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  • Hindawi Limited  (19)
  • Liu, Hao  (19)
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  • Hindawi Limited  (19)
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  • 1
    In: Human Mutation, Hindawi Limited, Vol. 41, No. 1 ( 2020-01), p. 212-221
    Type of Medium: Online Resource
    ISSN: 1059-7794 , 1098-1004
    URL: Issue
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2020
    detail.hit.zdb_id: 1498165-8
    SSG: 12
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  • 2
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2022 ( 2022-9-29), p. 1-19
    Abstract: Lung ischemia-reperfusion injury (LIRI) is a severe multifaceted pathological condition that can lead to poor patient outcome where oxidative stress and the resulting inflammatory response can trigger and exacerbate tissue damage in LIRI patients. Sirtuin3 (SIRT3), a member of the sirtuin family, protects against oxidative stress-related diseases. However, it remains unclear if and how SIRT3 alleviates lung injury induced by ischemia/reperfusion (I/R). Our previous study showed that lung tissue structures were severely damaged at 6 h after lung I/R in mice, however, repair of the injured lung tissue was significant at 24 h. In this study, we found that both SIRT3 mRNA and protein levels were markedly increased at 24 h after lung I/R in vivo. Meanwhile, inhibition of SIRT3 aggravated lung injury and inflammation, augmented mitochondrial fission and oxidative stress and increased Hypoxia-inducible factor-1α (HIF-1α) expression in vivo. The results suggest that SIRT3 may be an upstream regulator of HIF-1α expression. Knockdown of SIRT3 resulted in excessive mitochondrial fission and increased oxidative stress in vitro, and we found that knocking down the expression of HIF-1α alleviated these changes. This suggests that the SIRT3-HIF-1α signaling pathway is involved in regulating mitochondrial function and oxidative stress. Furthermore, inhibition of dynamin-related protein 1 (Drp-1) by the inhibitor of mitophagy, Mdivi-1, blocked mitochondrial fission and alleviated oxidative stress in vitro. Taken together, our results demonstrated that downregulation of SIRT3 aggravates LIRI by increasing mitochondrial fission and oxidative stress. Activation of SIRT3 inhibits mitochondrial fission and this mechanism may serve as a new therapeutic strategy to treat LIRI.
    Type of Medium: Online Resource
    ISSN: 1942-0994 , 1942-0900
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2022
    detail.hit.zdb_id: 2455981-7
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  • 3
    In: Pain Research and Management, Hindawi Limited, Vol. 2020 ( 2020-01-11), p. 1-7
    Abstract: Objective . To investigate the change of spinopelvic sagittal balance and clinical outcomes after posterior lumbar interbody fusion (PLIF) in patients with degenerative spondylolisthesis (DS), especially the relationship between sagittal spinopelvic parameters and persistent low back pain (PLBP). Methods . 107 patients who were diagnosed with DS and underwent PLIF in our department were enrolled retrospectively in the present study. Sagittal spinopelvic parameters including lumbar lordosis (LL), segmental lordosis (SL), height of the disc (HOD), sacral slope (SS), pelvic incidence (PI), and pelvic tilt (PT) were recorded pre- and postoperatively. Sagittal balance and clinical outcomes were compared between patients with and without PLBP. Pearson correlation was used to analyze the change of sagittal balance parameters and clinical functions. Logistic regression analysis was performed to examine the risk factors of PLBP. Results . It showed significant improvements of SL, HOD, and PT postoperatively. Both the Numeric Rating Scale (NRS) and Oswestry Disability Index (ODI) had significant improvement postoperatively. Change of PT and SL also differed observably between patients with and without PLBP. SL and PT were correlated with NRS and ODI, and insufficient restoration of PT was an independent factor for PLBP. Conclusion . The sagittal balance parameters and clinical outcomes can be improved markedly via PLIF for treating DS. Restoration of SL and PT was correlated with satisfactory outcomes, and adequate improvement of PT may have positive impact on reducing PLBP.
