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  • 1
    Online Resource
    Online Resource
    Elsevier BV ; 2023
    In:  Microbial Pathogenesis Vol. 181 ( 2023-08), p. 106197-
    In: Microbial Pathogenesis, Elsevier BV, Vol. 181 ( 2023-08), p. 106197-
    Type of Medium: Online Resource
    ISSN: 0882-4010
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2023
    detail.hit.zdb_id: 1471158-8
    SSG: 12
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  • 2
    In: Biology, MDPI AG, Vol. 12, No. 2 ( 2023-02-16), p. 317-
    Abstract: Background: RSV is closely correlated with post-infection airway hyperresponsive diseases (AHD), but the mechanism remains unclear. Objective: Due to the pivotal role of miRNAs in AHD, we analyzed the differentially expressed miRNAs (DEmiRs) in RSV-infected patients, asthma patients, and COPD patients from public datasets and explored the mechanisms of association between RSV and AHD. Methods: We obtained miRNA and mRNA databases of patients with RSV infection, as well as miRNA databases of asthma and COPD patients from the GEO database. Through integrated analysis, we screened DEmiRs and DEGs. Further analysis was carried out to obtain the hub genes through the analysis of biological pathways and enrichment pathways of DEGs targeted by DEmiRs and the construction of a protein-protein interaction (PPI) network. Results: The five differential molecules (miR-34b/c-5p, Cd14, Cxcl10, and Rhoh) were verified through in vivo experiments that had the same expression trend in the acute and chronic phases of RSV infection. Following infection of BEAS-2B cells with RSV, we confirmed that RSV infection down-regulated miR-34b/c-5p, and up-regulated the expression levels of CXCL10 and CD14. Furthermore, the results of the dual-luciferase reporter assay showed that CXCL10 was the target of hsa-miR-34c-5p. Conclusions: miR-34b/c-5p/CXCL10 axis mediates a mechanism of AHD.
    Type of Medium: Online Resource
    ISSN: 2079-7737
    Language: English
    Publisher: MDPI AG
    Publication Date: 2023
    detail.hit.zdb_id: 2661517-4
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  • 3
    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2023
    In:  Journal of Antimicrobial Chemotherapy Vol. 78, No. 1 ( 2023-01-05), p. 169-179
    In: Journal of Antimicrobial Chemotherapy, Oxford University Press (OUP), Vol. 78, No. 1 ( 2023-01-05), p. 169-179
    Abstract: Respiratory syncytial virus (RSV) infection is one of the three most common causes of death in the infants, pre-schoolers, immunocompromised patients and elderly individuals due to many complications and lack of specific treatment. During RSV infection, the fusion protein (F protein) mediates the fusion of the virus envelope with the host cell membrane. Therefore, the F protein is an effective target for viral inhibition. Methods We identified potential small-molecule inhibitors against RSV-F protein for the treatment of RSV infection using virtual screening and molecular dynamics (MD) simulations. The CCK8 assay was used to determine the cytotoxicity and quantitative RT–PCR and indirect fluorescence assay (IFA) were used to determine the viral replication and RSV-induced inflammation in vitro. An RSV-infected mouse model was established, and viral replication was assayed using real-time quantitative PCR and IFA. Virus-induced complications were also examined using histopathological analysis, airway resistance and the levels of IL-1β, IL-6 and TNF-α. Results The top three potential inhibitors against the RSV-F protein were screened from the FDA-approved drug database. Z65, Z85 and Z74 significantly inhibited viral replication and RSV-induced inflammation. They also significantly alleviated RSV infection and RSV-induced complications in vivo. Z65 and Z85 had no cytotoxicity and better anti-RSV effects than Z74. Conclusions Z65 and Z85 may be suitable candidates for the treatment of RSV and serve as the basis for the development of new drugs.
    Type of Medium: Online Resource
    ISSN: 0305-7453 , 1460-2091
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2023
    detail.hit.zdb_id: 1467478-6
    SSG: 15,3
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  • 4
    Online Resource
    Online Resource
    AME Publishing Company ; 2021
    In:  Annals of Translational Medicine Vol. 9, No. 5 ( 2021-3), p. 366-366
    In: Annals of Translational Medicine, AME Publishing Company, Vol. 9, No. 5 ( 2021-3), p. 366-366
    Type of Medium: Online Resource
    ISSN: 2305-5839 , 2305-5847
    Language: Unknown
    Publisher: AME Publishing Company
    Publication Date: 2021
    detail.hit.zdb_id: 2893931-1
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  • 5
    Online Resource
    Online Resource
    S. Karger AG ; 2016
    In:  Cellular Physiology and Biochemistry Vol. 39, No. 5 ( 2016), p. 1804-1812
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 39, No. 5 ( 2016), p. 1804-1812
    Abstract: Background: The present study was designed to observe the infection of human cytomegalovirus (HCMV) to human vascular smooth muscle cells (VSMCs), and the effect of viral infection on lipid metabolism in VSMCs. Methods: The cytopathic effects were observed by inverted microscopy and viral infection were examined by electron microscopy and RT-PCR. The lipid metabolism related gene profiling of VSMCs after HCMV infection was assayed by cDNA assay and the abnormal expression of genes were validated by quantitative RT-PCR. The content of cholesterol in VSMCs after HCMV infection was assayed by cholesterol detection kit. Results: VSMCs showed obvious cytopathic effects after HCMV infection. Intact viral particles could be detected in VSMCs using electron microscope. By use of RT-PCR technology, IE gene of HCMV could be amplified from VSMCs. The expression of cell lipid metabolism related gene profiling showed obvious disorders. The expression levels of HMG-CoA synthase and HMG-CoA reductase after infection increased significantly. The cellular cholesterol content (µmol/106 cells) was significantly higher than that of mock infected group at 72h post infection. Conclusion: HCMV can infect VSMCs and the infection can affect cellular lipid metabolism related gene expression, which get involved in the occurrence and development of atherosclerosis (AS).
