scholarly journals Calcium Peroxide-Containing Polydimethylsiloxane-Based Microwells for Inhibiting Cell Death in Spheroids through Improved Oxygen Supply

2021 ◽  
Vol 44 (10) ◽  
pp. 1458-1464
Author(s):  
Yuya Mizukami ◽  
Yuki Takahashi ◽  
Kazunori Shimizu ◽  
Satoshi Konishi ◽  
Yoshinobu Takakura ◽  
...  
2020 ◽  
Author(s):  
Yuya Mizukami ◽  
Yuki Takahashi ◽  
Kazunori Shimizu ◽  
Satoshi Konishi ◽  
Yoshinobu Takakura ◽  
...  

ESC CardioMed ◽  
2018 ◽  
pp. 1230-1232
Author(s):  
Pascal Vranckx

Myocardial infarction is the irreversible myocardial cell death (necrosis) secondary to a prolonged lack of oxygen supply (ischaemia) caused by a complete occlusion of a major coronary in the absence of forward or collateral flow. Within the perfusion area of the occluded artery, flow deprivation and myocardial ischaemia are usually most severe subendocardially (apart from the innermost cell layers nourished from the cavity) and, at least in dogs, cell death progresses from the subendocardium to the subepicardium in a time-dependent fashion.


2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
I. K. Hals ◽  
A. M. Rokstad ◽  
B. L. Strand ◽  
J. Oberholzer ◽  
V. Grill

Islet transplantation in diabetes is hampered by the need of life-long immunosuppression. Encapsulation provides partial immunoprotection but could possibly limit oxygen supply, a factor that may enhance hypoxia-induced beta cell death in the early posttransplantation period. Here we tested susceptibility of alginate microencapsulated human islets to experimental hypoxia (0.1–0.3% O2for 8 h, followed by reoxygenation) on viability and functional parameters. Hypoxia reduced viability as measured by MTT by33.8±3.5% in encapsulated and42.9±5.2% in nonencapsulated islets (P<0.2). Nonencapsulated islets released 37.7% (median) more HMGB1 compared to encapsulated islets after hypoxic culture conditions (P<0.001). Glucose-induced insulin release was marginally affected by hypoxia. Basal oxygen consumption was equally reduced in encapsulated and nonencapsulated islets, by22.0±6.1% versus24.8±5.7%. Among 27 tested cytokines/chemokines, hypoxia increased the secretion of IL-6 and IL-8/CXCL8 in both groups of islets, whereas an increase of MCP-1/CCL2 was seen only with nonencapsulated islets.Conclusion. Alginate microencapsulation of human islets does not increase susceptibility to acute hypoxia. This is a positive finding in relation to potential use of encapsulation for islet transplantation.


ESC CardioMed ◽  
2018 ◽  
pp. 1230-1232
Author(s):  
Pascal Vranckx

Myocardial infarction is the irreversible myocardial cell death (necrosis) secondary to a prolonged lack of oxygen supply (ischaemia) caused by a complete occlusion of a major coronary in the absence of forward or collateral flow. Within the perfusion area of the occluded artery, flow deprivation and myocardial ischaemia are usually most severe subendocardially (apart from the innermost cell layers nourished from the cavity) and, at least in dogs, cell death progresses from the subendocardium to the subepicardium in a time-dependent fashion.


Metallomics ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1330-1343 ◽  
Author(s):  
Joseph Ischia ◽  
Damien M. Bolton ◽  
Oneel Patel

Ischaemia (interruption in the blood/oxygen supply) and subsequent damage induced by reperfusion (restoration of blood/oxygen supply) ultimately leads to cell death, tissue injury and permanent organ dysfunction.


