scholarly journals Simulation of the effect of mucociliary clearance on the bronchial distribution of inhaled radon progenies and related cellular damage using a new deposition and clearance model for the lung

2020 ◽  
Vol 59 (4) ◽  
pp. 651-661
Author(s):  
Árpád Farkas
Keyword(s):  
Cell Death ◽  
Mucociliary Clearance ◽  
Cell Transformation ◽  
Alpha Decay ◽  
Cellular Damage ◽  
Biological Damage ◽  
Biophysical Models ◽  
Radon Decay ◽  
Airway Bifurcation ◽  
Clearance Model

Abstract Most of the current dosimetry models of inhaled short-lived radon decay products assume uniform activity distributions along the bronchial airways. In reality, however, both deposition and clearance patterns of inhaled radon progenies are highly inhomogeneous. Consequently, a new deposition-clearance model has been developed that accounts for such inhomogeneities and applied together with biophysical models of cell death and cell transformation. The scope of this study was to apply this model which is based on computational fluid and particle dynamics methods, in an effort to reveal the effect of mucociliary clearance on the bronchial distribution of deposited radon progenies. Furthermore, the influence of mucociliary clearance on the spatial distribution of biological damage due to alpha-decay of the deposited radon progenies was also studied. The results obtained demonstrate that both deposition and clearance of inhaled radon progenies are highly non-uniform within a human airway bifurcation unit. Due to the topology of the carinal ridge, a slow clearance zone emerged in this region, which is the location where most of the radio-aerosols deposit. In spite of the slow mucus movement in this zone, the initial degree of inhomogeneity of the activity due to the nonuniform deposition decreased by a factor of about 3 by considering the effect of mucociliary clearance. In the peak of the airway bifurcation, the computed cell death and cell transformation probabilities were lower when considering deposition and clearance simultaneously, compared to the case when only deposition was considered. However, cellular damage remained clustered.

Computational analysis of a 3D mucociliary clearance model predicting nasal drug uptake

2021 ◽  
Vol 155 ◽  
pp. 105757
Author(s):  
Sriram Chari ◽  
Karthik Sridhar ◽  
Ross Walenga ◽  
Clement Kleinstreuer
Keyword(s):  
Computational Analysis ◽  
Mucociliary Clearance ◽  
Drug Uptake ◽  
Clearance Model

scholarly journals Overexpression of Pto Induces a Salicylate-Independent Cell Death But Inhibits Necrotic Lesions Caused by Salicylate-Deficiency in Tomato Plants

2002 ◽  
Vol 15 (7) ◽  
pp. 654-661 ◽  
Author(s):  
Jianxiong Li ◽  
Libo Shan ◽  
Jian-Min Zhou ◽  
Xiaoyan Tang
Keyword(s):  
Cell Death ◽  
Disease Resistance ◽  
Pseudomonas Syringae ◽  
Virulent Strain ◽  
Gene Activation ◽  
Cellular Damage ◽  
Minor Role ◽  
Disease Resistance Gene ◽  
Tomato Plants ◽  
Spontaneous Cell Death

Tomato plants overexpressing the disease resistance gene Pto (35S∷Pto) exhibit spontaneous cell death, accumulation of salicylic acid (SA), elevated expression of pathogenesis-related genes, and enhanced resistance to a broad range of pathogens. Because salicylate plays an important role in the cell death and defense activation in many lesion mimic mutants, we investigated the interaction of SA-mediated processes and the 35S∷Pto-mediated defense pathway by introducing the nahG transgene that encodes salicylate hydroxylase. Here, we show that SA is not required for the 35S∷Pto-activated microscopic cell death and plays a minor role in defense gene activation and general disease resistance in 35S∷Pto plants. In contrast, temperature greatly affects the spontaneous cell death and general resistance in 35S∷Pto plants, and high temperature inhibits the cell death. The NahG tomato plants develop spontaneous, unconstrained necrotic lesions on leaves. These lesions also are initiated by the inoculation of a virulent strain of Pseudomonas syringae pv. tomato. However, the NahG-dependent necrotic lesions are inhibited in the NahG/35S∷Pto plants. This inhibition is most pronounced under conditions favoring the 35S∷Pto-mediated spontaneous cell death development. These results indicate that the signaling pathways activated by Pto overexpression suppress the cellular damage that is caused by SA depletion. We also found that ethylene is dispensable for the 35S∷Pto-mediated general defense.

