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  • 1
    Online Resource
    Online Resource
    BML-111, a Lipoxin Receptor Agonist, Attenuates Ventilator-Induced Lung Injury in Rats
    Ovid Technologies (Wolters Kluwer Health) ; 2014
    In:  Shock Vol. 41, No. 4 ( 2014-04), p. 311-316
    Details
    In: Shock, Ovid Technologies (Wolters Kluwer Health), Vol. 41, No. 4 ( 2014-04), p. 311-316
    Type of Medium: Online Resource
    ISSN: 1073-2322
    URL: Article
    DOI: 10.1097/SHK.0000000000000104
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2014
    detail.hit.zdb_id: 2011863-6
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  • 2
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    Table_2.XLSX
    Frontiers Media SA ; 2020
    In:  Frontiers in Microbiology Vol. 11 ( 2020-12-23)
    Details
    In: Frontiers in Microbiology, Frontiers Media SA, Vol. 11 ( 2020-12-23)
    Abstract: SARS-coronavirus-2–induced immune dysregulation and inflammatory responses are involved in the pathogenesis of coronavirus disease-2019 (COVID-19). However, very little is known about immune cell and cytokine alterations in specific organs of COVID-19 patients. Here, we evaluated immune cells and cytokines in postmortem tissues, i.e., lungs, intestine, liver, kidneys, and spleen of three patients with COVID-19. Imaging mass cytometry revealed monocyte, macrophage, and dendritic cell (DC) infiltration in the lung, intestine, kidney, and liver tissues. Moreover, in patients with COVID-19, natural killer T cells infiltrated the liver, lungs, and intestine, whereas B cells infiltrated the kidneys, lungs, and intestine. CD11b + macrophages and CD11c + DCs also infiltrated the lungs and intestine, a phenomenon that was accompanied by overproduction of the immunosuppressive cytokine interleukin (IL)-10. However, CD11b + macrophages and CD11c + DCs in the lungs or intestine of COVID-19 patients did not express human leukocyte antigen DR isotype. In contrast, tumor necrosis factor (TNF)-α expression was higher in the lungs, intestine, liver, and kidneys, but not in the spleen, of all COVID-19 patients (compared to levels in controls). Collectively, these findings suggested that IL-10 and TNF-α as immunosuppressive and pro-inflammatory agents, respectively,—might be prognostic and could serve as therapeutic targets for COVID-19.
    Type of Medium: Online Resource
    ISSN: 1664-302X
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fmicb.2020.600989
    DOI: 10.3389/fmicb.2020.600989.s001
    DOI: 10.3389/fmicb.2020.600989.s002
    DOI: 10.3389/fmicb.2020.600989.s003
    DOI: 10.3389/fmicb.2020.600989.s004
    DOI: 10.3389/fmicb.2020.600989.s005
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2020
    detail.hit.zdb_id: 2587354-4
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  • 3
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    Death-associated Protein Kinase 1 Mediates Ventilator-induced Lung Injury in Mice by Promoting Alveolar Epithelial Cell Apoptosis
    Ovid Technologies (Wolters Kluwer Health) ; 2020
    In:  Anesthesiology Vol. 133, No. 4 ( 2020-10-01), p. 905-918
    Details
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 133, No. 4 ( 2020-10-01), p. 905-918
    Abstract: Alveolar epithelial cell apoptosis is implicated in the onset of ventilator-induced lung injury. Death-associated protein kinase 1 (DAPK1) is associated with cell apoptosis. The hypothesis was that DAPK1 participates in ventilator-induced lung injury through promoting alveolar epithelial cell apoptosis. Methods Apoptosis of mouse alveolar epithelial cell was induced by cyclic stretch. DAPK1 expression was altered (knockdown or overexpressed) in vitro by using a small interfering RNA or a plasmid, respectively. C57/BL6 male mice (n = 6) received high tidal volume ventilation to establish a lung injury model. Adeno-associated virus transfection of short hairpin RNA and DAPK1 inhibitor repressed DAPK1 expression and activation in lungs, respectively. The primary outcomes were alveolar epithelial cell apoptosis and lung injury. Results Compared with the control group, the 24-h cyclic stretch group showed significantly higher alveolar epithelial cell apoptotic percentage (45 ± 4% fold vs. 6 ± 1% fold; P & lt; 0.0001) and relative DAPK1 expression, and this group also demonstrated a reduced apoptotic percentage after DAPK1 knockdown (27 ± 5% fold vs. 53 ± 8% fold; P & lt; 0.0001). A promoted apoptotic percentage in DAPK1 overexpression was observed without stretching (49 ± 6% fold vs. 14 ± 3% fold; P & lt; 0.0001). Alterations in B-cell lymphoma 2 and B-cell lymphoma 2–associated X are associated with DAPK1 expression. The mice subjected to high tidal volume had higher DAPK1 expression and alveolar epithelial cell apoptotic percentage in lungs compared with the low tidal volume group (43 ± 6% fold vs. 4 ± 2% fold; P & lt; 0.0001). Inhibition of DAPK1 through adeno-associated virus infection or DAPK1 inhibitor treatment appeared to be protective against lung injury with reduced lung injury score, resolved pulmonary inflammation, and repressed alveolar epithelial cell apoptotic percentage (47 ± 4% fold and 48 ± 6% fold; 35 ± 5% fold and 34 ± 4% fold; P & lt; 0.0001, respectively). Conclusions DAPK1 promotes the onset of ventilator-induced lung injury by triggering alveolar epithelial cell apoptosis through intrinsic apoptosis pathway in mice. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New
