GLORIA

GEOMAR Library Ocean Research Information Access

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    In: Frontiers in Cell and Developmental Biology, Frontiers Media SA, Vol. 9 ( 2021-11-8)
    Abstract: Circular RNAs (circRNAs) participate in the development of various kinds of diseases. However, the function and roles of circRNAs in obstructive sleep apnea (OSA)-induced cardiovascular disease remain poorly understood. Therefore, we sought to explore the circRNA expression profiles and predict their functions in OSA-induced cardiac injury with the use of bioinformatics analysis. The model of OSA was established in mouse treated by chronic intermittent hypoxia (CIH) exposure. Then, we screened the circRNA profile using circRNA microarray. By comparing circRNA expression in three matched pairs of CIH-treated cardiac tissues and controls, differentially expressed circRNAs were identified in the CIH groups. Comparison of the selected circRNAs expression levels was performed between qRT-PCR and microarray. Meanwhile, we employed Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses to predict the functions of these selected circRNAs. Finally, we constructed a circRNA-miRNA-mRNA network based on the target prediction. It was found that a total of 124 circRNAs were differentially expressed in CIH-treated cardiac tissues ( p ≤ 0.05, fold-change ≥ 1.5). Among them, 23 circRNAs were significantly down-regulated, and the other 101 were up-regulated. Then, ten circRNAs were randomly selected to validate the reliability of the microarray results by using qRT-PCR. Next, we conducted the GO and KEGG pathway analysis to explore the parental genes functions of differentially expressed circRNA. Finally, two significantly differentially expressed circRNAs (mmu_circRNA_014309 and mmu_circRNA_21856) were further selected to create a circRNA-miRNA-mRNA regulation network. Our study did first reveal that the differentially expressed circRNAs played a vital role in the pathogenesis of OSA-induced cardiac damage. Thus, our findings bring us closer to unraveling the pathophysiologic mechanisms and eliciting novel therapeutic targets for the treatment of OSA-associated cardiovascular diseases.
    Type of Medium: Online Resource
    ISSN: 2296-634X
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2737824-X
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
    In: Bioscience Reports, Portland Press Ltd., Vol. 41, No. 1 ( 2021-01-29)
    Abstract: Objective: Fibrinogen has been implicated to play a role in the pathophysiology of obstructive sleep apnea (OSA). Many studies have evaluated the effect of continuous positive airway pressure (CPAP) on plasma fibrinogen levels in OSA patients. However, results from different reports were not consistent. To assess the effect of CPAP treatment on plasma fibrinogen levels of patients with OSA, a meta-analysis was performed. Methods: A systematic search of Pubmed, Embase, Cochrane, Wanfang Database and Chinese National Knowledge Infrastructure was performed. Data were extracted, and then weighted mean difference (WMD) and 95% confidence intervals (CIs) were calculated using a random-effects model. Results: Twenty-two studies involving 859 patients were included in this meta-analysis. Combined data showed that plasma fibrinogen concentrations decreased after CPAP therapy (WMD = −0.38 g/l, 95% CI [−0.54 to −0.22 g/l], P & lt;0.001). In the subgroup analyses by therapy duration, plasma fibrinogen concentrations declined significantly in the long-term (≥1 month) CPAP therapy subgroup (WMD = −0.33 g/l, 95% CI [−0.49 to −0.16 g/l], P & lt;0.001) but not in the short-term ( & lt;1 month) CPAP therapy subgroup (WMD = −0.84 g/l, 95% CI [−1.70 to 0.03 g/l], P=0.058). Moreover, in patients with long-term CPAP therapy duration, plasma fibrinogen levels decreased with good CPAP compliance (≥4 h/night) (WMD = −0.37 g/l, 95% CI [−0.55 to −0.19 g/l] , P & lt;0.001) but not with poor CPAP compliance ( & lt;4 h/night) (WMD = 0.12 g/l, 95% CI [−0.09 to 0.33 g/l], P=0.247). Conclusion: Long-term CPAP treatment with good compliance can reduce the plasma fibrinogen levels in patients with OSA.
