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      Morphological and biochemical changes in the pancreas associated with acute systemic hypoxia

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          Abstract

          This study aimed to investigate the changes associated with acute systemic hypoxia in the endocrine system, particularly in pancreatic tissues. The investigation was based on macroscopic, pathohistological, biochemical, and molecular biological findings in cell lines and human cadavers. The results showed that cases of death due to asphyxia more frequently showed severe subcapsular/interstitial hemorrhage versus the other causes of death. Histological examination showed that asphyxia cases were associated with severe morphological changes. Although measured insulin levels in the asphyxia were higher compared to other causes of death, no differences were noted for the glucagon and amylase levels with regard to the cause of death. Increased blood insulin levels were not associated with macro- and micromorphological changes, and did not show any association with glucose or cortisol levels. The experiment conducted under hypoxic conditions in cultured cells demonstrated that insulin mRNA expression and insulin protein levels peaked at 10 min after hypoxia exposure. However, there were no changes in either the amylase mRNA or protein levels. Corticosterone level peaked at 120 min after exposure to hypoxic conditions. Overall, acute systemic hypoxic conditions can directly affect the mechanisms involved in pancreatic insulin secretion.

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          Hypoxia induces senescence of bone marrow mesenchymal stem cells via altered gut microbiota

          Systemic chronic hypoxia is a feature of many diseases and may influence the communication between bone marrow (BM) and gut microbiota. Here we analyse patients with cyanotic congenital heart disease (CCHD) who are experiencing chronic hypoxia and characterize the association between bone marrow mesenchymal stem cells (BMSCs) and gut microbiome under systemic hypoxia. We observe premature senescence of BMSCs and abnormal d-galactose accumulation in patients with CCHD. The hypoxia that these patients experience results in an altered diversity of gut microbial communities, with a remarkable decrease in the number of Lactobacilli and a noticeable reduction in the amount of enzyme-degraded d-galactose. Replenishing chronic hypoxic rats with Lactobacillus reduced the accumulation of d-galactose and restored the deficient BMSCs. Together, our findings show that chronic hypoxia predisposes BMSCs to premature senescence, which may be due to gut dysbiosis and thus induced d-galactose accumulation.
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            Early response of neurons and glial cells to hypoxia in the retina.

            The present study was undertaken to examine the involvement of nitric oxide (NO) and excitotoxicity in the development of hypoxia-induced retinopathy in adult rats. Retinas of adult rats were examined at 3 hours to 14 days after hypoxia. The mRNA and protein expression of endothelial, neuronal, and inducible nitric oxide synthase (eNOS, nNOS, and iNOS, respectively), hypoxia-inducible factor-1alpha (HIF-1alpha), vascular endothelial growth factor (VEGF), N-methyl-D-aspartate receptor subunit 1 (NMDAR1), and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid glutamate (AMPA GluR2 and GluR3) receptors in the retina was determined by real-time RT-PCR, Western blot analysis, and immunohistochemistry. The response of retinal microglial cells to hypoxia was also studied by immunohistochemistry. Hemorrhages were observed in the retina after hypoxia. Upregulated mRNA and protein expression of HIF-1alpha, NMDAR1, GluR2, GluR3, VEGF, eNOS, nNOS, and iNOS in the retina was observed in response to hypoxia. Complement type 3 (CR3) receptors and major histocompatibility complex (MHC) class I and II antigen expression on the microglial cells was increased after exposure to hypoxia. The findings of this study indicate that NO and excitotoxicity may produce damage to retina in response to hypoxia. Increased expressions of eNOS and VEGF in response to hypoxia are indicative of vasodilatation and increased permeability of retinal blood vessels. Increased phagocytosis by retinal microglial cells evidenced by increased expression of CR3 receptors may occur for the removal of hemorrhagic debris. Upregulation of MHC antigens indicates the readiness of these cells to participate in an immune response.
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              Self-Monitoring of Blood Glucose: The Basics

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                Author and article information

                Contributors
                fmorioka@med.osaka-cu.ac.jp
                Journal
                Hum Cell
                Hum Cell
                Human Cell
                Springer Singapore (Singapore )
                0914-7470
                1749-0774
                2 February 2021
                2 February 2021
                2021
                : 34
                : 2
                : 400-418
                Affiliations
                [1 ]GRID grid.261445.0, ISNI 0000 0001 1009 6411, Department of Legal Medicine, , Osaka City University Medical School, ; 1-4-3 Asahi-machi, Abeno, Osaka, 545-8585 Japan
                [2 ]Forensic Autopsy Section, Medico-Legal Consultation and Postmortem Investigation Support Center (MLCPI-SC), Osaka, Japan
                Author information
                http://orcid.org/0000-0002-1280-8643
                Article
                481
                10.1007/s13577-020-00481-0
                7900369
                33532907
                10d8707e-e075-4b19-ab66-b4368271ab5d
                © The Author(s) 2021

                Open AccessThis 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
                : 1 October 2020
                : 30 December 2020
                Categories
                Research Article
                Custom metadata
                © Japan Human Cell Society 2021

                Cell biology
                hypoxia,insulin,glucose,cortisol,cell culture
                Cell biology
                hypoxia, insulin, glucose, cortisol, cell culture

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