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2016
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
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  • 6
    Online Resource
    Online Resource
    MDPI AG ; 2023
    In:  Microbiology Research Vol. 14, No. 2 ( 2023-05-06), p. 627-634
    In: Microbiology Research, MDPI AG, Vol. 14, No. 2 ( 2023-05-06), p. 627-634
    Abstract: The aim of this study was to understand the molecular epidemiological characteristics and drug resistance mechanism of carbapenem-resistant Pseudomonas aeruginosa (CRPA) and to provide a theoretical basis for the prevention and treatment of CRPA infection in hospitals. A total of 34 CRPA strains were isolated, and resistance to 13 commonly used antibiotics was detected using the TDR-300B Plus VitEK-2 compact automatic bacterial identification instrument. Then, carbapenemase production was detected using the Carbe NP test. RT-qPCR was used to detect the expression of efflux pump MexA and outer membrane protein OprD, and PCR amplification and sequence analysis were used to detect class Ⅰ integrons carried by drug resistance genes. Our results showed that of the 34 CRPAs, 22 were multi-drug resistant (MDR), and five were extensively drug-resistant (XDR). Sequencing analysis showed that class Ⅰ integron mainly carried aminoglycosides or quinolones resistance genes. Multiple mechanisms play important roles in the formation and development of MDR or XDR.
    Type of Medium: Online Resource
    ISSN: 2036-7481
    Language: English
    Publisher: MDPI AG
    Publication Date: 2023
    detail.hit.zdb_id: 2571057-6
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  • 7
    Online Resource
    Online Resource
    SAGE Publications ; 2020
    In:  Experimental Biology and Medicine Vol. 245, No. 6 ( 2020-03), p. 512-521
    In: Experimental Biology and Medicine, SAGE Publications, Vol. 245, No. 6 ( 2020-03), p. 512-521
    Abstract: Studies have shown that metabolic diseases, such as obesity, are significantly associated with intestinal flora imbalance. The amplification of opportunistic pathogens induced by the glyoxylic acid cycle contributes to intestinal flora imbalance. Promising, though, is that saturated hydrogen can effectively improve the occurrence and development of metabolic diseases, such as obesity. However, the specific mechanism of how saturated hydrogen operates is still not very clear. In this study, after a high-fat diet, the level of total cholesterol, total glyceride, and low-density lipoprotein in the peripheral blood of mice increased, and that of high-density lipoprotein decreased. Intestinal fatty acid metabolism-related gene Apolipoprotein E (ApoE), fatty acid synthase (FAS), intestinal fatty acid-binding protein (I-FAPB), acetyl-CoA carboxylase 1 (ACC1), peroxisome proliferator-activated receptor γ (PPARγ), and stearoyl-CoA desaturase 1 (SCD1) increased significantly. Bacteroides, Bifidobacteria, and Lactobacillus counts in feces decreased considerably, while Enterobacter cloacae increased. The activity of isocitrate lyase in feces increased markedly. Treatment of mice with saturated hydrogen led to decreased total cholesterol, total glyceride, and low-density lipoprotein and increased high-density lipoprotein in the peripheral blood. FAS and I-FAPB gene expression in the small intestine decreased. Bacteroides, Bifidobacteria, and Lactobacillus in feces increased significantly, whereas Enterobacter cloacae decreased. The activity of isocitrate lyase also diminished remarkably. These results suggest that saturated hydrogen could improve intestinal structural integrity and lipid metabolism disorders by inhibiting the glyoxylic acid cycle of the intestinal flora. Impact statement Past studies have shown that hydrogen can improve metabolic disorders, but its mechanism of action remains unclear. It is well known that metabolic diseases, such as obesity, are significantly associated with changes in the intestinal flora. The glyoxylic acid cycle is an essential metabolic pathway in prokaryotes, lower eukaryotes, and plants and could be the portal for mechanisms related to metabolic disorders. Many opportunistic pathogenic bacteria can recycle fatty acids to synthesize sugars and other pathogenic substances using the glyoxylic acid cycle. So, the glyoxylic acid cycle may be involved in intestinal dysbacteriosis under high-fat diet. This study, therefore, seeks to provide the mechanism of how hydrogen improves metabolic diseases and a new basis for the use of hydrogen in the treatment of metabolic disorders.
