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  1. Article ; Online: Effect of topdressing time on spring maize yield and nitrogen utilization in black soil of northeast China.

    Zheng, Yu / Ji, Jinghong / Liu, Shuangquan

    Scientific reports

    2023  Volume 13, Issue 1, Page(s) 11841

    Abstract: Topdressing time is crucial to achieving a high yield. To determine the optimum topdressing time for spring maize in the black soil of northeast China in the "one base and one topdressing" mode, the effects of topdressing time of nitrogen (N) fertilizer ... ...

    Abstract Topdressing time is crucial to achieving a high yield. To determine the optimum topdressing time for spring maize in the black soil of northeast China in the "one base and one topdressing" mode, the effects of topdressing time of nitrogen (N) fertilizer on maize yield, N utilization, and inorganic N residue and distribution were investigated by using
    MeSH term(s) Zea mays ; Fertilizers ; China ; Nitrogen ; Soil
    Chemical Substances Fertilizers ; Nitrogen (N762921K75) ; Soil
    Language English
    Publishing date 2023-07-22
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-023-38724-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Chlamydia trachomatis T3SS effector CT622 induces proinflammatory cytokines through TLR2/TLR4-mediated MAPKs/NF-κB pathways in THP-1 cells.

    Lei, Wenbo / Wen, Yating / Yang, Yewei / Liu, Shuangquan / Li, Zhongyu

    The Journal of infectious diseases

    2023  

    Abstract: Background: The pathogenesis of Chlamydia trachomatis (C. trachomatis) is associated with the induction of the host inflammatory response; however, the precise underlying molecular mechanisms remain poorly understood.: Methods: CT622, a T3SS effector ...

    Abstract Background: The pathogenesis of Chlamydia trachomatis (C. trachomatis) is associated with the induction of the host inflammatory response; however, the precise underlying molecular mechanisms remain poorly understood.
    Methods: CT622, a T3SS effector protein, has an important role in the pathogenesis of C. trachomatis; however, little is understood as to whether CT622 can induce a host inflammatory response. Our findings demonstrate that CT622 induces the expression of interleukin-6 (IL-6) and interleukin-8 (IL-8). Mechanistically, these effects involved the activation of the mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-κB) signaling pathways.
    Results: Interestingly, we also demonstrated that the suppression of toll-like receptor 4 (TLR4) using small interfering RNA (siRNA) markedly reduced the phosphorylation of ERK, p38, JNK, and IκBα, concomitant with a significant decrease in IL-6 and IL-8 secretion. Conversely, disruption of Toll-like receptor 2 (TLR2) abrogated the CT622-induced upregulation of IL-8 and ERK activation, whereas IL-6 expression and p38, JNK, and IκBα phosphorylation were unaffected.
    Conclusions: Taken together, these results indicate that CT622 contributes to the inflammatory response through the TLR2/TLR4-mediated MAPKs/NF-κB pathway, which provides insight into the molecular pathology of Chlamydia trachomatis infection.
    Language English
    Publishing date 2023-12-26
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3019-3
    ISSN 1537-6613 ; 0022-1899
    ISSN (online) 1537-6613
    ISSN 0022-1899
    DOI 10.1093/infdis/jiad597
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: UCHL1 deficiency upon HCMV infection induces vascular endothelial inflammatory injury mediated by mitochondrial iron overload.

    Zhu, Wenbo / Zhu, Wentong / Wang, Shao / Liu, Shuangquan / Zhang, Hongbo

    Free radical biology & medicine

    2023  Volume 211, Page(s) 96–113

    Abstract: Human cytomeglovirus (HCMV) infection predisposes blood vessels to atherosclerosis (AS) and post-transplantation restenosis, but the underlying molecular basis remains elusive. Here, we found that HCMV infection activates AIM2 inflammasome and pyroptosis ...

