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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↑, 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 Rotating Magnetic Fields
Time-Scale Flag: TSF = P / R / G P: 0–30 min (physical / electron / radical effects) R: 30 min–3 hr (redox signaling & stress response) G: >3 hr (gene-regulatory adaptation)MPTP: opening represents a mitochondrial commitment event integrating ROS and Ca²⁺ stress; sustained opening indicates irreversible bioenergetic failure. |
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| Cytochrome c ** The term "release of cytochrome c" ** an increase in level for the cytosol. Small hemeprotein found loosely associated with the inner membrane of the mitochondrion where it plays a critical role in cellular respiration. Cytochrome c is highly water-soluble, unlike other cytochromes. It is capable of undergoing oxidation and reduction as its iron atom converts between the ferrous and ferric forms, but does not bind oxygen. It also plays a major role in cell apoptosis. The term "release of cytochrome c" refers to a critical step in the process of programmed cell death, also known as apoptosis. In its new location—the cytosol—cytochrome c participates in the apoptotic signaling pathway by helping to form the apoptosome, which activates caspases that execute cell death. Cytochrome c is a small protein normally located in the mitochondrial intermembrane space. Its primary role in healthy cells is to participate in the electron transport chain, a process that helps produce energy (ATP) through oxidative phosphorylation. Mitochondrial outer membrane permeability leads to the release of cytochrome c from the mitochondria into the cytosol. The release of cytochrome c is a pivotal event in apoptosis where cytochrome c moves from the mitochondria to the cytosol, initiating a chain reaction that leads to programmed cell death. On the one hand, cytochrome c can promote cancer cell survival and proliferation by regulating the activity of various signaling pathways, such as the PI3K/AKT pathway. This can lead to increased cell growth and resistance to apoptosis, which are hallmarks of cancer. On the other hand, cytochrome c can also induce apoptosis in cancer cells by interacting with other proteins, such as Apaf-1 and caspase-9. This can lead to the activation of the intrinsic apoptotic pathway, which can result in the death of cancer cells. Overexpressed in Breast, Lung, Colon, and Prostrate. Underexpressed in Ovarian, and Pancreatic. |
| 2259- | MFrot, | MF, | Method and apparatus for oncomagnetic treatment |
| - | in-vitro, | GBM, | NA |
| 3493- | MFrot, | MF, | Mechanical nanosurgery of chemoresistant glioblastoma using magnetically controlled carbon nanotubes |
| - | in-vivo, | GBM, | NA |
| 184- | MFrot, | MF, | Rotating Magnetic Fields Inhibit Mitochondrial Respiration, Promote Oxidative Stress and Produce Loss of Mitochondrial Integrity in Cancer Cells |
| - | in-vitro, | GBM, | GBM |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
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