scholarly journals POSTMORTEM PATHOLOGICALFEATURES IN LIVER TISSUE OF HIV PATIENTS

2019 ◽  
Vol 9 (1) ◽  
pp. 75-78
Author(s):  
Mariya Tuchina ◽  
Galina Reva ◽  
Ivan Reva ◽  
Vladimir Kozhukhar Kozhukhar ◽  
R. Nasyrov
Keyword(s):  
Carbon Dioxide ◽  
Cell Death ◽  
Liver Tissue ◽  
Oxygen Supply ◽  
Structural Elements ◽  
Pathological Changes ◽  
Free Hemoglobin ◽  
Pathogenetic Mechanism ◽  
Decay Products ◽  
Impaired Metabolism

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

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 ◽  
...  
Keyword(s):  
Cell Death ◽  
Oxygen Supply ◽  
Calcium Peroxide

Development of myocardial infarction

ESC CardioMed ◽  
2018 ◽  
pp. 1230-1232
Author(s):  
Pascal Vranckx
Keyword(s):  
Myocardial Infarction ◽  
Cell Death ◽  
Myocardial Ischaemia ◽  
Oxygen Supply ◽  
Myocardial Cell ◽  
Time Dependent ◽  
Collateral Flow ◽  
Complete Occlusion ◽  
Cell Layers ◽  
Artery Flow

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.

scholarly journals T-2 mycotoxin induced apoptosis in broiler’s liver tissue

2018 ◽  
Vol 27 (1) ◽  
pp. 9-16
Author(s):  
Piret Hussar ◽  
Tõnu Järveots ◽  
Lazo Pendovski ◽  
Katerina Blagoevska ◽  
Trpe Ristoski ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Liver Tissue ◽  
Immunohistochemical Staining ◽  
Mammalian Cells ◽  
Gallus Domesticus ◽  
Gallus Gallus Domesticus ◽  
Histopathological Changes ◽  
Induced Apoptosis ◽  
Multicellular Organisms

Apoptosis is a process of programmed cell death that occurs in multicellular organisms. As T-2 toxin is known to induce apoptosis in mammalian cells, the aim of the present experiment was to study the toxic effect of T-2 on chicken liver tissue using apoptosis-related antibodies p21 and p53 which are involved in the p53/p21-mediated apoptotic signalling pathway. The experiment was conducted on fourteen 40-day-old broilers (Gallus gallus domesticus) who were divided into control and T-2 toxin groups. For the T-2 toxin group, T-2 toxin (Sigma, Germany) was dissolved in water and given per os for three consecutive days. The material of the liver was taken 24 hours after the last application. The specimens were fixed with 10% formalin and embedded into paraffin; slices 5 μm in thickness were cut followed by immunohistochemical staining with polyclonal primary antibodies p21 and p53 (Abcam, UK) according to the manufacturer’s guidelines (IHC kit, Abcam, UK). Strong expression of p21 and p53 found in hepatocytes, endotheliocytes and around blood vessels together with large tissue destructions in T-2 toxin group birds’ liver indicates apoptosis and histopathological changes in liver tissue during T-2 mycotoxicosis.

scholarly journals Soluble Asialoglycoprotein Receptors Reflect the Apoptosis of Hepatocytes

2002 ◽  
Vol 11 (5) ◽  
pp. 407-415 ◽  
Author(s):  
Tetsuji Kakegawa ◽  
Hirohiko Ise ◽  
Nobuhiro Sugihara ◽  
Toshio Nikaido ◽  
Naoki Negishi ◽  
...  
Keyword(s):  
Cell Death ◽  
Liver Tissue ◽  
Liver Diseases ◽  
Culture Medium ◽  
Apoptotic Cell ◽  
Rabbit Serum ◽  
Mouse Serum ◽  
Apoptosis And Necrosis

Cell death is thought to take place through at least two distinct processes: apoptosis and necrosis. There is increasing evidence that dysregulation of the apoptotic program is involved in liver diseases. However, there is no method to simply evaluate apoptosis in the liver tissue at present. It has been reported that the expression of asialoglycoprotein receptors (AGPRs) increases with apoptosis, but there is no report until now that investigates the influence of soluble AGPRs on apoptosis of hepatocytes. Soluble AGPRs have been reported to be present in human serum under physiological conditions. In the present study, in order to investigate the correlation between apoptosis of hepatocytes and soluble AGPR, mouse soluble AGPRs were detected using SDS-PAGE and Western blot analysis was conducted using anti-extracellular mouse hepatic lectin-1 (Ex-MHL-1) antiserum (polyclonal rabbit serum). The mouse soluble AGPRs were present in culture medium and mouse serum when hepatocytes were damaged. The soluble AGPRs increased proportionately, as the number of dead hepatocytes increased. In addition, soluble AGPRs existed more when apoptotic cell death was observed in in vitro and in vivo than when necrotic cell death was observed. The extracellular moiety of MHL-1 exists in the culture medium and mouse serum as a soluble AGPR, but the detailed mechanism of releasing soluble AGPR from hepatocytes has not been revealed yet. We described the first evidence for the relation between quantity of soluble AGPRs with two kinds of cell death: necrosis and apoptosis. Based on the results of our study, soluble AGPRs might become a new marker of apoptosis in the liver tissue and be useful for clinical diagnosis and treatment for liver diseases.

scholarly journals Living on mars: how to produce oxygen and fuel to get home

2018 ◽  
Vol 49 (3) ◽  
pp. 15-18 ◽  
Author(s):  
Vasco Guerra ◽  
Tiago Silva ◽  
Olivier Guaitella
Keyword(s):  
Carbon Dioxide ◽  
Oxygen Supply ◽  
Space Exploration ◽  
Martian Atmosphere ◽  
Plasma Technology ◽  
Do So ◽  
The Way

Sending a manned mission to Mars is one of the next major steps in space exploration. Creating a breathable environment, however, is a substantial challenge. A sustainable oxygen supply on the red planet can be achieved by converting carbon dioxide directly from the Martian atmosphere. A new solution to do so is on the way: plasma technology.

scholarly journals Alginate Microencapsulation of Human Islets Does Not Increase Susceptibility to Acute Hypoxia

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
I. K. Hals ◽  
A. M. Rokstad ◽  
B. L. Strand ◽  
J. Oberholzer ◽  
V. Grill
Keyword(s):  
Cell Death ◽  
Oxygen Consumption ◽  
Beta Cell ◽  
Islet Transplantation ◽  
Oxygen Supply ◽  
Acute Hypoxia ◽  
Human Islets ◽  
Culture Conditions ◽  
Positive Finding ◽  
Potential Use

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.

Sign in / Sign up

Export Citation Format

Share Document