DEX2) group. Saline or dexmedetomidine were administered over 20 min. 30 min after injection, hemorrhage was initiated in the hemorrhagic shock, DEX1 and DEX2 group. Four hours after resuscitation, protein and cellular content in bronchoalveolar lavage fluid, and the lung histopathology were measured. The malondialdehyde, superoxide dismutase, Bcl-2, Bax and caspase-3 were also tested in the lung tissue. Results: Compare with hemorrhagic shock group, 5 ug.kg−1 dexmedetomidine pretreatment reduced the apoptosis (2.25 ± 0.24 vs. 4.12 ± 0.42%, p 0.05). Conclusion: Dexmedetomidine preconditioning has a protective effect against lung injury caused by hemorrhagic shock in rats. The potential mechanisms involved are the inhibition of cell death and improvement of antioxidation. But did not show a dose-dependent effect. Resumo: Justificativa e objetivos: Dexmedetomidina demonstrou efeitos protetores contra a lesão pulmonar in vitro. Neste estudo, investigamos se o pré-condicionamento com dexmedetomidina protege contra a lesão pulmonar em ratos com choque hemorrágico. Métodos: Ratos machos, Sprague-Dawley, foram aleatoriamente divididos em quatro grupos (n = 8): grupo controle, grupo com choque hemorrágico, grupo com 5 μg.kg−1 de dexmedetomidina (DEX1) e grupo com 10 μg.kg−1 de dexmedetomidina (DEX2). Solução salina ou dexmedetomidina foi administrada durante 20 minutos. Trinta minutos após a injeção, a hemorragia foi iniciada nos grupos choque hemorrágico, DEX1 e DEX2. Quatro horas após a ressuscitação, a proteína e o conteúdo celular no lavado broncoalveolar e a histopatologia pulmonar foram medidos. Malondialdeído, superóxido dismutase, Bcl-2, Bax e caspase-3 também foram testados no tecido pulmonar. Resultados: Na comparação com o grupo choque hemorrágico, o pré-tratamento com 5 ug.kg−1 de dexmedetomidina reduziu a apoptose (2,25 ± 0,24 vs. 4,12 ± 0,42%, p 0,05). Conclusão: O pré-condicionamento com dexmedetomidina tem um efeito protetor contra a lesão pulmonar causada por choque hemorrágico em ratos. Os potenciais mecanismos envolvidos são a inibição da morte celular e a melhora da antioxidação. Porém, não mostrou um efeito dose-dependente. Keywords: Dexmedetomidine, Hemorrhagic shock, Preconditioning, Lung injury, Rat, Palavras-chave: Dexmedetomidina, Choque hemorrágico, Pré-condicionamento, Lesão pulmonar, Rato
Published: 2019

24. Pré‐condicionamento com dexmedetomidina protege contra lesão pulmonar em ratos com choque hemorrágico

Author: Qian-Qian Qiao, Lei Zhang, Yi-Fan Jia, Wei Wang, Zhongyuan Xia, Xue-Shan Bu, Ling-Hua Tang, and Qing-Tao Meng
Subjects: 03 medical and health sciences, 0302 clinical medicine, Anesthesiology and Pain Medicine, 030202 anesthesiology
Abstract: Resumo Justificativa e objetivos Dexmedetomidina demonstrou efeitos protetores contra a lesao pulmonar in vitro. Neste estudo, investigamos se o pre‐condicionamento com dexmedetomidina protege contra a lesao pulmonar em ratos com choque hemorragico. Metodos Ratos machos, Sprague‐Dawley, foram aleatoriamente divididos em quatro grupos (n = 8): grupo controle, grupo com choque hemorragico, grupo com 5 μg.kg−1 de dexmedetomidina (DEX1) e grupo com 10 μg.kg−1 de dexmedetomidina (DEX2). Solucao salina ou dexmedetomidina foi administrada durante 20 minutos. Trinta minutos apos a injecao, a hemorragia foi iniciada nos grupos choque hemorragico, DEX1 e DEX2. Quatro horas apos a ressuscitacao, a proteina e o conteudo celular no lavado broncoalveolar e a histopatologia pulmonar foram medidos. Malondialdeido, superoxido dismutase, Bcl‐2, Bax e caspase‐3 tambem foram testados no tecido pulmonar. Resultados Na comparacao com o grupo choque hemorragico, o pre‐tratamento com 5 ug.kg−1 de dexmedetomidina reduziu a apoptose (2,25 ± 0,24 vs. 4,12 ± 0,42%, p 0,05). Conclusao O pre‐condicionamento com dexmedetomidina tem um efeito protetor contra a lesao pulmonar causada por choque hemorragico em ratos. Os potenciais mecanismos envolvidos sao a inibicao da morte celular e a melhora da antioxidacao. Porem, nao mostrou um efeito dose‐dependente.
Published: 2019

25. Diosgenin inhibited the expression of TAZ in hepatocellular carcinoma

Author: Zhize Chen, Shaoqing Lei, Yang Wu, Jingjing Xu, Qing-Tao Meng, Zhongyuan Xia, and Hui-min Liu
Subjects: 0301 basic medicine, Carcinoma, Hepatocellular, Biophysics, Antineoplastic Agents, Apoptosis, Diosgenin, Biochemistry, Structure-Activity Relationship, 03 medical and health sciences, chemistry.chemical_compound, 0302 clinical medicine, Transcription (biology), medicine, Humans, Molecular Biology, Cell Proliferation, Wound Healing, Hippo signaling pathway, Dose-Response Relationship, Drug, Cell growth, Liver Neoplasms, Cell migration, Cell Cycle Checkpoints, Hep G2 Cells, Cell Biology, medicine.disease, 030104 developmental biology, chemistry, 030220 oncology & carcinogenesis, Hepatocellular carcinoma, Cancer research, Drug Screening Assays, Antitumor, Liver cancer, Acyltransferases, Transcription Factors
Abstract: Emerging evidence has supported that TAZ (transcriptional co-activator with PDZ binding motif), one transcription co-activator in Hippo signaling pathway, plays an oncogenic role in liver carcinogenesis. Targeting TAZ could be a potential therapeutic approach for liver cancer patients. In the current study, we aim to determine whether diosgenin could be an inhibitor of TAZ in liver cancer cells. We found that diosgenin inhibited the expression of TAZ in liver cancer cells. Moreover, we found that diosgenin inhibited cell growth, induced apoptosis, suppressed cell migration and invasion in part via inhibition of TAZ in liver cancer cells. Our study provides the evidence to support that diosgenin could be a potential agent for treating human liver cancer.
Published: 2018

26. BNP facilitates NMB-mediated histaminergic itch via NPRC-NMBR crosstalk

Author: Jun Yin, Ailin Tao, Admire Munanairi, Kai-Feng Shen, Devin M. Barry, Yu Sun, Hua Jin, Xian-Yu Liu, Qianyi Yang, Qing-Tao Meng, Jin-Hua Jin, Zhou-Feng Chen, Raymond J. Kim, Xue-Ting Liu, and Li Wan
Subjects: medicine.drug_class, HEK 293 cells, Histaminergic, Neuropeptide, Neuromedin B receptor, Pharmacology, chemistry.chemical_compound, chemistry, Gastrin-releasing peptide, Natriuretic peptide, medicine, skin and connective tissue diseases, Receptor, hormones, hormone substitutes, and hormone antagonists, Histamine
Abstract: B-type natriuretic peptide (BNP) binds to its two cognate receptors NPRA and NPRC, encoded by Npr1 and Npr3, respectively, with equal potency and both are expressed in the spinal cord. Moreover, natriuretic peptides (NP) signal through the inhibitory cGMP pathway, raising the question of how BNP may transmit itch information. We report that Npr3 is highly restricted to laminae I-II of the dorsal horn, and partially overlaps with neuromedin B receptor (NMBR) that encodes histaminergic itch. Functional studies indicate that NPRC is required for itch evoked by histamine but not chloroquine (CQ), a nonhistaminergic pruritogen. Importantly, BNP significantly facilitates scratching behaviors mediated by NMB, but not gastrin releasing peptide (GRP) that encodes nonhistaminergic itch. Consistently, BNP evoked Ca2+ response in NMBR/NPRC HEK 293 cells and BNP-saporin that ablated both Npr1 and Npr3 neurons impaired histamine-, but not CQ-evoked, itch. These results reveal a previously unknown mechanism by which BNP changes its inhibitory mode of action to the facilitation of itch through a novel NPRC-NMBR cross-talk. Our studies suggest that neuropeptides encode histaminergic and nonhistaminergic itch not only through distinct modes but also in synergy.
Published: 2021

27. Avoiding health worker infection and containing the coronavirus disease 2019 pandemic: Perspectives from the frontline in Wuhan

Author: Shan Tang, Shi Zhang, Zhongyuan Xia, Xiao-liang Chen, Rong Chen, Hui-min Liu, Wei Li, Yong Xiong, Qing-Tao Meng, and Ling-Hua Tang
Subjects: Government, business.industry, Victory, Outbreak, General Medicine, Dilemma, 03 medical and health sciences, 0302 clinical medicine, 030220 oncology & carcinogenesis, Environmental health, Pandemic, Infection control, Medicine, 030211 gastroenterology & hepatology, Surgery, China, business, Personal protective equipment
Abstract: Coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has caused great public concern worldwide due to its high rates of infectivity and pathogenicity. The Chinese government responded in a timely manner, alleviated the dilemma, achieved a huge victory and lockdown has now been lifted in Wuhan. However, the outbreak has occurred in more than 200 other countries. Globally, as of 9:56 am CEST on 19 May 2020, there have been 4,696,849 confirmed cases of COVID-19, including 315,131 deaths, reported to Word Health Organization (WHO). The spread of COVID-19 overwhelmed the healthcare systems of many countries and even crashed the fragile healthcare systems of some. Although the situation in each country is different, health workers play a critical role in the fight against COVID-19. In this review, we highlight the status of health worker infections in China and other countries, especially the causes of infection in China and the standardised protocol to protect health workers from the perspective of an anaesthesiologist, in the hope of providing references to reduce medical infections and contain the COVID-19 epidemic.
Published: 2020
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28. Anaesthetic managment and clinical outcomes of parturients with COVID-19: a multicentre, retrospective, propensity score matched cohort study

Author: Xiangdong Chen, Daqing Ma, Qin Zhou, Hui-hui Cheng, Rong Chen, Yuan Zhang, Yuan Gong, Qing-Tao Meng, Jie Wang, and Zhongyuan Xia
Subjects: Regimen, Neonatal intensive care unit, Nausea, business.industry, Anesthesia, Propensity score matching, Cohort, medicine, General anaesthesia, Chills, Apgar score, medicine.symptom, business
Abstract: ObjectiveTo analyse the clinical features of COVID-19 parturients, and to compare anaesthetic regimen and clinical outcomes in parturients with or without COVID-19 undergoing cesarean delivery.MethodData were extracted from the electronic medical record of 3 medical institutions in Hubei Province, China, from June 1, 2019 to March 20, 2020 according to inclusion and exclusion criteria. After propensity score matching with demographics, the clinical and laboratory characteristics of parturients with or without COVID-19 were analysed. The anaesthetic regimen and clinical outcomes of themselves and their infants were compared in these two groups of parturients.ResultsA total of 1,588 patients without SARS-CoV-2 infection undergoing cesarean delivery were retrospectively included. After achieving a balanced cohort through propensity score matching, 89 patients (COVID-19 group), who were diagnosed with COVID-19 by SARS-CoV-2 nucleic acid test and CT scan matched with 173 patients without COVID-19 (Control group). The SARS-CoV-2 infected parturients in the early stages of COVID-19 outbreak was much more than during the later stage. The main clinical characteristics of parturients with COVID-19 were fever (34.8%), cough (33.7%), an increased plasma CRP (52.8%) and a decreased lymphocyte counting (33.7%). A high rate of emergency and a high incidence of anaesthesia-related complications, such as pharyngalgia, multiple puncture, intraoperative hypotension, nausea, vomiting, vertigo and chills in the COVID-19 parturients. In addition, the parturients with COVID-19 had a long duration of operation and hospital stay, and an increased intraoperative oxytocin utilization and postoperative oxygen therapy. The newborns from the SARS-CoV-2 infected mothers, who received general anaesthesia, had a high risk of Apgar score ≤ 8 at 1 and 5 minutes after delivery and a higher rate of neonatal intensive care unit (NICU) admission.ConclusionsAnaesthesia-related complications occur more frequently in the COVID-19 parturients and their newborns have a high risk of distress.
Published: 2020

29. Safety and efficacy of different anesthetic regimens for parturients with COVID-19 undergoing Cesarean delivery: a case series of 17 patients

Author: Bi-Heng Cheng, Lei Huang, Zhongyuan Xia, Rong Chen, Yuan Zhang, and Qing-Tao Meng
Subjects: Anesthesia, Epidural, medicine.medical_specialty, Infectious Disease Transmission, Patient-to-Professional, medicine.medical_treatment, Pneumonia, Viral, Anesthesia, General, 03 medical and health sciences, 0302 clinical medicine, Pregnancy, 030202 anesthesiology, Anesthesiology, medicine, Humans, Infection control, 030212 general & internal medicine, Pandemics, Retrospective Studies, Asphyxia, Infection Control, Cesarean Section, business.industry, Incidence (epidemiology), Tracheal intubation, Infant, Newborn, COVID-19, Retrospective cohort study, General Medicine, medicine.disease, Treatment Outcome, Anesthesiology and Pain Medicine, Anesthesia, Anesthetic, Female, medicine.symptom, Coronavirus Infections, business, medicine.drug
Abstract: To assess the management and safety of epidural or general anesthesia for Cesarean delivery in parturients with coronavirus disease (COVID-19) and their newborns, and to evaluate the standardized procedures for protecting medical staff.We retrospectively reviewed the cases of parturients diagnosed with severe acute respiratory syndrome coronavirus (SARS-CoV-2) infection disease (COVID-19). Their epidemiologic history, chest computed tomography scans, laboratory measurements, and SARS-CoV-2 nucleic acid positivity were evaluated. We also recorded the patients' demographic and clinical characteristics, anesthesia and surgery-related data, maternal and neonatal complications, as well as the health status of the involved medical staff.The clinical characteristics of 17 pregnant women infected with SARS-CoV-2 were similar to those previously reported in non-pregnant adult patients. All of the 17 patients underwent Cesarean delivery with anesthesia performed according to standardized anesthesia/surgery procedures. Fourteen of the patients underwent continuous epidural anesthesia with 12 experiencing significant intraoperative hypotension. Three patients received general anesthesia with tracheal intubation because emergency surgery was needed. Three of the parturients are still recovering from their Cesarean delivery and are receiving in-hospital treatment for COVID-19. Three neonates were born prematurely. There were no deaths or serious neonatal asphyxia events. All neonatal SARS-CoV-2 nucleic acid tests were negative. No medical staff were infected throughout the patient care period.Both epidural and general anesthesia were safely used for Cesarean delivery in the parturients with COVID-19. Nevertheless, the incidence of hypotension during epidural anesthesia appeared excessive. Proper patient transfer, medical staff access procedures, and effective biosafety precautions are important to protect medical staff from COVID-19.RéSUMé: OBJECTIF: Évaluer la gestion et la sécurité de l’anesthésie péridurale ou de l’anesthésie générale pour un accouchement par césarienne chez des parturientes infectées par la maladie à coronavirus 2019 (COVID-19) et pour leurs nouveau-nés, et évaluer les procédures standardisées visant la protection du personnel médical. MéTHODES: Nous avons revu de manière rétrospective les cas de parturientes ayant un diagnostic de syndrome respiratoire aigu sévère lié à l’infection (SARS-CoV-2) par le coronavirus (COVID-19). L’enquête épidémiologique, leurs examens de tomodensitométrie thoracique, les analyses de laboratoire et leur positivité pour l’acide nucléique du SARS-CoV-2 ont été évalués. Nous avons également consigné les caractéristiques démographiques et cliniques des patientes, les données liées à l’anesthésie et à la chirurgie, les complications maternelles et néonatales, ainsi que l’état de santé du personnel médical concerné. RéSULTATS: Les caractéristiques cliniques des 17 femmes enceintes infectées par le SARS-CoV-2 étaient semblables à celles précédemment rapportées chez des patientes adultes non enceintes. Les 17 patientes ont subi un accouchement par césarienne sous anesthésie effectué selon les procédures standardisées d’anesthésie et de chirurgie. Parmi les quatorze patientes ayant eu une anesthésie péridurale continue, 12 patientes ont présenté une hypotension peropératoire significative. Trois patientes ont accouché sous anesthésie générale avec intubation trachéale, car nécessitant une chirurgie d’urgence. Trois parturientes sont encore en convalescence après leur accouchement par césarienne et reçoivent un traitement à l’hôpital pour la COVID-19. Trois nouveau-nés sont nés prématurément. Il n’y a pas eu de décès ou d’événement asphyxique néonatal grave. Toutes les recherches d’acide nucléique du SARS-CoV-2 chez les nouveau-nés ont été négatives. Aucun membre du personnel médical n’a été infecté pendant la durée des soins aux patientes. CONCLUSIONS: L’anesthésie par péridurale et l’anesthésie générale ont été utilisées sans danger pour l’accouchement par césarienne de parturientes atteintes de COVID-19. Cependant, l’incidence de l’hypotension au cours de l’anesthésie péridurale a paru excessive. Un transfert approprié des patientes, les procédures d’accès du personnel médical et des précautions efficaces de biosécurité sont importants pour protéger le personnel médical contre la COVID-19.
Published: 2020
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30. Ischemic Postconditioning Alleviates Intestinal Ischemia-Reperfusion Injury by Enhancing Autophagy and Suppressing Oxidative Stress through the Akt/GSK-3β/Nrf2 Pathway in Mice