    Type of Medium: Online Resource
    ISSN: 1535-3702 , 1535-3699
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2020
    detail.hit.zdb_id: 2020856-X
    SSG: 12
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  • 8
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 37, No. 5 ( 2015), p. 2012-2022
    Abstract: Background/Aims: The previous study in our lab showed that Nodal molecule on bronchial epithelial cells (BECs) was modulated by all kinds of lung microbes. The present study was designed to determine the effects of Nodal on proliferation of BECs and BECs-induced differentiation of T-helper (Th) cells. The epigenetic mechanisms of Nodal expression following treatments of different lung microbes were also identified. Methods: Real-time polymerization chain reaction (PCR) and western blot were used to determine the expression of Nodal. Flow cytometry was used to observe the effects of proliferation of BECs and subsequent BECs-induced differentiation of Th cells. Methylation levels of CpG islands in Nodal promoters were also analyzed by time of flight mass spectrometry. Results: The results showed that Nodal promoted proliferation of BECs and BECs-induced differentiation of Th cell from Th1 to Th2 and Th17. Nodal promoter showed a hyper-methylation in normal BECs. Through methylation modification in the promoter, P. aeruginosa or A.baumanni inhibited the expression of Nodal while RSV promoted the expression of Nodal. Conclusions: Our data showed that Nodal promoted Th2 and Th17 differentiation and inhibited Th1 differentiation which may cause imbalance of airway microenvironment. P. aeruginosa or A.baumanni may be hopeful for the treatment of airway hyperresponsveness by inhibition Nodal expression through DNA methylation modification in the promoter.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2015
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
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  • 9
    Online Resource
    Online Resource
    Frontiers Media SA ; 2016
    In:  Frontiers in Cellular and Infection Microbiology Vol. 6 ( 2016-11-30)
    In: Frontiers in Cellular and Infection Microbiology, Frontiers Media SA, Vol. 6 ( 2016-11-30)
    Type of Medium: Online Resource
    ISSN: 2235-2988
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2016
    detail.hit.zdb_id: 2619676-1
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  • 10
    Online Resource
    Online Resource
    Wiley ; 2023
    In:  Journal of Medical Virology Vol. 95, No. 1 ( 2023-01)
    In: Journal of Medical Virology, Wiley, Vol. 95, No. 1 ( 2023-01)
    Abstract: Lots of epidemiological and clinical studies have shown that human cytomegalovirus (HCMV) is related to the pathogenesis of atherosclerosis. Released by inflammatory cells and vascular smooth muscle cell (VSMCs), metalloproteinases are observed in many pathological vessel conditions, including atherosclerosis and restenosis. This study was designed to investigate the effect of HCMV infection on the expression of metalloproteinases and their involvements in the HCMV‐induced functional changes of VSMCs. Differential metalloproteinase after HCMV infection was assayed using reverse transcription‐polymerase chain reaction (RT‐PCR) microarray. The most significant increased a disintegrin and metalloprotease 9 (ADAM9) was chosen to investigate the mechanism of its specific increase after infection using the treatment of UV‐irradiated replication‐deficient HCMV, HCMV‐infected cell lysate filters or Foscarnet. The function of proliferation, migration, production of inflammatoty factors and phenotypic transformation were determined by using cell counting kit‐8, transwell, Enzyme‐linked immunosorbent assay, RT‐quantitative PCR (qPCR) and Western blot, respectively. Moreover, the effect of ADAM9 deficiency on HCMV replication was also determined using RT‐qPCR and immunofluorescence. The expression levels of 6 genes were upregulated and 14 genes were downregulated at different time points after HCMV infection. Among these, the expression level of ADAM9 increased most significantly at each time point and the abnormal expression of ADAM9 might be induced by the early gene products of HCMV. Further studies found that ADAM9 promoted the proliferation, the migration, the production of inflammatory factors and the transit from the contractile phenotype (decreased ACTA2 expression) to the synthetic phenotype (increased osteopontin [OPN] expression). Knockdown theADAM9 expression could rescue the decreased ACTA2 expression, but has no effect on OPN expression. ADAM‐9 deficiency didn't affect the replication of HCMV. The findings of our study suggest that HCMV infection changed VSMC function through ADAM9 expression, which may contribute to the understanding of the underlying pathological mechanisms of HCMV‐induced atherosclerosis.
    Type of Medium: Online Resource
    ISSN: 0146-6615 , 1096-9071
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 752392-0
    detail.hit.zdb_id: 1475090-9
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