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      Investigation of the stent induced deformation on hemodynamic of internal carotid aneurysms by computational fluid dynamics

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          Abstract

          Application of the stent for treatment of the internal carotid artery (ICA) aneurysms has been extensively increased in recent decades. In the present work, stent-induced deformations of the parent vessel of ICA aneurysms are fully investigated. This study tries to visualize blood stream and calculated hemodynamic factors inside the four ICA aneurysms after deformations of parent vessel. For the simulation of the non-Newtonian blood stream, computational fluid dynamic is applied with one-way Fluid–Solid interaction (FSI) approach. Four ICA aneurysms with different ostium sizes and neck vessel angle are selected for this investigation. Wall shear stress on wall of aneurysm is analyzed in two angles of deformation due to application of the stent. Blood flow investigation shows that the deformation of the aneurysm limited blood entrance to the sac region and this decreases the blood velocity and consequently oscillatory shear index (OSI) on the sac wall. It is also observed that the stent-induced deformation is more effective on those cases with extraordinary OSI values on aneurysm wall.

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          webTWAS: a resource for disease candidate susceptibility genes identified by transcriptome-wide association study

          The development of transcriptome-wide association studies (TWAS) has enabled researchers to better identify and interpret causal genes in many diseases. However, there are currently no resources providing a comprehensive listing of gene-disease associations discovered by TWAS from published GWAS summary statistics. TWAS analyses are also difficult to conduct due to the complexity of TWAS software pipelines. To address these issues, we introduce a new resource called webTWAS, which integrates a database of the most comprehensive disease GWAS datasets currently available with credible sets of potential causal genes identified by multiple TWAS software packages. Specifically, a total of 235 064 gene-diseases associations for a wide range of human diseases are prioritized from 1298 high-quality downloadable European GWAS summary statistics. Associations are calculated with seven different statistical models based on three popular and representative TWAS software packages. Users can explore associations at the gene or disease level, and easily search for related studies or diseases using the MeSH disease tree. Since the effects of diseases are highly tissue-specific, webTWAS applies tissue-specific enrichment analysis to identify significant tissues. A user-friendly web server is also available to run custom TWAS analyses on user-provided GWAS summary statistics data. webTWAS is freely available at http://www.webtwas.net .
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            Atractylenolide I enhances responsiveness to immune checkpoint blockade therapy by activating tumor antigen presentation

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              Homocysteine inhibits pro-insulin receptor cleavage and causes insulin resistance via protein cysteine-homocysteinylation.

              Elevation in homocysteine (Hcy) level is associated with insulin resistance; however, the causality between them and the underlying mechanism remain elusive. Here, we show that Hcy induces insulin resistance and causes diabetic phenotypes by protein cysteine-homocysteinylation (C-Hcy) of the pro-insulin receptor (pro-IR). Mechanistically, Hcy reacts and modifies cysteine-825 of pro-IR in the endoplasmic reticulum (ER) and abrogates the formation of the original disulfide bond. C-Hcy impairs the interaction between pro-IR and the Furin protease in the Golgi apparatus, thereby hindering the cleavage of pro-IR. In mice, an increase in Hcy level decreases the mature IR level in various tissues, thereby inducing insulin resistance and the type 2 diabetes phenotype. Furthermore, inhibition of C-Hcy in vivo and in vitro by overexpressing protein disulfide isomerase rescues the Hcy-induced phenotypes. In conclusion, C-Hcy in the ER can serve as a potential pharmacological target for developing drugs to prevent insulin resistance and increase insulin sensitivity.
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                Author and article information

                Contributors
                am.abazari@urmia.ac.ir
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                2 May 2023
                2 May 2023
                2023
                : 13
                : 7155
                Affiliations
                [1 ]GRID grid.5970.b, ISNI 0000 0004 1762 9868, Mathematics Area, MathLab, , International School for Advanced Studies (SISSA), ; Trieste, Italy
                [2 ]GRID grid.472236.6, ISNI 0000 0004 1784 8702, Department of Civil Engineering, College of Engineering, , Cihan University-Erbil, ; Erbīl, Iraq
                [3 ]GRID grid.411496.f, ISNI 0000 0004 0382 4574, Department of Mechanical Engineering, , Babol Noshirvani University of Technology, ; Babol, Iran
                [4 ]GRID grid.5371.0, ISNI 0000 0001 0775 6028, Department of Space, Earth and Environment, , Chalmers University of Technology, ; Gothenburg, Sweden
                [5 ]GRID grid.412763.5, ISNI 0000 0004 0442 8645, Department of Mechanical Engineering, Faculty of Engineering, , Urmia University, ; Urmia, Iran
                Article
                34383
                10.1038/s41598-023-34383-6
                10154420
                37130902
                4c90f724-7a33-49b4-8129-b1ea38faca05
                © The Author(s) 2023

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 23 January 2023
                : 28 April 2023
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                © The Author(s) 2023

                Uncategorized
                biomedical engineering,mechanical engineering
                Uncategorized
                biomedical engineering, mechanical engineering

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