Author: Jia-Nan Lan, Jiabao Hou, Qing-Tao Meng, Yang Wu, Wei Li, Ling-Hua Tang, Zhongyuan Xia, Yun-Yan Zhang, Yan Leng, Qian Sun, Tao Sun, Zi Zeng, Hui-min Liu, and Rong Chen
Subjects: Male, Aging, Article Subject, H&E stain, Ischemia, Pharmacology, medicine.disease_cause, Biochemistry, Mice, GSK-3, medicine, Autophagy, Animals, Ischemic Postconditioning, Protein kinase B, Barrier function, Glycogen Synthase Kinase 3 beta, QH573-671, business.industry, Cell Biology, General Medicine, medicine.disease, Oxidative Stress, Reperfusion Injury, business, Cytology, Reperfusion injury, Proto-Oncogene Proteins c-akt, Oxidative stress, Research Article
Abstract: Aims. Ischemic postconditioning (IPO) has a strong protective effect against intestinal ischemia-reperfusion (IIR) injury that is partly related to autophagy. However, the precise mechanisms involved are unknown. Methods. C57BL/6J mice were subjected to unilateral IIR with or without IPO. After 45 min ischemia and 120 min reperfusion, intestinal tissues and blood were collected for examination. HE staining and Chiu’s score were used to evaluate pathologic injury. We test markers of intestinal barrier function and oxidative stress. Finally, we used WB to detect the expression of key proteins of autophagy and the Akt/GSK-3β/Nrf2 pathway. Results. IPO significantly attenuated IIR injury. Expression levels of LC3 II/I, Beclin-1, and p62 were altered during IIR, indicating that IPO enhanced autophagy. IPO also activated Akt, inhibited GSK-3β, induced Nrf2 nuclear translocation, and upregulated HO-1 and NQO1 expression, thus providing protective effects against IIR injury by suppressing oxidative stress. Consistently, the beneficial effects of IPO were abolished by pretreatment with 3-methyladenine, SC66, and brusatol, potent inhibitors of autophagy, Akt, and Nrf2, respectively. Conclusion. Our study indicates that IPO can ameliorate IIR injury by evoking autophagy, activating Akt, inactivating GSK-3β, and activating Nrf2. These findings may provide novel insights for the alleviation of IIR injury.
Published: 2020

31. Epigenetic modulation of the MAPK pathway prevents isoflurane-induced neuronal apoptosis and cognitive decline in aged rats

Author: Hui‑Hui Cheng, Yao Lv, Qing-Tao Meng, Yun‑Ping Cheng, Sheng‑Lan Mei, Zhongyuan Xia, Lei Huang, and Hai‑Bin Fang
Subjects: 0301 basic medicine, MAPK/ERK pathway, Cancer Research, medicine.medical_specialty, hippocampus, p38 mitogen-activated protein kinases, Morris water navigation task, Biology, cognitive, 03 medical and health sciences, isoflurane, 0302 clinical medicine, Immunology and Microbiology (miscellaneous), Internal medicine, medicine, histone-deacetylase, Cognitive decline, epigenetics, apoptosis, General Medicine, Articles, MAPK, 030104 developmental biology, Endocrinology, Isoflurane, Apoptosis, 030220 oncology & carcinogenesis, Anesthetic, Histone deacetylase, medicine.drug
Abstract: Isoflurane is a broadly used inhalation anesthetic that causes cognitive impairment in rodent models as well as humans. Although previous studies suggested an association between isoflurane exposure and neuro-inflammation, apoptosis and mitochondrial dysfunction, the pathogenesis of isoflurane-induced cognitive decline remains elusive. In the present study, 22-month-old male Sprague-Dawley male rats (n=96) were divided into three groups: Control (Cont), isoflurane (ISO) and MS-275 pre-treated groups. The rats were sacrificed following exposure to isoflurane and a cognitive test. The hippocampus of each animal was harvested for quantitative PCR, TUNEL staining and western blot analysis. Histone deacetylases (HDAC)-1, -2 and -3 exhibited a significant increase at the gene and protein expression levels, whereas negligible mRNA expressions were observed for genes HDAC 4-11 (P>0.05; compared with Cont). Pre-treatment with the HDAC inhibitor MS-275 significantly inhibited the increase in TUNEL-positive cells induced by isoflurane exposure (70.72% decrease; P
Published: 2019

32. Involvement of poly(ADP-ribose) polymerase-1 in development of spinal cord injury in Chinese individuals: a Chinese clinical study

Author: Wei Zhou, Hong-De Yu, Li Jiang, Jing-Bo Shang, Guang Yang, Qing-Tao Meng, Bo Chen, Jing-Xin Nie, and Ren-Bo Li
Subjects: Adult, Male, China, medicine.medical_specialty, Adolescent, Genotype, Poly ADP ribose polymerase, Poly (ADP-Ribose) Polymerase-1, Pharmaceutical Science, poly(ADP-ribose) polymerase-1, Gastroenterology, polymorphism, Clinical study, Young Adult, Asian People, Risk Factors, Internal medicine, Drug Discovery, medicine, Humans, Allele, Spinal cord injury, Spinal Cord Injuries, Original Research, Aged, Pharmacology, Polymorphism, Genetic, Drug Design, Development and Therapy, Plasma samples, business.industry, NF-kappa B, Odds ratio, Middle Aged, medicine.disease, spinal cord injury, Confidence interval, Female, business
Abstract: Qing-Tao Meng,* Guang Yang,* Ren-Bo Li, Jing-Xin Nie, Wei Zhou, Hong-De Yu, Bo Chen, Li Jiang, Jing-Bo Shang Department of Spine Surgery, The Third People’s Hospital of Dalian, Dalian, People’s Republic of China *These authors contributed equally to this work Objective: We aimed to evaluate whether the polymorphism of poly(ADP-ribose) polymerase-1 (PARP-1) is involved as potential risk factor in the development of spinal cord injury (SCI) among Chinese individuals.Patients and methods: Patients with a confirmed diagnosis of SCI (other than traumatic injury) and healthy individuals with no clinical symptoms of SCI were enrolled at Spinal Cord Injury Care Center, The Third People’s Hospital of Dalian, China. Genetic polymorphisms were studied in plasma samples by polymerase chain reaction-restriction fragment length polymorphism assay.Results: A total of 130 Chinese patients with SCI and 130 healthy Chinese individuals were included. We found that patients with the GG genotype (odds ratio [OR]: 4.09, 95% confidence interval [CI] 2.42–6.90, P
Published: 2017

33. Pré‐condicionamento com dexmedetomidina protege contra lesões induzidas por lipopolissacarídeos em células epiteliais alveolares humanas

Author: Lei Zhang, Zhongyuan Xia, Bo Zhao, Liying Zhan, Qing-Tao Meng, Wen-Lan Li, Xian-jin Zhou, and Xiaojing Wu
Subjects: 0301 basic medicine, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Anesthesiology and Pain Medicine, Chemistry, 030220 oncology & carcinogenesis, Alveolar epithelial cell, Molecular biology
Abstract: Resumo Justificativa e objetivos Dexmedetomidina (DEX) demonstrou ter efeito pre‐condicionante e tambem efeitos protetores contra lesao organizada. Neste estudo, com celulas A549 (celulas epiteliais alveolares humanas), investigamos se o pre‐condicionamento com DEX proporcionaria protecao contra lesao pulmonar aguda (LPA) in vitro. Metodos Celulas A549 foram aleatoriamente distribuidas em quatro grupos (n = 5): controle, DEX, lipopolissacarideos (LPS) e D‐LPS (DEX + LPS). Administramos solucao de PBS (tampao fosfato‐alcalino) ou DEX. Apos 2 h de pre‐condicionamento, o meio foi renovado e as celulas desafiadas com LPS por 24 h nos grupos LPS e D‐LPS. Em seguida, malondialdeido (MDA), superoxido dismutase (SOD), Bcl‐2, Bax, caspase‐3 e em A549 foram testados. Apoptose tambem foi avaliada nas celulas. Resultados Em comparacao com o grupo LPS, o pre‐condicionamento com DEX reduziu a apoptose (26,43% ± 1,05% vs. 33,58% ± 1,16%, p Conclusao O pre‐condicionamento com DEX tem efeito protetor contra LPA in vitro. Os potenciais mecanismos envolvidos sao inibicao da morte celular e melhoria da antioxidacao.
Published: 2017

34. Transcription factors Nrf2 and NF-κB contribute to inflammation and apoptosis induced by intestinal ischemia-reperfusion in mice

Author: Qing-Tao Meng, Cheng Chen, Ling-Hua Tang, Qian Sun, Jiabao Hou, Rui Xue, Yang Wu, Rong Chen, Ke Su, Wei Li, Zhongyuan Xia, Yan Leng, and Hui-min Liu
Subjects: 0301 basic medicine, Male, intestinal ischemia/reperfusion, NF-E2-Related Factor 2, Retinoic acid, nuclear factor-κB, Inflammation, Biology, Proinflammatory cytokine, 03 medical and health sciences, chemistry.chemical_compound, Mice, 0302 clinical medicine, brusatol, Genetics, medicine, Animals, Intestinal Mucosa, t-butylhydroquinone, Transcription factor, Oncogene, Activator (genetics), apoptosis, NF-kappa B, NF-κB, General Medicine, Articles, all-trans retinoic acid, Intestines, Mice, Inbred C57BL, Intestinal Diseases, 030104 developmental biology, chemistry, nuclear factor erythroid 2-related factor 2, Apoptosis, 030220 oncology & carcinogenesis, Reperfusion Injury, Cancer research, Cytokines, medicine.symptom
Abstract: Intestinal ischemia/reperfusion (IIR) is a common pathological event associated with intestinal injury and apoptosis with high mortality. Nuclear factor (NF)-E2-related factor-2 (Nrf2) is a key transcription factor that interacts with NF-κB and has a vital anti-inflammatory effect. However, whether Nrf2 has a role in IIR-induced apoptosis and the possible underlining mechanisms, such as modulation of the inflammation regulation pathway, have remained to be fully elucidated. In the present study, IIR was identified to cause significant intestinal injury and apoptosis, with high expression levels of inflammatory cytokines, as well as the apoptotic proteins B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax) and caspase-3, while simultaneously decreasing the protein levels of Bcl-2. The effect was more pronounced after pretreatment of the animals with all-trans retinoic acid or brusatol, potent inhibitors of Nrf2. t-Butylhydroquinone, an Nrf2 activator, significantly attenuated IIR-induced intestinal injury and apoptosis, with inhibition of the overexpression of the inflammatory cytokines, Bax and caspase-3 protein and partial restoration of Bcl-2 protein expression. Taken together, these results indicated that increased Nrf2 expression reduced IIR-induced intestinal apoptosis and that the protective function of Nrf2 may be based on its anti-inflammatory effects through the inhibition of the NF-κB pathway.
Published: 2017

35. BNP facilitates NMB-encoded histaminergic itch via NPRC-NMBR crosstalk.

Author: Qing-Tao Meng, Xian-Yu Liu, Xue-Ting Liu, Juan Liu, Munanairi, Admire, Barry, Devin M., Benlong Liu, Hua Jin, Yu Sun, Qianyi Yang, Fang Gao, Li Wan, Jiahang Peng, Jin-Hua Jin, Kai-Feng Shen, Ray Kim, Jun Yin, Ailin Tao, and Zhou-Feng Chen
Subjects: *ITCHING, *NATRIURETIC peptides, *NEURAL pathways, *PEPTIDES, *SPINAL cord, *NEUROPEPTIDES
Abstract: Histamine-dependent and -independent itch is conveyed by parallel peripheral neural pathways that express gastrin-releasing peptide (GRP) and neuromedin B (NMB), respectively, to the spinal cord of mice. B-type natriuretic peptide (BNP) has been proposed to transmit both types of itch via its receptor NPRA encoded by Npr1. However, BNP also binds to its cognate receptor, NPRC encoded by Npr3 with equal potency. Moreover, natriuretic peptides (NP) signal through the Gi-couped inhibitory cGMP pathway that is supposed to inhibit neuronal activity, raising the question of how BNP may transmit itch information. Here, we report that Npr3 expression in laminae I-II of the dorsal horn partially overlaps with NMB receptor (NMBR) that transmits histaminergic itch via Gq-couped PLCß-Ca2+ signaling pathway. Functional studies indicate that NPRC is required for itch evoked by histamine but not chloroquine (CQ), a nonhistaminergic pruritogen. Importantly, BNP significantly facilitates scratching behaviors mediated by NMB, but not GRP. Consistently, BNP evoked Ca2+ responses in NMBR/NPRC HEK 293 cells and NMBR/NPRC dorsal horn neurons. These results reveal a previously unknown mechanism by which BNP facilitates NMB-encoded itch through a novel NPRC-NMBR cross-signaling in mice. Our studies uncover distinct modes of action for neuropeptides in transmission and modulation of itch in mice. [ABSTRACT FROM AUTHOR]
Published: 2022
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36. Critical care admission following elective surgery was not associated with survival benefit