    Type of Medium: Online Resource
    ISSN: 0003-3022 , 1528-1175
    URL: Article
    DOI: 10.1097/ALN.0000000000003464
    RVK:
    XA 22600
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2020
    detail.hit.zdb_id: 2016092-6
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  • 4
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    Protectin DX increases survival in a mouse model of sepsis by ameliorating inflammation and modulating macrophage phenotype
    Springer Science and Business Media LLC ; 2017
    In:  Scientific Reports Vol. 7, No. 1 ( 2017-03-07)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 7, No. 1 ( 2017-03-07)
    Abstract: Recently, a serial of studies have demonstrated that lipid mediators derived from Omega-3 fatty acid docosahexaenoic acid have pro-resolving or anti-inflammatory effects in many inflammatory diseases. Here, we sought to evaluate whether Protectin DX (PDX, an isomer of Protecin D1), a newly identified lipid mediator, could protect mice against sepsis and explore the underling mechanism. Animal model of sepsis was established by cecum ligation and puncture (CLP). We found that PDX increased overall survival rate within eight days and attenuated multiple organ injury in septic mice. In addition, PDX reduced pro-inflammatory cytokines and bacterial load 24 h after CLP. Moreover, PDX promoted phagocytosis of peritoneal macrophages and increased the percentage of M2 macrophages in peritoneum of septic mice. In vitro , M2 macrophage markers (Arg1 and Ym1) and its transcriptional regulator (peroxisome proliferator-activated receptor-γ, PPAR-γ) were upregulated in Raw264.7 macrophages challenged with PDX. GW9662 (a PPAR-γ inhibitor) and PPAR-γ siRNA abrogated the induction of Arg1 and Ym1 by PDX in Raw264.7 cells. Taken together, our results suggest that PDX is able to promote M2 polarization, enhance phagocytosis activity of macrophage and accelerate resolution of inflammation, finally leading to increased survival rate of septic mice.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/s41598-017-00103-0
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2017
    detail.hit.zdb_id: 2615211-3
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  • 5
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    Resolvin D1 attenuates mechanical stretch-induced pulmonary fibrosis via epithelial-mesenchymal transition
    American Physiological Society ; 2019
    In:  American Journal of Physiology-Lung Cellular and Molecular Physiology Vol. 316, No. 6 ( 2019-06-01), p. L1013-L1024
    Details
    In: American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society, Vol. 316, No. 6 ( 2019-06-01), p. L1013-L1024
    Abstract: Mechanical ventilation-induced pulmonary fibrosis plays an important role in the high mortality rate of acute respiratory distress syndrome (ARDS). Resolvin D1 (RvD1) displays potent proresolving activities. Epithelial-mesenchymal transition (EMT) has been proved to be an important pathological feature of lung fibrosis. This study aimed to investigate whether RvD1 can attenuate mechanical ventilation-induced lung fibrosis. Human lung epithelial (BEAS-2B) cells were pretreated with RvD1 for 30 min and exposed to acid for 10 min before being subjected to mechanical stretch for 48 h. C57BL/6 mice were subjected to intratracheal acid aspiration followed by mechanical ventilation 24 h later (peak inspiratory pressure 22 cmH 2 O, positive end-expiratory pressure 2 cmH 2 O, and respiratory rate 120 breaths/min for 2 h). RvD1 was injected into mice for 5 consecutive days after mechanical ventilation. Treatment with RvD1 significantly inhibited mechanical stretch-induced mesenchymal markers (vimentin and α-smooth muscle actin) and stimulated epithelial markers (E-cadherin). Tert-butyloxycarbonyl 2 (BOC-2), a lipoxin A4 receptor/formyl peptide receptor 2 (ALX/FPR2) antagonist, is known to inhibit ALX/FPR2 function. BOC-2 could reverse the beneficial effects of RvD1. The antifibrotic effect of RvD1 was associated with the suppression of Smad2/3 phosphorylation. This study demonstrated that mechanical stretch could induce EMT and pulmonary fibrosis and that treatment with RvD1 could attenuate mechanical ventilation-induced lung fibrosis, thus highlighting RvD1 as an effective therapeutic agent against pulmonary fibrosis associated with mechanical ventilation.