scholarly journals Staphylococcus aureus Induces Hypoxia and Cellular Damage in Porcine Dermal Explants

2015 ◽  
Vol 83 (6) ◽  
pp. 2531-2541 ◽  
Author(s):  
Abdul G. Lone ◽  
Erhan Atci ◽  
Ryan Renslow ◽  
Haluk Beyenal ◽  
Susan Noh ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Death ◽  
Effective Diffusion ◽  
Oxygen Demand ◽  
Shotgun Proteomics ◽  
Cellular Damage ◽  
Label Free ◽  
Content Type ◽  
Dermal Tissue ◽  
The Difference

We developed a porcine dermal explant model to determine the extent to whichStaphylococcus aureusbiofilm communities deplete oxygen, change pH, and produce damage in underlying tissue. Microelectrode measurements demonstrated that dissolved oxygen (DO) in biofilm-free dermal tissue was 4.45 ± 1.17 mg/liter, while DO levels for biofilm-infected tissue declined sharply from the surface, with no measurable oxygen detectable in the underlying dermal tissue. Magnetic resonance imaging demonstrated that biofilm-free dermal tissue had a significantly lower relative effective diffusion coefficient (0.26 ± 0.09 to 0.30 ± 0.12) than biofilm-infected dermal tissue (0.40 ± 0.12 to 0.48 ± 0.12;P< 0.0001). Thus, the difference in DO level was attributable to biofilm-induced oxygen demand rather than changes in oxygen diffusivity. Microelectrode measures showed that pH within biofilm-infected explants was more alkaline than in biofilm-free explants (8.0 ± 0.17 versus 7.5 ± 0.15, respectively;P< 0.002). Cellular and nuclear details were lost in the infected explants, consistent with cell death. Quantitative label-free shotgun proteomics demonstrated that both proapoptotic programmed cell death protein 5 and antiapoptotic macrophage migration inhibitory factor accumulated in the infected-explant spent medium, compared with uninfected-explant spent media (1,351-fold and 58-fold, respectively), consistent with the cooccurrence of apoptosis and necrosis in the explants. Biofilm-origin proteins reflected an extracellular matrix-adapted lifestyle ofS. aureus. S. aureusbiofilms deplete oxygen, increase pH, and induce cell death, all factors that contribute to impede wound healing.

scholarly journals MicroRNA-21 promotes cell transformation by targeting the programmed cell death 4 gene

Oncogene ◽  
2008 ◽  
Vol 27 (31) ◽  
pp. 4373-4379 ◽  
Author(s):  
Z Lu ◽  
M Liu ◽  
V Stribinskis ◽  
C M Klinge ◽  
K S Ramos ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Cell Transformation ◽  
Programmed Cell Death 4

scholarly journals Curcumin Scavenges Peroxynitrite in RAW 264.7 Macrophages through Phenolic Hydroxyl Groups

2021 ◽  
pp. 66-77
Author(s):  
Mustafa Kassim ◽  
Nazeh M Al-abd ◽  
Mohd Shahnaz Hasan ◽  
Marzida Mansor ◽  
Mohamed Izham Mohamed Ibrahim
Keyword(s):  
Cell Death ◽  
Tissue Injury ◽  
Statistical Significance ◽  
Phenolic Hydroxyl ◽  
Cellular Damage ◽  
Hydroxyl Groups ◽  
No Production ◽  
Raw 264.7 ◽  
Raw 264.7 Macrophages ◽  
Ifn Γ