    Abstract Human cytomeglovirus (HCMV) infection predisposes blood vessels to atherosclerosis (AS) and post-transplantation restenosis, but the underlying molecular basis remains elusive. Here, we found that HCMV infection activates AIM2 inflammasome and pyroptosis in vascular endothelial cells by inducing mitochondrial iron overload. Mechanistically, under normal conditions, ubiquitin carboxyl terminal hydrolase-L1 (UCHL1) was identified as a DUB enzyme that interacts with, deubiquitylates, and stabilizes ferredoxin reductase (FDXR), an important mitochondrial protein that regulates mitochondral iron homeostasis. However, HCMV infection induces the aberrantly elevated m6A modification and R-loops, the three-stranded DNA-DNA:RNA hybrid structures. The expression of UCHL1 was remarkably reduced by m6A modification-mediated mRNA decay and R-loop-dependent transcriptional termination after HCMV infection. Deficiency of UCHL1 causes ubiquitination and degradation of FDXR. Loss of FDXR induces the mitochondrial iron overload, which consequently leads to AIM2 inflammasome activation and endothelial injury. Moreover, both downregulation expression of UCHL1 and related inflammatory injury in vascular endothelium was observed in MCMV-infected mice. Notably, STM2457, a METTL3 specific inhibitor, restores the expression of UCHL1 upon HCMV infection, thereby inhibiting the inflammatory injury of vascular endothelial cells. Our findings delineate a novel mechnism involved in HCMV-induced inflammatory injury to vascular endothelium and implicate the role of METTL3 inhibitor as a potential therapeutic approach.
    MeSH term(s) Animals ; Humans ; Mice ; DNA/metabolism ; Endothelial Cells/metabolism ; Inflammasomes/metabolism ; Iron Overload/genetics ; Methyltransferases/genetics ; Methyltransferases/metabolism ; Ubiquitin Thiolesterase/genetics ; Ubiquitination
    Chemical Substances DNA (9007-49-2) ; Inflammasomes ; Methyltransferases (EC 2.1.1.-) ; METTL3 protein, human (EC 2.1.1.62) ; Ubiquitin Thiolesterase (EC 3.4.19.12) ; UCHL1 protein, human ; Uchl1 protein, mouse (EC 3.4.19.12)
    Language English
    Publishing date 2023-12-09
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 807032-5
    ISSN 1873-4596 ; 0891-5849
    ISSN (online) 1873-4596
    ISSN 0891-5849
    DOI 10.1016/j.freeradbiomed.2023.12.002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: The role of human cytomegalovirus in atherosclerosis: a systematic review.

    Zhu, Wenbo / Liu, Shuangquan

    Acta biochimica et biophysica Sinica

    2020  Volume 52, Issue 4, Page(s) 339–353

    Abstract: Atherosclerosis is a progressive vascular disease with increasing morbidity and mortality year by year in modern society. Human cytomegalovirus (HCMV) infection is closely associated with the development of atherosclerosis. HCMV infection may accelerate ... ...

    Abstract Atherosclerosis is a progressive vascular disease with increasing morbidity and mortality year by year in modern society. Human cytomegalovirus (HCMV) infection is closely associated with the development of atherosclerosis. HCMV infection may accelerate graft atherosclerosis and the development of transplant vasculopathy in organ transplantation. However, our current understanding of HCMV-associated atherosclerosis remains limited and is mainly based on clinical observations. The underlying mechanism of the involvement of HCMV infection in atherogenesis remains unclear. Here, we summarized current knowledge regarding the multiple influences of HCMV on a diverse range of infected cells, including vascular endothelial cells, vascular smooth muscle cells, monocytes, macrophages, and T cells. In addition, we described potential HCMV-induced molecular mechanisms, such as oxidative stress, endoplasmic reticulum stress, autophagy, lipid metabolism, and miRNA regulation, which are involved in the development of HCMV-associated atherogenesis. Gaining an improved understanding of these mechanisms will facilitate the development of novel and effective therapeutic strategies for the treatment of HCMV-related cardiovascular disease.
    MeSH term(s) Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Atherosclerosis/virology ; Cytomegalovirus/metabolism ; Cytomegalovirus Infections/metabolism ; Cytomegalovirus Infections/pathology ; Endoplasmic Reticulum Stress ; Endothelial Cells/metabolism ; Endothelial Cells/pathology ; Endothelial Cells/virology ; Humans ; Lipid Metabolism ; Macrophages/metabolism ; Macrophages/pathology ; Macrophages/virology ; MicroRNAs/metabolism ; Monocytes/metabolism ; Monocytes/pathology ; Monocytes/virology ; Oxidative Stress ; T-Lymphocytes/metabolism ; T-Lymphocytes/pathology ; T-Lymphocytes/virology
    Chemical Substances MicroRNAs
    Language English
    Publishing date 2020-05-20
    Publishing country China
    Document type Journal Article ; Systematic Review
    ZDB-ID 2175256-4
    ISSN 1745-7270 ; 0582-9879 ; 1672-9145
    ISSN (online) 1745-7270
    ISSN 0582-9879 ; 1672-9145
    DOI 10.1093/abbs/gmaa005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Influenza virus causes lung immunopathology through down-regulating PPARγ activity in macrophages.

    Zhang, Hongbo / Alford, Taylor / Liu, Shuangquan / Zhou, Dongming / Wang, Jieru

    Frontiers in immunology

    2022  Volume 13, Page(s) 958801

    Abstract: Fatal influenza (flu) virus infection often activates excessive inflammatory signals, leading to multi-organ failure and death, also referred to as cytokine storm. PPARγ (Peroxisome proliferator-activated receptor gamma) agonists are well-known ... ...

