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| Rotary Magnetic field can be generated by a spinning magnet or magnets. Or it can be implemented with 2 or more coils, power with a phase shift between them (90 deg for 2 coil implementation) (60deg for 3 coil implementation) Targets affected are mostly the same as for Magnet fields Main differences - may enhance the EPR effect allowing targeting of drugs to cancer cells - acts as wireless stirrer, especially on magnetic particles(inducing eddy currents in water media) - research for use in nano surgery, and mechanical destruction of cancer cells - continue to highlight ability to raise ROS in cancer cell and lower ROS in normal cells - RMF may be responsible for Ca2+ distribution to pass across the plasma membrane(differental affected for cancer and normal cells) Pathways: - induce ROS production in cancer cells, while decreasing ROS in normal cells. Ca2+ is critical and the Ca2+ balance is increased in cancer cells while decreased in normal cells (example for wound healing) - ROS↑ related: MMP↓(ΔΨm), Ca+2↑">Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, cl-PARP↑, HSP↓, Prx, - Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑, - lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : TNF-α↓, IL-6↓, - inhibit Growth/Metastases : TumMeta↓, TumCG↓, MMPs↓, MMP2↓, MMP9↓, IGF-1↓, RhoA↓, NF-κB↓, TGF-β↓, ERK↓ - cause Cell cycle arrest : TumCCA↑, - inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, ERK↓, - Others: PI3K↓, AKT↓, Wnt↓, AMPK, ERK↓, JNK, - Synergies: < Others(review target notes), Neuroprotective, Cognitive, - Selectivity: Cancer Cells vs Normal Cells |
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| In all eukaryotic cells, intracellular Ca2+ levels are maintained at low resting concentrations (approximately 100 nM) by the activity of the major Ca2+ extrusion system, the plasma membrane Ca2+-ATPase (PMCA), which exchanges extracellular protons (H+) for cytosolic Ca2+. Indeed, sustained elevation of [Ca2+]C in the form of overload, saturating all Ca2+-dependent effectors, prolonged decrease in [Ca2+]ER, causing ER stress response, and high [Ca2+]M, inducing mitochondrial permeability transition (MPT), are considered to be pro-death factors. In cancer the Ca2+-handling toolkit undergoes profound remodelling (figure 1) to favour activation of Ca2+-dependent transcription factors, such as the nuclear factor of activated T cells (NFAT), c-Myc, c-Jun, c-Fos that promote hypertrophic growth via induction of the expression of the G1 and G1/S phase transition cyclins (D and E) and associated cyclin-dependent kinases (CDK4 and CDK2). Thus, cancer cells may evade apoptosis through decreasing calcium influx into the cytoplasm. This can be achieved by either downregulation of the expression of plasma membrane Ca2+-permeable ion channels or by reducing the effectiveness of the signalling pathways that activate these channels. Such protective measures would largely diminish the possibility of Ca2+ overload in response to pro-apoptotic stimuli, thereby impairing the effectiveness of mitochondrial and cytoplasmic apoptotic pathways. Voltage-Gated Calcium Channels (VGCCs): Overexpression of VGCCs has been associated with increased tumor growth and metastasis in various cancers, including breast and prostate cancer. Store-Operated Calcium Entry (SOCE): SOCE mechanisms, such as STIM1 and ORAI1, are often upregulated in cancer cells, contributing to enhanced cell survival and proliferation. High intracellular calcium levels are associated with increased cell proliferation and migration, leading to a poorer prognosis. Calcium signaling can also influence hormone receptor status, affecting treatment responses. Increased Ca²⁺ signaling is associated with advanced disease and metastasis. Patients with higher CaSR expression may have a worse prognosis due to enhanced tumor growth and resistance to apoptosis. -Ca2+ is an important regulator of the electric charge distribution of bio-membranes. |
| 3491- | MFrot, | MF, | Magnetically controlled cyclic microscale deformation of in vitro cancer invasion models |
| - | in-vitro, | BC, | MDA-MB-231 |
| 3499- | MFrot, | MF, | Rotating magnetic field delays human umbilical vein endothelial cell aging and prolongs the lifespan of Caenorhabditis elegans |
| - | in-vitro, | Nor, | HUVECs |
| 3535- | MFrot, | MF, | Pulsed Electromagnetic Field Stimulation in Osteogenesis and Chondrogenesis: Signaling Pathways and Therapeutic Implications |
| - | Review, | Nor, | NA |
| 203- | MFrot, | MF, | Rotating Magnetic Field Induced Oscillation of Magnetic Particles for in vivo Mechanical Destruction of Malignant Glioma |
| - | vitro+vivo, | GBM, | U87MG |
| 199- | MFrot, | MF, | Modulation of Cellular Response to Different Parameters of the Rotating Magnetic Field (RMF)—An In Vitro Wound Healing Study |
| - | in-vivo, | Wounds, | L929 | - | NA, | NA, | HaCaT |
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