Author: Kahan, Brennan C., Desponia, Koulenti, Kostoula, Arvaniti, Vanessa, Beavis, Douglas, Campbell, Matthew, Chan, Rui, Moreno, Pearse, Rupert M., Scott, Beattie, Pierre-Alain, Clavien, Nicolas, Demartines, Lee, A Fleisher, Mike, Grocott, James, Haddow, Andreas, Hoeft, Peter, Holt, Naomi, Pritchard, Andrew, Rhodes, Duminda, Wijeysundera, Matt, Wilson, Tahania, Ahmed, Kirsty, Everingham, Russell, Hewson, Marta, Januszewska, Rupert, M Pearse, Mandeep-Kaur, Phull, Richard, Halliwell, Mark, Shulman, Paul, Myles, Werner, Schmid, Michael, Hiesmayr, Patrick, Wouters, Stefan de Hert, Suzana, Lobo, Xiangming, Fang, Lars, Rasmussen, Emmanuel, Futier, Matthieu, Biais, Aurélien, Venara, Karem, Slim, Michael, Sander, Despoina, Koulenti, Mathew, Chan, Atul, Kulkarni, Susilo, Chandra, Aida, Tantri, Emad, Geddoa, Muntadhar, Abbas, Giorgio Della Rocca, Datin, Sivasakthi, Marzida, Mansor, Pastor, Luna, Arthur, Bouwman, Wolfgang, Buhre, Tim, Short, Tunde, Osinaike, Ricardo, Matos, Ioana, Grigoras, Mikhail, Kirov, Denis, Protsenko, Bruce, Biccard, Cesar, Aldecoa, Michelle, Chew, Christoph, Hofer, Martin, Hubner, James, Ditai, Tamas, Szakmany, Lee, Fleisher, Marissa, Ferguson, Michael, Macmahon, Ritchie, Cherian, Helen, Currow, Kathirgamanathan, Kanathiban, David, Gillespie, Edward, Pathmanathan, Katherine, Phillips, Jenifer, Reynolds, Joanne, Rowley, Jeanene, Douglas, Ross, Kerridge, Sameer, Garg, Michael, Bennett, Megha, Jain, David, Alcock, Nico, Terblanche, Rochelle, Cotter, Kate, Leslie, Marcelle, Stewart, Nicolette, Zingerle, Antony, Clyde, Oliver, Hambidge, Adam, Rehak, Sharon, Cotterell, Wilson Binh Quan Huynh, Timothy, Mcculloch, Erez, Ben-Menachem, Thomas, Egan, Jennifer, Cope, Paul, Fellinger, Simone, Haselberger, Caroline, Holaubek, Paul, Lichtenegger, Florian, Scherz, Franz, Hoffer, Veronika, Cakova, Andreas, Eichwalder, Norbert, Fischbach, Reinhold, Klug, Elisabeth, Schneider, Martin, Vesely, Reinhart, Wickenhauser, Karl Gernot Grubmueller, Marion, Leitgeb, Friedrich, Lang, Nancy, Toro, Marlene, Bauer, Friedrich, Laengle, Thomas, Mayrhofer, Christian, Buerkle, Karin, Forstner, Reinhard, Germann, Harald, Rinoesl, Elke, Schindler, Ernst, Trampitsch, Gerhard, Fritsch, Christian, Szabo, Jawad, Bidgoli, Hans, Verdoodt, Patrice, Forget, David, Kahn, Fernande, Lois, Mona, Momeni, Caroline, Prégardien, Audrey, Pospiech, Arnaud, Steyaert, Laurent, Veevaete, Dirk De Kegel, Karen De Jongh, Luc, Foubert, Carine, Smitz, Marcel, Vercauteren, Jan, Poelaert, Veerle Van Mossevelde, Jacques, Abeloos, Stefaan, Bouchez, Marc, Coppens, Luc De Baerdemaeker, Isabel, Deblaere, Ann De Bruyne, Stefan De Hert, Kristine, Fonck, Bjorn, Heyse, Tom, Jacobs, Koen, Lapage, Anneliese, Moerman, Martine, Neckebroek, Aliaksandra, Parashchanka, Nathalie, Roels, Nancy Van Den Eynde, Michael, Vandenheuvel, Jurgen Van Limmen, Ann, Vanluchene, Caroline, Vanpeteghem, Piet, Wyffels, Christel, Huygens, Punitha, Vandenbempt, Marc Van de Velde, Dimitri, Dylst, Bruno, Janssen, Evelien, Schreurs, Fábia Berganton Aleixo, Keulle, Candido, Hugo Dias Batista, Mario, Guimarães, Jaqueline, Guizeline, João, Hoffmann, Suzana, M Lobo, Francisco Ricardo Lobo, Vinícius, Nascimento, Katia, Nishiyama, Lucas, Pazetto, Daniela, Souza, Rodrigo Souza Rodrigues, Ana Maria Vilela Dos Santos, Jaquelline, Jardim, Joao, Silva, Paulo do Nascimento Junior, Thalissa Hermínia Baio, Gabriel Isaac Pereira de Castro, Henri Roger Watanabe Oliveira, Cristina Prata Amendola, Gutemberg, Cardoso, Daniela, Ortega, Ana Flavia Brotto, Mirella Cristine De Oliveira, Álvaro, Réa-Neto, Fernando, Dias, Pedro, Azambuja, Marcos Freitas Knibel, Antonio, Martins, William, Almeida, Calim Neder Neto, Maria Angela Tardelli, Eliana, Caser, Marcio, Machado, Crisitiano, Aguzzoli, Sérgio, Baldisserotto, Fernanda Beck Tabajara, Fernanda, Bettega, La Hore Correa Rodrigues Júnior, Julia de Gasperi, Lais, Faina, Marcos Farias Nolasco, Bruna Ferreira da Costa Fischer, Mariana Fosch de Campos Ferreira, Cristina, Hartmann, Marta, Kliemann, Gustavo Luis Hubert Ribeiro, Julia Merladete Fraga, Thiago Motta Netto, Laura Valduga Pozza, Paulo Rafael Wendling, Caroline, Azevedo, Juliana, Garcia, Marcel, Lopes, Bernardo, Maia, Paula, Maselli, Ralph, Melo, Weslley, Mendes, Matheus, Neves, Jacqueline, Ney, Claudio, Piras, Christopher, Applewhaite, Adrienne, Carr, Lorraine, Chow, Kaylene, Duttchen, Julena, Foglia, Michael, Greene, Ashley, Hinther, Kendra, Houston, Thomas Jared McCormick, Jennifer, Mikhayel, Sam, Montasser, Alex, Ragan, Andrew, Suen, Adrianna, Woolsey, Hai Chuan Yu, Duane, Funk, Stephen, Kowalski, Regina, Legaspi, Heather, Mcdonald, Faisal, Siddiqui, Jeremy, Pridham, Bernadette, Rowe, Sonia, Sampson, Barton, Thiessen, Geoff, Zbitnew, Andre, Bernard, Ronald, George, Philip, Jones, Rita, Moor, Naveed, Siddiqui, Alexandra, Wolfer, Diem, Tran, Denyse, Winch, Gary, Dobson, Thomas, Mccormick, Osama, Montasser, Richard, Hall, Leyla, Baghirzada, Si Yuan Dai, Gregory, Hare, Esther, Lee, Uma, Shastri, Albert, Tsui, Anmol, Yagnik, Danielle, Alvares, Stephen, Choi, Heather, Dwyer, Kathrina, Flores, Colin, Mccartney, Priya, Somascanthan, Carroll, Jo, Janneth, Pazmino-Canizares, Noam, Ami, Vincent, Chan, Anahi, Perlas, Ruth, Argue, Katie, Lavis, Kelly, Mayson, Ying, Cao, Hong, Gao, Tingju, Hu, Jie, Lv, Jian, Yang, Yang, Yang, Zhong, Yi, Jing, Zhou, Xiaohua, Zou, Miao, He, Xiaoying, Li, Dihuan, Luo, Haiying, Wang, Tian, Yu, Liyong, Chen, Lijun, Wang, Yunfei, Cai, Zhongming, Cao, Yanling, Li, Jiaxin, Lian, Haiyun, Sun, Sheng, Wang, Zhipeng, Wang, Kenru, Wang, Zhu, Yi, Xindan, Du, Hao, Fan, Yunbin, Fu, Lixia, Huang, Yanming, Huang, Haifang, Hwan, Hong, Luo, Pi-Sheng, Qu, Fan, Tao, Zhen, Wang, Guoxiang, Wang, Shun, Wang, Yan, Zhang, Xiaolin, Zhang, Chao, Chen, Weixing, Wang, Zhengyuan, Liu, Lihua, Fan, Jing, Tang, Yijun, Chen, Yongjie, Chen, Yangyang, Han, Changshun, Huang, Guojin, Liang, Jing, Shen, Jun, Wang, Qiuhong, Yang, Jungang, Zhen, Haidong, Zhou, Junping, Chen, Zhang, Chen, Xiaoyu, Li, Meng, Bo, Haiwang, Ye, Xiaoyan, Zhang, Yanbing, Bi, Jianqiao, Cao, Fengying, Guo, Hong, Lin, Yang, Liu, Meng, Lv, Pengcai, Shi, Xiumei, Song, Chuanyu, Sun, Yongtao, Sun, Yuelan, Wang, Shenhui, Wang, Min, Zhang, Rong, Chen, Jiabao, Hou, Yan, Leng, Qing-Tao, Meng, Qian, Li, Zi-Ying, Shen, Zhong-Yuan, Xia, Rui, Xue, Yuan, Zhang, Zhao, Bo, Xian-Jin, Zhou, Qiang, Chen, Huinan, Guo, Yongqing, Guo, Yuehong, Qi, Zhi, Wang, Jianfeng, Wei, Weiwei, Zhang, Lina, Zheng, Bao, Qi, Yaqiu, Chen, Yijiao, Chen, Yue, Fei, Nianqiang, Hu, Xuming, Hu, Min, Lei, Xiaoqin, Li, Xiaocui, Lv, Fangfang, Miao, Lingling, Ouyang, Qian, Lu, Conyu, Shen, Sun, Yu, Yuting, Wang, Dong, Wang, Chao, Wu, Liyuan, Xu, Jiaqi, Yuan, Lina, Zhang, Huan, Zhang, Yapping, Zhang, Jinning, Zhao, Chong, Zhao, Lei, Zhao, Tianzhao, Zheng, Dachun, Zhou, Haiyan, Zhou, Zhou, Ce, Kaizhi, Lu, Ting, Zhao, Changlin, He, Hong, Chen, Shasha, Chen, Baoli, Cheng, Jie, He, Lin, Jin, Caixia, Li, Hui, Li, Yuanming, Pan, Yugang, Shi, Xiao Hong Wen, Shuijing, Wu, Guohao, Xie, Kai, Zhang, Bing, Zhao, Xianfu, Lu, Feifei, Chen, Qisheng, Liang, Xuewu, Lin, Yunzhi, Ling, Gang, Liu, Jing, Tao, Yang, Lu, Jialong, Zhou, Fumei, Chen, Yunlin, Feng, Benchao, Hou, Jiamei, Lin, Mei, Liu, Foquan, Luo, Xiaoyun, Shi, Yingfen, Xiong, Lin, Xu, Shuangjia, Yang, Qin, Zhang, Huaigen, Zhang, Weihong, Zhao, Weilu, Zhao, Yun, Bai, Linbi, Chen, Sijia, Chen, Qinxue, Dai, Wujun, Geng, Kunyuan, Han, Xin, He, Luping, Huang, Binbin, Ji, Danyun, Jia, Shenhui, Jin, Qianjun, Li, Dongdong, Liang, Shan, Luo, Lulu, Lwang, Yunchang, Mo, Yuanyuan, Pan, Xinyu, Qi, Meizi, Qian, Jinling, Qin, Yelong, Ren, Yiyi, Shi, Junlu, Wang, Junkai, Wang, Leilei, Wang, Junjie, Xie, Yixiu, Yan, Yurui, Yao, Mingxiao, Zhang, Jiashi, Zhao, Xiuxiu, Zhuang, Yanqiu, Ai, Fang, Du, Long, He, Ledan, Huang, Zhisong, Li, Huijuan, Li, Yetong, Li, Liwei, Li, Meng, Su, Yazhuo, Yuan, Enman, Zhang, Jie, Zhang, Shuna, Zhao, Zhenrong, Ji, Ling, Pei, Wang, Li, Chen, Chen, Beibei, Dong, Jing, Li, Ziqiang, Miao, Hongying, Mu, Chao, Qin, Lin, Su, Zhiting, Wen, Keliang, Xie, Yonghao, Yu, Fang, Yuan, Xianwen, Hu, Zhang, Ye, Wangpin, Xiao, Zhipeng, Zhu, Qingqing, Dai, Kaiwen, Fu, Rong, Hu, Xiaolan, Hu, Song, Huang, Yaqi, Li, Yingping, Liang, Shuchun, Yu, Zheng, Guo, Yan, Jing, Tang, Na, Jie, Wu, Dajiang, Yuan, Ruilin, Zhang, Xiaoying, Zhao, Yuhong, Li, Hui-Ping, Bai, Chun-Xiao, Liu, Fei-Fei, Liu, Wei, Ren, Xiu-Li, Wang, Guan-Jie, Xu, Na, Hu, Bo, Li, Yangwen, Ou, Yongzhong, Tang, Shanglong, Yao, Shihai, Zhang, Cui-Cui, Kong, Bei, Liu, Tianlong, Wang, Wei, Xiao, Bo, Lu, Yanfei, Xia, Jiali, Zhou, Fang, Cai, Pushan, Chen, Shuangfei, Hu, Hongfa, Wang, Qiong, Xu, Liu, Hu, Liang, Jing, Bin, Li, Qiang, Liu, Yuejiang, Liu, Xinjian, Lu, Zhen Dan Peng, Xiaodong, Qiu, Quan, Ren, Youliang, Tong, Jin, Wang, Yazhou, Wen, Qiong, Wu, Jiangyan, Xia, Jue, Xie, Xiapei, Xiong, Shixia, Xu, Tianqin, Yang, Hui, Ye, Ning, Yin, Jing, Yuan, Qiuting, Zeng, Baoling, Zhang, Kang, Zheng, Jing, Cang, Shiyu, Chen, Fan, Yu, Shuying, Fu, Xiaodong, Ge, Baolei, Guo, Wenhui, Huang, Linghui, Jiang, Xinmei, Jiang, Liu, Yi, Yan, Pan, Yun, Ren, Shan, Qi, Jiaxing, Wang, Fei, Wang, Chi, Wu, Xiaoguang, Zhang, Ida Cecilie Christiansen, Simon Nørgaard Granum, Bodil Steen Rasmussen, Morten, Daugaard, Rajiv, Gambhir, Guðný Erla Steingrímsdóttir, Peter, Jensen-Gadegaard, Karsten Skovgaard Olsen, Hanna, Siegel, Katrine Zwicky Eskildsen, Mona Ring Gätke, Ida, Wibrandt, Simon Bisgaard Heintzelmann, Kai Henrik Wiborg Lange, Rune Sarauw Lundsgaard, Louise, Amstrup-Hansen, Claus, Hovendal, Michael, Larsen, Mette, Lenstrup, Tina, Kobborg, Jens Rolighed Larsen, Anette Barbre Pedersen, Søren Hübertz Smith, Rebecca Monett Oestervig, Arash, Afshari, Cheme, Andersen, Kim, Ekelund, Erik Lilja Secher, Birgitte, Brandsborg, Helene, Beloeil, Sigismond, Lasocki, Alexandre, Ouattara, Marlene, Sineus, Serge, Molliex, Marie Lim Legouge, Florent, Wallet, Antoine, Tesniere, Christophe, Gaudin, Paul, Lehur, Emma, Forsans, Stéphane de Rudnicki, Valerie Serra Maudet, Didier, Mutter, Ghassan, Sojod, Mehdi, Ouaissi, Jean-Marc, Regimbeau, Jacques, Desbordes, Nicolas, Comptaer, Diae El Manser, Sabine, Ethgen, Gilles, Lebuffe, Patrick, Auer, Christine, Härtl, Maria, Deja, Kirill, Legashov, Susanne, Sonnemann, Carola, Wiegand-Loehnert, Elke, Falk, Marit, Habicher, Stefan, Angermair, Beatrix, Laetsch, Katrin, Schmidt, Christian Von Heymann, Axel, Ramminger, Florian, Jelschen, Svenja, Pabel, Andreas, Weyland, Elke, Czeslick, Jochen, Gille, Michael, Malcharek, Armin, Sablotzki, Katharina, Lueke, Peter, Wetzel, Joerg, Weimann, Franz-Peter, Lenhart, Florian, Reichle, Frederike, Schirmer, Michael, Hüppe, Karl, Klotz, Carla, Nau, Julika, Schön, Thomas, Mencke, Christina, Wasmund, Carla, Bankewitz, Georg, Baumgarten, Andreas, Fleischer, Vera, Guttenthaler, Yvonne, Hack, Katharina, Kirchgaessner, Olja, Männer, Marlen, Schurig-Urbaniak, Rafael, Struck, Rebekka van Zyl, Maria, Wittmann, Ulrich, Goebel, Sarah, Harris, Siegfried, Veit, Evangelia, Andreadaki, Flora, Souri, Ioannis, Katsiadramis, Anthi, Skoufi, Maria, Vasileiou, Eleni, Aimoniotou-Georgiou, Anastasios, Katsourakis, Fotini, Veroniki, Glyceria, Vlachogianni, Konstantina, Petra, Dimitra, Chlorou, Eirini, Oloktsidou, Vasileios, Ourailoglou, Konstantinos, Papapostolou, Georgia, Tsaousi, Panagoula, Daikou, Georgia, Dedemadi, Ioannis, Kalaitzopoulos, Christos, Loumpias, Sotirios, Bristogiannis, Nikolaos, Dafnios, Georgios, Gkiokas, Elissaios, Kontis, Dimitra, Kozompoli, Aspasia, Papailia, Theodosios, Theodosopoulos, Christol, Bizios, Anastasia, Koutsikou, Aleaxandra, Moustaka, Ioannis, Plaitakis, Apostolos, Armaganidis, Theodora, Christodoulopoulou, Mihail, Lignos, Maria, Theodorakopoulou, Andreas, Asimakos, Eleni, Ischaki, Angeliki, Tsagkaraki, Spyros, Zakynthinos, Eleni, Antoniadou, Ioannis, Koutelidakis, Dimitrios, Lathyris, Irene, Pozidou, Nikolaos, Voloudakis, Maria, Dalamagka, Elena, Gkonezou, Christos, Chronis, Dimitra, Manolakaki, Dimitris, Mosxogiannidis, Tatiana, Slepova, Isaia-Sissy, Tsakiridou, Claire Lampiri Lampiri, Anastasia Vachlioti Vachlioti, Christos Panagiotakis Panagiotakis, Dimitrios Sfyras Sfyras, Fotios Tsimpoukas Tsimpoukas, Athanasia, Tsirogianni, Elena, Axioti, Andreas, Filippopoulos, Elli, Kalliafa, George, Kassavetis, Petros, Katralis, Ioannis, Komnos, Georgios, Pilichos, Ifigenia, Ravani, Antonis, Totis, Eymorfia, Apagaki, Andromachi, Efthymiadi, Nikolaos, Kampagiannis, Theoniki, Paraforou, Agoritsa, Tsioka, Georgios, Georgiou, Aristeidis, Vakalos, Aggeliki, Bairaktari, Efthimios, Charitos, George, Markou, Panagiota, Niforopoulou, Nikolaos, Papakonstantinou, Evdoxia, Tsigou, Archontoula, Xifara, Menelaos, Zoulamoglou, Panagiota, Gkioni, Stylianos, Karatzas, Aikaterini, Kyparissi, Efstratios, Mainas, Ioannis, Papapanagiotou, Theonymfi, Papavasilopoulou, George, Fragandreas, Eleni, Georgopoulou, Eleni, Katsika, Kyriakos, Psarras, Eirini, Synekidou, Maria, Verroiotou, Evangelia, Vetsiou, Donika, Zaimi, Athina, Anagnou, Konstantinos, Apostolou, Theodora, Melissopoulou, Theophilos, Rozenberg, Christos, Tsigris, Georgios, Boutsikos, Vasileios, Kalles, Nikolaos, Kotsalas, Christina, Lavdaiou, Fotini, Paikou, Georgia-Laura, Panagou, Anna, Spring, Ioannis, Botis, Maria, Drimala, Georgios, Georgakakis, Ellada, Kiourtzieva, Panagiota, Ntouma, Apostolos, Prionas, Kyriakos, Xouplidis, Eleftheria, Dalampini, Chrysavgi, Giannaki, Christina, Iasonidou, Orestis, Ioannidis, Athina, Lavrentieva, Athena, Lavrentieva, George, Papageorgiou, Maria, Kokkinoy, Maria, Stafylaraki, Stylianos, Gaitanakis, Periclis, Karydakis, Josef, Paltoglou, Panagiotis, Ponireas, Panagiotis, Chaloulis, Athanasios, Provatidis, Anisoglou, Sousana, Varvara Vanessa Gardikou, Maria, Konstantivelli, Olga, Lataniotou, Elisavet, Lisari, Maria, Margaroni, Konstantinos, Stamatiou, Edouardos, Nikolaidis, Ioannis, Pnevmatikos, Eleni, Sertaridou, Alexandros, Andreou, Eleni, Arkalaki, Elias, Athanasakis, Fotini, Chaniotaki, Aikaterini, Chatzimichali, Maria, Christofaki, Despina, Dermitzaki, Klara, Fiorentza, Georgios, Frantzeskos, Elisavet, Geromarkaki, Kalliopi, Kafkalaki, Marina, Kalogridaki, Konstyllia, Karydi, Sofia, Kokkini, Georgios, Kougentakis, Tatiana, Lefaki, Emmanouhl, Lilitsis, Aikaterini, Makatounaki, Polychronis, Malliotakis, Dimosthenis, Michelakis, Maria, Neonaki, Vasileia, Nyktari, Iliana, Palikyra, Eleftherios, Papadakis, Alexandra, Papaioannou, Konstantinos, Sfakianakis, Maria, Sgouraki, Xenia, Souvatzis, Anastasia, Spartinou, Nefeli, Stefanidou, Paulina, Syrogianni, Georgia, Tsagkaraki, Elena, Arnaoutoglou, Christina, Arnaoutoglou, Christina, Bali, Vasilios, Bouris, Rodamanthos, Doumos, Konstantia-Paraskevi, Gkini, Clio, Kapaktsi, Vasilios, Koulouras, Arian, Lena, Dimitra, Lepida, Evangelos, Michos, Dimitrios, Papadopoulos, Minas, Paschopoulos, Vaia