    Type of Medium: Online Resource
    ISSN: 1203-6765 , 1918-1523
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2020
    detail.hit.zdb_id: 2048409-4
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  • 4
    Online Resource
    Online Resource
    Hindawi Limited ; 2022
    In:  Oxidative Medicine and Cellular Longevity Vol. 2022 ( 2022-6-6), p. 1-11
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2022 ( 2022-6-6), p. 1-11
    Abstract: Millions of people worldwide suffer from osteoporosis, which causes bone fragility and increases the risk of fractures. Osteoporosis is closely related to the inhibition of osteogenesis and the enhancement of osteoclastogenesis. In addition, chronic inflammation and macrophage polarization may contribute to osteoporosis as well. Macrophages, crucial to inflammatory responses, display different phenotypes under the control of microenvironment. There are two major phenotypes, classically activated macrophages (M1) and alternatively activated macrophages (M2). Generally, M1 macrophages mainly lead to bone resorption, while M2 macrophages result in osteogenesis. M1/M2 ratio reflects the “fluid” state of macrophage polarization, and the imbalance of M1/M2 ratio may cause disease such as osteoporosis. Additionally, antioxidant drugs, such as melatonin, are applied to change the state of macrophage polarization and to treat osteoporosis. In this review, we introduce the mechanisms of macrophage polarization-mediated bone resorption and bone formation and the contribution to the clinical strategies of osteoporosis treatment.
    Type of Medium: Online Resource
    ISSN: 1942-0994 , 1942-0900
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2022
    detail.hit.zdb_id: 2455981-7
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  • 5
    In: International Journal of Clinical Practice, Hindawi Limited, Vol. 2022 ( 2022-2-16), p. 1-11
    Abstract: Introduction. This is a retrospective comparative study that aims to compare the benefits of different surgical approaches for patients with multilevel cervical canal stenosis (CCS) without cervical fracture or dislocation of acute traumatic central cord syndrome (ATCCS). Methods. From January 2015 to December 2018, 59 patients were included in the study. Among them, 35 patients (Group A) received anterior surgery and 24 patients (Group B) received posterior surgery. Primary outcome measures were American Spinal Cord Injury Association (Asia) grade, Japanese Orthopaedic Association (JOA) score, and recovery rate (RR). Secondary outcome measures included operation time, intraoperative blood loss, visual analogue scale (VAS) score, cervical sagittal parameters, and complications. Multivariate linear regression was used to analyze prognostic determinants. Results. Compared with Group B, Group A had longer operation time and more intraoperative blood loss ( P 〈 0.05 ). However, the VAS score of Group B was higher than that of Group A at discharge ( P 〈 0.05 ). There was no significant difference in cervical sagittal plane parameters between the two groups ( P 〉 0.05 ). Postoperative complications were different in the two groups. During follow-up, the Asia grade, the JOA score, and RR of both groups improved ( P 〈 0.05 ), but there were no significant differences between the two groups ( P 〉 0.05 ). Younger age, earlier surgery, and better preoperative Asia grade were correlated with better prognosis. Conclusions. For patients with multilevel CCS without cervical fracture or dislocation of ATCCS, both surgical approaches had good outcomes. Although no significant differences were found in the primary outcome measures between the two groups, there were different recommendations for the secondary outcome measures. Younger age, earlier surgery, and better preoperative Asia grade were protective factors for better prognosis.
    Type of Medium: Online Resource
    ISSN: 1742-1241 , 1368-5031
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2022
    detail.hit.zdb_id: 2135320-7
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  • 6
    Online Resource
    Online Resource
    Hindawi Limited ; 2020
    In:  Complexity Vol. 2020 ( 2020-10-29), p. 1-11
    In: Complexity, Hindawi Limited, Vol. 2020 ( 2020-10-29), p. 1-11
    Abstract: Brain networks provide essential insights into the diagnosis of functional brain disorders, such as Alzheimer’s disease (AD). Many machine learning methods have been applied to learn from brain images or networks in Euclidean space. However, it is still challenging to learn complex network structures and the connectivity of brain regions in non-Euclidean space. To address this problem, in this paper, we exploit the study of brain network classification from the perspective of graph learning. We propose an aggregator based on extreme learning machine (ELM) that boosts the aggregation ability and efficiency of graph convolution without iterative tuning. Then, we design a graph neural network named GNEA (Graph Neural Network with ELM Aggregator) for the graph classification task. Extensive experiments are conducted using a real-world AD detection dataset to evaluate and compare the graph learning performances of GNEA and state-of-the-art graph learning methods. The results indicate that GNEA achieves excellent learning performance with the best graph representation ability in brain network classification applications.