    Type of Medium: Online Resource
    ISSN: 1040-0605 , 1522-1504
    URL: Article
    DOI: 10.1152/ajplung.00415.2018
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2019
    detail.hit.zdb_id: 1477300-4
    SSG: 12
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  • 6
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    Death-Associated Protein Kinase 1 Promotes Alveolar Epithelial Cell Apoptosis and Ventilator-Induced Lung Injury Through P53 Pathway
    Ovid Technologies (Wolters Kluwer Health) ; 2022
    In:  Shock Vol. 57, No. 1 ( 2022-01), p. 140-150
    Details
    In: Shock, Ovid Technologies (Wolters Kluwer Health), Vol. 57, No. 1 ( 2022-01), p. 140-150
    Abstract: Mechanical stretch-induced alveolar epithelial cell (AEC) apoptosis participates in the onset of ventilator-induced lung injury (VILI). In this study, we explored whether death-associated protein kinase 1 (DAPK1) mediated cyclic stretch (CS)-induced AEC apoptosis and VILI though P53 pathway. Materials and Methods: AEC apoptosis was induced by CS using the FX-5000T Flexercell Tension Plus system. C57BL/6 mouse received high tidal volume ventilation to build VILI model. DAPK1 inhibitor, P53 inhibitor, or DAPK1 plasmid was used to regulate the expression of DAPK1 and P53, respectively. Flow cytometery was performed to assay cell apoptosis and the changes of mitochondrial membrane potential (MMP); immunoblotting was adopted to analyze related protein expression. The binding of related proteins was detected by coimmunoprecipitation; AEC apoptosis in vivo was determined by immunohistochemistry assay. Results: CS promoted AEC apoptosis, increased DAPK1 and P53 expression, and induced the binding of DAPK1 and P53; inhibition of DAPK1 or P53 reduced CS-induced AEC apoptosis, suppressed the expression of Bax, increased Bcl-2 level, and stabilized MMP; AEC apoptosis and the level of P53 were both increased after overexpressing of DAPK1. Moreover, DAPK1 plasmid transfection also promoted the expression of Bax and the change of MMP, but decreased the level of Bcl-2. Inhibition of DAPK1 or P53 in vivo alleviated high tidal volume ventilation-induced AEC apoptosis and lung injury. Conclusions: DAPK1 contributes to AEC apoptosis and the onset of VILI though P53 and its intrinsic pro-apoptotic pathway. Inhibition of DAPK1 or P53 alleviates high tidal volume ventilation-induced lung injury and AEC apoptosis.
    Type of Medium: Online Resource
    ISSN: 1073-2322 , 1540-0514
    URL: Article
    DOI: 10.1097/SHK.0000000000001831
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2022
    detail.hit.zdb_id: 2011863-6
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  • 7
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    Online Resource
    Maresin 1 Maintains the Permeability of Lung Epithelial Cells In Vitro and In Vivo
    Springer Science and Business Media LLC ; 2016
    In:  Inflammation Vol. 39, No. 6 ( 2016-12), p. 1981-1989
    Details
    In: Inflammation, Springer Science and Business Media LLC, Vol. 39, No. 6 ( 2016-12), p. 1981-1989
    Type of Medium: Online Resource
    ISSN: 0360-3997 , 1573-2576
    URL: Article
    DOI: 10.1007/s10753-016-0433-0
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2016
    detail.hit.zdb_id: 2015610-8
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  • 8
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    Maresin 1 Inhibits Epithelial-to-Mesenchymal Transition in Vitro and Attenuates Bleomycin Induced Lung Fibrosis in Vivo
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Shock Vol. 44, No. 5 ( 2015-11), p. 496-502
    Details
    In: Shock, Ovid Technologies (Wolters Kluwer Health), Vol. 44, No. 5 ( 2015-11), p. 496-502
    Type of Medium: Online Resource
    ISSN: 1073-2322
    URL: Article
    DOI: 10.1097/SHK.0000000000000446
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 2011863-6
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  • 9
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    Plasma metabolomic and lipidomic alterations associated with COVID-19
    Oxford University Press (OUP) ; 2020
    In:  National Science Review Vol. 7, No. 7 ( 2020-07-01), p. 1157-1168
    Details
    In: National Science Review, Oxford University Press (OUP), Vol. 7, No. 7 ( 2020-07-01), p. 1157-1168
    Abstract: The pandemic of the coronavirus disease 2019 (COVID-19) has become a global public health crisis. The symptoms of COVID-19 range from mild to severe, but the physiological changes associated with COVID-19 are barely understood. In this study, we performed targeted metabolomic and lipidomic analyses of plasma from a cohort of patients with COVID-19 who had experienced different symptoms. We found that metabolite and lipid alterations exhibit apparent correlation with the course of disease in these patients, indicating that the development of COVID-19 affected their whole-body metabolism. In particular, malic acid of the TCA cycle and carbamoyl phosphate of the urea cycle result in altered energy metabolism and hepatic dysfunction, respectively. It should be noted that carbamoyl phosphate is profoundly down-regulated in patients who died compared with patients with mild symptoms. And, more importantly, guanosine monophosphate (GMP), which is mediated not only by GMP synthase but also by CD39 and CD73, is significantly changed between healthy subjects and patients with COVID-19, as well as between the mild and fatal cases. In addition, dyslipidemia was observed in patients with COVID-19. Overall, the disturbed metabolic patterns have been found to align with the progress and severity of COVID-19. This work provides valuable knowledge about plasma biomarkers associated with COVID-19 and potential therapeutic targets, as well as an important resource for further studies of the pathogenesis of COVID-19.