Aliki Rompou, Ioanna, Siouti, Stavros, Tsampalas, Ourania, Ververidou, Georgios, Zilis, Alexandra, Charlalampidoy, Gregory, Christodoulidis, Andreas, Flossos, Konstantinos, Stamoulis, Man Shing Caleb Tsang, Man Shing Tsang, Man Ling Lai, Chi Pang Yip, Hey Man Heymans Chan, Bassanio, Law, Wing Sze Li, Hiu Man Chu, Emily Gar Yee Koo, Chi Cheong Joe Lam, Ka Ho Cheng, Tracy, Lam, Susanna, Chu, Wing Yan Lam, Kin Wai Kevin Wong, Dilys, Kwok, Ching Yue Janice Hung, Wai Kit Jacky Chan, Wing, Lamwong, Chun Kwong Eric Chung, Shu Kai Ma, Shuchi, Kaushik, Bhagyesh, Shah, Dhiren, Shah, Sanjay, Shah, Praburaj, Ar, Radhakrishnan, Muthuchellappan, Vandana, Agarwal, Jigeeshu, Divatia, Sanghamitra, Mishra, Ganesh, Nimje, Swati, Pande, Sukhada, Savarkar, Aditi, Shrivastava, Martin, Thomas, Shashikant, Yegnaram, Rahmat, Hidayatullah, Nasman, Puar, Sumara, Niman, Imai, Indra, Zulkarnain, Hamzah, Annika, Yuliana, Ucu Nurhadiat Abidin, Ade Nurkacan Dursin, Andri, Kurnia, Ade, Susanti, Dini, Handayani, Mahaalit Alit Aribawa, Aryabiantara, Arya, Tjokorda Gde Agung Senapathi, Utara Hartawan Utara, Widnyana Made Wid, Semarawima, Wima, Wiryana Made Wir, 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Hongying, Qin, Chao, Su, Lin, Wen, Zhiting, Xie, Keliang, Yu, Yonghao, Yuan, Fang, Hu, Xianwen, Zhang, Ye, Xiao, Wangpin, Zhu, Zhipeng, Dai, Qingqing, Fu, Kaiwen, Hu, Rong, Hu, Xiaolan, Huang, Song, Li, Yaqi, Liang, Yingping, Yu, Shuchun, Guo, Zheng, Jing, Yan, Tang, Na, Wu, Jie, Yuan, Dajiang, Zhang, Ruilin, Zhao, Xiaoying, Li, Yuhong, Bai, Hui-Ping, Liu, Chun-Xiao, Liu, Fei-Fei, Ren, Wei, Wang, Xiu-Li, Xu, Guan-Jie, Hu, Na, Li, Bo, Ou, Yangwen, Tang, Yongzhong, Yao, Shanglong, Zhang, Shihai, Kong, Cui-Cui, Liu, Bei, Wang, Tianlong, Xiao, Wei, Lu, Bo, Xia, Yanfei, Zhou, Jiali, Cai, Fang, Chen, Pushan, Hu, Shuangfei, Wang, Hongfa, Xu, Qiong, Hu, Liu, Jing, Liang, Li, Bin, Liu, Qiang, Liu, Yuejiang, Lu, Xinjian, Peng, Zhen Dan, Qiu, Xiaodong, Ren, Quan, Tong, Youliang, Wang, Jin, Wen, Yazhou, Wu, Qiong, Xia, Jiangyan, Xie, Jue, Xiong, Xiapei, Xu, Shixia, Yang, Tianqin, Ye, Hui, Yin, Ning, Yuan, Jing, Zeng, Qiuting, Zhang, Baoling, Zheng, Kang, Cang, Jing, Chen, Shiyu, Fan, Yu, Fu, Shuying, Ge, Xiaodong, Guo, Baolei, Huang, Wenhui, Jiang, Linghui, Jiang, Xinmei, Liu, Yi, Pan, Yan, Ren, Yun, Shan, Qi, Wang, Jiaxing, Wang, Fei, Wu, Chi, Zhang, Xiaoguang, Christiansen, Ida Cecilie, Granum, Simon Nørgaard, Rasmussen, Bodil Steen, Daugaard, Morten, Gambhir, Rajiv, Steingrímsdóttir, Guðný Erla, Jensen-Gadegaard, Peter, Olsen, Karsten Skovgaard, Siegel, Hanna, Zwicky Eskildsen, Katrine, Gätke, Mona Ring, Wibrandt, Ida, Heintzelmann, Simon Bisgaard, Lange, Kai Henrik Wiborg, Lundsgaard, Rune Sarauw, Amstrup-Hansen, Louise, Hovendal, Clau, Larsen, Michael, Lenstrup, Mette, Kobborg, Tina, Larsen, Jens Rolighed, Pedersen, Anette Barbre, Smith, Søren Hübertz, Oestervig, Rebecca Monett, Afshari, Arash, Andersen, Cheme, Ekelund, Kim, Secher, Erik Lilja, Brandsborg, Birgitte, Beloeil, Helene, Lasocki, Sigismond, Ouattara, Alexandre, Sineus, Marlene, Molliex, Serge, Legouge, Marie Lim, Wallet, Florent, Tesniere, Antoine, Gaudin, Christophe, Lehur, Paul, Forsans, Emma, de 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Siegfried, Andreadaki, Evangelia, Souri, Flora, Katsiadramis, Ioanni, Skoufi, Anthi, Vasileiou, Maria, Aimoniotou-Georgiou, Eleni, Katsourakis, Anastasio, Veroniki, Fotini, Vlachogianni, Glyceria, Petra, Konstantina, Chlorou, Dimitra, Oloktsidou, Eirini, Ourailoglou, Vasileio, Papapostolou, Konstantino, Tsaousi, Georgia, Daikou, Panagoula, Dedemadi, Georgia, Kalaitzopoulos, Ioanni, Loumpias, Christo, Bristogiannis, Sotirio, Dafnios, Nikolao, Gkiokas, Georgio, Kontis, Elissaio, Kozompoli, Dimitra, Papailia, Aspasia, Theodosopoulos, Theodosio, Bizios, Christol, Koutsikou, Anastasia, Moustaka, Aleaxandra, Plaitakis, Ioanni, Armaganidis, Apostolo, Christodoulopoulou, Theodora, Lignos, Mihail, Theodorakopoulou, Maria, Asimakos, Andrea, Ischaki, Eleni, Tsagkaraki, Angeliki, Zakynthinos, Spyro, Antoniadou, Eleni, Koutelidakis, Ioanni, Lathyris, Dimitrio, Pozidou, Irene, Voloudakis, Nikolao, Dalamagka, Maria, Gkonezou, Elena, Chronis, Christo, Manolakaki, Dimitra, Mosxogiannidis, Dimitri, 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Despina, Fiorentza, Klara, Frantzeskos, Georgio, Geromarkaki, Elisavet, Kafkalaki, Kalliopi, Kalogridaki, Marina, Karydi, Konstyllia, Kokkini, Sofia, Kougentakis, Georgio, Lefaki, Tatiana, Lilitsis, Emmanouhl, Makatounaki, Aikaterini, Malliotakis, Polychroni, Michelakis, Dimostheni, Neonaki, Maria, Nyktari, Vasileia, Palikyra, Iliana, Papadakis, Eleftherio, Papaioannou, Alexandra, Sfakianakis, Konstantino, Sgouraki, Maria, Souvatzis, Xenia, Spartinou, Anastasia, Stefanidou, Nefeli, Syrogianni, Paulina, Tsagkaraki, Georgia, Arnaoutoglou, Elena, Arnaoutoglou, Christina, Bali, Christina, Bouris, Vasilio, Doumos, Rodamantho, Gkini, Konstantia-Paraskevi, Kapaktsi, Clio, Koulouras, Vasilio, Lena, Arian, Lepida, Dimitra, Michos, Evangelo, Papadopoulos, Dimitrio, Paschopoulos, Mina, Rompou, Vaia Aliki, Siouti, Ioanna, Tsampalas, Stavro, Ververidou, Ourania, Zilis, Georgio, Charlalampidoy, Alexandra, Christodoulidis, Gregory, Flossos, Andrea, Stamoulis, Konstantino, Tsang, Man Shing Caleb, Tsang, Man Shing, Lai, Man Ling, Yip, Chi Pang, Chan, Hey Man Heyman, Law, Bassanio, Li, Wing Sze, Chu, Hiu Man, Koo, Emily Gar Yee, Lam, Chi Cheong Joe, Cheng, Ka Ho, Lam, Tracy, Chu, Susanna, Lam, Wing Yan, Wong, Kin Wai Kevin, Kwok, Dily, Hung, Ching Yue Janice, Chan, Wai Kit Jacky, LamWong, Wing, Chung, Chun Kwong Eric, Ma, Shu Kai, Kaushik, Shuchi, Shah, Bhagyesh, Shah, Dhiren, Shah, Sanjay, Ar, Praburaj, Muthuchellappan, Radhakrishnan, Agarwal, Vandana, Divatia, Jigeeshu, Mishra, Sanghamitra, Nimje, Ganesh, Pande, Swati, Savarkar, Sukhada, Shrivastava, Aditi, Thomas, Martin, Yegnaram, Shashikant, Hidayatullah, Rahmat, Puar, Nasman, Niman, Sumara, Indra, Imai, Hamzah, Zulkarnain, Yuliana, Annika, Abidin, Ucu Nurhadiat, Dursin, Ade Nurkacan, Kurnia, Andri, Susanti, Ade, Handayani, Dini, Aribawa, Mahaalit Alit, Arya, Aryabiantara, Senapathi, Tjokorda Gde Agung, Utara, Utara Hartawan, Wid, Widnyana Made, Wima, Semarawima, Wir, Wiryana Made, Jehosua, Brillyan, Kaunang, Jonathan, 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Sarki, Adamu Muhammad, Adekola, Oyebola, Akanmu, Olanrewaju, Durodola, Akanmu, Olukoju, Olusegun, Raji, Victor, Olajumoke, Tokunbo, Oyebamiji, Emmanuel, Adenekan, Anthony, Adetoye, Adenekan, Faponle, Folayemi, Olateju, Simeon, Owojuyigbe, Afolabi, Talabi, Ademola, Adenike, Odewabi, Adewale, Badru, Collins, Nwokoro, Ezekiel, Emmanuel, Fatungase, Oluwabunmi Motunrayo, Grace, Anuforo, Sola, Sotannde, Stella, Ogunmuyiwa, Ademola, Adeyinka, Adeolu, Augustine A., Adigun, Tinuolac, Akinwale, Mukaila, Fasina, Oluyemi, Gbolahan, Olalere, Idowu, Olusola, Olonisakin, Rotimi Peter, Osinaike, Babatunde Babasola, Asudo, Felicia, Mshelia, Danladi, Abdur-Rahman, Lukman, Agodirin, Olayide, Bello, Jibril, Bolaji, Benjamin, Oyedepo, Olanrewaju Olubukola, Ezike, Humphrey, Iloabachie, Ikechukwu, Okonkwo, Ikemefuna, Onuora, Elia, Onyeka, Tonia, Ugwu, Innocent, Umeh, Friday, Alagbe-Briggs, Olubusola, Dodiyi-Manuel, Amabra, Echem, Richard, Obasuyi, Bright, Onajin-Obembe, Bisola, Bandeira, Maria Expedito, 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Diaconescu, Ciresica, Iosep, Gabriel Florin, Pulbere, Dorin, Ursu, Irina, Balanescu, Andreea, Grintescu, Ioana, Mirea, Liliana, Rentea, Irina, Vartic, Mihaela, Lupu, Mary-Nicoleta, Stanescu, Dorin, Streanga, Lavinea, Antal, Oana, Hagau, Natalia, Patras, Dumitru, Petrisor, Cristina, Tosa, Flaviu, Tranca, Sebastian, Copotoiu, Sanda Maria, Ungureanu, Liviu Lucian, Harsan, Cristian Remu, Papurica, Mariu, Cernea, Daniela Denisa, Dragoescu, Nicoleta Alice, Aflori, Laura, Vaida, Carmen, Ciobotaru, Oana Roxana, Aignatoaie, Mariana, Carp, Cristina Paula, Cobzaru, Isabelle, Mardare, Oana, Purcarin, Bianca, Tutunaru, Valentin, Ionita, Victor, Arustei, Mirela, Codita, Anisoara, Busuioc, Mihai, Chilinciuc, Ion, Ciobanu, Cristina, Belciu, Ioana, Tincu, Eugen, Blaj, Mihaela, Grosu, Ramona-Mihaela, Sandu, Gigel, Bruma, Dana, Corneci, Dan, Dutu, Madalina, Krepil, Adriana, Copaciu, Elena, Dumitrascu, Clementina Oana, Jemna, Ramona, Mihaescu, Florentina, Petre, Raluca, Tudor, Cristina, Ursache, Elena, Kulikov, Alexander, Lubnin, Andrey, Grigoryev, Evgeny, Pugachev, Stanislav, Tolmasov, Alexander, Hussain, Ayyaz, Ilyina, Yana, Roshchina, Anna, Iurin, Aleksandr, Chazova, Elena, Dunay, Artem, Karelov, Alexey, Khvedelidze, Irina, Voldaeva, Olga, Belskiy, Vladislav, Dzhamullaev, Parvin, Grishkowez, Elena, Kretov, Vladimir, Levin, Valeriy, Molkov, Aleksandr, Puzanov, Sergey, Samoilenko, Aleksandr, Tchekulaev, Aleksandr, Tulupova, Valentina, Utkin, Ivan, Allorto, Nikki Leigh, Bishop, David Gray, Builu, Pierre Monji, Cairns, Carel, Dasrath, Ashish, de Wet, Jacque, den Hoedt, Marielle, Grey, Ben, Hayes, Morgan Philip, Küsel, Belinda Senta, Shangase, Nomcebo, Wise, Robert, Cacala, Sharon, Farina, Zane, Govindasamy, Vishendran, Kruse, Carl-Heinz, Lee, Carolyn, Marais, Leonard, Naidoo, Thinagrin Dhasarthun, Rajah, Chantal, Rodseth, Reitze Nil, Ryan, Lisa, von Rhaden, Richard, Adam, Suwayba, Alphonsus, Christella, Ameer, Yusuf, Anderson, Frank, Basanth, Sujith, Bechan, Sudha, Bhula, Chettan, Biccard, Bruce M., Biyase, Thuli, Buccimazza, Ine, Cardosa, Jorge, Chen, Jame, Daya, Bhavika, Drummond, Leanne, Elabib, Ali, Goad, Ehab Helmy Abdel, Goga, Ismail E., Goga, Riaz, Harrichandparsad, R., Hodgson, Richard E., Jordaan, J., Kalafatis, Nicky, Kampik, Christian, Landers, At, Loots, Emil, Madansein, Rajhmum, Madaree, Anil, Madiba, Thandinkosi E., Manzini, Vukani T., Mbuyisa, Mbali, Moodley, Rajan, Msomi, Mduduzi, Mukama, Innocent, Naidoo, Desigan, Naidoo, Rubeshan, Naidu, Tesuven K., Ntloko, Sindiswa, Padayachee, Eneshia, Padayachee, Lucelle, Phaff, Martijn, Pillay, Bala, Pillay, Desigan, Pillay, Lutchmee, Ramnarain, Anupa, Ramphal, Suren R., Ryan, Paul, Saloojee, Ahmed, Sebitloane, Motshedisi, Sigcu, Noluyolo, Taylor, Jenna L., Torborg, Alexandra, Visser, Linda, Anderson, Philip, Conradie, Alae, de Swardt, Mathew, de Villiers, Martin, Eikman, Johan, Liebenberg, Riaan, Mouton, Johan, Paton, Abbey, van der Merwe, Louwrence, Wilscott-Davids, Candice, Barrett, Wendy Joan, Bester, 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Dempsey, Ged, Seasman, Colette, Basit Nawaz Khan, Raja, Kurasz, Claire, Macgregor, Mark, Shawki, Burhan, Hariharan, Vimal, Chau, Simon, Ellis, Kate, Butt, Georgina, Chicken, Dennis-Wayne, Christmas, Natasha, Allen, Samantha, Daniel, Gayatri Daniel, Dempster, Angie, Kemp, Juliette, Matthews, Lewi, Mcglone, Philip, Tambellini, Joanne, Trodd, Dawn, Freitas, Katie, Garg, Atul, Karpate, Shilpaja, Kulkarni, Aditi, O’Hara, Chloe, Troko, Jtroko, Angus, Kirsty, Bradley, Jacqueline, Brennan, Emma, Brooks, Carolyn, Brown, Janette, Brown, Gemma, Finch, Amanda, Gratrix, Karen, Hesketh, Sue, Hill, Gillian, Jeffs, Carol, Morgan, Maureen, Pemberton, Chri, Slawson, Nicola, Spickett, Helen, Swarbrick, Gemma, Thomas, Megan, Van Duyvenvoorde, Greta, Brennan, Andrew, Briscoe, Richard, Cooper, Sarah, Lawton, Tom, Northey, Martin, Senaratne, Rashmi, Stanworth, Helen, Burrows, Lorna, Cain, Helen, Craven, Rachael, Davies, Keith, Jonas, Attila, Pachucki, Marcin, Walkden, Graham, Davies, Helen, Gudaca, Mariethel, Hobrok, Maria, Arawwawala, Dilshan, Fergey, Lauren, Gardiner, Matthew, Gunn, Jacqueline, Johnson, Lyndsay, Lofting, Amanda, Lyle, Amanda, Mc Neela, Fiona, Smolen, Susan, Topliffe, Joanne, Williams, Sarah, Bland, Martin, Kaura, Vika, Lanka, Prasad, Naylor, Chardé, Smith, Neil, Ahmed, Ahmed, Myatt, John, Shenoy, Ravikiran, Soon, Wai Cheong, Tan, Jessica, Karadia, Sunny, Self, Jame, Durant, Emma, Tripathi, Shiva, Bullock, Clare, Campbell, Debbie, Ghosh, Alison, Hughes, Thoma, Zsisku, Lajo, Bengeri, Sheshagiri, Cowton, Amanda, Khalid, Mohammed Shazad, Limb, Jame, McAdam, Colin, Porritt, Mandy, Rafi, M. Amir, Shekar, Priya, Harden, Catherine, Hollands, Heidi, King, Angela, March, Linda, Minto, Gary, Patrick, Abigail, Waugh, Darren, Kumara, Paramesh, Simeson, Karen, Yarwood, Jamie, Browning, Julie, Hatton, Jonathan, Julian, Howe, Mitra, Atideb, Newton, Maria, Pernu, Pawan, Wilson, Alison, Commey, Thelma, Foot, Helen, Glover, Lyn, Gupta, Ajay, Lancaster, Nicola, Levin, Jill, Mackenzie, Felicity, Mestanza, Claire, Nofal, Emma, Pout, Lauren, Varden, Rosanna, Wild, Jonathan, Jones, Stephanie, Moreton, Sarah, Pulletz, Mark, Davies, Charlotte, Martin, Matthew, Thomas, Sian, Burns, Karen, McArthur, Carol, Patel, Panna, Lau, Gary, Rich, Natalie, Davis, Fiona, Lyons, Rachel, Port, Beth, Prout, Rachel, Smith, Christopher, Adelaja, Yemi, Bennett, Victoria, Bidd, Heena, Dumitrescu, Alexandra, Murphy, Jacqui Fox, Keen, Abigail, Mguni, Nhlanhla, Ong, Cheng, Adams, George, Boshier, Pier, Brown, Richard, Butryn, Izabella, Chatterjee, Jayanta, Freethy, Alexander, Lockwood, Geoffrey, Tsakok, Maria, Tsiligiannis, Sophia, Peat, William, Stephenson, Lorraine, Bradburn, Mike, Pick, Sara, Cunha, Pedro, Olagbaiye, Olufemi, Tayeh, Salim, Abernethy, Caroline, Balasubramaniam, Madhu, Bennett, Rachael, Bolton, David, Martinson, Victoria, Naylor, Charde, Bell, Stephanie, Heather, Blaylock, Kushakovsky, Vlad, Alcock, Liam, Alexander, Hazel, Anderson, Colette, Baker, Paul, Brookes, Morag, Cawthorn, Louise, Cirstea, Emanuel, Colling, Kerry, Coulter, Ian, Das, Suparna, Haigh, Kathryn, Hamdan, Alhafidz, Hugill, Keith, Kottam, Lucksy, Lisseter, Emily, Mawdsley, Matthew, McGivern, Julie, Padala, Krishnaveni, Phelps, Victoria, kumar, Vineshykaa Ramesh, Stewart, Kirsten, Towse, Kayley, Tregonning, Julie, Vahedi, Ali, Walker, Alycon, Baines, Duncan, Bilolikar, Anjali, Chande, Shiv, Copley, Edward, Dunk, Nigel, Kulkarni, Raghavendra, Kumar, Pawan, Metodiev, Yavor, Ncomanzi, Dumisani, Raithatha, Bhavesh, Raymode, Parizade, Szafranski, Jan, Twohey, Linda, Watt, Philip, Weatherall, Lucie, Weatherill, J., Whitman, Zoe, Wighton, Elinor, Abayasinghe, Chamika, Chan, Alexander, Darwish, Sharif, Gill, Jame, Glasgow, Emma, Hadfield, Daniel, Harris, Clair, Kochhar, Arun, Mellis, Clare, Pool, Andrew, Riozzi, Paul, Selman, Andrew, Smith, Emma-Jane, Vele, Liana, Gercek, Yuksel, Guy, Kramer, Holden, Dougla, Watson, Nichola, Whysall, Karen, Andreou, Prematie, Hales, Dawn, Thompson, Jonathan, Bowrey, Sarah, McDonald, Shara, Gilmore, Jemma, Hills, Vicky, Kelly, Chan, Kelly, Sinead, Lloyd, Geraint, Abbott, Tom, Gall, Lewi, Torrance, Hew, Vivian, Mark, Berntsen, Emer, Nolan, Tracey, Turner, Angu, Vohra, Akbar, Brown, Andrew, Clark, Richard, Coughlan, Elaine, Daniel, Conway, Patvardhan, Chinmay, Pearson, Rachel, Predeep, Sheba, Saad, Hesham, Shanmugam, Mohanakrishnan, Varley, Simon, Wylie, Katharine, Cooper, Lucy, Makowski, Arystarch, Misztal, Beata, Moldovan, Eliza, Pegg, Claire, Donovan, Andrew, Foot, Jayne, Large, Simon, Claxton, Andrew, Netke, Bhagyashree, Armstrong, Richard, Calderwood, Claire, Kwok, Andy, Mohr, Otto, Oyeniyi, Peter, Patnaik, Lisa, Post, Benjamin, Ali, Sarah, Arshad, Homa, Baker, Gerard, Brenner, Laura, Brincat, Maximilian, Brunswicker, Annemarie, Cox, Hannah, Cozar, Octavian