    Abstract Fatal influenza (flu) virus infection often activates excessive inflammatory signals, leading to multi-organ failure and death, also referred to as cytokine storm. PPARγ (Peroxisome proliferator-activated receptor gamma) agonists are well-known candidates for cytokine storm modulation. The present study identified that influenza infection reduced PPARγ expression and decreased PPARγ transcription activity in human alveolar macrophages (AMs) from different donors. Treatment with PPARγ agonist Troglitazone ameliorated virus-induced proinflammatory cytokine secretion but did not interfere with the IFN-induced antiviral pathway in human AMs. In contrast, PPARγ antagonist and knockdown of PPARγ in human AMs further enhanced virus-stimulated proinflammatory response. In a mouse model of influenza infection, flu virus dose-dependently reduced PPARγ transcriptional activity and decreased expression of PPARγ. Moreover, PPARγ agonist troglitazone significantly reduced high doses of influenza infection-induced lung pathology. In addition, flu infection reduced PPARγ expression in all mouse macrophages, including AMs, interstitial macrophages, and bone-marrow-derived macrophages but not in alveolar epithelial cells. Our results indicate that the influenza virus specifically targets the PPARγ pathway in macrophages to cause acute injury to the lung.
    MeSH term(s) Acute Lung Injury/drug therapy ; Acute Lung Injury/genetics ; Acute Lung Injury/immunology ; Animals ; Antiviral Agents/immunology ; Antiviral Agents/therapeutic use ; Cytokine Release Syndrome/drug therapy ; Cytokine Release Syndrome/genetics ; Cytokine Release Syndrome/immunology ; Humans ; Influenza, Human/drug therapy ; Influenza, Human/genetics ; Influenza, Human/immunology ; Lung/immunology ; Macrophages/immunology ; Mice ; Orthomyxoviridae ; Orthomyxoviridae Infections/drug therapy ; Orthomyxoviridae Infections/genetics ; Orthomyxoviridae Infections/immunology ; Orthomyxoviridae Infections/virology ; PPAR gamma/agonists ; PPAR gamma/genetics ; PPAR gamma/immunology ; Troglitazone/immunology ; Troglitazone/therapeutic use
    Chemical Substances Antiviral Agents ; PPAR gamma ; PPARG protein, human ; Pparg protein, mouse ; Troglitazone (I66ZZ0ZN0E)
    Language English
    Publishing date 2022-08-25
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.958801
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  6. Article ; Online: Research and practice of the BOPPPS teaching model based on the OBE concept in clinical basic laboratory experiment teaching.

    Li, Pei / Lan, Xiaopeng / Ren, Lin / Xie, Xiaoping / Xie, Haitao / Liu, Shuangquan

    BMC medical education

    2023  Volume 23, Issue 1, Page(s) 882

    Abstract: Clinical basic inspection technology" is one of the essential courses in the medical laboratory profession. Combining the characteristics of the discipline itself, the research and practice of the BOPPPS model based on the OBE concept in clinical basic ... ...

    Abstract "Clinical basic inspection technology" is one of the essential courses in the medical laboratory profession. Combining the characteristics of the discipline itself, the research and practice of the BOPPPS model based on the OBE concept in clinical basic laboratory experiment teaching are discussed, and the reform of in teaching objectives, teaching contents, and teaching design path is implemented. The "student-centered" teaching process is divided into six stages: before, during, and after class, and the teaching process is continuously improved to achieve the desired teaching effect. Results of the experiment teaching show that the model has improved students' active participation and developed their clinical thinking skills, and more than 95% of students are satisfied with this teaching model.
    MeSH term(s) Humans ; Students ; Medicine ; Thinking ; Clinical Competence ; Laboratories
    Language English
    Publishing date 2023-11-17
    Publishing country England
    Document type Journal Article
    ZDB-ID 2044473-4
    ISSN 1472-6920 ; 1472-6920
    ISSN (online) 1472-6920
    ISSN 1472-6920
    DOI 10.1186/s12909-023-04822-z
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  7. Article ; Online: Transfer of HBV genomes to bone marrow using adenovirus vectors leads to alteration of the hematopoietic status in mice.

    Zhu, Wenbo / Zhou, Xiangping / Liu, Shuangquan

    Acta biochimica et biophysica Sinica

    2021  Volume 53, Issue 6, Page(s) 796–799

    MeSH term(s) Adenoviridae ; Animals ; Bone Marrow/metabolism ; Genetic Vectors ; Hematopoiesis ; Hepatitis B virus/genetics ; Hepatitis B virus/metabolism ; Mice ; Transduction, Genetic
    Language English
    Publishing date 2021-03-19
    Publishing country China
    Document type Journal Article
    ZDB-ID 2175256-4
    ISSN 1745-7270 ; 0582-9879 ; 1672-9145
    ISSN (online) 1745-7270
    ISSN 0582-9879 ; 1672-9145
    DOI 10.1093/abbs/gmab033
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  8. Article ; Online: Robust and Durable Superhydrophobic Coatings with Antipollution Flashover Performance via Silane-Modified Polyurea.

