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Studies of the Primate Inflammatory Hemostatic Axis and Its Response to Inflammatory Mediators
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
Figure 4A shows that Stage III begins at T = +6 hours with a rise of the plasma concentrations of markers of cell injury (e.g., SGPT), which are accompanied by a continuing steady decline in blood pressure and platelet count. Figure 4B shows that in this process the combined inflammatory and coagulopathic events of Stage I and II drives the microvascular endothelium deeper into a dysfunctional state leading to abnormal function as reflected by a more severe DIC (luminal surface) and by capillary leak (abluminal surface). This results in intra- and extracellular edema of parenchymal tissues and a transition from reversible to the irreversible cell injury of Stage IV beginning at approximately 10–12 hours. These two later stages are termed cell injury (reversible) and cell degeneration (irreversible). They coincide with the hypodynamic or cold shock phase of the baboon response to LD100E. coli (Fig. 4A).
Cellular Injury Associated with Organ Cryopreservation: Chemical Toxicity and Cooling Injury
Published in John J. Lemasters, Constance Oliver, Cell Biology of Trauma, 2020
Gregory M. Fahy, Carla da Mouta, Latchezar Tsonev, Bijan S. Khirabadi, Patrick Mehl, Harold T. Meryman
Thus far, our approach has been to deal with the direct forms of injury rather than the role of secondary types of injury such as reperfusion injury or ischemic injury. Our progress in minimizing direct forms of injury, however, now heightens the importance of attending to these secondary factors, and the spectacular advances in understanding and reversing cell injury that are documented in the previous contributions to this volume provide exciting opportunities for obviating these sources of injury. At the same time, we hope our focus on unusual types of injury and their mechanisms will open additional avenues of thought for those studying more conventional problems, and will therefore be of assistance outside the specific realm of organ cryopreservation.
Quantitative Evaluation of Minimal Injuries
Published in Joan Gil, Models of Lung Disease, 2020
Although morphometric studies can provide evidence of population shifts, they measure only static characteristics of the cell population. No kinetic data about cell death, cell proliferation, or cell differentiation can be detailed by morphometric studies alone. Cytodynamic studies, however, can be a highly sensitive index of cell injury. The sample of NO2-induced epithelial changes demonstrated that hypertrophy can be offset by cell spreading and cell proliferation. Cell proliferation can in turn be offset by cell differentiation. In mild injuries, the rate of cell proliferation and differentiation (repair) may keep pace with the rate of cell injury so that no overt injury can be detected, unless the rate of cell death is measured.
In vitro exposure of human lens epithelial cells to X-rays at varied dose-rates leads to protein-level changes relevant to cataractogenesis
Published in International Journal of Radiation Biology, 2021
Vinita Chauhan, Ngoc Q. Vuong, Simran Bahia, Nazila Nazemof, Premkumari Kumarathasan
The initiation of oxidative stress response following a radiation insult was expected since the human epithelial cell layer is primarily responsible for defense against oxidative stress. We have previously reported on oxidative stress-related metabolite changes in HLE cells after similar radiation exposures (Bahia et al. 2018). The protein network interconnectivities also highlighted indirect interactions with TP53, a central protein involved in DNA damage and repair processes consistent with our earlier report. It has been shown that a cell’s defense against oxidative stress can also involve the activation of molecular changes related to DNA repair mechanisms (Wilson et al. 2003), further highlighting oxidative stress as an important component to HLE cell injury from radiation exposure. This response combined with mitochondrial dysregulation shows that radiation exposure may also hinder the natural underlying protective mechanisms involved in scavenging free radicals.
The cytokine storm of COVID-19: a spotlight on prevention and protection
Published in Expert Opinion on Therapeutic Targets, 2020
Lucie Pearce, Sean M. Davidson, Derek M. Yellon
COVID-19 is no longer just an infection confined to the pulmonary epithelium, but a multi-system inflammatory disorder causing end-organ failure [28]. Although anti-viral agents such as Remdesivir have reduced disease severity in case studies [47], there is still no definitive cure for COVID-19. We must, therefore, turn our attention to other modalities of preventing end-organ destruction, whilst perfecting pharmacological options. As is evident from critical care reports, multi-organ ischemia in COVID-19 occurs as a result of cardio-renal syndrome, cytokine release and global hypoperfusion due to loss of vascular integrity [60]. It may be possible to apply the principles of organ protection, utilized in other ischemic conditions to limit cell injury and apoptosis. The aforementioned observation that RIC can influence cytokine release in animal models, provides an excellent foundation for further research in COVID-19 [61].
‘Relationship between thermal dose and cell death for “rapid” ablative and “slow” hyperthermic heating’
Published in International Journal of Hyperthermia, 2019
Petros X. E. Mouratidis, Ian Rivens, John Civale, Richard Symonds-Tayler, Gail ter Haar
The activation energy (ΔE) and frequency factor (A) of the ‘slow’ hyperthermic and ‘rapid’ ablative reactions were calculated using a method described in [18]. Briefly assuming a ‘top-hat’ thermal history for both ‘slow’ hyperthermic and ‘rapid’ ablative thermal exposures, the cell injury rate (k) was calculated using: −1) and t is the treatment time of cells (sec) at a constant temperature. An Arrhenius plot of Ln (k) versus the inverse of the absolute temperature 1/T (10−3 K−1) was then drawn. The activation energy (ΔE) is a function of the slope of the straight line fit of the data in the Arrhenius plot and the frequency factor can be calculated from its y-intercept using Equation (5): −1), A is the frequency factor (sec−1), ΔE is the activation energy (J mole−1), Rg is the universal gas constant (8.314 J mole−1 K−1), and T is the absolute temperature (K). To convert between the Arrhenius and the TID model, RCEM was calculated: CEM(T) is the RCEM value at temperature T, T is the absolute temperature (K) [8]. Inserting RCEM(T) into Equation (1) allows calculation of a temperature-dependent TID for comparison with the standard method of calculation.