Ionut, Durst, Alexander, Fengas, Lior, Flatt, Jim, Glister, Georgina, Narwani, Vishal, Photi, Evangelo, Rankin, Adeline, Rosbergen, Melissa, Tan, Mark, Beaton, Ceri, Horn, Rachel, Hunt, Jane, Rousseau, Guy, Stancombe, Lucia, Absar, Mohammed, Allsop, Joanne, Drinkwater, Zoe, Hodgkiss, Tracey, Smith, Kirsty, Brown, Jamie, Alexander-Sefre, Farhad, Campey, Lorraine, Dudgeon, Lucy, Hall, Kathryn, Hitchcock, Rachael, James, Lynne, Smith, Kate, Winstone, Ulrika, Ahmad, Norfaizan, Bauchmuller, Kri, Harrison, Jonathan, Jeffery, Holly, Miller, Duncan, Pinder, Angela, Pothuneedi, Sailaja, Rosser, Jonathan, Sanghera, Sumayer, Swift, Diane, Walker, Rachel, Bester, Delia, Cavanagh, Sarah, Cripps, Heather, Daniel, Harvey, Lynch, Julie, Paton, Alison, Pyke, Shirley, Scholefield, John, Whitworth, Helen, Bottrill, Fiona, Ramalingam, Ganesh, Webb, Stephen, Akerman, Nik, Antill, Philip, Bourner, Lynsey, Buckley, Sarah, Castle, Gail, Charles, Rob, Eggleston, Christopher, Foster, Rebecca, Gill, Satwant, Lindley, Kate, Lklouk, Mohamed, Lowery, Tracey, Martin, Oliver, Milne, David, O’Connor, Patrick, Ratcliffe, Andrew, Rose, Alastair, Smith, Annie, Varma, Sandeep, Ward, Jackie, Barcraft-Barnes, Helena, Camsooksai, Julie, Colvin, Carolyn, Reschreiter, Henrik, Tbaily, Lee, Venner, Nicola, Hamilton, Caroline, Kelly, Lewi, Toth-Tarsoly, Piroska, Dodsworth, Kerry, Foord, Denise, Gordon, Paul, Hawes, Elizabeth, Lamb, Nikki, Mouland, Johanna, Nightingale, Jeremy, Rose, Steve, Schrieber, Joe, Al ‘Amri, Khalid, Aladin, Hafiz, Arshad, Mohammed Asif, Barraclough, Jame, Bentley, Conor, Bergin, Colin, Carrera, Ronald, Clarkson, Aisling, Collins, Michelle, Cooper, Lauren, Denham, Samuel, Griffiths, Ewen, Ip, Peter, Jeyanthan, Somasundaram, Joory, Kavita, Kaur, Satwant, Marriott, Paul, Mitchell, Natalie, Nagaiah, Sukumar, Nilsson, Annette, Parekh, Nilesh, Pope, Martin, Seager, Joseph, Serag, Hosam, Tameem, Alifia, Thomas, Anna, Thunder, Joanne, Torrance, Andrew, Vohra, Ravinder, whitehouse, Arlo, Wong, Tony, Blunt, Mark, Wong, Kate, Giles, Julian, Reed, Isabelle, Weller, Debbie, Bell, Gillian, Birch, Julie, Damant, Rose, Maiden, Jane, Mewies, Clare, Prince, Claire, Radford, Jane, Balain, Birender, Banerjee, Robin, Barnett, Andrew, Burston, Ben, Davies, Kirsty, Edwards, Jayne, Evans, Chri, Ford, David, Gallacher, Pete, Hill, Simon, Jaffray, David, Karlakki, Sudheer, Kelly, Cormac, Kennedy, Julia, Kiely, Nigel, Lewthwaite, Simon, Marquis, Chri, Ockendon, Matthew, Phillips, Stephen, Pickard, Simon, Richardson, Jame, Roach, Richard, Smith, Tony, Spencer-Jones, Richard, Steele, Niall, Steen, Julie, Van Liefland, Marck, White, Steve, Faulds, Matthew, Harris, Meredyth, Kelly, Carrie, Nicol, Scott, Pearson, Sally Anne, Chukkambotla, Srikanth, Andrew, Alyson, Attrill, Elizabeth, Campbell, Graham, Datson, Amanda, Fouracres, Anna, Graterol, Juan, Graves, Lynne, Hong, Bosun, Ishimaru, Alexander, Karthikeyan, Arvind, King, Helen, Lawson, Tom, Lee, Gregory, Lyons, Saoirse, Macalister Hall, Andrew, Mathoulin, Sophie, Mcintyre, Eilidh, Mclaughlin, Danny, Mulcahy, Kathleen, Ratcliffe, Anna, Robbins, Jame, Sung, Weilin, Tayo, Adeoluwa, Trembath, Lisa, Venugopal, Suneetha, Walker, Robert, Wigmore, Geoffrey, Boereboom, Catherine, Downes, Charlotte, Humphries, Ryan, Melbourne, Susan, Smith, Coral, Tou, Samson, Ullah, Shafa, Batchelor, Nick, Boxall, Leigh, Broomby, Rupert, Deen, Tariq, Hellewell, Alistair, Helliwell, Laurence, Hutchings, Melanie, Hutchins, David, Keenan, Samantha, Mackie, Donna, Donna, Alison, Smith, France, Stone, Lucy, Thorpe, Kevin, Wassall, Richard, Woodgate, Andrew, Baillie, Shelley, Campbell, Tara, James, Sarah, King, Chri, Marques de Araujo, Daniela, Martin, Daniel, Morkane, Clare, Neely, Julia, Rajendram, Rajkumar, Burton, Megan, James, Kathryn, Keevil, Edward, Minik, Orsolya, Morgan, Jenna, Musgrave, Anna, Rajanna, Harish, Roberts, Tracey, Adamson, Michael, Jumbe, Sandra, Kendall, Jennie, Muthuswamy, Mohan Babu, Anderson, Charlotte, Cruikshanks, Andrew, Wrench, Ian, Zeidan, Lisa, Ardern, Diane, Harris, Benjamin, Hellstrom, Johanna, Martin, Jane, Thomas, Richard, Varsani, Nimu, Wrey Brown, Caroline, Docherty, Philip, Gillies, Michael, McGregor, Euan, Usher, Helen, Craig, Jayne, Smith, Andrew, Ahmad, Tahania, Bodger, Phoebe, Creary, Thai, Fowler, Alexander, Hewson, Ru, Ijuo, Eke, Jones, Timothy, Kantsedikas, Ilya, Lahiri, Sumitra, McLean, Aaron Lawson, Niebrzegowska, Edyta, Phull, Mandeep, Wang, Difei, Wickboldt, Nadine, Baldwin, Jacqueline, Doyle, Donna, Mcmullan, Sean, Oladapo, Michelle, Owen, Thoma, Williams, Alexandra, Daniel, Hull, Gregory, Peter, Husain, Tauqeer, Kirk-Bayley, Justin, Mathers, Edward, Montague, Laura, White, Stuart, Avis, Joanne, Cook, Tim, Dali-Kemmery, Lola, Kerslake, Ian, Lambourne, Victoria, Pearson, Annabel, Boyd, Christine, Callaghan, Mark, Lawson, Cathy, McCrossan, Roopa, Nesbitt, Vanessa, O’connor, Laura, Scott, Julia, Sinclair, Rhona, Farid, Nahla, Morgese, Ciro, Bhatia, Kailash, Karmarkar, Swati, Ahmed, Jamil, Branagan, Graham, Hutton, Monica, Swain, Andrew, Brookes, Jamie, Cornell, Jonathan, Dolan, Rachael, Hulme, Jonathan, Jansen van Vuuren, Amanda, Jowitt, Tom, Kalashetty, Gunasheela, Lloyd, Fran, Patel, Kiran, Sherwood, Nichola, Brown, Lynne, Chandler, Ben, Deighton, Kerry, Emma, Temlett, Haunch, Kirsty, Cheeseman, Michelle, Dent, Kathy, Garg, Sanjeev, Gray, Carol, Hood, Marion, Jones, Dawn, Juj, Joanne, Rao, Roshan, Walker, Tara, Al Anizi, Mashel, Cheah, Clarissa, Cheing, Yushio, Coutinho, Francisco, Gondo, Prisca, Hadebe, Bernard, Onie Hove, Mazvangu, khader, Ahamed, Krishnachetty, Bobby, Rhodes, Karen, Sokhi, Jagdish, Baker, Katie-Anne, Bertram, Wendy, Looseley, Alex, Mouton, Ronelle, Arnold, Glenn, Arya, Shobhit, Balfoussia, Danai, Baxter, Linden, Harris, Jame, Jones, Craig, Knaggs, Alison, Markar, Sheraz, Perera, Anisha, Scott, Alasdair, Shida, Asako, Sirha, Ravneet, Wright, Sally, Frost, Victoria, Gray, Catherine, MacGregor, Mark, Andrews, Emma, Arrandale, Lindsay, Barrett, Stephen, Cifra, Elna, Cooper, Mariese, Dragnea, Drago, Elna, Cifra, Maclean, Jennifer, Meier, Sonja, Milliken, Donald, Munns, Christopher, Ratanshi, Nadir, Salvana, Abegail, Watson, Anthony, Ali, Hani, Campbell, Gill, Critchley, Rebecca, Hicks, Catherine, Liddle, Alison, Pass, Marc, Ritchie, Charlotte, Thomas, Charlotte, Too, Lingxi, Welsh, Sarah, Gill, Talvinder, Johnson, Joanne, Reed, Joanne, Davis, Edward, Papadopoullos, Sam, Attwood, Clare, Biffen, Andrew, Boulton, Kerenza, Gray, Sophie, Hay, David, Mills, Sarah, Montgomery, Jane, Riddell, Rory, Simpson, Jame, Bhardwaj, Neeraj, Paul, Elaine, Uwubamwen, Nosakhare, Alexander, Maini, Arrich, Jame, Arumugam, Swarna, Blackwood, Dougla, Boggiano, Victoria, Brown, Robyn, Lam Chan, Yik, Chatterjee, Devnandan, Chhabra, Ashok, Christian, Rachel, Costelloe, Hannah, Coxwell Matthewman, Madeline, Dalton, Emma, Darko, Julia, Davari, Maria, Dave, Tejal, Deacon, Matthew, Deepak, Shantal, Edmond, Holly, Ellis, Jessica, El-Sayed, Ahmed, Eneje, Philip, English, Rose, Ewe, Renee, Foers, William, Franklin, John, Gallego, Laura, Garrett, Emily, Goldberg, Olivia, Goss, Harry, Greaves, Rosanna, Harris, Rudy, Hennings, Charle, Jones, Eleanor, Kamali, Nelson, Kokkinos, Naomi, Lewis, Cary, Lignos, Leda, Malgapo, Evaleen Victoria, Malik, Rizwana, Milne, Andrew, Mulligan, John-Patrick, Nicklin, Philippa, Palipane, Natasha, Parsons, Thoma, Piper, Rebecca, Prakash, Rohan, Ramesh, Byron, Rasip, Sarah, Reading, Jacob, Rela, Mariam, Reyes, Anna, Robert, Stephen, Rooms, Martin, Shah, Karishma, Simons, Henry, Solanki, Shalil, Spowart, Emma, Stevens, Amy, Thomas, Christopher, Waggett, Helena, Yassaee, Arrash, Kennedy, Anthony, Scott, Sara, Somanath, Sameer, Berg, Andrew, Hernandez, Miguel, Nanda, Rajesh, Tank, Ghanshyambhai, Wilson, Natalie, Wilson, Debbie, Al-Soudaine, Yassr, Baldwin, Matthew, Cornish, Julie, Davies, Zoe, Davies, Leigh, Edwards, Marc, Frewer, Natasha, Gallard, Sian, Glasbey, Jame, Harries, Rhiannon, Hopkins, Luke, Kim, Taeyang, Koompirochana, Vilavan, Lawson, Simon, Lewis, Megan, Makzal, Zaid, Scourfield, Sarah, Ahmad, Yousra, Bates, Sarah, Blackwell, Clare, Bryant, Helen, Coulter, Suzanne, Cruickshank, Ro, Daniel, Sonya, Daubeny, Thoma, Edwards, Mark, Golder, Kim, Hawkins, Lesley, Helen, Bryant, Hinxman, Honor, Levett, Denny, Skinner, Ben, Walsgrove, Joseph, Dickson, Jane, Constantin, Kathryn, Karen, Markwell, O’Brien, Peter, O’Donohoe, Lynn, Payne, Hannah, Sundayi, Saul, Walker, Elaine, Brooke, Jenny, Cardy, Jon, Humphreys, Sally, Kessack, Laura, Kubitzek, Christiane, Kumar, Suha, Cotterill, Donna, Hodzovic, Emil, Hosdurga, Gurunath, Miles, Edward, Saunders, Glenn, Campbell, Marta, Chan, Peter, Jemmett, Kim, Raj, Ashok, Naik, Aditi, Ramamoorthy, Rajarajan, Shah, Nimesh, Sylvan, Axel, Blyth, Katharine, 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J., Rua, F., Martins, I., Pinho-Oliveira, V.M., Rodrigues, C.M., Cabral, R., Marques, S., Rêgo, S., Teixeira Jesus, J.S., Conceição Marques, M., Romao, C., Dias, S., Santos, A.M., Alves, M.J., Salta, C., Cruz, S., Duarte, C., Furtado Paiva, A.A., do Nascimento Cabral, T., Fariae Maia, D., Correia da Silva, RFM, Langner, A., Oliveira Resendes, H., da Conceição Soares, M., Abrunhosa, A., Faria, F., Miranda, L., Pereira, H., Serra, S., Ionescu, D., Margarit, S., Mitre, C., Vasian, H., Manga, G., Stefan, A., Tomescu, D., Filipescu, D., Paunescu, M.A., Stefan, M., Stoica, R., Gavril, L., Pătrăşcanu, E., Ristescu, I., Rusu, D., Diaconescu, C., Iosep, G.F., Pulbere, D., Ursu, I., Balanescu, A., Grintescu, I., Mirea, L., Rentea, I., Vartic, M., Lupu, M.N., Stanescu, D., Streanga, L., Antal, O., Hagau, N., Patras, D., Petrisor, C., Tosa, F., Tranca, S., Copotoiu, S.M., Ungureanu, L.L., Harsan, C.R., Papurica, M., Cernea, D.D., Dragoescu, N.A., Aflori, L., Vaida, C., Ciobotaru, O.R., Aignatoaie, 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Banner-Goodspeed, V., Boone, M., Campbell, K., Lu, F., Scannell, J., Sobol, J., Balajonda, N., Clemmons, K., Conde, C., Funk, B., Hopkins, T., Olaleye, O., Omer, O., Pender, M., Porto, A., Waweru, P., Yeh, E., Bodansky, D., Evans, A., Kleopoulos, S., Maril, R., Mathney, E., Sanchez, A., Tinuoye, E., Bateman, B., Eng, K., Jiang, N., Ladha, K., Needleman, J., Chen, L.L., Lane, R., Robinowitz, D., Ghushe, N., Irshad, M., Patel, S., Takemoto, S., Wallace, A., Mazzeffi, M., Rock, P., Wallace, K., Zhu, X., Chua, P., Mattera, M., Sharar, R., Thilen, S., Treggiari, M., Morgan, A., Sofjan, I., Subramaniam, K., Avidan, M., Maybrier, H., Muench, M., and Wildes, T.
Subjects: Male, HSJ UCI, Critical Care and Intensive Care Medicine, law.invention, Perioperative Care/methods, 0302 clinical medicine, Surgical procedures, 030202 anesthesiology, law, Critical care/utilisation, Postoperative care/methods, Postoperative care/statistics and numerical data, Surgical procedures, operative/mortality, statistics and numerical data, Prospective Studies, Postoperative Period, Postoperative care/methods, education.field_of_study, Postoperative care/method, Elective Surgical Procedures/mortality, fluid output, Middle Aged, fluid administration, Intensive care unit, Hospitalization, Length of Stay/statistics & numerical data, operative/mortality, Intensive Care Units/statistics & numerical data, outcome, Female, Elective Surgical Procedure, Human, Adult, medicine.medical_specialty, Logistic Model, Postoperative care/statistics and numerical data, Critical care/utilisation, Population, Intensive Care Unit, Elective Surgical Procedures/statistics & numerical data, Hospitalization/statistics & numerical data, Humans, Logistic Models, Surgical procedures, operative/mortality, Postoperative care, methods, Perioperative Care, NO, 03 medical and health sciences, Anesthesiology, Intensive care, medicine, Elective surgery, Intensive care medicine, education, business.industry, 030208 emergency & critical care medicine, Perioperative, Length of Stay, Clinical trial, Prospective Studie, septic shock, business
Abstract: PURPOSE: As global initiatives increase patient access to surgical treatments, there is a need to define optimal levels of perioperative care. Our aim was to describe the relationship between the provision and use of critical care resources and postoperative mortality. METHODS: Planned analysis of data collected during an international 7-day cohort study of adults undergoing elective in-patient surgery. We used risk-adjusted mixed-effects logistic regression models to evaluate the association between admission to critical care immediately after surgery and in-hospital mortality. We evaluated hospital-level associations between mortality and critical care admission immediately after surgery, critical care admission to treat life-threatening complications, and hospital provision of critical care beds. We evaluated the effect of national income using interaction tests. RESULTS: 44,814 patients from 474 hospitals in 27 countries were available for analysis. Death was more frequent amongst patients admitted directly to critical care after surgery (critical care: 103/4317 patients [2%], standard ward: 99/39,566 patients [0.3%]; adjusted OR 3.01 [2.10-5.21]; p < 0.001). This association may differ with national income (high income countries OR 2.50 vs. low and middle income countries OR 4.68; p = 0.07). At hospital level, there was no association between mortality and critical care admission directly after surgery (p = 0.26), critical care admission to treat complications (p = 0.33), or provision of critical care beds (p = 0.70). Findings of the hospital-level analyses were not affected by national income status. A sensitivity analysis including only high-risk patients yielded similar findings. CONCLUSIONS: We did not identify any survival benefit from critical care admission following surgery. info:eu-repo/semantics/publishedVersion
Published: 2017