    Type of Medium: Online Resource
    ISSN: 0144-8463 , 1573-4935
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 2021
    detail.hit.zdb_id: 2014993-1
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 3
    Online Resource
    Online Resource
    Frontiers Media SA ; 2023
    In:  Frontiers in Endocrinology Vol. 14 ( 2023-8-21)
    In: Frontiers in Endocrinology, Frontiers Media SA, Vol. 14 ( 2023-8-21)
    Abstract: As important organelles of energetic and metabolism, changes in the dynamic state of mitochondria affect the homeostasis of cellular metabolism. Mitochondrial dynamics include mitochondrial fusion and mitochondrial fission. The former is coordinated by mitofusin-1 (Mfn1), mitofusin-2 (Mfn2), and optic atrophy 1 (Opa1), and the latter is mediated by dynamin related protein 1 (Drp1), mitochondrial fission 1 (Fis1) and mitochondrial fission factor (MFF). Mitochondrial fusion and fission are generally in dynamic balance and this balance is important to preserve the proper mitochondrial morphology, function and distribution. Diabetic conditions lead to disturbances in mitochondrial dynamics, which in return causes a series of abnormalities in metabolism, including decreased bioenergy production, excessive production of reactive oxygen species (ROS), defective mitophagy and apoptosis, which are ultimately closely linked to multiple chronic complications of diabetes. Multiple researches have shown that the incidence of diabetic complications is connected with increased mitochondrial fission, for example, there is an excessive mitochondrial fission and impaired mitochondrial fusion in diabetic cardiomyocytes, and that the development of cardiac dysfunction induced by diabetes can be attenuated by inhibiting mitochondrial fission. Therefore, targeting the restoration of mitochondrial dynamics would be a promising therapeutic target within type II diabetes (T2D) and its complications. The molecular approaches to mitochondrial dynamics, their impairment in the context of T2D and its complications, and pharmacological approaches targeting mitochondrial dynamics are discussed in this review and promise benefits for the therapy of T2D and its comorbidities.
    Type of Medium: Online Resource
    ISSN: 1664-2392
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2592084-4
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 4
    Online Resource
    Online Resource
    American Scientific Publishers ; 2020
    In:  Journal of Medical Imaging and Health Informatics Vol. 10, No. 1 ( 2020-01-01), p. 76-80
    In: Journal of Medical Imaging and Health Informatics, American Scientific Publishers, Vol. 10, No. 1 ( 2020-01-01), p. 76-80
    Type of Medium: Online Resource
    ISSN: 2156-7018
    Language: English
    Publisher: American Scientific Publishers
    Publication Date: 2020
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 5
    In: Inorganic Chemistry Communications, Elsevier BV, Vol. 106 ( 2019-08), p. 144-150
    Type of Medium: Online Resource
    ISSN: 1387-7003
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2019
    detail.hit.zdb_id: 2026959-6
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 6
    In: Environmental Research, Elsevier BV, Vol. 241 ( 2024-01), p. 117262-
    Type of Medium: Online Resource
    ISSN: 0013-9351
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2024
    detail.hit.zdb_id: 205699-9
    detail.hit.zdb_id: 1467489-0
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 7
    In: Evidence-Based Complementary and Alternative Medicine, Hindawi Limited, Vol. 2021 ( 2021-11-2), p. 1-14
    Abstract: Objectives. Ulcerative colitis (UC) is a chronic inflammatory disease affecting the colon, and its incidence is rising worldwide. This study was designed to uncover the healing effect of friedelin, a bioactive compound against UC through bioinformatics of network pharmacology and experimental verification of UC model mice. Materials and Methods. Targets of friedelin and potential mechanism of friedelin on UC were predicted through target searching, PPI network establishing, and enrichment analyzing. We explored effects of friedelin on dextran sulfate sodium (DSS)-induced colitis. Severity of UC was investigated by body weight, disease activity index (DAI), and length of the colon. Inflammation severity was examined by determination of proinflammatory and anti-inflammatory cytokines. The numbers of autophagosome around the epithelial cells were observed by autophagy inhibition via a transmission electron microscope. The expressions of autophagy-related ATG5 protein and AMPK-mTOR signaling pathway were determined by immunofluorescence staining. Results. In this study, 17 potential targets of friedelin and 1111 UC-related targets were identified. 10 therapeutic targets of friedelin against UC were acquired from overlapped targets of UC and friedelin. PPI network construction filtered 14 core targets through target amplification and confidence enhancement. The results of molecular docking showed that the docking scores of the top 5 active targets were higher than the threshold values. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were carried out, showing friedelin alleviates UC through anti-inflammatory pathways and molecular function of autophagy. Subsequently, animal-based experiments revealed the intraperitoneal injection of friedelin ameliorated DSS-induced body weight loss, DAI decrease, colon length shortening and colonic pathological damage with lower myeloperoxidase and proinflammatory cytokines (IL-1β and IL-6) and higher IL-10 levels, and more autophagosomes in transmission electron microscope results. The AMPK-mTOR signaling pathway plays important role in the friedelin’s effect in autophagy as KEGG pathway result and experiment verification. Furthermore, the 3 ma validated the role of autophagy as an improvement in the friedelin’s pharmacologic effect to UC model mice. Conclusions. Friedelin ameliorated DSS-induced colitis in mice through of inflammatory inhibition and regulation of autophagy.