    Type of Medium: Online Resource
    ISSN: 2095-5138 , 2053-714X
    URL: Article
    DOI: 10.1093/nsr/nwaa086
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2020
    detail.hit.zdb_id: 2745465-4
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  • 10
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    The rate of missed diagnosis of lower-limb DVT by ultrasound amounts to 50% or so in patients without symptoms of DVT : A meta-analysis
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Medicine Vol. 98, No. 37 ( 2019-09), p. e17103-
    Details
    In: Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 98, No. 37 ( 2019-09), p. e17103-
    Abstract: To assess whether the ultrasound (US) is a reliable approach in detecting lower-limb deep-vein thrombosis (DVT) in patients without symptoms of DVT. Methods: The research team performed a systematic search in PubMed, Ovid, Cochrane, and Web of Science without language or date restrictions. Full-text reports on prospective diagnostic studies involve the detection of lower-limb proximal and distal DVT in patients without symptoms of DVT using US and venography. A meta-analysis was performed using Meta-DiSc (version 1.4), providing the pooled sensitivity, specificity, positive (LR+) and negative (LR–) likelihood ratios of the detection accuracy of US. There were 4 different classes of subgroup analysis—the class of patients stratified by location of US exam (proximal, distal, whole leg), the class stratified by technique (color/doppler, compression, both modalities), the class stratified by kind of surgery (orthopedic, otherwise hospitalized) and the class stratified by era of publishing (1980s, 1990s, 2000s). The study quality and the risk of bias were evaluated using QUADAS-2, with heterogeneity was assessed and quantified by the Q score and I 2 statistics, respectively. Results: The meta-analysis included 26 articles containing 41 individual studies with a total of 3951 patients without symptoms of DVT. Using venography as the gold standard, US for proximal DVT had a pooled sensitivity of 59% (95% confidence interval (CI) = 51%–66%) and a pooled specificity of 98% (95% CI = 97%–98%), US for distal DVT had a poor sensitivity of 43% (95% CI = 38%–48%) and a pooled specificity of 95% (95% CI = 94%–96%), US for whole-leg DVT had a pooled sensitivity of 59% (95% CI = 54%–64%) and a pooled specificity of 95% (95% CI = 94%–96%), US for post-major orthopedic surgery patients had a pooled sensitivity of 52% (95% CI = 49%–55%), and US for other types of patients had a pooled sensitivity of 58% (95% CI = 43%–72%). Pure compression technique for DVT had a poor sensitivity of 43% (95% CI = 39%–48%), pure color/doppler technique for DVT had a pooled sensitivity of 58% (95% CI = 53%–63%), compression and color/doppler technique for DVT had a pooled sensitivity of 61% (95% CI = 48%–74%). Conclusion: US could be a useful tool for diagnosing DVT, but it has a lower positive rate and a higher false negative rate. The rate of missed diagnosis of lower-limb DVT by US amounts to 50% or so in the patients without symptoms of DVT. The negative results do not preclude the possibility of DVT and if appropriate heightened surveillance and continued monitoring or try a more accurate inspection method is warranted. The whole leg evaluation and color/doppler technique should be the preferred approach.
    Type of Medium: Online Resource
    ISSN: 0025-7974 , 1536-5964
    URL: Article
    DOI: 10.1097/MD.0000000000017103
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 2049818-4
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