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  • Chen, Yangxin  (4)
  • 1
    In: BMJ Open, BMJ, Vol. 12, No. 6 ( 2022-06), p. e060258-
    Abstract: We aimed to develop an effective tool for predicting severe acute kidney injury (AKI) in patients admitted to the cardiac surgery recovery unit (CSRU). Design A retrospective cohort study. Setting Data were extracted from the Medical Information Mart for Intensive Care (MIMIC)-III database, consisting of critically ill participants between 2001 and 2012 in the USA. Participants A total of 6271 patients admitted to the CSRU were enrolled from the MIMIC-III database. Primary and secondary outcome Stages 2–3 AKI. Result As identified by least absolute shrinkage and selection operator (LASSO) and logistic regression, risk factors for AKI included age, sex, weight, respiratory rate, systolic blood pressure, diastolic blood pressure, central venous pressure, urine output, partial pressure of oxygen, sedative use, furosemide use, atrial fibrillation, congestive heart failure and left heart catheterisation, all of which were used to establish a clinical score. The areas under the receiver operating characteristic curve of the model were 0.779 (95% CI: 0.766 to 0.793) for the primary cohort and 0.778 (95% CI: 0.757 to 0.799) for the validation cohort. The calibration curves showed good agreement between the predictions and observations. Decision curve analysis demonstrated that the model could achieve a net benefit. Conclusion A clinical score built by using LASSO regression and logistic regression to screen multiple clinical risk factors was established to estimate the probability of severe AKI in CSRU patients. This may be an intuitive and practical tool for severe AKI prediction in the CSRU.
    Type of Medium: Online Resource
    ISSN: 2044-6055 , 2044-6055
    Language: English
    Publisher: BMJ
    Publication Date: 2022
    detail.hit.zdb_id: 2599832-8
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  • 2
    In: Molecular Genetics & Genomic Medicine, Wiley, Vol. 8, No. 10 ( 2020-10)
    Abstract: Coronary atherosclerotic heart disease (CHD) is the most common cardiovascular disease and has become a leading cause of death globally. Various molecular typing methods are available for the diagnosis and treatment of tumors. However, molecular typing results are not routinely used for CHD. Methods and Results Aiming to uncover the underlying molecular features of different types of CHD, we screened the differentially expressed genes (DEGs) associated with CHD based on the Gene Expression Omnibus (GEO) data and expanded those with the NCBI‐gene and OMIM databases to finally obtain 2021 DEGs. The weighted gene co‐expression analysis (WGCNA) was performed on the candidate genes, and six distinctive WGCNA modules were identified, two of which were associated with CHD. Moreover, DEGs were mined as key genes for co‐expression based on the module network relationship. Furthermore, the differentially expressed miRNAs in CHD and interactions in the database were mined in the GEO data set to build a multifactor regulatory network of key genes for co‐expression. Based on the network, the CHD samples were further classified into five clusters and we defined FTH1, HCAR3, RGS2, S100A9, and TYROBP as the top genes of the five subgroups. Finally, the mRNA levels of FTH1, S100A9, and TYROBP were found to be significantly increased, while the expression of HCAR3 was decreased in the blood of CHD patients. We did not detect measurable levels of RGS2. Conclusion The screened core clusters of genes may be a target for the diagnosis and treatment of CHD as a molecular typing module.
    Type of Medium: Online Resource
    ISSN: 2324-9269 , 2324-9269
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2734884-2
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  • 3
    In: Cell Proliferation, Wiley, Vol. 51, No. 6 ( 2018-12)
    Abstract: Yes‐associated protein ( YAP ) has been reported to regulate cell proliferation and differentiation. We aimed to characterize the role of YAP in angiotensin II (Ang II )‐induced hypertensive vascular remodelling ( HVR ) and vascular smooth muscle cells ( VSMC s) phenotypic modulation and to explore the underlying mechanisms. Materials and methods An HVR rat model was established by continuous Ang II infusion for 2 weeks. Western blotting, qRT ‐ PCR , and confocal microscopy were conducted to assess YAP expression. YAP ‐sh RNA interfering plasmid and adenovirus were constructed to knock down YAP . We used cell proliferation and migration assays, accompanied by pathway inhibitors, to evaluate the biological function and underlying mechanisms. Results Ang II upregulated YAP expression in the media of carotid artery; however, in vivo YAP silencing significantly mitigated HVR , independent of the blood pressure level. Ang II upregulated YAP expression and promoted YAP nuclear accumulation in a dose‐ and time‐dependent manner in rat VSMC s. YAP knockdown ameliorated Ang II ‐induced VSMC s phenotypic modulation. The regulation of YAP by Ang II could be blocked by pretreatment with angiotensin receptor type 1 antagonist losartan or F‐actin depolymerizing agent latrunculin B but not the AT 2R antagonist PD 123319. Disrupting the YAP ‐ TEA domain ( TEAD ) interaction with verteporfin inhibited Ang II ‐induced VSMC s phenotypic modulation. Conclusions Yes‐associated protein mediated angiotensin II ‐induced VSMC s phenotypic modulation and vascular remodelling. YAP is a potential therapeutic target for HVR beyond blood pressure control.
    Type of Medium: Online Resource
    ISSN: 0960-7722 , 1365-2184
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 2019986-7
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Frontiers Media SA ; 2022
    In:  Frontiers in Cell and Developmental Biology Vol. 9 ( 2022-1-5)
    In: Frontiers in Cell and Developmental Biology, Frontiers Media SA, Vol. 9 ( 2022-1-5)
    Abstract: Atheroclerosis refers to a chronic inflammatory disease featured by the accumulation of fibrofatty lesions in the intima of arteries. Cardiovasular events associated with atherosclerosis remain the major causes of mortality worldwide. Recent studies have indicated that ferroptosis, a novel programmed cell death, might participate in the process of atherosclerosis. However, the ferroptosis landscape is still not clear. In this study, 59 genes associated with ferroptosis were ultimately identified in atherosclerosis in the intima. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed for functional annotation. Through the construction of protein–protein interaction (PPI) network, five hub genes ( TP53 , MAPK1 , STAT3 , HMOX1 , and PTGS2 ) were then validated histologically. The competing endogenous RNA (ceRNA) network of hub genes was ultimately constructed to explore the regulatory mechanism between lncRNAs, miRNAs, and hub genes. The findings provide more insights into the ferroptosis landscape and, potentially, the therapeutic targets of atherosclerosis.
    Type of Medium: Online Resource
    ISSN: 2296-634X
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2737824-X
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