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  1. Article ; Online: Findings of lung ultrasonography of novel corona virus pneumonia during the 2019-2020 epidemic.

    Peng, Qian-Yi / Wang, Xiao-Ting / Zhang, Li-Na

    Intensive care medicine

    2020  Volume 46, Issue 5, Page(s) 849–850

    MeSH term(s) COVID-19 ; Epidemics ; Humans ; Lung/diagnostic imaging ; Pneumonia ; SARS-CoV-2 ; Ultrasonography
    Keywords covid19
    Language English
    Publishing date 2020-03-12
    Publishing country United States
    Document type Letter
    ZDB-ID 80387-x
    ISSN 1432-1238 ; 0340-0964 ; 0342-4642 ; 0935-1701
    ISSN (online) 1432-1238
    ISSN 0340-0964 ; 0342-4642 ; 0935-1701
    DOI 10.1007/s00134-020-05996-6
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    Zs.A 1089: Show issues Location:
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  2. Article ; Online: Using echocardiography to guide the treatment of novel coronavirus pneumonia.

    Peng, Qian-Yi / Wang, Xiao-Ting / Zhang, Li-Na

    Critical care (London, England)

    2020  Volume 24, Issue 1, Page(s) 143

    MeSH term(s) Betacoronavirus ; COVID-19 ; Coronavirus Infections/physiopathology ; Coronavirus Infections/therapy ; Critical Illness ; Echocardiography ; Heart/physiology ; Humans ; Pandemics ; Pneumonia, Viral/physiopathology ; Pneumonia, Viral/therapy ; SARS-CoV-2
    Keywords covid19
    Language English
    Publishing date 2020-04-10
    Publishing country England
    Document type Editorial
    ZDB-ID 2041406-7
    ISSN 1466-609X ; 1364-8535
    ISSN (online) 1466-609X
    ISSN 1364-8535
    DOI 10.1186/s13054-020-02856-z
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    Zs.A 5517: Show issues Location:
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  3. Article ; Online: Hippocampus-prefrontal cortex inputs modulate spatial learning and memory in a mouse model of sepsis induced by cecal ligation puncture.

    Ge, Cheng-Long / Chen, Wei / Zhang, Li-Na / Ai, Yu-Hang / Zou, Yu / Peng, Qian-Yi

    CNS neuroscience & therapeutics

    2022  Volume 29, Issue 1, Page(s) 390–401

    Abstract: Aims: Sepsis-associated encephalopathy (SAE) often leads to cognitive impairments. However, the pathophysiology of SAE is complex and unclear. Here, we investigated the role of hippocampus (HPC)-prefrontal cortex (PFC) in cognitive dysfunction in sepsis ...

    Abstract Aims: Sepsis-associated encephalopathy (SAE) often leads to cognitive impairments. However, the pathophysiology of SAE is complex and unclear. Here, we investigated the role of hippocampus (HPC)-prefrontal cortex (PFC) in cognitive dysfunction in sepsis induced by cecal ligation puncture (CLP) in mice.
    Methods: The neural projections from the HPC to PFC were first identified via retrograde tracing and viral expression. Chemogenetic activation of the HPC-PFC pathway was shown via immunofluorescent staining of c-Fos-positive neurons in PFC. Morris Water Maze (MWM) and Barnes maze (BM) were used to evaluate cognitive function. Western blotting analysis was used to determine the expression of glutamate receptors and related molecules in PFC and HPC.
    Results: Chemogenetic activation of the HPC-PFC pathway enhanced cognitive dysfunction in CLP-induced septic mice. Glutamate receptors mediated the effects of HPC-PFC pathway activation in CLP mice. The activation of the HPC-PFC pathway resulted in significantly increased levels of NMDAR, AMPAR, and downstream signaling molecules including CaMKIIa, pCREB, and BDNF in PFC. However, inhibition of glutamate receptors using 2,3-dihydroxy-6-nitro-7-sulphamoyl-benzo (F)quinoxaline (NBQX), which is an α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR inhibitor), or D-2-amino-5-phosphonopentanoate (D-AP5), which is an NMDA receptor antagonist abolished this increase.
    Conclusion: Our study reveals the important role of the HPC-PFC pathway in improving cognitive dysfunction in a mouse model of CLP sepsis and provides a novel pathogenetic mechanism for SAE.
    MeSH term(s) Mice ; Animals ; Spatial Learning ; Sepsis/complications ; Sepsis/metabolism ; Sepsis-Associated Encephalopathy ; Hippocampus/metabolism ; Prefrontal Cortex/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Punctures
    Chemical Substances Receptors, N-Methyl-D-Aspartate
    Language English
    Publishing date 2022-11-15
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2423461-8
    ISSN 1755-5949 ; 1755-5930
    ISSN (online) 1755-5949
    ISSN 1755-5930
    DOI 10.1111/cns.14013
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    Zs.A 4537: Show issues Location:
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  4. Article ; Online: Effect of β-blockers on mortality in patients with sepsis: A propensity-score matched analysis.