    Type of Medium: Online Resource
    ISSN: 1099-0526 , 1076-2787
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2020
    detail.hit.zdb_id: 2004607-8
    SSG: 11
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  • 7
    In: BioMed Research International, Hindawi Limited, Vol. 2021 ( 2021-12-22), p. 1-16
    Abstract: Lung ischemia reperfusion injury (LIRI) is a complex pathophysiological process with high morbidity and mortality. An important pathophysiological characteristic of LIRI is endothelial barrier dysfunction, although the mechanism involved in this process remains unclear. VX765, a specific caspase-1 inhibitor, has been shown to have a protective effect against several diseases including sepsis, atherosclerosis, and glial inflammatory disease. The objective of this study was to determine whether VX765 had a protective effect in LIRI. The results showed that lung ischemia/reperfusion (I/R) and oxygen/glucose deprivation and reoxygenation (OGD/R) induced endothelial pyroptosis and barrier dysfunction characterized by an inflammatory response. Treatment with VX765 successfully alleviated I/R- and OGD/R-induced endothelial pyroptosis and barrier dysfunction by inhibiting caspase-1 in vivo and in vitro. In conclusion, these findings showed that VX765 provided effective protection against lung I/R-induced endothelial pyroptosis and barrier dysfunction.
    Type of Medium: Online Resource
    ISSN: 2314-6141 , 2314-6133
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2021
    detail.hit.zdb_id: 2698540-8
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  • 8
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2022 ( 2022-1-18), p. 1-22
    Abstract: Accumulation of senescent bone marrow-derived mesenchymal stem cells (BMMSCs) has led to an age-related bone loss. However, the role of stem cell senescence in estrogen deficiency-induced osteoporosis remains elusive. Though melatonin plays a vital role in bone metabolism regulation, the underlying mechanisms of melatonin-mediated antiosteoporosis are partially elucidated. Therefore, this study purposed to explore (1) whether estrogen deficiency causes cellular senescence of BMMSCs, and if so, (2) the potential of melatonin in preventing bone loss via senescence signaling inhibition. BMMSCs derived from ovariectomized (OVX) rats (OVX BMMSCs) showed an impaired osteogenic capacity, albeit having comparable levels of senescence biomarkers than the sham cells. When exposed to low levels of hydrogen peroxide (H2O2), OVX BMMSCs rapidly exhibited senescence-associated phenotypes such as the increased activity of senescence-associated β-galactosidase (SA-β-gal) and upregulation of cell cycle inhibitors. Notably, the in vitro treatment with melatonin hindered H2O2-induced senescence in OVX BMMSCs and restored their osteogenic capacity. Treatment with either SIRT1 inhibitor (sirtinol) or melatonin receptor antagonists (luzindole and 4-P-PDOT) eliminated melatonin protective effects, thus indicating its potential in preventing stem cell senescence via SIRT1 activation through the melatonin membrane receptors. Following in vivo intravenous administration with melatonin, it successfully protected the bone microstructure and preserved the antisenescence property of BMMSCs in OVX rats. Collectively, our findings demonstrated that melatonin protected against estrogen deficiency-related bone loss by improving the resistance of BMMSCs to cellular senescence. Therefore, melatonin-mediated antisenescence effect on stem cells provides vital information to facilitate the development of a novel and effective strategy for treating postmenopausal OP.
