China
Africa
Explore chapters and articles related to this topic
History of the Frank Reidy Research Center for Bioelectrics
Published in Marko S. Markov, James T. Ryaby, Erik I. Waldorff, Pulsed Electromagnetic Fields for Clinical Applications, 2020
Additional steps were made that clearly showed that nsPEFs induced apoptosis in Jurkat cells and did it by intrinsic mechanisms – that is from the inside. One of those was induction of cytochrome c release from mitochondria into the cytoplasm (Beebe et al., 2003). Like cell permeabilization and caspase activation in the previous paper (Beebe et al., 2002) and repeated in this paper, nsPEF induced cytochrome c release and annexin-V externalization, another apoptosis marker. All of these cell responses were independent of energy and directly proportional to charging effects. When conditions were 10, 60, and 300 ns durations at 150, 60, and 26 kV/cm electric fields (1–2 J/cc), respectively, caspase activation and cytochrome c release were greater as the pulse duration increased, indicating that these nsPEF-induced responses were energy independent. Using a scaling law that later defined effects of nsPEFs as charging effects expressed in Vs/cm {electric field (E as V/cm) × pulse duration (τ in seconds) × pulse number (n) or Eτn1/2} (Schoenbach et al., 2009), caspase activation and cytochrome c release were directly proportional to the Vs/cm.
Analysis of Single Cells Using Lab-on-a-Chip Systems
Published in Frances S. Ligler, Jason S. Kim, The Microflow Cytometer, 2019
Figure 2.4 shows that data obtained using the microfluidic system in apoptosis experiments compares well with data obtained using a standard flow cytometer. Jurkat cells were treated with camptothecin at different time points to induce apoptosis. The percentage of apoptotic cells detected was almost identical at a given timepoint of induction independently of staining for caspase-3 or PS (compare ~70% apoptotic cells in Fig. 2.4 E, F at 2h). This indicates a nearly simultaneous induction of active caspase-3 and display of phosphatidylserine on the outer leaflet of the cell membrane. A concern of LOC-based flow cytometry is the small channel dimensions which could lead to clogging and possible cell-channel wall interactions. For microfluidic cell analysis, a variety of cell lines have been tested ranging from yeast and fungal spores11 to mammalian cells9 without any adverse effects. To avoid cell-channel interactions the microfluidic channels can either be covalently or dynamically coated with charge-neutral compounds (as in the case of glass chips) or manufactured from an inert material (polymer chips).
Magnetic Separation in Integrated Micro-Analytical Systems
Published in Nguyễn T. K. Thanh, Clinical Applications of Magnetic Nanoparticles, 2018
Yu et al.17 fabricated 9-μm-thick nickel patterns through electroplating. They were magnetized with two permanent magnets placed in parallel with opposite NS poles to create a uniform magnetic field. The pattern has sharp edges to control local magnetic field distribution. Different sizes of microbeads, including 500-nm-diameter beads (02150 AdemTech, Pessac) and 1.05-μm-diameter beads (MyOne carboxylic acid magnetic beads, Dynal), were tested. Lung cancer cells (A549) were labelled with wheat germ agglutinin functionalized magnetic beads and captured by micromagnets. Deng et al.39 used electroplated nickel posts (7 μm in height and 15 μm in diameter, and 40 μm spacing) in a microfluidic channel. A film of UV-curable polyurethane transferred onto a substrate using a PDMS mould was used as a mask of electroplating. Tested in the microchannel were 4.5-μm-diameter magnetic beads (M-450 Dynal). Liu et al.40 deposited a 6-μm-thick permalloy wave form pattern on the substrate through electroplating and encapsulated it with polystyrene. Live Jurkat cells, which were 10 μm in average diameter, labelled with StemCell Technologies EasySep Human CD3 positive selection cocktail, were captured in the microchannel. Permanent magnets were used to magnetize the pattern.
A comparative study of the bispecific monoclonal antibody, blinatumomab expression in CHO cells and E. coli
Published in Preparative Biochemistry and Biotechnology, 2018
Fatemeh Naddafi, Farshad H. Shirazi, Yeganeh Talebkhan, Maryam Tabarzad, Farzaneh Barkhordari, Zahra Aliabadi Farahani, Elham Bayat, Reza Moazzami, Fereidoun Mahboudi, Fatemeh Davami
Binding specificities of the bispecific mAB to CD3 and CD19 were indicated by In-Cell ELISA. Two cell lines were used. Jurkat cells as CD3 + and NALM-6 cells as CD19+ cells. The cells were treated with decreasing dilutions of expressed BsAb (12.5, 6.25, 3.125, 1.56, and 0.78 pg/mL) (Figure 8). It has been indicated that the binding activity of the purified BsAb supernatants from CHO was more than that of purified supernatants from BL21strain (Figures 9 and 10). We found that the binding affinity of expressed mAb to CD19 antigen was higher than its binding affinity to CD3 antigen (Figure 11). The highest binding activity was at 12.5 pg/mL of expressed BsAb in CHO cells and BL21 strain.