37. Protective effects of SOCS3 overexpression in high glucose-induced lung epithelial cell injury through the JAK2/STAT3 pathway

Author: Zhongyuan Xia, Yan Leng, Qing‑Tao Meng, Shao‑Qing Lei, Xiao‑Jing Wu, Qian Sun, Wei‑Na Duan, and Min Liu
Subjects: 0301 basic medicine, STAT3 Transcription Factor, Cancer Research, injury, Cell Survival, medicine.medical_treatment, Respiratory Mucosa, Lung injury, Biology, Biochemistry, Stat3 Signaling Pathway, Proinflammatory cytokine, 03 medical and health sciences, human lung epithelial cells, Genetics, medicine, Humans, Viability assay, SOCS3, STAT3, Molecular Biology, Lung, A549 cell, Inflammation, Articles, Lung Injury, Janus Kinase 2, high glucose, Up-Regulation, 030104 developmental biology, Cytokine, Glucose, Oncology, suppressor of cytokine signaling 3, A549 Cells, Suppressor of Cytokine Signaling 3 Protein, Hyperglycemia, Cancer research, biology.protein, Molecular Medicine, Janus kinase2/signal transducers and activators of transcription 3, Signal Transduction
Abstract: Previous studies have suggested that the Janus kinase (JAK)/signal transducers and activators of transcription (STAT) pathway is involved in hyperglycemia‑induced lung injury. The present study aimed to investigate the roles of suppressor of cytokine signaling3 (SOCS3) in the regulation of JAK2/STAT3 activation following high glucose (HG) treatment in A549 human pulmonary epithelial cells. Cell viability was evaluated using Cell Counting Kit-8 and lactate dehydrogenase assays. HG‑induced inflammatory injury in A549 cells was assessed through the evaluation of interleukin‑6 (IL‑6) and tumor necrosis factor‑α (TNF‑α) levels using ELISA. The protein expression levels of SOCS3, JAK2, STAT3, phosphorylated (p)‑JAK2 and p‑STAT3 were determined using western blot analysis. Cellular viability was significantly decreased, whereas IL‑6 and TNF‑α levels were significantly increased, following HG stimulation of A549 cells. In addition, the protein levels of SOCS3, p‑JAK2 and p‑STAT3 were significantly increased in HG‑treated cells. Treatment with the JAK2/STAT3 inhibitor tyrphostin AG490, or SOCS3 overexpression, appeared to prevent the HG‑induced alterations in protein expression. Furthermore, cellular viability was enhanced, whereas the levels of proinflammatory cytokines were suppressed. These finding suggested the involvement of the SOCS3/JAK2/STAT3 signaling pathway in HG‑induced responses in lung cells. Therefore, it may be hypothesized that the inhibition of the JAK2/STAT3 pathway through SOCS3 overexpression may prevent hyperglycemia‑induced lung injury, and may have therapeutic potential for the treatment of patients with diabetic lung injury.
Published: 2017