    Ge, Cheng-Long / Zhang, Li-Na / Ai, Yu-Hang / Chen, Wei / Ye, Zhi-Wen / Zou, Yu / Peng, Qian-Yi

    Frontiers in cellular and infection microbiology

    2023  Volume 13, Page(s) 1121444

    Abstract: Objectives: We aimed to evaluate the association between β-blocker therapy and mortality in patients with sepsis.: Methods: Patients with sepsis were selected from the Medical Information Mart for Intensive Care (MIMIC)-III. Propensity score matching ...

    Abstract Objectives: We aimed to evaluate the association between β-blocker therapy and mortality in patients with sepsis.
    Methods: Patients with sepsis were selected from the Medical Information Mart for Intensive Care (MIMIC)-III. Propensity score matching (PSM) was used to balance the baseline differences. A multivariate Cox regression model was used to assess the relationship between β-blocker therapy and mortality. The primary outcome was the 28-day mortality.
    Results: A total of 12,360 patients were included in the study, involving 3,895 who received β-blocker therapy and 8,465 who did not. After PSM, 3,891 pairs of patients were matched. The results showed that β-blockers were associated with improved 28- (hazards ratio (HR) 0.78) and 90-day (HR 0.84) mortality. Long-acting β-blockers were associated with improved 28-day survival (757/3627 [20.9%] vs. 583/3627 [16.1%],
    Conclusions: β-blockers were associated with improved 28- and 90-day mortality in patients with sepsis and septic shock. Long-acting β-blocker therapy may have a protective role in patients with sepsis, reducing the 28-day and 90-day mortality. However, short-acting β-blocker (esmolol) treatment did not reduce the mortality in sepsis.
    MeSH term(s) Humans ; Propensity Score ; Sepsis/drug therapy ; Adrenergic beta-Antagonists/therapeutic use ; Shock, Septic/drug therapy ; Retrospective Studies
    Chemical Substances Adrenergic beta-Antagonists
    Language English
    Publishing date 2023-03-28
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2619676-1
    ISSN 2235-2988 ; 2235-2988
    ISSN (online) 2235-2988
    ISSN 2235-2988
    DOI 10.3389/fcimb.2023.1121444
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Inhibition of CD38/Cyclic ADP-ribose Pathway Protects Rats against Ropivacaine-induced Convulsion.

    Zou, Yu / He, Xin / Peng, Qian-Yi / Guo, Qu-Lian

    Chinese medical journal

    2017  Volume 130, Issue 19, Page(s) 2354–2360

    Abstract: Background: The CD38/cyclic ADP-ribose (cADPR) pathway plays a role in various central nervous system diseases and in morphine tolerance, but its role in local anesthetic intoxication is unknown. The aim of this study was to determine the role of the ... ...

    Abstract Background: The CD38/cyclic ADP-ribose (cADPR) pathway plays a role in various central nervous system diseases and in morphine tolerance, but its role in local anesthetic intoxication is unknown. The aim of this study was to determine the role of the CD38/cADPR pathway in ropivacaine-induced convulsion.
    Methods: Forty male Sprague-Dawley rats were randomly divided into five groups (n = 8 per group): sham group, ropivacaine group, ropivacaine+8-Br-cADPR (5 nmol) group, ropivacaine+8-Br-cADPR (10 nmol) group, and ropivacaine+8-Br-cADPR (20 nmol) group (no rats died). Rats were intracerebroventricularly injected with normal saline or 8-Br-cADPR 30 min before receiving an intraperitoneal injection of ropivacaine. Electroencephalography and convulsion behavior scores were recorded. The hippocampus was harvested from each group and subjected to nicotinamide adenine dinucleotide and cADPR assays, Western blotting analysis, and malondialdehyde (MDA) and superoxide dismutase (SOD) assays.
    Results: Intraperitoneal injection of ropivacaine (33.8 mg/kg) induced convulsions in rats. CD38 and cADPR levels increased significantly following ropivacaine-induced convulsion (P = 0.031 and 0.020, respectively, compared with the sham group). Intraventricular injection of 8-Br-cADPR (5, 10, and 20 nmol) significantly prolonged convulsion latency (P = 0.037, 0.034, and 0.000, respectively), reduced convulsion duration (P = 0.005, 0.005, and 0.005, respectively), and reduced convulsion behavior scores (P = 0.015, 0.015, and 0.000, respectively). Intraventricular injection of 8-Br-cADPR (10 nmol) also increased the B-cell lymphoma-2 (Bcl-2)/Bcl-2-associated X protein ratio (P = 0.044) and reduced cleaved Caspase 3/Caspase 3 ratio, inducible nitric oxide synthase, MDA and SOD levels (P = 0.014, 0.044, 0.001, and 0.010, respectively) compared with the ropivacaine group.
    Conclusions: The CD38/cADPR pathway is activated in ropivacaine-induced convulsion. Inhibiting this pathway alleviates ropivacaine-induced convulsion and protects the brain from apoptosis and oxidative stress.
    Language English
    Publishing date 2017-10-05
    Publishing country China
    Document type Journal Article
    ZDB-ID 127089-8
    ISSN 0366-6999 ; 1002-0187
    ISSN 0366-6999 ; 1002-0187
    DOI 10.4103/0366-6999.215333
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  8. Article ; Online: Lung ultrasound score based on the BLUE-plus protocol is associated with the outcomes and oxygenation indices of intensive care unit patients.

