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Radiotherapy Physics
Published in Debbie Peet, Emma Chung, Practical Medical Physics, 2021
Andrea Wynn-Jones, Caroline Reddy, John Gittins, Philip Baker, Anna Mason, Greg Jolliffe
Radiation damage and cancer cell death, while minimising damage to healthy cells, is the main purpose of radiotherapy treatment. Ionising radiation reduces the ability of cells to live and reproduce by damaging their DNA. To further understand the radiobiological ideas underpinning radiotherapy, it is useful to introduce the concepts of lethal damage, potentially lethal damage and sub-lethal damage. In lethal damage, the cellular repair is not possible and cell death becomes inevitable. Potentially, lethal damage could lead to cellular death, but this depends on post-irradiation conditions, whereas sub-lethal damage is damage that could be repaired given time. Sub-lethal damage can result in increased normal cell survival, especially if the total dose is split into fractions with a suitable time interval between fractions. The prescribed dose of radiation is usually divided into multiple smaller doses called fractions. This allows healthy cells to recover between treatments.
Cognition Enhancers
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Ramneek Kaur, Rashi Rajput, Sachin Kumar, Harleen Kaur, R. Rachana, Manisha Singh
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.
Oxidative Stress: Relevance, Evaluation, and Management
Published in Botros Rizk, Ashok Agarwal, Edmund S. Sabanegh, Male Infertility in Reproductive Medicine, 2019
Kristian Leisegang, Ralf Henkel
Phenolic compounds intake particularly is associated with reduced CVD, T2DM, and various malignancies. However, the molecular mechanisms are complex, mediated through numerous different pathways directly and indirectly. This may include gene modulation and transcription factor regulation in various cell-signaling cascades, particularly involved in cell survival and apoptosis [99]. Polyphenols are well characterized plant-derived antioxidants [80,100]. This is more complex, and the mechanisms of cellular activity are not well known. There is evidence of mild oxidative activity that results in a beneficial cellular response and may modulate signaling between mitochondria and endoplasmic reticulum relevant to cellular energy regulation and ROS generation [80]. Polyphenols further regulate eicosanoid production exerting anti-inflammatory activity. These compounds are therefore increasingly investigated with supporting benefit for inflammatory-mediated chronic disorders [100]. Flavonoids are able to react with and neutralize superoxide, lipid peroxide radicals, protecting cellular structures, and conversely may generate H2O2 with cytotoxic consequences [101]. As a flavonoid group, anthocyanins have anti-inflammatory and antioxidant activity, mediated in part through modulation of nuclear factor-kappa (NF-kβ) and mitogen-activated protein kinase signaling, regulating inflammatory gene transcription, and molecular activity [102].
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.
Preparing the spinal cord – priming or preconditioning? A systematic review of experimental studies
Published in Scandinavian Cardiovascular Journal, 2023
Johanna Herajärvi, Tatu Juvonen
Spinal cord and collateral network priming aim to stimulate the collateral blood flow to spinal cord by means of permanent altering of its neighboring vasculature, however not leading to ischemic tissue injury. A recent extensive review by Simon et al. introduced different signaling pathways such as phosphoinositide 3 kinase, the antiapoptotic kinase, the endothelial nitric oxide synthase, the Erk1, the delta-like ligand, the jagged NOTCH and the midkine regulatory cytokine in association with priming and its potential underlying mechanism of arteriogenesis [22]. Their conclusions of networks were extrapolated from lower limb ischemia studies i.e. occluding femoral artery, and thus no direct spinal cord priming studies were included [22]. After stress stimulus several cascades are initiated, and these key pathways involve with coordination and remodeling of the collaterals, metabolism, apoptosis, cell survival, proliferation and growth and inflammatory response [22]. The hints and suggestions of arteriogenetic stimulus base on experimental imaging and resin cast studies with segmental artery sacrifice showing increased density of intramuscular paraspinous vessels, a shift of size distribution from small to larger arterioles, parallel realignment of arterioles, dilatation of anterior spinal artery (ASA) and proliferation of small collateral vessels [15,21]. Recently, Lewis et al. reported that in a microarray analysis and gene expression profiling study, several modified cell-signaling cascades were detected in the biopsies of paraspinal muscles after selective segmental artery occlusion in a pig model [43].
Desmoplastic small round cell tumor: from state of the art to future clinical prospects
Published in Expert Review of Anticancer Therapy, 2023
Shushan Hovsepyan, Claudia Giani, Sandro Pasquali, Angela Di Giannatale, Stefano Chiaravalli, Chiara Colombo, Daniel Orbach, Luca Bergamaschi, Sabina Vennarini, Susanne Andrea Gatz, Patrizia Gasparini, Pablo Berlanga, Michela Casanova, Andrea Ferrari
A phase II study was designed to consider the neuroendocrine phenotype and genotype of DSRCT. ONC201 is an antagonist of the tumor dopamine-like DRD2, and an agonist of the antagonist/caseinolytic protease P (ClpP) that causes an increased integrated stress response, a decreased Ras signaling (lower ERK/AKT), and TRAIL induction. These mechanisms result in more cell death signals and fewer cell survival signals in cancer cells. In a preclinical study on DSRCT cell lines and orthotropic peritoneal xenotransplants, ONC201 induced the protein expression of TRAIL and DR5, a receptor that – together with DR4 – triggers TRAIL-induced apoptosis. This orally administered drug was subsequently tested in a phase II clinical trial on patients with neuroendocrine tumors or DSRCT [111]. Two of 10 patients with DSRCT enrolled in this study were treated, one for more than a year, the other for more than 4 years. A further patient, who had limited disease progression at 3 months, came off the study and was given radiotherapy for progressive lung metastases: he has remained off any therapy and without any relapse for more than 3 years.