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      Gray level co-occurrence matrix and wavelet analyses reveal discrete changes in proximal tubule cell nuclei after mild acute kidney injury

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          Abstract

          Acute kidney injury (AKI) relates to an abrupt reduction in renal function resulting from numerous conditions. Morbidity, mortality, and treatment costs related to AKI are relatively high. This condition is strongly associated with damage to proximal tubule cells (PTCs), generating distinct patterns of transcriptional and epigenetic alterations that result in structural changes in the nuclei of this epithelium. To this date, AKI-related nuclear chromatin redistribution in PTCs is poorly understood, and it is unclear whether changes in PTC chromatin patterns can be detected using conventional microscopy during mild AKI, which can progress to more debilitating forms of injury. In recent years, gray level co-occurrence matrix (GLCM) analysis and discrete wavelet transform (DWT) have emerged as potentially valuable methods for identifying discrete structural changes in nuclear chromatin architecture that are not visible during the conventional histopathological exam. Here we present findings indicating that GLCM and DWT methods can be successfully used in nephrology to detect subtle nuclear morphological alterations associated with mild tissue injury demonstrated in rodents by inducing a mild form of AKI through ischemia–reperfusion injury. Our results show that mild ischemic AKI is associated with the reduction of local textural homogeneity of PTC nuclei quantified by GLCM and the increase of nuclear structural heterogeneity indirectly assessed with DWT energy coefficients. This rodent model allowed us to show that mild ischemic AKI is associated with the significant reduction of textural homogeneity of PTC nuclei, indirectly assessed by GLCM indicators and DWT energy coefficients.

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          Most cited references47

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          Scikit-learn: machine learning in Python

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            Cellular pathophysiology of ischemic acute kidney injury.

            Ischemic kidney injury often occurs in the context of multiple organ failure and sepsis. Here, we review the major components of this dynamic process, which involves hemodynamic alterations, inflammation, and endothelial and epithelial cell injury, followed by repair that can be adaptive and restore epithelial integrity or maladaptive, leading to chronic kidney disease. Better understanding of the cellular pathophysiological processes underlying kidney injury and repair will hopefully result in the design of more targeted therapies to prevent the injury, hasten repair, and minimize chronic progressive kidney disease.
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              Apoptosis and acute kidney injury.

              Improved mechanistic understanding of renal cell death in acute kidney injury (AKI) has generated new therapeutic targets. Clearly, the classic lesion of acute tubular necrosis is not adequate to describe the consequences of renal ischemia, nephrotoxin exposure, or sepsis on glomerular filtration rate. Experimental evidence supports a pathogenic role for apoptosis in AKI. Interestingly, proximal tubule epithelial cells are highly susceptible to apoptosis, and injury at this site contributes to organ failure. During apoptosis, well-orchestrated events converge at the mitochondrion, the organelle that integrates life and death signals generated by the BCL2 (B-cell lymphoma 2) protein family. Death requires the 'perfect storm' for outer mitochondrial membrane injury to release its cellular 'executioners'. The complexity of this process affords new targets for effective interventions, both before and after renal insults. Inhibiting apoptosis appears to be critical, because circulating factors released by the injured kidney induce apoptosis and inflammation in distant organs including the heart, lung, liver, and brain, potentially contributing to the high morbidity and mortality associated with AKI. Manipulation of known stress kinases upstream of mitochondrial injury, induction of endogenous, anti-apoptotic proteins, and improved understanding of the timing and consequences of renal cell apoptosis will inevitably improve the outcome of human AKI.
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                Author and article information

                Contributors
                peter.corridon@ku.ac.ae
                Journal
                Sci Rep
                Sci Rep
                Scientific Reports
                Nature Publishing Group UK (London )
                2045-2322
                10 March 2023
                10 March 2023
                2023
                : 13
                : 4025
                Affiliations
                [1 ]GRID grid.7149.b, ISNI 0000 0001 2166 9385, Faculty of Medicine, Department of Medical Physiology, Laboratory for Cellular Physiology, , University of Belgrade, ; Visegradska 26/II, 11129 Belgrade, Serbia
                [2 ]GRID grid.18098.38, ISNI 0000 0004 1937 0562, University of Haifa, ; 199 Abba Hushi Blvd, Mount Carmel, 3498838 Haifa, Israel
                [3 ]GRID grid.440568.b, ISNI 0000 0004 1762 9729, Department of Pharmacology, College of Medicine and Health Sciences, , Khalifa University of Science and Technology, ; PO Box 127788, Abu Dhabi, UAE
                [4 ]GRID grid.7149.b, ISNI 0000 0001 2166 9385, Faculty of Medicine, , University of Belgrade, University Clinical Center of Serbia, ; Dr. Koste Todorovica 8, 11129 Belgrade, Serbia
                [5 ]GRID grid.440568.b, ISNI 0000 0004 1762 9729, Department of Immunology and Physiology, College of Medicine and Health Sciences, , Khalifa University of Science and Technology, ; PO Box 127788, Abu Dhabi, UAE
                [6 ]GRID grid.440568.b, ISNI 0000 0004 1762 9729, Healthcare Engineering Innovation Center, , Biomedical Engineering, Khalifa University of Science and Technology, ; PO Box 127788, Abu Dhabi, UAE
                [7 ]GRID grid.440568.b, ISNI 0000 0004 1762 9729, Center for Biotechnology, , Khalifa University of Science and Technology, ; PO Box 127788, Abu Dhabi, UAE
                [8 ]GRID grid.257413.6, ISNI 0000 0001 2287 3919, Indiana Center for Biological Microscopy, , Indiana University School of Medicine, ; Indianapolis, IN USA
                Author information
                http://orcid.org/0000-0002-6796-4301
                Article
                31205
                10.1038/s41598-023-31205-7
                10006226
                36899130
                97a6bdbd-c395-4422-847b-9cb37cf795b4
                © 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
                : 15 June 2022
                : 8 March 2023
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100016047, Science Fund of the Republic of Serbia;
                Award ID: #7739645
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/100000002, National Institutes of Health;
                Award ID: NIH P-30 O’Brien Center (DK 079312)
                Award Recipient :
                Funded by: FundRef http://dx.doi.org/10.13039/501100004070, Khalifa University of Science, Technology and Research;
                Award ID: FSU-2020-25
                Award Recipient :
                Categories
                Article
                Custom metadata
                © The Author(s) 2023

                Uncategorized
                imaging,computational biology and bioinformatics,biomarkers,health care,nephrology
                Uncategorized
                imaging, computational biology and bioinformatics, biomarkers, health care, nephrology

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