    Peng, Qian-Yi / Liu, Li-Xia / Zhang, Qian / Zhu, Ying / Zhang, Hong-Min / Yin, Wan-Hong / He, Wei / Shang, Xiu-Ling / Chao, Yan-Gong / Lv, Li-Wen / Wang, Xiao-Ting / Zhang, Li-Na

    Journal of clinical ultrasound : JCU

    2021  Volume 49, Issue 7, Page(s) 704–714

    Abstract: Purpose: The primary objective was to demonstrate the relationship between lung ultrasound (LUS) manifestations and the outcomes of intensive care unit (ICU) patients. The secondary objective was to determine the characteristics of LUS manifestations in ...

    Abstract Purpose: The primary objective was to demonstrate the relationship between lung ultrasound (LUS) manifestations and the outcomes of intensive care unit (ICU) patients. The secondary objective was to determine the characteristics of LUS manifestations in different subgroups of ICU patients.
    Methods: This prospective multi-center cohort study was conducted in 17 ICUs. A total of 1702 patients admitted between August 31, 2017 and February 16, 2019 were included. LUS was performed according to the bedside lung ultrasound in emergency (BLUE)-plus protocol, and LUS scores were calculated. Data on the outcomes and oxygenation indices were analyzed and compared between different primary indication groups.
    Results: The LUS scores were significantly higher for non-survivors than for survivors and were significantly different between the oxygenation index groups, with higher scores in the lower oxygenation index groups. The LUS score was an independent risk factor for the 28-day mortality. The area under the receiver operating characteristic curve was 0.663 for prediction of the 28-day mortality and 0.748 for prediction of an oxygenation index ≤100.
    Conclusions: The LUS score based on the BLUE-plus protocol was an independent risk factor for the 28-day mortality and was important for the prediction of an oxygenation index ≤100. An early LUS score within 24 hours of ICU admission helps predicting the outcome of ICU patients.
    MeSH term(s) Cohort Studies ; Humans ; Intensive Care Units ; Lung/diagnostic imaging ; Prospective Studies ; Ultrasonography
    Language English
    Publishing date 2021-06-11
    Publishing country United States
    Document type Journal Article ; Multicenter Study
    ZDB-ID 189393-2
    ISSN 1097-0096 ; 0091-2751
    ISSN (online) 1097-0096
    ISSN 0091-2751
    DOI 10.1002/jcu.23024
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  9. Article: Blocking Cyclic Adenosine Diphosphate Ribose-mediated Calcium Overload Attenuates Sepsis-induced Acute Lung Injury in Rats.

    Peng, Qian-Yi / Zou, Yu / Zhang, Li-Na / Ai, Mei-Lin / Liu, Wei / Ai, Yu-Hang

    Chinese medical journal

    2016  Volume 129, Issue 14, Page(s) 1725–1730

    Abstract: Background: Acute lung injury (ALI) is a common complication of sepsis that is associated with high mortality. Intracellular Ca2+ overload plays an important role in the pathophysiology of sepsis-induced ALI, and cyclic adenosine diphosphate ribose ( ... ...