Background: Overproduction of free radicals is implicated in cell death and tissue injury. Peroxynitrite (PN) is a highly oxidizing and short-lived free radical that is formed by the interaction of nitric oxide (NO) with superoxide. Curcumin is a natural compound obtained from Curcuma longa and has high antioxidant and anti-inflammatory activities. Aim: We investigated the PN scavenging ability of curcumin to determine its potential as a therapeutic agent for chronic diseases caused by highly oxidative molecules. Methodology: We examined the PN scavenging ability of curcumin either by directly incubating lipopolysaccharide (LPS)+interferon (IFN)-γ-stimulated RAW 264.7 murinacrophages with PN or indirectly through incubation with a PN donor (the artificial substrate SIN-1). Student t-test and one-way ANOVA were used to determine the statistical significance of differences between the experimental and control groups.  Results: The results demonstrate that curcumin inhibits PN and the synthesis of PN from SIN-1. Curcumin also significantly improved the viability of LPS+IFN-γ-treated RAW 264.7 macrophages and inhibited NO production. In macrophages, curcumin inhibited cellular PN synthesis, as evidenced by the absence of 3-nitrotyrosine, a marker of PN-oxidized proteins.  Conclusion: Curcumin attenuates the immune responses that lead to cellular damage and cell death through suppression or scavenging of cytotoxic molecules such as NO and PN. The role of the phenolic hydroxyl of curcumin is critical in PN scavenging.

scholarly journals Enhanced Biomass and Astaxanthin Production of Haematococcus pluvialis by a Cell Transformation Strategy with Optimized Initial Biomass Density

Marine Drugs ◽  
2020 ◽  
Vol 18 (7) ◽  
pp. 341
Author(s):  
Feng Li ◽  
Minggang Cai ◽  
Mingwei Lin ◽  
Xianghu Huang ◽  
Jun Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Transformation ◽  
Haematococcus Pluvialis ◽  
Cost Effective ◽  
Control Group ◽  
Biomass Density ◽  
Cost Effective Method ◽  
Astaxanthin Production ◽  
The Stability ◽  
Transformation Strategy

Astaxanthin from H. pluvialis is an antioxidant and presents a promising application in medicine for human health. The two-stage strategy has been widely adopted to produce astaxanthin by the Haematococcus industry and research community. However, cell death and low astaxanthin productivity have seriously affected the stability of astaxanthin production. This study aims to test the effect of cell transformation strategies on the production of astaxanthin from H. pluvialis and determine the optimal initial biomass density (IBD) in the red stage. The experimental design is divided into two parts, one is the vegetative growth experiment and the other is the stress experiment. The results indicated that: (1) the cell transformation strategy of H. pluvialis can effectively reduce cell death occurred in the red stage and significantly increase the biomass and astaxanthin production. (2) Compared with the control group, the cell mortality rate of the red stage in the treatment group was reduced by up to 81.6%, and the biomass and astaxanthin production was increased by 1.63 times and 2.1 times, respectively. (3) The optimal IBD was determined to be 0.5, and the highest astaxanthin content can reach 38.02 ± 2.40 mg·g−1. Thus, this work sought to give useful information that will lead to an improved understanding of the cost-effective method of cultivation of H. pluvialis for natural astaxanthin. This will be profitable for algal and medicine industry players.

In vivo measurements of mitochondrial function and cell death following hypoxic/ischaemic damage to the new-born brain

1999 ◽  
Vol 66 ◽  
pp. 123-140 ◽  
Author(s):  
Chris E. Cooper
Keyword(s):  
Cell Death ◽  
Magnetic Resonance ◽  
Mitochondrial Function ◽  
Apoptotic Cell ◽  
Cellular Damage ◽  
Resonance Spectroscopy ◽  
Advantages And Disadvantages ◽  
Non Invasive ◽  
The Brain

Critically impaired gas exchange to the brain due to decreased oxygen (hypoxia) or reduced blood flow (ischaemia) is a major cause of brain injury in the perinatal period. There is an accumulating body of evidence suggesting that the irreversible cellular damage in the neonatal brain that occurs subsequent to an hypoxic/ischaemic insult is at the level of the mitochondria. Much of this evidence has been obtained by novel non-invasive measurements of mitochondrial function in vivo. This review focuses on four techniques: near-infrared spectroscopy, magnetic resonance spectroscopy, magnetic resonance imaging and electron paramagnetic resonance spectroscopy. The advantages and disadvantages of these in vivo methods are described in patients and animal models. The picture that emerges is of a slow (1-2 day) energy failure, occurring at the level of the brain mitochondria and leading to a primarily apoptotic cell death. Moderate post-insult hypothermia prevents this damage by an unknown mechanism. It is stressed that isolated cell studies alone are not sufficient to understand the processes occurring at the biochemical and physiological levels. The use of the non-invasive techniques described to understand the biochemistry occurring in vivo is therefore an invaluable aid in integrating cellular and organismal studies of the role of mitochondria in cell death.

