Quantifying cell kill and cell survival
Michael C. Joiner, Albert J. van der Kogel in Basic Clinical Radiobiology, 2018
The continually downward bending form of a cell survival can simply be fitted by a second-order polynomial, with a zero constant term to ensure that S = 1 at zero dose. This is exactly the formulation that is termed the linear-quadratic (LQ) model. Although we can regard this as based on pure mathematics (i.e. the simplest formula which can describe a curve), it has often been possible to usefully link radiobiological mechanisms to this model, most notably with the increase in number of dicentric or centric-ring chromosomes with dose (17). The formula for cell survival is and the cell survival curve is drawn in Figure 4.5b. Although the shapes of the LQ model and the more complicated two-component model are superficially similar (compare Figures 4.5a and 4.5b), the simple LQ formula gives a better description of radiation response in the low-dose region (0–3 Gy): LQ survival curves are continuously bending with no straight portion either at low or high radiation doses. The shape (or ‘bendiness’) is determined by the value of α/β.
Cognition Enhancers
Sahab Uddin, Rashid Mamunur in Advances in Neuropharmacology, 2020
If a neuron is stressed or injured, it might undergo apoptosis. It may be either extrinsic (which can be started by activating the receptors of cell surface) or intrinsic (involving the ER and the mitochondria). Cell death can be triggered by either of the losses of factors responsible for cell survival. Further, damage of DNA, which may thereby, cause the pro-apoptotic proteins from the mitochondria to stimulate caspase proteases and eventually, caspase activated DNase. Apoptosis can also be induced in caspase independent manner by triggering apoptosis-inducing factor (AIF) which is protein present in the intermembrane of the mitochondria. Attenuation of cell death can be triggered by stimulation of PKCγ in the hippocampus. Therefore, it is suggested that the activators of PKCγ inhibits apoptosis (Sun et al., 2009), thereby, increasing the usefulness as CE that can act on the patients specifically suffering from stroke, brain injury, and acute radiation sickness.
The genetics of breast and ovarian cancer
J. K. Cowell in Molecular Genetics of Cancer, 2003
Current concepts suggest that cancers arise due to deregulation of critical cellular pathways, enabling the cancer cell to evade normal control of cell growth and death. Consistent with this, primary tumors of the breast and ovary frequently show alterations in genes involved in cell cycle control, signaling and cell survival pathways. Breast and ovarian cancer patients who succumb to their disease generally die of complications associated with metastatic disease rather than their primary cancer, and primary tumors often show altered expression of genes associated with extracellular matrix interactions and motility which may be indicative of poor prognosis. In this chapter, we will review the more commonly described genetic changes associated with hereditary and nonhereditary forms of breast and ovarian cancer and their relationship to prognosis.
Pentadecanal inspired molecules as new anti-biofilm agents against Staphylococcus epidermidis
Published in Biofouling, 2018
Annarita Ricciardelli, Angela Casillo, Rosanna Papa, Daria Maria Monti, Paola Imbimbo, Gianluca Vrenna, Marco Artini, Laura Selan, Maria Michela Corsaro, Maria Luisa Tutino, Ermenegilda Parrilli
Immortalized human keratinocyte cells (HaCaT), and mouse fibroblasts (BALB/c3T3) were from ATCC. These cell lines are commonly used for biocompatibility and cytotoxicity assay, as reported by Wiegand and Hipler (2009), and are particularly appropriate cell lines for use in cytotoxicity and tolerance tests concerning the skin because they represent dermal fibroblasts and epidermal keratinocytes, both targets of S. epidermidis. Cells were cultured in Dulbecco’s modified Eagle’s medium (Sigma-Aldrich), supplemented with 10% foetal bovine serum (HyClone, Logan, UT, USA), 2 mM L-glutamine and antibiotics. Cells were grown in a 5% CO2 humidified atmosphere at 37 °C. To test the biocompatibility of the molecules, cells were seeded in 96-well plates at a density of 2.5 × 103 well−1. Twenty-four hours after seeding, cells were incubated with increasing amounts of the molecule under test (from 10 to 100 μg ml−1) for 24, 48 and 72 h. At the end of incubation, cell viability was assessed by the MTT assay as previously described (Arciello et al. 2011). Cell survival was expressed as a percentage of viable cells in the presence of the analysed molecule, with respect to the control cells. Control cells were represented by cells grown in the absence of the molecule and by cells supplemented with identical volumes of DMSO. Two-way ANOVA was performed as a statistical analysis.
Hypoxic preconditioning reduces propofol-induced neuroapoptosis via regulation of Bcl-2 and Bax and downregulation of activated caspase-3 in the hippocampus of neonatal rats
Published in Neurological Research, 2018
Jing Lv, Yubing Liang, Youbing Tu, Jing Chen, Yubo Xie
Several protein families are involved in apoptotic cell death regulation [19]. The Bcl family proteins are an intrinsic, mitochondrial pathway, and Bcl-2 functions as an anti-apoptotic factor and Bax as a pro-apoptotic factor [20]. Thus, the relative expression levels of these factors determine cell survival. Caspase-3 is a key executor of apoptosis and a widely studied member of the caspase family. Cleaved-caspase-3 is the hallmark indicator of caspase-3 activation to measure apoptosis [21]. In the current study, cleaved-caspase-3 levels increased in propofol-induced immature neuron cell death [22]. Bcl-2 can migrate from the cytoplasm to mitochondria to act as an upstream inhibitor of caspase-3, which is consistent with the release of cytochrome c in mitochondria [23]. Bax can eliminate the mitochondrial membrane potential by affecting the permeability of the transition pore and the release of cytochrome c [24].
Novel predictive model of cell survival/death related effects of Extracellular Signal-Regulated kinase protein
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2023
Shruti Jain, Ayodeji Olalekan Salau
The experimental data of cell survival or cell death for ERK-MAPK proteins was taken from [3,16] for HT carcinoma cells and was treated with ten cytokine combinations of different input proteins. In every combination, there are 13 different platelets. From every platelet, 10 values were drawn randomly for further consideration. The authors have used perl software to write the code for selecting random values. For the ERK protein, the signal values were normalised (1: red; 0.5: black; 0: green) to the maximum value for ten combinations of three input proteins (ng/mL) for a period of 0–24 h. Since cell survival/death is highly context-dependent and changes with the stress faced by cells, it must be experimentally determined. The authors have performed similar experimental work for ERK protein in [18,19]. Preprocessing of data was done using visual tests, uniformity tests, and Pearson correlation coefficient tests. Normality AD test was used for two different approaches: based on different concentrations and the basis of samples.