2019 ◽  
Vol 9 (1) ◽  
pp. 75-78
Author(s):  
Mariya Tuchina ◽  
Galina Reva ◽  
Ivan Reva ◽  
Vladimir Kozhukhar Kozhukhar ◽  
R. Nasyrov

Study of morbid anatomy material from dead patients suffering from HIV-related illnesses, including hepatitis С, provided an opportunity to identify substantial pathological changes in the structural elements liver that suggested other pathogenetic mechanism of development changes in patients with HIV and hepatitis С associated with impaired metabolism in erythrocytes that are collapsing, hemoglobin in the plasma of blood blood vessels of the liver. As a result of the destruction of erythrocytes, free, not associated with erythrocytes, hemoglobin cannot carry carbon dioxide from cells, hypoxia ensues the structural elements of the liver and cells are forced to use the free dissolved in plasma oxygen, which further exacerbates the occurrence of hypoxia and Anoxia and then the appearance of intoxication of the massive destruction of hemoglobin and the advent of plasma transferrin. The last captured by macrophages. The free hemoglobin in the bloodstream increases its toxic effect on tissue cells, causing cell death in the resultant ischemia, thus worsening the oxygen supply of them. As a result of the subsequent destruction of haemoglobin are formed its decay products in the form of iron рorphyrin, bilirubin, The latter contributed to the development of jaundice or acute porfirii owing to the death of hepatocytes, which manifest is to develop cirrhosis or cancer


2016 ◽  
Vol 4 (2) ◽  
Author(s):  
Clifford Lapian ◽  
Sunny Wangko ◽  
Djon Wongkar

Abstract: Cell death occurs after somatic death. The aerobic process of cells would be halted as a result of somatic death, whereas the anaerobic process will continue. Therefore, the cells do not die in a short time although the oxygen supply has been depleted. This anaerobic process will have an impact on the morphology and activity of cells. This study was aimed to obtain the microscopic changes of large intestine for 24 hours postmortem. This was a descriptive observational study. A domestic pig weighed 20 kg was used as sample. The microscopic examinations were performed at several interval times as follow: 0, 1, 2, 3, 4, 5, 6, 7, 8, 9, 12, 14, 16, 18, 20, 22, and 24 hours postmortem. The results showed that the microscopic changes of the large intestine were identified the earliest at 2 hours postmortem as congestion with dilatation of the intestinal crypt lumen; lysis of a number of intestinal crypts at 6 hours postmortem; all intestinal crypts were lysis leaving empty areas; and the mucosal layer and intestinal crypts could not be identified at 24 hours postmortem. Conclusion: The earliest microscopic changes of the large intestine occured at 2 hours postmortem. Lysis of the intestinal crypts began at 6 hours postmortem and became complete at 12 hours postmortem. Keywords: large intestine, postmortem, intestinal crypt Abstrak: Kematian sel terjadi setelah kematian somatis. Proses aerobik sel-sel akan terhenti akibat kematian somatis, sedangkan proses anaerobik akan tetap berlangsung. Hal tersebut mengakibatkan sel-sel tidak mati dalam waktu yang singkat meskipun pasokan oksigen telah habis. Proses anaerobik ini akan berdampak pada morfologi dan aktivitas sel. Penelitian ini bertujuan untuk mendapatkan perubahan gambaran histologik usus besar pada hewan coba selama 24 jam postmortem. Jenis penelitian ialah deskriptif observasional. Sampel penelitian ialah satu ekor babi domestik dengan berat 20 kg. Pengamatan mikroskopik terhadap sampel dilakukan pada beberapa interval waktu, yaitu: 0 jam, 1 jam, 2 jam, 3 jam, 4 jam, 5 jam, 6 jam, 7 jam, 8 jam, 9 jam, 12 jam, 14, 16 jam, 18 jam, 20 jam, 22 jam, dan 24 jam postmortem. Hasil penelitian mendapatkan perubahan mikroskopik postmortem paling awal pada usus besar terjadi pada 2 jam postmortem berupa kongesti dengan lumen kripta Lieberkuhn yang berdilatasi; pada 6 jam postmortem tampak sebagian kripta Lieberkuhn telah lisis; pada 12 jam postmortem seluruh kripta Lieberkuhn telah lisis; dan pada 24 jam postmortem lapisan epitel dan kripta Lieberkuhn tidak dapat diidentifikasi lagi. Simpulan: Perubahan histologik postmortem paling awal pada 3 jam postmortem, lisis kripta Lieberkuhn telah tampak sejak 6 jam postmortem, dan menyeluruh pada 12 jam postmortem.Kata kunci: usus besar, postmortem, kripta Lieberkuhn


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