38. (−)-Epigallocatechin-3-gallate attenuates myocardial injury induced by ischemia/reperfusion in diabetic rats and in H9c2 cells under hyperglycemic conditions

Author: Zhongyuan Xia, Yan Leng, Zhize Chen, Bo Zhao, Jie Zhu, Yang Wu, Juan Dou, Shaoqing Lei, and Qing-Tao Meng
Subjects: Male, 0301 basic medicine, medicine.medical_specialty, Pathology, Cardiotonic Agents, Cardiac fibrosis, Myocardial Infarction, Ischemia, Apoptosis, Myocardial Reperfusion Injury, ischemia, medicine.disease_cause, complex mixtures, Catechin, Diabetes Mellitus, Experimental, Rats, Sprague-Dawley, Superoxide dismutase, 03 medical and health sciences, chemistry.chemical_compound, Sirtuin 1, Malondialdehyde, Internal medicine, Diabetes mellitus, Diabetic cardiomyopathy, Genetics, medicine, Animals, Myocytes, Cardiac, diabetes, biology, Superoxide Dismutase, business.industry, (−)-epigallocatechin-3-gallate, food and beverages, Articles, General Medicine, Hypoxia (medical), medicine.disease, reperfusion, Oxidative Stress, 030104 developmental biology, Endocrinology, chemistry, Hyperglycemia, biology.protein, medicine.symptom, business, Oxidative stress
Abstract: (−)-Epigallocatechin gallate (EGCG) exerts multiple beneficial effects on cardiovascular performance. In this study, we aimed to examine the effects of EGCG on diabetic cardiomyopathy during myocardial ischemia/reperfusion (I/R) injury. EGCG (100 mg/kg/day) was administered at week 6 for 2 weeks to diabetic rats following the induction of type 1 diabetes by streptozotocin (STZ). At the end of week 8, the animals were subjected to myocardial I/R injury. The EGCG-elicited structural and functional effects were analyzed. Additionally, EGCG (20 μM) was administered for 24 h to cultured cardiac H9c2 cells under hyperglycemic conditions (30 mM glucose) prior to hypoxia/reoxygenation (H/R) challenge, and its effects on oxidative stress were compared to H9c2 cells transfecteed with silent information regulator 1 (SIRT1) small interfering RNA (siRNA). In rats with STZ-induced diabetes, EGCG treatment ameliorated post-ischemic cardiac dysfunction, decreased the myocardial infarct size, apoptosis and cardiac fibrosis, and reduced the elevated lactate dehydrogenase (LDH) and malonaldehyde (MDA) levels, and attenuated oxidative stress. Furthermore, EGCG significantly reduced H/R injury in cardiac H9c2 cells exposed to high glucose as evidenced by reduced apoptotic cell death and oxidative stress. The protein expression levels of SIRT1 and manganese superoxide dismutase (MnSOD) were reduced in the diabetic rats and the H9c2 cells under hyperglycemic conditions, compared with the control rats following I/R injury and H9c2 cells under normal glucose conditions. EGCG pre-treatment significantly upregulated the levels of htese proteins in vitro and in vivo. However, treatment with EX527 and SIRT1 siRNA blocked the EGCG-mediated cardioprotective effects. Taken together, our data indicate that SIRT1 plays a critical role in the EGCG-mediated amelioration of I/R injury in diabetic rats, which suggests that EGCG may be a promising dietary supplement for the prevention of diabetic cardiomyopathy.
Published: 2017

39. Propofol protects against hepatic ischemia/reperfusion injury via miR-133a-5p regulating the expression of MAPK6

Author: Zhongyuan Xia, Shaoqing Lei, Wei Hao, Zhi-hui Zhao, Qing-Tao Meng, and Mu-Er Tie
Subjects: 0301 basic medicine, medicine.diagnostic_test, Chemistry, Ischemia, Cell Biology, General Medicine, Pharmacology, Hypoxia (medical), medicine.disease, 03 medical and health sciences, 030104 developmental biology, 0302 clinical medicine, Downregulation and upregulation, Western blot, Apoptosis, In vivo, 030220 oncology & carcinogenesis, medicine, medicine.symptom, Propofol, Reperfusion injury, medicine.drug
Abstract: Propofol has been found to play an important role in hepatic ischemia/reperfusion (I/R) injury with the antioxidant effects. However, the molecular mechanism of propofol in hepatic I/R injury has not been fully understood. Male Sprague-Dawley rats were randomly assigned into Sham group, hepatic I/R group, and propofol treatment group. I/R injury was attained by ischemia for 1 h and reperfusion for 2 h. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activity were detected. QSG-7701 cells were cultured in hypoxia condition for 15 h and then in reoxygenation condition for 6 h to imitate hypoxia/reoxygenation (H/R) injury in vitro. Real-time RT-PCR and Western blot were performed to determine the expression of miR-133a-5p and MAPK6. Luciferase reporter assay was used to determine the regulation of miR-133a-5p on MAPK6. Propofol significantly reduced the activities of serum AST and ALT induced by hepatic I/R injury in rats. Propofol increased the level of miR-133a-5p and decreased the expression of MAPK6 in vivo and in vitro. Luciferase reporter assay showed that MAPK6 was a target of miR-133a-5p. Knockdown of miR-133a-5p abrogated the effect of propofol on the upregulation of MAPK6 induced by H/R. MAPK6 overexpression promoted the cell apoptosis induced by H/R which could be attenuated by propofol. Finally, we found that miR-133a-5p reversed the protective effect of propofol in rats with hepatic I/R injury. Propofol showed protective roles for hepatic I/R injury in vivo and H/R injury in vitro, which involved with miR-133a-5p regulating the expression of MAPK6.
Published: 2017

40. Suppression of Excessive Histone Deacetylases Activity in Diabetic Hearts Attenuates Myocardial Ischemia/Reperfusion Injury via Mitochondria Apoptosis Pathway

Author: Rui Xue, Yang Wu, Zhongyuan Xia, Yan Leng, Liying Zhan, Bo Zhao, and Qing-Tao Meng
Subjects: Male, 0301 basic medicine, medicine.medical_specialty, Article Subject, Endocrinology, Diabetes and Metabolism, Ischemia, Apoptosis, Myocardial Reperfusion Injury, 030204 cardiovascular system & hematology, Mitochondrion, Biology, Hydroxamic Acids, lcsh:Diseases of the endocrine glands. Clinical endocrinology, Histone Deacetylases, Diabetes Mellitus, Experimental, Rats, Sprague-Dawley, 03 medical and health sciences, 0302 clinical medicine, Endocrinology, Internal medicine, medicine, Animals, Myocytes, Cardiac, Protein kinase B, Membrane Potential, Mitochondrial, lcsh:RC648-665, Hypoxia (medical), medicine.disease, Mitochondria, Rats, Histone Deacetylase Inhibitors, 030104 developmental biology, Trichostatin A, Mitochondrial permeability transition pore, medicine.symptom, Reperfusion injury, Research Article, medicine.drug
Abstract: Background. Histone deacetylases (HDACs) play a pivotal role in signaling modification and gene transcriptional regulation that are essential for cardiovascular pathophysiology. Diabetic hearts with higher HDACs activity were more vulnerable to myocardial ischemia/reperfusion (MI/R) injury compared with nondiabetic hearts. We are curious about whether suppression of excessive HDACs activity in diabetic heart protects against MI/R injury. Methods. Diabetic rats were subjected to 45 min of ischemia, followed by 3 h of reperfusion. H9C2 cardiomyocytes were exposed to high glucose for 24 h, followed by 4 h of hypoxia and 2 h of reoxygenation (H/R). Results. Both MI/R injury and diabetes mellitus elevated myocardium HDACs activity. MI/R induced apoptotic cell death was significantly decreased in diabetic rats treated with HDACs inhibitor trichostatin A (TSA). TSA administration markedly moderated dissipation of mitochondrial membrane potential, protected the integrity of mitochondrial permeability transition pore (mPTP), and decreased cell apoptosis. Notably, cotreatment with Akt inhibitor partly or absolutely inhibited the protective effect of TSA in vivo and in vitro. Furthermore, TSA administration activated Akt/Foxo3a pathway, leading to Foxo3a cytoplasm translocation and attenuation proapoptosis protein Bim expression. Conclusions. Both diabetes mellitus and MI/R injury increased cardiac HDACs activity. Suppression of HDACs activity triggered protective effects against MI/R and H/R injury under hyperglycemia conditions through Akt-modulated mitochondrial apoptotic pathways via Foxo3a/Bim.
Published: 2017

41. In reply: Spinal anesthesia for Cesarean delivery in women with COVID-19 infection: questions regarding the cause of hypotension

Author: Qing-Tao Meng, Rong Chen, Qin Zhou, and Yun-Yan Zhang
Subjects: 2019-20 coronavirus outbreak, Pregnancy, medicine.medical_specialty, Coronavirus disease 2019 (COVID-19), business.industry, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Spinal anesthesia, General Medicine, medicine.disease, Anesthesiology and Pain Medicine, Anesthesia, Anesthesiology, Medicine, Cesarean delivery, business, Coronavirus Infections
Published: 2020

42. In reply: Uncertainty in using chest computed tomography in early coronavirus disease (COVID-19)

Author: Qing tao Meng and Rong Chen
Subjects: medicine.medical_specialty, 2019-20 coronavirus outbreak, Coronavirus disease 2019 (COVID-19), Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Pneumonia, Viral, Computed tomography, Disease, medicine.disease_cause, Betacoronavirus, Medicine, Pandemics, Tomography, Coronavirus, medicine.diagnostic_test, SARS-CoV-2, business.industry, Uncertainty, COVID-19, General Medicine, Anesthesiology and Pain Medicine, Anesthesia, Radiology, Coronavirus Infections, business
Published: 2020

43. Chest computed tomography images of early coronavirus disease (COVID-19)

Author: Rong Chen, Qing-Tao Meng, and Jun Chen
Subjects: Adult, Male, medicine.medical_specialty, 2019-20 coronavirus outbreak, Coronavirus disease 2019 (COVID-19), Pneumonia, Viral, Computed tomography, medicine.disease_cause, Pregnancy, X ray computed, medicine, Humans, Pregnancy Complications, Infectious, Pandemics, Coronavirus, medicine.diagnostic_test, Cesarean Section, business.industry, Disease progression, Infant, Newborn, COVID-19, General Medicine, medicine.disease, Infectious Disease Transmission, Vertical, Pneumonia, Anesthesiology and Pain Medicine, Anesthesia, Disease Progression, Female, Radiology, Tomography, Coronavirus Infections, Tomography, X-Ray Computed, business
Published: 2020

44. Long non-coding RNA MALAT1 functions as a mediator in cardioprotective effects of fentanyl in myocardial ischemia-reperfusion injury

Author: Zhongyuan Xia, Zhi-hui Zhao, Shaoqing Lei, Xiao-bing Du, Qing-Tao Meng, and Wei Hao
Subjects: 0301 basic medicine, Gene knockdown, Cell, Cell Biology, General Medicine, Pharmacology, Hypoxia (medical), medicine.disease, 03 medical and health sciences, chemistry.chemical_compound, 030104 developmental biology, medicine.anatomical_structure, Downregulation and upregulation, chemistry, Apoptosis, Lactate dehydrogenase, medicine, medicine.symptom, Reperfusion injury, Cardiac muscle cell
Abstract: Long non-coding (lncRNA) MALAT1 can be increased by hypoxia or ischemic limbs. Also, downregulation of MALAT1 contributes to reduction of cardiomyocyte apoptosis. However, the functional involvement of MALAT1 in myocardial ischemia-reperfusion (I/R) injury has not been defined. This study investigated the functional involvement of lncRNA-MALAT1 in cardioprotective effects of fentanyl. HL-1, a cardiac muscle cell line from the AT-1 mouse atrial cardiomyocyte tumor lineage was pre-treated with fentanyl and generated cell model of hypoxia-reoxygenation (H/R). Relative expression of MALAT1, miR-145, and Bnip3 mRNA in cells was determined by quantitative real-time PCR. Cardiomyocyte H/R injury was indicated by lactate dehydrogenase (LDH) release and cell apoptosis. The results showed that fentanyl abrogates expression of responsive gene for H/R and induces downregulation of MALAT1 and Bnip3 and upregulation of miR-145. We found that miR-145/Bnip3 pathway was negatively regulated by MALAT1 in H/R-HL-1 cell with or without fentanyl treatment. Moreover, both MALAT1 overexpression and miR-145 knockdown reverse cardioprotective effects of fentanyl, as indicated by increase in LDH release and cell apoptosis. The reversal effect of MALAT1 for fentanyl is confirmed in cardiac ischemia/reperfusion (I/R) mice. In summary, lncRNA-MALAT1 is sensitive to H/R injury and abrogates cardioprotective effects of Fentanyl by negatively regulating miR-145/Bnip3 pathway.
Published: 2016

