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Environmental Disease
Published in Gary S. Moore, Kathleen A. Bell, Living with the Earth, 2018
Gary S. Moore, Kathleen A. Bell
Many human diseases are associated with genetic defects. These defects can occur as (1) single-gene defects known as a point mutations or base substitutions or (2) cytogenetic defects in which there are abnormalities in the number or structure of chromosomes. A point mutation occurs when a single nucleotide base is replaced at one point in the DNA molecule with a different base. The DNA replicates with a substituted base pair such that A:T might be substituted for C:G. This base substitution could result in the incorporation of an incorrect amino acid into a synthesized protein, thereby rendering the protein less active or inactive. The resulting effect may be imperceptible or neutral or may result in one of many serious human ailments such as cystic fibrosis (CF), phenylketonuria (PKU), hereditary spherocytosis, alpha-1-antitrypsin deficiency, Gaucher’s disease, achondroplastic dwarfism, hemophilia, or certain forms of diabetes (Figure 4.5). Point mutations may occur spontaneously because of occasional mistakes in the process of DNA replication, without any intervention of external factors. There are also agents in the environment including chemicals or radiation that promote or cause such mutations. These agents are called mutagens. When such mutations occur, they become part of all the daughter cells of that cell. If the mutations occur in the cells that lead to reproductive cells, these defective genes may be inherited just as are healthy genes.
Monitoring, Controlling, and Improving Engineered Tissues Nanoscale Technologies and Devices for Tissue Engineering
Published in Šeila Selimovic, Nanopatterning and Nanoscale Devices for Biological Applications, 2017
Irina Pascu, Hayriye Ozcelik, Albana NdreuHalili, Yurong Liu, Nihal Engin Vrana
The elasticity of cells is determined by their cytoskeleton. Actin microfilaments, intermediate filaments, and microtubules are the major constituents of the cyto-skeleton in eukaryotic cells. Changes in the amount of cytoskeletal proteins and their associated networks are reflected in the cellular function. Cancer is only one example of a disease in which the altered cytoskeleton is diagnostic. There are many other examples that show a strong connection between disease and the cytoskeletal status: circulatory problems [73]; genetic disorders of intermediate filaments and their cytoskeletal networks [74]; various blood diseases, including sickle-cell anemia, hereditary spherocytosis, or immune hemolytic anemia; and certain autoimmune diseases [75]. TE structures allow the modeling of such disease states, which provides a robust tool to understand the effect of cell mechanical properties on the progression of the disease state.
Effect of collision, size, and oscillation of RBCs on blood heat transfer in a bifurcated vessel
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2022
Sidharth Sankar Das, Swarup Kumar Mahapatra
Axial migration of RBCs towards the center of a blood vessel creates a plasma and platelets rich layer near the wall, which is termed as plasma skimming effect. This migration of RBCs towards the center of blood vessel also depends on RBC surface area, collision frequency with both particle and wall, and also collision type (elastic or inelastic) (Munn and Dupin 2008). Due to presence of strong curved streamlines in the bifurcated channel, inter-particle and particle wall collision is much more frequent compared to tube flow. Normally RBCs have a surface area to volume ratio of 1.5 (Namvar et al. 2020), but this ratio changes when osmotic pressure in blood is altered. The causes of this alteration, which subsequently changes the deformability of RBCs, are hereditary spherocytosis, haemolytic-anaemia, and malaria infection (Ebrahimi and Bagchi 2022). The coefficient of restitution between RBCs changes according to the deformability. So, to understand how inter particle collision affects the heat transfer in bifurcated blood vessel, analysis is done in this section. At the inlet of branch vessel-1, the effect of RBC-RBC collision on radial variation of blood heat transfer and temperature is studied. In this study to understand the effect of collision, two different values (of coefficient of restitution (e) (0.6 and 0.95) are taken for analysis purpose.
The expression of Phase II drug-metabolizing enzymes in human B-lymphoblastoid TK6 cells
Published in Journal of Environmental Science and Health, Part C, 2022
Xilin Li, Yuxi Li, Kylie G. Ning, Si Chen, Lei Guo, Jessica A. Bonzo, Nan Mei
In vitro genotoxicity testing has been successfully used to predict genotoxicity and plays an important role in chemical risk assessment. The human B-lymphoblastoid TK6 cell line was established in 1978 from the parental WI-L2 cells, which are diploid lymphoblast cells derived from a 5-year-old male with hereditary spherocytosis. The relevance of TK6 cells to genetic toxicology stems from their heterozygosity at the thymidine kinase (TK) locus on human chromosome 17 and the presence of the hypoxanthine phosphoribosyl transferase (HPRT) gene on the X chromosome. Due to these specific features, the TK6 cell line was originally used in the TK mutation assay to detect point mutations, deletions, and recombination, and is also well suited for the HPRT gene mutation assay. Both TK and HPRT gene mutation assays have been recommended by international authorities such as the Organization for Economic Co-operation and Development (OECD) and described in the OECD testing guidelines (TG) 476 and 490.1,2 Currently, the human TK6 cell line is widely used as a standard cell line for regulatory safety assessments to conduct TK and HPRT gene mutation assays, chromosome aberration tests (e.g., OECD TG473), micronucleus assays (e.g., OECD TG487), and comet assays.3 In fact, a recent international survey indicated that the human TK6 cells and mouse lymphoma L5178Y cells are the most used cell lines for in vitro genotoxicity testing.4 In addition, TK6 cells not only demonstrate negligible genetic variability to the human reference genome, but also harbor a homozygous wild type p53 gene, making them more physiologically relevant than other cell models used in genotoxicity testing.5 TK6 cells have the potential for high-throughput genotoxicity screening since they readily expand in standard RPMI 1640 cell culture media in suspension.6