Perfluorooctanesulfonate (PFOS) and perfluorooctanoic acid (PFOA) modify in vitro mitogen- and antigen-induced human peripheral blood mononuclear cell (PBMC) responses
Published in Journal of Toxicology and Environmental Health, Part A, 2022
Jane Kasten-Jolly, David A. Lawrence
An in vitro study measuring inhibition of IL-2 secretion by PFOA and PFOS in a human T cell line (Jurkat cells) noted that the PPARα agonist, GW5471, exerted no marked effect on IL-2 secretion by these cells exposed to 0.05–100 µg/ml PFOA or PFOS and stimulated with phytohemagglutinin and phorbol myristate acetate (PHA/PMA) (Midgett et al. 2015). Further, numerous epidemiological studies were conducted on humans to examine the impact of PFOA and PFOS on antibody production in response to vaccination and these have been reviewed (Chang et al. 2016; DeWitt, Blossom, and Schaider 2019; Mumtaz, Buser, and Pohl 2021; United States Department of Health and Human Services-National Toxicology Program [USDHHS-NTP] 2016; Von Holst et al. 2021). The results of a few recent reports are summarized here. A study of children (13 year) reported an approximate 25% reduction in Ab titers to diphtheria vaccine antigens (Ags) with respect to each doubling of PFOA exposure (Grandjean et al. 2017b). Pilkerton et al. (2018) found that PFOA and PFOS serum concentrations exerted no significant effects on Ab titers to rubella Ags for adults, but for children (≥12 year) the Ab titers were negatively associated with serum PFOA concentrations in males, but not females accompanied by no marked association with the rubella Ab titer detected for PFOS. Grandjean et al. (2017a) noted a 19–20% decrease in Ab titer to the tetanus and diphtheria vaccines in children (5 year) for each doubling of PFOA and PFOS exposure in early infancy. A study by Abraham et al. (2020) of healthy children (1 year) showed significant associations between PFOA and Ab titers against the Heamophilus influenza type b (r = 0.32), tetanus (r = 0.25), and diphtheria (r = 0.23) vaccines. Further, PFOA exposure was inversely associated with interferon gamma (IFN-γ) production by ex vivo analysis of lymphocytes stimulated with tetanus or diphtheria toxoid. Pennings et al. (2016) in a study of cord blood gene expression with respect to mothers with elevated serum PFOA and PFOS levels demonstrated affected genes were associated with immunological and developmental functions. Conversely, Stein et al. (2016) found no significant association between serum PFOA and PFOS concentrations in healthy adults for Ab titers, cytokine, chemokine, and mucosal IgA concentrations after immunization with the FluMist vaccine. Consistent findings across these studies indicate that PFOA and PFOS exposures impact Ab responses to vaccination during childhood, while the immune system is still developing.
Anti-apoptotic effect of a static magnetic field in human cells that had been treated with sodium fluoride
Published in Journal of Environmental Science and Health, Part A, 2020
Magdalena Kimsa-Dudek, Agnieszka Synowiec-Wojtarowicz, Agata Krawczyk, Celina Kruszniewska-Rajs, Stanisław Gawron, Monika Paul-Samojedny, Joanna Gola
Before attempting to use a static magnetic field effectively, both the negative and positive effects of exposure to it should be assessed. One of the processes that can be affected by both fluoride and a static magnetic field is apoptosis. Many previous studies, both in vitro and in vivo, have found that fluoride induced the apoptosis of various cells that were exposed to it. [28–30] It has been shown that fluoride induces apoptosis in cells, including human lymphocytes, e.g. by generating ROS[31], human umbilical vein endothelial cells via disturbance to the redox homeostasis[32], ameloblasts via the caspase pathways[33] and H9c2 cardiomyocytes via the mitochondrial pathway.[34] In turn, research on the effect of a constant magnetic field on the apoptosis process has so far yielded dissonant results. Research published by Tenuzzo et al.[35] confirmed that a static magnetic field with an intensity of 6 mT had a preventive action in human lymphocytes in which apoptosis had been elicited. These authors observed a change in the expression of the genes that are associated with apoptosis such as bcl-2, bax, p53 and hsp70. It has also been shown that in liver cancer cells (Bel-7402 and Hep G-2) that were under the influence of a 0.2 T static magnetic field, the activity of caspase 3 and 9 was enhanced and the amount of the anti-apoptotic bcl-2 protein was decreased, thus implying the induction of apoptosis in these cells in such exposure conditions.[36] The initiation of programed cell death by a static magnetic field (5.1 mT) has also been manifested in two malignancies – nephroblastoma and neuroblastoma, occuring in early childhood.[37] Moreover, after static magnetic field exposure (6 mT) elevated apoptosis of Jurkat cells was observed.[38] Studies on the induction of apoptosis by static magnetic field have also been carried out in vivo in an animal model. A static magnetic field with a 128 mT magnetic induction was shown to trigger apoptosis in rat hepatocytes, but via a caspase-independent pathway. However, this effect was not seen in the rat brain, kidneys and muscles.[39,40] It seems that cancer cells are prompted to apoptosis by a static magnetic field while normal cells are usually protected against cell death under these conditions.