    Type of Medium: Online Resource
    ISSN: 1942-0994 , 1942-0900
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2022
    detail.hit.zdb_id: 2455981-7
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  • 9
    Online Resource
    Online Resource
    Hindawi Limited ; 2021
    In:  Evidence-Based Complementary and Alternative Medicine Vol. 2021 ( 2021-03-20), p. 1-9
    In: Evidence-Based Complementary and Alternative Medicine, Hindawi Limited, Vol. 2021 ( 2021-03-20), p. 1-9
    Abstract: This study aimed to evaluate the efficacy of cinobufotalin combined with gefitinib in the treatment of lung cancer. A549 cells were treated with gefitinib, cinobufotalin, or cinobufotalin plus gefitinib. MTT assay, annexin-V/PI staining and flow cytometry, TUNEL staining, DCFH-DA staining, Western blot, and real-time RT-PCR were performed to investigate the synergistic inhibitory effect of cinobufotalin combined with gefitinib on the growth of A549 cells. Results showed that cinobufotalin synergized with gefitinib displayed inhibited cell viability and enhanced apoptosis in the combination group. Cinobufotalin combined with gefitinib induced a significant enhancement in reactive oxygen species (ROS) production accompanied by cell cycle arrest in the S phase arrest, characterized by upregulation of p21 and downregulation of cyclin A, cyclin E, and CDK2. Besides, cinobufotalin plus gefitinib downregulated the levels of HGF and c-Met. In summary, cinobufotalin combined with gefitinib impedes viability and facilitates apoptosis of A549 cells, indicating that the combined therapy might be a new promising treatment for lung cancer patients who are resistant to gefitinib.
    Type of Medium: Online Resource
    ISSN: 1741-4288 , 1741-427X
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2021
    detail.hit.zdb_id: 2148302-4
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  • 10
    Online Resource
    Online Resource
    Hindawi Limited ; 2019
    In:  Oxidative Medicine and Cellular Longevity Vol. 2019 ( 2019-04-17), p. 1-15
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2019 ( 2019-04-17), p. 1-15
    Abstract: Background . Activation of cell apoptosis is a major form of cell death during myocardial ischemia/reperfusion injury (I/RI). Therefore, examining ways to control cell apoptosis has important clinical significance for improving postischemic recovery. Clinical evidence demonstrated that miR-181c-5p was significantly upregulated in the early phase of myocardial infarction. However, whether or not miR-181c-5p mediates cardiac I/RI through cell apoptosis pathway is unknown. Thus, the present study is aimed at investigating the role and the possible mechanism of miR-181c-5p in apoptosis during I/R injury by using H9C2 cardiomyocytes. Methods and Results . The rat origin H9C2 cardiomyocytes were subjected to hypoxia/reoxygenation (H/R, 6 hours hypoxia followed by 6 hours reoxygenation) to induce cell injury. The results showed that H/R significantly increased the expression of miR-181c-5p but not miR-181c-3p in H9C2 cells. In line with this, in an in vivo rat cardiac I/RI model, miR-181c-5p expression was also significantly increased. The overexpression of miR-181c-5p by its agomir transfection significantly aggravated H/R-induced cell injury (increased lactate dehydrogenase level and reduced cell viability) and exacerbated H/R-induced cell apoptosis (greater cleaved caspases 3 expression, Bax/Bcl-2 and more TUNEL-positive cells). In contrast, inhibition of miR-181c-5p in vitro had the opposite effect. By using computational prediction algorithms, protein tyrosine phosphatase nonreceptor type 4 (PTPN4) was predicted as a potential target gene of miR-181c-5p and was verified by the luciferase reporter assay. The overexpression of miR-181c-5p significantly attenuated the mRNA and protein expression of PTPN4 in H9C2 cardiomyocytes. Moreover, knockdown of PTPN4 significantly aggravated H/R-induced enhancement of LDH level, cleaved caspase 3 expression, and apoptotic cell death, which mimicked the proapoptotic effects of miR-181c-5p in H9C2 cardiomyocytes. Conclusions . These findings suggested that miR-181c-5p exacerbates H/R-induced cardiomyocyte injury and apoptosis via targeting PTPN4 and that miR-181c-5p/PTPN4 signaling may yield novel strategies to combat myocardial I/R injury.
    Type of Medium: Online Resource
    ISSN: 1942-0900 , 1942-0994
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2019
    detail.hit.zdb_id: 2455981-7
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