45. Pri-miR-34b/c rs4938723 Polymorphism is Associated with Decreased Risk and Better Prognosis for Colorectal Cancer Patients

Author: Xiaobo Li, Mirza Muhammad Faran Ashraf Baig, Said Abasse Kassim, Chengcheng Zhang, Rui Chen, Muhammad Abbas, Xi Yang, Shenshen Wu, and Qing Tao Meng
Subjects: 0301 basic medicine, Adult, Male, Risk, medicine.medical_specialty, Genotype, Colorectal cancer, Single-nucleotide polymorphism, medicine.disease_cause, Gastroenterology, Polymorphism, Single Nucleotide, 03 medical and health sciences, 0302 clinical medicine, Asian People, Internal medicine, medicine, Odds Ratio, Humans, In patient, Genetic Predisposition to Disease, Promoter Regions, Genetic, business.industry, General Medicine, Odds ratio, Middle Aged, medicine.disease, Prognosis, MicroRNAs, 030104 developmental biology, Apoptosis, 030220 oncology & carcinogenesis, Colonic Neoplasms, Female, Carcinogenesis, business, Mir 34b c
Abstract: Colorectal cancer (CRC) is a major cause of cancer-related deaths worldwide. miR-34 induces changes of its downstream genes and plays a key role in altering the apoptotic cycle and pathways of downstream cells and therefore influences carcinogenesis.The present study investigated whether the single nucleotide polymorphism rs4938723TC in the promoter of region of miR-34b/c may increase the risk of CRC and influence outcome in patients with CRC.We enrolled 1078 CRC patients and 1175 cancer-free controls subjects from the Chinese population. miR-34b/c rs4938723TC polymorphisms were genotyped using a TaqMan PCR method.We found that subjects carrying rs4938723CT/CC genotypes have significantly decreased risk of CRC (adjusted odds ratios (AOR) = 0.75, 95% CI (0.63-0.90) for CT vs.TT; AOR = 0.61, 95% CI (0.46-0.83) for CC vs. TT and AOR = 0.73,95% CI (0.61-0.86) for CT/CC vs. TT) and a significant increased median survival time (MST) compared with those with TT genotypes (MST = 96.500; 75.883 and 71.370 months for CT, CC and CT/CC respectively vs. MST = 54.300 months for TT, p0.0001). Stratified analysis by both life style and clinicopathological risks revealed that subjects carrying rs4938723CT/CC genotypes were remained significantly associated with increased survival and low risk of CRC compared with those with TT genotypes in all subgroup (all p0.05). Similar observation was also reported for the prognostic value of rs4938723TC/CC genotypes across all subgroups.These findings indicate that the miR-34b/c rs4938723TC polymorphism is an independent variable and associated with a decreased risk of CRC in Chinese population. This study provides evidence of the protective effects of rs4938723CT/CC genotypes in the development of CRC.
Published: 2019

46. The Pathway of Let-7a-1/2-3p and HMGB1 Mediated Dexmedetomidine Inhibiting Microglia Activation in Spinal Cord Ischemia-Reperfusion Injury Mice

Author: Qing-Tao Meng, Zhongyuan Xia, Ming Nuo, and Ha Sen Ta Na
Subjects: 0301 basic medicine, Male, Stimulation, Pharmacology, HMGB1, 03 medical and health sciences, Cellular and Molecular Neuroscience, Mice, 0302 clinical medicine, Downregulation and upregulation, medicine, Animals, HMGB1 Protein, Cells, Cultured, Gene knockdown, biology, Microglia, Chemistry, Interleukin-6, Tumor Necrosis Factor-alpha, General Medicine, Analgesics, Non-Narcotic, Spinal cord, medicine.disease, Mice, Inbred C57BL, Microglial cell activation, MicroRNAs, 030104 developmental biology, medicine.anatomical_structure, Spinal Cord, Reperfusion Injury, biology.protein, Reperfusion injury, 030217 neurology & neurosurgery, Dexmedetomidine
Abstract: Microglial cell activation after spinal cord ischemia-reperfusion injury (SCIRI) commonly causes the secondary nerve motion function injury. This study aims to study the mechanism by which the drug dexmedetomidine (DEX) inhibits microglial cell activation and improves motion function of SCIRI mice. Mice SCIRI model was established, and microglia from spinal cord were isolated and cultured for subsequent molecule analysis of let-7a-1-3p, let-7a-2-3p, HMGB1, TNF-α, and IL-6. DEX was given by intraperitoneal injection. Mice motion function was evaluated by Basso mouse score. In vitro microglial cells were subjected to oxygen and glucose deprivation/reoxygenation (OGD/R) to imitate ischemia-reperfusion injury stimulation. DEX injection improves the mouse motion function in SCIRI model and upregulates let-7a-1/2-3p expression in the isolated activated microglia from SCIRI mice. In OGD/R-stimulated microglia, DEX treatment also caused the inactivation of cells, the upregulation of let-7a-1/2-3p expression, and the downregulation of HMGB1 expression. While the co-silencing of let-7a-1/2-3p in microglia in addition to DEX treatment restored the activation of microglia. HMGB1 is a targeted gene for let-7a-1/2-3p and negatively regulated by them. HMGB1 knockdown abrogates the pro-activation impact on microglial cell by let-7a-1/2-3p silencing. DEX inhibits the activation of microglial cell in the spinal cord of SCIRI mice, mediated by the let-7a-1/2-3p/HMGB1 pathway.
Published: 2019

47. Propofol alleviates oxidative stress via upregulating lncRNA-TUG1/Brg1 pathway in hypoxia/reoxygenation hepatic cells

Author: Ha Sen Ta Na, Nuo Ming, Qing-Tao Meng, Zhongyuan Xia, and Jin-Ling He
Subjects: Male, Immunoprecipitation, Pharmacology, medicine.disease_cause, Biochemistry, 03 medical and health sciences, Mice, 0302 clinical medicine, Downregulation and upregulation, medicine, Gene silencing, Animals, Viability assay, Hypoxia, Molecular Biology, Propofol, 030304 developmental biology, 0303 health sciences, Chemistry, DNA Helicases, Nuclear Proteins, General Medicine, Hypoxia (medical), medicine.disease, Up-Regulation, Mice, Inbred C57BL, Oxygen, Oxidative Stress, 030220 oncology & carcinogenesis, Hepatic stellate cell, Hepatocytes, RNA, Long Noncoding, medicine.symptom, Reperfusion injury, Oxidative stress, Transcription Factors
Abstract: Reducing oxidative stress is an effective method to prevent hepatic ischaemia/reperfusion injury (HIRI). This study focuses on the role of propofol on the oxidative stress of hepatic cells and the involved lncRNA-TUG1/Brahma-related gene 1 (Brg1) pathway in HIRI mice. The mouse HIRI model was established and was intraperitoneally injected with propofol postconditioning. Hepatic injury indexes were used to evaluate HIRI. The oxidative stress was indicated by increasing 8-isoprostane concentration. Mouse hepatic cell line AML12 was treated with hypoxia and subsequent reoxygenation (H/R). The targeted regulation of lncRNA-TUG1 on Brg1 was proved by RNA pull-down, RIP (RNA-binding protein immunoprecipitation) and the expression level of Brg1 responds to silencing or overexpression of lncRNA-TUG1. Propofol alleviates HIRI and induces the upregulation of lncRNA-TUG1 in the mouse HIRI model. Propofol increases cell viability and lncRNA-TUG1 expression level in H/R-treated hepatic cells. In H/R plus propofol-treated hepatic cells, lncRNA-TUG1 silencing reduces cell viability and increased oxidative stress. LncRNA-TUG1 interacts with Brg1 protein and keeps its level via inhibiting its degradation. Brg1 overexpression reverses lncRNA-TUG1 induced the reduction of cell viability and the increase in oxidative stress. LncRNA-TUG1 silencing abrogates the protective role of propofol against HIRI in the mouse HIRI model. LncRNA-TUG1 has a targeted regulation of Brg1, and thereby affects the oxidative stress induced by HIRI. This pathway mediates the protective effect of propofol against HIRI of hepatic cell.
Published: 2019

48. Histone Deacetylase Inhibitor MS-275 Alleviates Postoperative Cognitive Dysfunction in Rats by Inhibiting Hippocampal Neuroinflammation

Author: Jiabao Hou, Yang Wu, Yan Leng, Bo Zhao, Lili Chen, Xu-Ke Liu, Juan Dou, Qing-Tao Meng, Xing Wan, and Qianni Shen
Subjects: 0301 basic medicine, Male, medicine.drug_class, Pyridines, Morris water navigation task, Hippocampus, Pharmacology, Neuroprotection, Histone Deacetylases, Histones, Rats, Sprague-Dawley, 03 medical and health sciences, 0302 clinical medicine, Postoperative Cognitive Complications, medicine, Animals, Maze Learning, Neuroinflammation, Inflammation, business.industry, Histone deacetylase 2, General Neuroscience, Histone deacetylase inhibitor, Transcription Factor RelA, medicine.disease, Rats, Histone Deacetylase Inhibitors, 030104 developmental biology, Benzamides, Cytokines, Histone deacetylase, business, Postoperative cognitive dysfunction, 030217 neurology & neurosurgery
Abstract: Neuroinflammation in the hippocampus plays essential roles in postoperative cognitive dysfunction (POCD). Histone deacetylases (HDACs) have recently been identified as key regulators of neuroinflammation. MS-275, an inhibitor of HDAC, has been reported to have neuroprotective effects. Therefore, the present study aimed to test the hypothesis that pretreatment with MS-275 prevents POCD by inhibiting neuroinflammation in rats. In this study, anesthesia/surgery impaired cognition, demonstrated by an increase escape latency and reduction in the number of platform crossings in Morris water maze (MWM) trials, through activating microglia neuroinflammation and decreasing PSD-95 expression. However, pretreatment with MS-275 attenuated postoperative cognitive impairment severity. Furthermore, pretreatment with MS-275 decreased activated microglia levels and increased PSD95 protein expression in the hippocampus. Pretreatment with MS-275 reduced NF-κB-p65 protein expression and nuclear accumulation as well as the neuroinflammatory response (production of proinflammatory cytokines including TNF-α and IL-1β) in the hippocampus. Additionally, MS-275 reduced HDAC2 expression and HDAC activity in the hippocampus, which were enhanced in vehicle-treated rats. These results suggest that MS-275 alleviates postoperative cognitive dysfunction by reducing neuroinflammation in the hippocampus of rats via HDAC inhibition.
Published: 2018

49. DOCOSAHEXAENOIC ACID PROTECTS RAT ASTROCYTES FROM OXYGEN-GLUCOSE DEPRIVATION/REPERFUSION INJURY BY ACTIVATING PPARG AND DOWNSTREAM ANG/TIE2 AND PI3K/AKT SIGNALING PATHWAYS.

Author: YAN-LI YU, HAI-BIN FANG#, ZHEN QIU, QING-TAO MENG, and BIN ZHOU
Subjects: DOCOSAHEXAENOIC acid, ASTROCYTES, OXYGEN, REPERFUSION injury, ANGIOPOIETIN-2, APOPTOSIS
Abstract: Docosahexaenoic acid (DHA) has been shown to alleviate cerebral ischemia/reperfusion (I/R) injury, but the underlying mechanisms remain unclear. Increasing the angiopoietin 1 (Ang1)/ angiopoietin 2 (Ang2) ratio and activating angiopoietin (Ang)/tyrosine 2 kinase (Tie2) signaling and its downstream PI3K/Akt pathway in the early stages of brain ischemic injury are considered promising strategies. However, whether DHA could activate Ang/Tie2 and PI3K/Akt signaling and then reduce apoptosis and provide protective effects to the brain after I/R injury remains to be studied. Rat primary astrocytes cultured in vitro were divided into groups, treated with or without DHA, and then subjected to 24 h of oxygenglucose deprivation (OGD) followed by 6 h of reoxygenation (R). Cell viability was tested by CCK-8 kits; the release of lactate dehydrogenase (LDH), Ang-1, Ang-2, PPARγ and vascular endothelial growth factor (VEGF) was detected by using ELISA kits; the cell apoptosis rate was assessed by TUNEL flow cytometry; and the expression of the Bcl-2, Bax and Caspase-3 proteins was evaluated by western blotting. Astrocytes subjected to OGD/R exhibited lower cell viability and higher lactate dehydrogenase (LDH) activity. Pretreatment with DHA notably reduced rat astrocyte OGD/R injury, as evidenced by increased cell viability and a decreased apoptosis rate and LDH activity, accompanied by increased levels of Ang1, phosphorylated Tie2, phosphorylated Akt, PPARγ and Bcl-2 and decreased levels of Ang2, Bax and Caspase- 3. However, these effects were completely reversed by the inhibitor of peroxisome-proliferator- -activated receptors (PPARγ) GW9662. Thus, DHA could exert protective effects against OGD/R injury by activating PPARγ and the downstream Ang/Tie2 and PI3K/Akt signaling pathways. [ABSTRACT FROM AUTHOR]
Published: 2021
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50. Overexpression of DJ-1 reduces oxidative stress and attenuates hypoxia/reoxygenation injury in NRK-52E cells exposed to high glucose

Author: Shaoqing Lei, Qing-Tao Meng, Rui Xue, Ling-Hua Tang, Zhongyuan Xia, Bo Zhao, Zi-ying Shen, Qian Sun, and Rong Chen
Subjects: 0301 basic medicine, DJ-1, Time Factors, Protein Deglycase DJ-1, medicine.disease_cause, Antioxidants, Kidney Tubules, Proximal, chemistry.chemical_compound, Malondialdehyde, oxidative stress, Articles, General Medicine, Cell Hypoxia, high glucose, Cystine, medicine.symptom, medicine.medical_specialty, Cell Survival, NF-E2-Related Factor 2, Blotting, Western, Biology, Transfection, Cell Line, Superoxide dismutase, 03 medical and health sciences, Lactate dehydrogenase, Internal medicine, Genetics, medicine, Animals, Viability assay, Dose-Response Relationship, Drug, Renal ischemia, Superoxide Dismutase, NRK-52E cells, Epithelial Cells, hypoxia/reoxygenation injury, Hypoxia (medical), Molecular biology, Rats, Oxygen, Glucose, 030104 developmental biology, Endocrinology, chemistry, Apoptosis, biology.protein, Heme Oxygenase-1, Oxidative stress
Abstract: Patients with diabetes are more vulnerable to renal ischemia/reperfusion (I/R) injury, which is implicated in hyperglycemia-induced oxidative stress. We previously reported that the hyperglycemia-induced inhibition of DJ-1, a novel oncogene that exhibits potent antioxidant activity, is implicated in the severity of myocardial I/R injury. In the present study, we aimed to explore the role of DJ-1 in hypoxia/reoxygenation (H/R) injury in renal cells exposed to high glucose (HG). For this purpose, NRK-52E cells were exposed to HG (30 mM) for 48 h and then exposed to hypoxia for 4 h and reoxygenation for 2 h, which significantly decreased cell viability and superoxide dismutase (SOD) activity, and increased the malondialdehyde (MDA) content, accompanied by a decrease in DJ-1 protein expression. The overexpression of DJ-1 by transfection with a DJ-1 overexpression plasmid exerted protective effects against HG-induced H/R injury, as evidenced by increased CCK-8 levels and SOD activity, the decreased release of lactate dehydrogenase (LDH) and the decreased MDA content, and increased nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and heme oxygenase-1 (HO-1) expression. Similar effects were observed following treatment with the antioxidant, N-acetylcysteine. These results suggest that the overexpression of DJ-1 reduces oxidative stress and attenuates H/R injury in NRK-52E cells exposed to HG.
Published: 2016

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