    Abstract Background: Acute lung injury (ALI) is a common complication of sepsis that is associated with high mortality. Intracellular Ca2+ overload plays an important role in the pathophysiology of sepsis-induced ALI, and cyclic adenosine diphosphate ribose (cADPR) is an important regulator of intracellular Ca2+ mobilization. The cluster of differentiation 38 (CD38)/cADPR pathway has been found to play roles in multiple inflammatory processes but its role in sepsis-induced ALI is still unknown. This study aimed to investigate whether the CD38/cADPR signaling pathway is activated in sepsis-induced ALI and whether blocking cADPR-mediated calcium overload attenuates ALI.
    Methods: Septic rat models were established by cecal ligation and puncture (CLP). Rats were divided into the sham group, the CLP group, and the CLP+ 8-bromo-cyclic adenosine diphosphate ribose (8-Br-cADPR) group. Nicotinamide adenine dinucleotide (NAD+), cADPR, CD38, and intracellular Ca2+ levels in the lung tissues were measured at 6, 12, 24, and 48 h after CLP surgery. Lung histologic injury, tumor necrosis factor (TNF)-μ, malondialdehyde (MDA) levels, and superoxide dismutase (SOD) activities were measured.
    Results: NAD+, cADPR, CD38, and intracellular Ca2+ levels in the lungs of septic rats increased significantly at 24 h after CLP surgery. Treatment with 8-Br-cADPR, a specific inhibitor of cADPR, significantly reduced intracellular Ca2+ levels (P = 0.007), attenuated lung histological injury (P = 0.023), reduced TNF-μ and MDA levels (P < 0.001 and P = 0.002, respectively) and recovered SOD activity (P = 0.031) in the lungs of septic rats.
    Conclusions: The CD38/cADPR pathway is activated in the lungs of septic rats, and blocking cADPR-mediated calcium overload with 8-Br-cADPR protects against sepsis-induced ALI.
    MeSH term(s) ADP-ribosyl Cyclase 1/metabolism ; Acute Lung Injury/chemically induced ; Acute Lung Injury/drug therapy ; Animals ; Calcium/metabolism ; Cyclic ADP-Ribose/analogs & derivatives ; Cyclic ADP-Ribose/antagonists & inhibitors ; Cyclic ADP-Ribose/metabolism ; Cyclic ADP-Ribose/therapeutic use ; Male ; Malondialdehyde/metabolism ; Rats ; Rats, Sprague-Dawley ; Sepsis/complications ; Superoxide Dismutase/metabolism ; Tumor Necrosis Factor-alpha/metabolism
    Chemical Substances 8-bromo-cyclic-ADP-ribose ; Tumor Necrosis Factor-alpha ; Cyclic ADP-Ribose (119340-53-3) ; Malondialdehyde (4Y8F71G49Q) ; Superoxide Dismutase (EC 1.15.1.1) ; ADP-ribosyl Cyclase 1 (EC 3.2.2.6) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2016-07-20
    Publishing country China
    Document type Journal Article
    ZDB-ID 127089-8
    ISSN 0366-6999 ; 1002-0187
    ISSN 0366-6999 ; 1002-0187
    DOI 10.4103/0366-6999.185854
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  10. Article ; Online: Hemin protects against oxygen-glucose deprivation-induced apoptosis activation via neuroglobin in SH-SY5Y cells.

    Wang, Yun-Jia / Peng, Qian-Yi / Deng, Song-Yun / Chen, Cai-Xia / Wu, Long / Huang, Li / Zhang, Li-Na

    Neurochemical research

    2017  Volume 42, Issue 8, Page(s) 2208–2217

    Abstract: This study aimed to investigate the mechanism underlying the neuroprotective effect of hemin in oxygen-glucose deprivation (OGD)-treated neurons. OGD-treated SH-SY5Y cells (human neuroblastoma cells) were used in the study. The cellular viability of SH- ... ...

    Abstract This study aimed to investigate the mechanism underlying the neuroprotective effect of hemin in oxygen-glucose deprivation (OGD)-treated neurons. OGD-treated SH-SY5Y cells (human neuroblastoma cells) were used in the study. The cellular viability of SH-SY5Y cells was assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, and the cell apoptosis rate was determined by flow cytometry analysis with Annexin V-fluorescein isothiocyanate and propidium iodide staining with or without hemin pretreatment. Cell viability and apoptotic activation were detected after hemin administration combined with neuroglobin (Nqb), thioredoxin-1, peroxiredoxin-2, or heme oxygenase-1 siRNA transient transfection. The release of cytochrome c from mitochondria and the interaction between Ngb and cytochrome c were examined with hemin pretreatment. Hemin had a neuroprotective effect in OGD-treated SH-SY5Y cells, which was mainly mediated by the upregulation of Ngb. Moreover, the release of cytochrome c from mitochondria was inhibited by hemin-induced Ngb expression through facilitating the interaction of Ngb with cytochrome c in mitochondria. The present findings provided new insights into the neuroprotective mechanisms of hemin. It was concluded that low-dose hemin pretreatment had a neuroprotective effect in OGD-treated SH-SY5Y cells, through inhibiting cell apoptosis. The neuroprotective effects of hemin following hypoxic-ischemic neuronal damage were mainly mediated by Ngb. One underlying mechanism was hemin-induced overexpression of mitochondrial Ngb, which inhibited endogenous apoptosis via the association with cytochrome c.
    Language English
    Publishing date 2017-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 199335-5
    ISSN 1573-6903 ; 0364-3190
    ISSN (online) 1573-6903
    ISSN 0364-3190
    DOI 10.1007/s11064-017-2230-z
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