    Li, Xu / Tan, Xinyu / Chen, Weifeng / Xiao, Ting / Li, Xinyi / Jiang, Lihua / Liu, Shuangquan / Tan, Xin / Li, Tao

    Langmuir : the ACS journal of surfaces and colloids

    2024  Volume 40, Issue 10, Page(s) 5151–5161

    Abstract: The inadequate hydrophobicity and the degradation in usage seriously hampered the applications of the existing antipollution flashover coatings. In this paper, a superhydrophobic polyurea coating with antipollution flashover ability was fabricated ... ...

    Abstract The inadequate hydrophobicity and the degradation in usage seriously hampered the applications of the existing antipollution flashover coatings. In this paper, a superhydrophobic polyurea coating with antipollution flashover ability was fabricated through chemically grafting the silica onto the chains of polyurea by utilizing silane coupling agent and hydrophobic modification. It is demonstrated that the coating exhibits outstanding antipollution flashover performances. Noteworthy, the surface pollution flashover voltage has been increased by 33.8% compared with the room temperature vulcanizing silicone rubber (RTV silicone rubber). In addition, the volume resistivity is above 1.0 × 10
    Language English
    Publishing date 2024-02-29
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2005937-1
    ISSN 1520-5827 ; 0743-7463
    ISSN (online) 1520-5827
    ISSN 0743-7463
    DOI 10.1021/acs.langmuir.3c03243
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  9. Article ; Online: Correction: Temporally and spatially resolved molecular profiling in fingerprint analysis using indium vanadate nanosheets-assisted laser desorption ionization mass spectrometry.

    Zhu, Yanli / Wang, Jikai / Fu, Chengxiao / Liu, Shuangquan / Awasthi, Pragati / Zeng, Pengfei / Chen, Danjun / Sun, Yiyang / Mo, Ziyi / Liu, Hailing

    Journal of nanobiotechnology

    2024  Volume 22, Issue 1, Page(s) 42

    Language English
    Publishing date 2024-01-30
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2100022-0
    ISSN 1477-3155 ; 1477-3155
    ISSN (online) 1477-3155
    ISSN 1477-3155
    DOI 10.1186/s12951-023-02292-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Progression of unfolded protein response and ferroptosis in angiogenesis.

    He, Bisha / Hu, Yibao / Cao, Qian / Li, Yue / Tang, Yun / Cao, Ting / Zhou, Xiangping / Liu, Shuangquan

    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

    2024  Volume 173, Page(s) 116354

    Abstract: Angiogenesis is the growth of new blood vessels on preexisting ones. It is the outcome of a multifactorial effect involving several cells, which can be brought on by different stress reactions.The accumulation of unfolded proteins in the endoplasmic ... ...

    Abstract Angiogenesis is the growth of new blood vessels on preexisting ones. It is the outcome of a multifactorial effect involving several cells, which can be brought on by different stress reactions.The accumulation of unfolded proteins in the endoplasmic reticulum occurs when cells are stressed due to environmental changes, where physical or chemical stimuli induce endoplasmic reticulum stress, thereby activating the unfolded protein response (UPR), a homeostasis response designed to re-establish protein balance. Ferroptosis is a planned death of lipid peroxidation and anomalies in metabolism that is dependent on iron. Large concentrations of iron ions accumulate there, along with high concentrations of lipid peroxides and reactive oxygen species, all of which can contribute to the development of several diseases. Through the production of growth factors, adhesion factors, and inflammatory factors that trigger the start of angiogenesis, both UPR and Ferroptosis can be implicated in angiogenesis.To set the stage for further research on angiogenesis, this work concentrated on the effects of Ferroptosis and UPR on angiogenesis, respectively.
    MeSH term(s) Ferroptosis ; Angiogenesis ; Unfolded Protein Response ; Endoplasmic Reticulum Stress/physiology ; Iron
    Chemical Substances Iron (E1UOL152H7)
    Language English
    Publishing date 2024-03-04
    Publishing country France
    Document type Journal Article ; Review
    ZDB-ID 392415-4
    ISSN 1950-6007 ; 0753-3322 ; 0300-0893
    ISSN (online) 1950-6007
    ISSN 0753-3322 ; 0300-0893
    DOI 10.1016/j.biopha.2024.116354
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