    Type of Medium: Online Resource
    ISSN: 1741-4288 , 1741-427X
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2021
    detail.hit.zdb_id: 2148302-4
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 8
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2023
    In:  Inflammatory Bowel Diseases Vol. 29, No. 5 ( 2023-05-02), p. 818-829
    In: Inflammatory Bowel Diseases, Oxford University Press (OUP), Vol. 29, No. 5 ( 2023-05-02), p. 818-829
    Abstract: Inflammatory bowel diseases (IBDs), including ulcerative colitis and Crohn’s disease, are characterized by chronic idiopathic inflammation of gastrointestinal tract. Although the pathogenesis of IBD remains unknown, intestinal immune dysfunction has been considered as the core pathogenesis. In the intestinal immune system, T helper 1 (Th1) and Th17 cells are indispensable for intestine homeostasis via preventing pathogenic bacteria invasion, regulating metabolism and functions of intestinal epithelial cells (IECs), and promoting IEC self-renewal. However, during the development of IBD, Th1 and Th17 cells acquire the pathogenicity and change from the maintainer of intestinal homeostasis to the destroyer of intestinal mucosa. Because of coexpressing interferon-γ and interleukin-17A, Th17 cells with pathogenicity are named as pathogenic Th17 cells. In disease states, Th1 cells impair IEC programs by inducing IEC apoptosis, recruiting immune cells, promoting adhesion molecules expression of IECs, and differentiating to epithelial cell adhesion molecule–specific interferon γ–positive Th1 cells. Pathogenic Th17 cells induce IEC injury by triggering IBD susceptibility genes expression of IECs and specifically killing IECs. In addition, Th1 and pathogenic Th17 cells could cooperate to induce colitis. The evidences from IBD patients and animal models demonstrate that synergistic action of Th1 and pathogenic Th17 cells occurs in the diseases development and aggravates the mucosal inflammation. In this review, we focused on Th1 and Th17 cell programs in homeostasis and intestine inflammation and specifically discussed the impact of Th1 and Th17 cell pathogenicity and their synergistic action on the onset and the development of IBD. We hoped to provide some clues for treating IBD.
    Type of Medium: Online Resource
    ISSN: 1078-0998 , 1536-4844
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 9
    Online Resource
    Online Resource
    Frontiers Media SA ; 2020
    In:  Frontiers in Cell and Developmental Biology Vol. 8 ( 2020-12-4)
    In: Frontiers in Cell and Developmental Biology, Frontiers Media SA, Vol. 8 ( 2020-12-4)
    Abstract: Primary Sjögren’s syndrome (pSS) is a chronic systemic autoimmune disease characterized by exocrine gland damage and extraglandular involvements. To identify potential biomarkers for the early detection of pSS and to further investigate the potential roles of the biomarkers in the progression of pSS, our previous RNA sequencing data and four microarray data of salivary glands (SGs) were combined for integrative transcriptome analysis between pSS and non-pSS. Differential gene expression analysis, gene co-expression network analysis, and pathway analysis were conducted to detect hub genes, which were subsequently investigated in peripheral blood mononuclear cell (PBMC) and plasma. Correlation analysis, single-gene Gene Set Enrichment Analysis, and receiver operating characteristic (ROC) curve were applied to investigate the potential function of the hub genes and their classification capacity for pSS. A total of 51 common up-regulated genes were identified among different pSS cohorts. A key module was found to be the most closely linked to pSS, which was significantly associated with inflammation-related pathways. Seven overlapped hub genes ( ICOS , SELL , CR2 , BANK1 , MS4A1 , ZC3H12D , and CCR7 ) were identified, among which ICOS was demonstrated to be involved in most crucial immune pathways. ICOS was up-regulated not only in SGs but also in PBMC and plasma in pSS, and the expression of ICOS was closely associated with lymphocytic infiltration in SGs and disease activity of pSS patients. It showed a strong classification capacity with classic clinical index in SGs (ROC curve 0.9821) and significant distinct discrimination in PBMC (ROC curve 0.9107). These findings are expected to gain a further insight into the pathogenesis of pSS and provide a promising candidate for the early detection of pSS.
    Type of Medium: Online Resource
    ISSN: 2296-634X
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2020
    detail.hit.zdb_id: 2737824-X
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 10
    Online Resource
    Online Resource
    Springer Science and Business Media LLC ; 2016
    In:  Molecular and Cellular Biochemistry Vol. 411, No. 1-2 ( 2016-1), p. 143-150
    In: Molecular and Cellular Biochemistry, Springer Science and Business Media LLC, Vol. 411, No. 1-2 ( 2016-1), p. 143-150
    Type of Medium: Online Resource
    ISSN: 0300-8177 , 1573-4919
    RVK:
    RVK:
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2016
    detail.hit.zdb_id: 2003615-2
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...