scholarly journals Momordica charantia Ethanol Extract Attenuates H2O2-Induced Cell Death by Its Antioxidant and Anti-Apoptotic Properties in Human Neuroblastoma SK-N-MC Cells

Nutrients ◽  
2018 ◽  
Vol 10 (10) ◽  
pp. 1368 ◽  
Author(s):  
Kkot Kim ◽  
SeonAh Lee ◽  
Inhae Kang ◽  
Jung-Hee Kim
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Ethanol Extract ◽  
Momordica Charantia ◽  
Mitogen Activated Protein Kinase ◽  
Cellular Damage ◽  
Protective Effects ◽  
Human Neuroblastoma

Oxidative stress, which is induced by reactive oxygen species (ROS), causes cellular damage which contributes to the pathogenesis of neurodegenerative diseases. Momordica charantia (MC), a traditional medicinal plant, is known to have a variety of health benefits, such as antidiabetic, anti-inflammatory, and antioxidant effects. However, it is unknown whether MC has protective effects against oxidative stress-induced neuronal cell death. The aim of this study was to investigate the potential action of MC on oxidative stress induced by H2O2. First, we tested whether the pretreatment of Momordica charantia ethanol extract (MCEE) attenuates H2O2-induced cell death in human neuroblastoma SK-N-MC cells. MCEE pretreatment significantly improved cell viability and apoptosis that deteriorated by H2O2. Further, MCEE ameliorated the imbalance between intracellular ROS production and removal through the enhancement of the intracellular antioxidant system. Intriguingly, the inhibition of apoptosis was followed by the blockage of mitochondria-dependent cell death cascades and suppression of the phosphorylation of the mitogen-activated protein kinase signaling (MAPKs) pathway by MCEE. Taken together, MCEE was shown to be effective in protecting against H2O2-induced cell death through its antioxidant and anti-apoptotic properties.

scholarly journals Transformation by myc prevents fusion but not biochemical differentiation of C2C12 myoblasts: mechanisms of phenotypic correction in mixed culture with normal cells.

1994 ◽  
Vol 125 (5) ◽  
pp. 1137-1145 ◽  
Author(s):  
M Crescenzi ◽  
D H Crouch ◽  
F Tatò
Keyword(s):  
Cell Death ◽  
Cell Transformation ◽  
Muscle Differentiation ◽  
Retroviral Vectors ◽  
C2c12 Cells ◽  
C2c12 Myotubes ◽  
Myc Oncogene ◽  
Differentiated Cells ◽  
Murine Skeletal Muscle ◽  
Biochemical Differentiation

To study the effects of myc oncogene on muscle differentiation, we infected the murine skeletal muscle cell line C2C12 with retroviral vectors encoding various forms of avian c- or v-myc oncogene. myc expression induced cell transformation but, unlike many other oncogenes, prevented neither biochemical differentiation, nor commitment (irreversible withdrawal from the cell cycle). Yet, myotube formation by fusion of differentiated cells was strongly inhibited. Comparison of uninfected C2C12 myotubes with differentiated myc-expressing C2C12 did not reveal consistent differences in the expression of several muscle regulatory or structural genes. The present results lead us to conclude that transformation by myc is compatible with differentiation in C2C12 cells. myc expression induced cell death under growth restricting conditions. Differentiated cells escaped cell death despite continuing expression of myc, suggesting that the muscle differentiation programme interferes with the mechanism of myc-induced cell death. Cocultivation of v-myc-transformed C2C12 cells with normal fibroblasts or myoblasts restored fusion competence and revealed two distinguishable mechanisms that lead to correction of the fusion defect.

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